ARTV US Equity☆

10-K

UNITED STATES

SECURITIES AND EXCHANGE COMMISSION

Washington, D.C. 20549

FORM 10-K

(Mark One)

For the fiscal year ended December 31, 2024

OR

Commission File Number 001-42179

Artiva Biotherapeutics, Inc.

(Exact name of Registrant as specified in its Charter)

(Address of principal executive offices) (Zip Code)

Registrant’s telephone number, including area code: (858) 267-4467

Securities registered pursuant to Section 12(b) of the Act:

Title of each class TradingSymbol(s) Name of each exchange on which registered

Common Stock, par value $0.0001 per share ARTV The Nasdaq Global Market

Securities registered pursuant to Section 12(g) of the Act: None

Indicate by check mark if the Registrant is a well-known seasoned issuer, as defined in Rule 405 of the Securities Act. Yes ☐ No☒

Indicate by check mark if the Registrant is not required to file reports pursuant to Section 13 or 15(d) of the Act. Yes ☐ No☒

Indicate by check mark whether the Registrant: (1) has filed all reports required to be filed by Section 13 or 15(d) of the Securities Exchange Act of 1934 during the preceding 12 months (or for such shorter period that the Registrant was required to file such reports), and (2) has been subject to such filing requirements for the past 90 days. Yes☒ No ☐

Indicate by check mark whether the Registrant has submitted electronically every Interactive Data File required to be submitted pursuant to Rule 405 of Regulation S-T (§232.405 of this chapter) during the preceding 12 months (or for such shorter period that the Registrant was required to submit such files). Yes ☒ No ☐

Indicate by check mark whether the registrant is a large accelerated filer, an accelerated filer, a non-accelerated filer, smaller reporting company, or an emerging growth company. See the definitions of “large accelerated filer,” “accelerated filer,” “smaller reporting company,” and “emerging growth company” in Rule 12b-2 of the Exchange Act.

Large accelerated filer ☐ Accelerated filer ☐

Non-accelerated filer ☒ Smaller reporting company ☒

Emerging growth company ☒

If an emerging growth company, indicate by check mark if the registrant has elected not to use the extended transition period for complying with any new or revised financial accounting standards provided pursuant to Section 13(a) of the Exchange Act. ☐

Indicate by check mark whether the registrant has filed a report on and attestation to its management’s assessment of the effectiveness of its internal control over financial reporting under Section 404(b) of the Sarbanes-Oxley Act (15 U.S.C. 7262(b)) by the registered public accounting firm that prepared or issued its audit report. ☐

If securities are registered pursuant to Section 12(b) of the Act, indicate by check mark whether the financial statements of the registrant included in the filing reflect the correction of an error to previously issued financial statements. ☐

Indicate by check mark whether any of those error corrections are restatements that required a recovery analysis of incentive-based compensation received by any of the registrant’s executive officers during the relevant recovery period pursuant to §240.10D-1(b). ☐

Indicate by check mark whether the Registrant is a shell company (as defined in Rule 12b-2 of the Exchange Act). Yes ☐ No☒

The Registrant did not have an aggregate market value for the common equity held by non-affiliates of the Registrant on the last business day of its most recently completed second fiscal quarter because there was no public market for the Registrant’s common equity as of such date.

The number of shares of Registrant’s Common Stock outstanding as of March 19, 2025 was 24,363,119.

DOCUMENTS INCORPORATED BY REFERENCE

Portions of the Registrant’s definitive proxy statement relating to its 2025 annual meeting of shareholders (the Proxy Statement) are incorporated by reference into Part III of this Annual Report on Form 10-K where indicated. The Proxy Statement will be filed with the U.S. Securities and Exchange Commission within 120 days after the end of the fiscal year to which this report relates.

Artiva Biotherapeutics, Inc.

Table of Contents

Page

PART I

Item 1. Business 1

Item 1A. Risk Factors 56

Item 1B. Unresolved Staff Comments 123

Item 1C. Cybersecurity 123

Item 2. Properties 125

Item 3. Legal Proceedings 125

Item 4. Mine Safety Disclosures 125

PART II

Item 6. [Reserved] 127

Item 7A. Quantitative and Qualitative Disclosures About Market Risk 145

Item 8. Financial Statements and Supplementary Data 145

Item 9A. Controls and Procedures 146

Item 9B. Other Information 146

Item 9C. Disclosure Regarding Foreign Jurisdictions that Prevent Inspections 146

PART III

Item 10. Directors, Executive Officers and Corporate Governance 147

Item 11. Executive Compensation 147

Item 14. Principal Accounting Fees and Services 147

PART IV

Item 15. Exhibits, Financial Statement Schedules 148

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SPECIAL NOTE REGARDING FORWARD-LOOKING STATEMENTS

This Annual Report on Form 10-K contains forward-looking statements about us and our industry that involve substantial risks and uncertainties. All statements other than statements of historical facts contained in this Annual Report on Form 10-K, including statements regarding future events, our business strategy, and the plans and objectives of management for future operations, are forward-looking statements. We have based these forward-looking statements largely on our current expectations and projections. In some cases, you can identify forward-looking statements because they contain words such as “anticipate,” “believe,” “contemplate,” “continue,” “could,” “estimate,” “expect,” “intend,” “may,” “plan,” “potential,” “predict,” “project,” “should,” “target,” “will,” or “would,” or the negative of these words or other similar terms or expressions.

These statements involve known and unknown risks, uncertainties and other factors which may cause our actual results, performance or achievements to be materially different from any future results, performance or achievements expressed or implied by the forward-looking statements. Forward-looking statements include, but are not limited to, statements about:

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the success, cost, timing and potential indications of our product development activities and clinical trials, including the ongoing clinical trials of AlloNK;

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the timing of our planned Investigational New Drug application (IND) submissions to the United States Food and Drug Administration (FDA) for our product candidates, including AlloNK;

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the timing of the initiation, enrollment and completion of planned clinical trials;

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the ability to obtain regulatory approval for our manufacturing facility in San Diego, California and the cost and timing associated therewith;

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our ability to obtain and maintain regulatory approval of our product candidates, including AlloNK, in any of the indications for which we plan to develop them, and any related restrictions, limitations and/or warnings in the label of an approved product candidate;

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our ability to obtain funding for our operations, including funding necessary to complete the clinical trials of any of our product candidates, including AlloNK;

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our plans to research and develop our product candidates, including AlloNK;

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our ability to attract and retain collaborators with development, regulatory and commercialization expertise;

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the size of the markets for our product candidates, and our ability to serve those markets;

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our ability to successfully commercialize our product candidates, including AlloNK;

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the rate and degree of market acceptance of our product candidates, including AlloNK;

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our ability to develop and maintain sales and marketing capabilities, whether alone or with potential future collaborators;

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the performance of our third-party suppliers and manufacturers;

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the success of competing therapies that are or become available;

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existing regulations and regulatory developments in the United States and other jurisdictions;

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the implementation of our business model and strategic plans for our business and operations;

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our ability to attract and retain key scientific or management personnel;

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the accuracy of our estimates regarding expenses, future revenues, capital requirements and needs for additional financing;

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our expectations regarding the impact of global health pandemics, geopolitical conflicts and economic uncertainty, including rising interest rates and inflation on our business and operations, including clinical trials, collaborators, contract research organizations (CROs) and employees;

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our expectations regarding the period during which we will qualify as an emerging growth company under the Jumpstart Our Business Startups Act (JOBS Act); and

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our expectations regarding our ability to obtain and maintain intellectual property protection for our product candidates and our ability to operate our business without infringing on the intellectual property rights of others.

These forward-looking statements reflect our management’s beliefs and views with respect to future events and are based on estimates and assumptions as of the date of this Annual Report on Form 10-K and are subject to risks and uncertainties. In addition, statements that “we believe” and similar statements reflect our beliefs and opinions on the relevant subject. These statements are based upon information available to us as of the date of this Annual Report on Form 10-K, and while we believe such information forms a reasonable basis for such statements, such information may be limited or incomplete, and our statements should not be read to indicate that we have conducted an exhaustive inquiry into, or review of, all potentially available relevant information. These statements are inherently uncertain and investors are cautioned not to unduly rely upon these statements. We discuss many of the risks associated with the forward-looking statements in greater detail under the heading “Risk Factors” and elsewhere in this Annual Report on Form 10-K. Moreover, we operate in a very competitive and rapidly changing environment. New risks emerge from time to time. It is not possible for our management to predict all risks, nor can we assess the impact of all factors on our business or the extent to which any factor, or combination of factors, may cause actual results to differ materially from those contained in any forward-looking statements we may make. Given these uncertainties, you should not place undue reliance on these forward-looking statements. Except as required by law, we undertake no obligation to update these forward-looking statements publicly, or to update the reasons actual results could differ materially from those anticipated in any forward-looking statements, whether as a result of new information, future events or otherwise.

We may use our website as a means of disclosing material non-public information and for complying with our disclosure obligations under Regulation Fair Disclosure promulgated by the U.S. Securities and Exchange Commission (SEC). These disclosures will be included on our website under the “Investors” section.

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Risk Factor Summary

Below is a summary of the principal risks and uncertainties that make an investment in our securities speculative or risky. Importantly, this summary does not address all of the risks that we face. Additional discussion of the risks and uncertainties summarized in this risk factor summary, as well as other risks that we face, follows this summary, and should be carefully considered, together with other information in this Annual Report on Form 10-K and our other filings with the SEC before making investment decisions regarding our securities. This summary is qualified in its entirety by that more complete discussion of such risks and uncertainties.

The following is a summary of the principal risks and uncertainties described in more detail in this Annual Report:

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We have a limited operating history, have not completed any clinical trials and have no products approved for commercial sale, which may make it difficult for you to evaluate our current business and predict our future success and viability.

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We will need to obtain substantial additional funding to complete the development and any commercialization of our current and any future product candidates, which may cause dilution to our stockholders. If we are unable to raise this capital when needed, we may be forced to delay, reduce or eliminate our research and development programs or other operations.

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Our approach to the development of NK cell-based product candidates is unproven, and we do not know whether we will be able to develop any products of commercial value, or if competing technological approaches will limit the commercial value of our product candidates or render our platform obsolete.

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Our product candidates are based on novel technologies, which makes it difficult to predict the time and cost of developing product candidates and obtaining regulatory approval for any product candidates that we develop.

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We are early in our development efforts and are substantially dependent on the success of our lead product candidate, AlloNK, which is in early clinical development. Although we have other product candidates in our pipeline being developed by our partners, all of our other internally developed product candidates are in the preclinical or discovery stage. If we are unable to advance our product candidates in clinical development, obtain regulatory approval and ultimately commercialize our product candidates, or experience significant delays in doing so, our business will be materially harmed.

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Current clinical data regarding the efficacy of NK cell therapies against autoimmune diseases are limited, raising uncertainties about the therapeutic benefits of treatments like AlloNK for conditions such as SLE, LN, RA, PV, GPA / MPA and other autoimmune diseases. Moreover, these therapies may not prove to be competitive compared to existing treatments for autoimmune diseases.

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Clinical trials are expensive, time-consuming, difficult to design and implement, and have an uncertain outcome. Further, we may encounter substantial delays in our clinical trials.

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Our product candidates may cause serious adverse events or undesirable side effects or have other properties that may delay or prevent regulatory approval, cause us to suspend or discontinue clinical trials, limit the commercial profile of an approved label, or result in significant negative consequences following marketing approval, if any.

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Enrollment and retention of patients in clinical trials is an expensive and time-consuming process subject to various external factors beyond our control that may cause delays or complications.

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Results of any patient who receives our product candidate in an investigator initiated trial should not be viewed as representative of how the product candidate will perform in our clinical trials and may not be able to be used to establish safety or efficacy for regulatory approval.

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The affected populations for our product candidates may be smaller than we or third parties currently project, which may affect the addressable markets for our product candidates.

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Our collaboration agreements with Affimed GmbH, a subsidiary of Affimed N.V. (Affimed), GC Cell Corporation (GC Cell) and any future collaborations with third parties to develop or commercialize our product candidates, mean that our prospects with respect to the product candidates involved will depend in significant part on the success of those collaborations.

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The manufacture of cell therapy products is novel, complex and subject to multiple risks. We could experience manufacturing problems, and/or we could be required to or choose to modify our manufacturing processes, which could result in delays in the development or commercialization of our product candidates or otherwise harm our business.

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We currently rely on GC Cell for the manufacturing of certain of our product candidates. While we have built our own clinical manufacturing facility and may decide to operate our manufacturing facility at commercial-scale, we may encounter delays, quality or other issues if and when we begin to use our manufacturing facility for supply, and will continue to rely on GC Cell at least partially for manufacturing of our product candidates in the near term.

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Our partial reliance on third parties for manufacturing increases the risk that supply of our product candidates may become limited or interrupted or may not be of satisfactory quality and quantity.

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We are dependent on third parties to acquire, ship and store our cord blood units, NK cell master cell banks and drug product lots, viral vectors, and master and working feeder cell banks, and any disruption, quality concerns, damage or loss would cause delays in replacement and our business could suffer.

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Our cell therapy products depend on the availability of reagents and specialized materials and equipment, including cord blood and viral vectors, which in each case are required to be acceptable to the FDA and comparable foreign regulatory authorities, and such reagents, materials, and equipment may not be available to us on acceptable terms or at all. We and our third-party manufacturers rely on third-party suppliers for various components, materials and equipment required for the manufacture of our product candidates, some of which are single-source products, and do not have supply arrangements for certain of these components.

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We face significant competition from other biotechnology and pharmaceutical companies, and our operating results will suffer if we fail to compete effectively.

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We depend substantially on intellectual property rights granted under our agreements with GC Cell. If we lose our existing licenses or are unable to acquire or license additional proprietary rights from third parties, we may not be able to continue developing our product candidates.

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We will need to expand our organization, and we may experience significant challenges in managing this growth as we build our capabilities, which could disrupt our operations.

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Our future success depends on our ability to retain our key personnel and to attract, retain and motivate qualified personnel.

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PART I

Item 1. Business.

Overview

We are a clinical-stage biotechnology company focused on developing natural killer (NK) cell-based therapies for patients suffering from devastating autoimmune diseases and cancers. Our product candidates are derived from donor cells (allogeneic) rather than a patient’s own cells (autologous) and are pre-manufactured, and stored frozen and ready to ship to a patient’s treatment location, making them what we believe to be “off-the-shelf.” Our lead product candidate, AlloNK, is a non-genetically modified, cryopreserved NK cell therapy being evaluated in combination with B-cell targeted monoclonal antibodies (mAbs) in an ongoing Phase 1/1b trial in SLE with or without lupus nephritis (LN) and a basket investigator-initiated trial (IIT) in multiple autoimmune indications. Seminal peer-reviewed clinical studies using autologous CD19 chimeric antigen receptor (CAR) T-cell therapy (auto-CAR-T) for the treatment of autoimmune diseases have demonstrated that deep B-cell depletion in the periphery and in the lymphoid tissue can lead to drug free disease remission. We have already demonstrated that AlloNK in combination with rituximab was able to drive deep B-cell depletion in the periphery and observed complete responses (CRs) in heavily pre-treated patients naïve to auto-CAR-T in our ongoing Phase 1/2 clinical trial in patients with relapsed or refractory B-cell-non-Hodgkin lymphoma (B-NHL). We believe the preliminary results from our Phase 1/2 clinical trial evaluating AlloNK in combination with rituximab in patients with B-NHL provide a readthrough to autoimmune disease because efficacy in both diseases appears to be accomplished with a shared mechanism of action involving B-cell depletion in the periphery and in the lymphoid tissues, followed by an immunological reset and B-cell reconstitution. We expect to report initial data on autoimmune indications from at least one of our Phase 1/1b trial or the basket IIT in the first half of 2025.

To our knowledge, AlloNK was the first allogeneic, off-the-shelf NK cell therapy candidate to receive Investigational New Drug application (IND) clearance to be administered to a patient with an autoimmune disease in a U.S. clinical trial, and to receive United States Food and Drug Administration (FDA) Fast Track designation in an autoimmune disease. Additionally, to our knowledge, AlloNK is the first allogeneic NK cell therapy candidate in the United States to receive IND clearance for a basket trial in autoimmune diseases, and specifically the first to be evaluated in rheumatoid arthritis (RA), pemphigus vulgaris (PV), and the anti-neutrophil cytoplasmic antibody (ANCA) associated vasculitis (AAV) subtypes granulomatosis with polyangiitis (GPA) / microscopic polyangiitis (MPA), which we are exploring through a basket IIT. We believe as we continue to execute on our strategic plan that these critical first mover advantages will solidify our leadership in multiple autoimmune diseases with high unmet need. Receiving IND clearance and any special designations, such as Fast Track designation, does not guarantee an accelerated review of AlloNK or increase the likelihood of approval of AlloNK by the FDA. Given our early stage of development, it will take several years before we complete clinical development and receive regulatory approval of AlloNK or any of our product candidates, if at all.

B-Cell Driven Autoimmune Disease Background, Prevalence and Unmet Need

Many autoimmune diseases occur when autoreactive B-cells produce autoantibodies that target the body’s own healthy cells and tissues, which can lead to significant morbidity and long-term steroid use. This presents an opportunity to develop treatments that deplete B-cells in a variety of autoimmune diseases such as RA, multiple sclerosis (MS), systemic lupus erythematosus (SLE), LN, AAV, systemic sclerosis (SSc), myasthenia gravis (MG), and myositis, which together account for approximately 6.8 million patients in the United States and Europe alone. Global sales for autoimmune disease, treatments for which in 2023 reached approximately $160 billion (including $65 billion for the topten immunology and inflammation drugs focused on rheumatology) and represent the second-largest class of spending behind oncology, are expected to continue to grow.

Approved treatments for autoimmune diseases encompass various classes of therapies, including steroids, mycophenolate mofetil (MMF), anti-tumor necrosis factor alpha (TNFa) agents and interleukin (IL) inhibitors. Even though these therapies largely provide general immunosuppression and manage symptoms of disease, many patients still suffer from disease progression, leading to worsening complications. Furthermore, chronic use of these therapies typically creates secondary complications for patients, including, but not limited to, increased risk of infections and cancer, cardiovascular disease, hypertension, Cushing’s disease, diabetes and osteoporosis.

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While auto-CAR-T cell therapies have demonstrated the transformative potential of cell therapy, adoption has been limited since their initial approvals due to several factors, including but not limited, to safety, patient access, and scalability. We believe AlloNK in combination with B-cell targeted mAbs represents the next-generation of B-cell depleting therapies because it aims to address important limitations of auto-CAR-T, including:

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Scalability: AlloNK can be manufactured at scale, cryopreserved, easily transported through cold-chain logistics, and we believe be made readily available for patients. In contrast, auto-CAR-T requires a complex, costly, and lengthy manufacturing process that is individualized for each patient. The need for hospitalization further compounds the challenges of scalability and access, adding financial burden to the healthcare system. For example, toxicity and extended hospitalization from treatment with auto-CAR-T could add an incremental financial burden of over $1 million per patient. The scalability of our process creates the potential to expand treatment access to the many autoimmune patients annually who currently live with the consequences of long-term steroid use.

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Safety: As a result of autologous and allogeneic CAR-T cell therapies’ association with immune effector cell-associated neurotoxicity syndrome (ICANS), cytokine release syndrome (CRS) and other severe adverse events, treatment is generally only available at advanced clinical centers capable of supporting these patients. Conversely, in our clinical trial of AlloNK in combination with rituximab in patients with relapsed or refractory B-NHL, as of April 8, 2024, more than two thirds of the patients were not hospitalized within 30 days of dosing AlloNK. We believe this demonstrates, the ability of AlloNK to be administered and managed in an outpatient setting, with limited risk of required hospitalization.

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Cost: Cost of goods sold (COGS) to manufacture auto-CAR-Ts is estimated at over $100,000 per treatment course, limiting flexibility in therapy pricing. Assuming a range of one billion to four billion AlloNK cells per dose and three doses for a treatment regimen of an aggregate of three billion to twelve billion AlloNK cells total per patient with autoimmune disease, AlloNK’s COGS per patient would be below a range of $3,000 to $12,000, approximately an order of magnitude below the current COGS of auto-CAR-T. As auto-CAR-Ts move from their currently marketed indication of hematological malignancies towards chronic and more prevalent autoimmune diseases, AlloNK’s extremely competitive commercial COGS could allow for advantageous pricing flexibility and payor coverage, if approved.

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Our Pipeline

Our lead product candidate, AlloNK, is currently being evaluated in combination with B-cell targeted mAbs in patients with autoimmune diseases and cancers, such as SLE, LN, RA, PV, the ANCA-associated vasculitis subtypes GPA / MPA and B-NHL. In addition, we are also pursuing AlloNK and our CAR-NK product candidates in multiple indications through collaborator-funded trials. Our current pipeline is depicted below.

Note: Artiva holds ex-APAC rights to all programs.

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The IIT will initially enroll patients with RA, PV, GPA / MPA, and SLE.

AlloNK Overview

AlloNK is an allogeneic, off-the-shelf, cryopreserved NK cell therapy candidate designed to enhance the antibody-dependent cellular cytotoxicity (ADCC) effect of mAbs to drive B-cell depletion and to be administered in the community setting. Using our proprietary cell therapy manufacturing platform, we can generate thousands of doses of cryopreserved, infusion-ready AlloNK from a single cord blood unit.

Our lead product candidate, AlloNK, is being evaluated in combination with B-cell targeted mAbs in an ongoing Phase 1/1b trial in patients with SLE with or without LN, a type of kidney disease that manifests from SLE, and a basket IIT in multiple autoimmune indications. LN is reported to affect approximately half of all patients with SLE. There are an estimated 210,000 SLE patients with LN across the United States and Europe, and approximately 30% do not respond to currently available treatments and can develop end stage renal disease and require dialysis.

We have begun dosing and are continuing to enroll our Phase 1/1b open-label multi-center clinical trial in combination with rituximab or obinutuzumab in patients with SLE with or without LN who previously failed treatment. In addition, AlloNK in combination with rituximab or obinutuzumab has been granted Fast Track designation by the FDA to improve disease activity in patients with class III or class IV LN. We also received Fast Track designation for AlloNK for intravenous (IV) infusion in combination with rituximab for the treatment of relapsed or refractory B-NHL to improve cancer response rates. Fast Track designation does not guarantee an accelerated review of AlloNK or increase the likelihood that AlloNK will receive regulatory approval by the FDA.

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In April 2024, the FDA cleared an IND submitted by Integral Rheumatology & Immunology Specialists (IRIS), a large community practice rheumatology clinic in Florida, to conduct a basket IIT to assess the safety, tolerability and clinical activity of AlloNK in combination with rituximab in patients with RA, PV, the ANCA-associated vasculitis subtypes GPA / MPA and SLE. We supply AlloNK and funding for the IIT, but unlike our sponsored clinical trials, IRIS is the regulatory sponsor of, and responsible for, the conduct of the IIT. Treatment of the first patient in the basket IIT was initiated in August 2024.

We intend to pursue additional autoimmune diseases with AlloNK in combination with B-cell targeted mAbs.

Because AlloNK can be used with mAbs that target different antigens based on the target cell’s antigen expression, we believe we have the versatility to use AlloNK in combination with different mAbs to deplete distinct B-cell subpopulations. AlloNK has the potential to be used with a CD19 or CD20 targeting mAb to determine which drives a more robust response. Furthermore, emerging evidence with auto-CAR-T targeting B-cell maturation antigen (BCMA), a plasma cell antigen, either alone or dual-targeted with CD19, has shown distinct therapeutic activity in several indications when compared with CD19-only auto-CAR-T. We believe AlloNK in combination with approved anti-CD38 mAbs could target a similar plasma cell population. We believe this versatility will enable us to pursue a wider range of indications than cell therapies engineered against specific targets.

Our Collaborator-Funded Trials

We have a collaboration with Affimed, whereby we are investigating AlloNK in a Phase 2 trial in combination with acimtamig, a CD30-targeted NK cell engager, in CD30+ Hodgkin lymphoma (HL). In addition, we own exclusive worldwide rights (excluding Asia, Australia and New Zealand (ex-APAC)) for AB-201, a human epidermal growth factor receptor 2 (HER2) targeting CAR-NK cell product candidate, and for AB-205, a CD5 directed CAR-NK cell product candidate.

Manufacturing Capabilities

We have a manufacturing-first approach, referencing the fact that even before we were founded, our strategic partner, GC Cell, had already invested years pioneering the manufacturing process that we use today. Unlike most other companies in the NK field who started clinical development before establishing a scalable manufacturing process, we started clinical development with a mature and robust process in place. Our process is designed to allow us to produce off-the-shelf, allogeneic NK cell therapy candidates and to potentially meet the scale of commercial demand, with the mission to make these therapies broadly accessible for patients with devastating autoimmune diseases and cancers. We leveraged our deep expertise in NK cell biology to establish an end-to-end proprietary process in collaboration with GC Cell. In our San Diego headquarters, we have established a 9,000 square foot, purpose-built cell production center that is compliant with current Good Manufacturing Practices (cGMP) and capable of producing enough vials to treat over 250 to 1,000 autoimmunity patients annually, depending on the cells per dose used. Furthermore, assuming a range of one billion to four billion AlloNK cells per dose and three doses for a treatment regimen of an aggregate of three billion to twelve billion AlloNK cells total per patient with autoimmune disease, AlloNK COGS per patient would be below a range of $3,000 to $12,000, approximately an order of magnitude below the current COGS of auto-CAR-T.

Our Management Team, History and Investors

We were founded in 2019 as a spin out of GC Cell, formerly GC Lab Cell Corporation, a leading healthcare company in the Republic of Korea (Korea), pursuant to a strategic partnership granting us exclusive, worldwide, ex-APAC, rights to GC Cell’s NK cell manufacturing technology and programs. GC Cell has an established track record in cell therapy, with over two decades of cell therapy research, process development and manufacturing experience, as well as a clinical and commercial track-record outside the United States with the first ever marketed T-cell product, Immuncell-LC, which received South Korean Ministry of Food and Drug Safety (MFDS) approval for hepatocellular carcinoma in 2017. An investigational version of the product candidate also received FDA Orphan Drug Designation for pancreatic cancer, liver cancer and glioblastoma in 2018. In addition, GC Cell spent over a decade optimizing the manufacturing process for NK cell therapeutics, including selection of cord blood as a starting material, expanding process scale and enabling cryopreservation. GC Cell utilizes a custom-built

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300,000 square foot cell therapy research, process development and cGMP manufacturing facility from which we were able to produce drug product for our first clinical trials in the United States.

Our team is led by executives who have deep experience in their respective functions in cell therapy with multi-faceted experience across a company’s life cycle. Our leadership team has extensive combined experience in therapeutics, medical devices and diagnostics companies. We have also assembled scientific advisors with deep experience in both cell therapy and autoimmune disease who are actively involved in our drug development process and programs.

Our Mission

Our mission is to develop effective, safe and accessible cell therapies for patients with devastating autoimmune diseases and cancers.

Our Strengths

We believe that our company and therapeutic candidates possess the following competitive strengths.

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Autoimmune disease treatment approach supported through scientific publications and our ongoing clinical trial. Our conviction in the transferability of our proposed mechanism of action from treatment of B-NHL to treatment of autoimmune diseases is driven by both the peer reviewed scientific publication of clinical trial results of auto-CAR-T in autoimmune diseases as well as preliminary data from our ongoing Phase 1/2 clinical trial of AlloNK in combination with rituximab in patients with relapsed or refractory B-NHL. In all 29 patients in our trial with samples analyzed, as of March 26, 2024, following the first cycle of treatment, all patients achieved non-quantifiable peripheral B-cell levels by Day 8 (except for one patient who achieved such B-cell depletion by Day 15) following the start of therapy, regardless of B-cell levels at baseline. We believe this data provides support for a B-cell depleting mechanism of action of AlloNK in combination with B-cell targeted mAbs. AlloNK in combination with rituximab has also demonstrated CRs in B-NHL patients as measured by imaging of tumor lesions. Because of the common tissues of interest, principally the lymphoid tissues, in B-NHL and autoimmune diseases, we believe data in these B-NHL patients provides supporting evidence for our proposed mechanism of action in autoimmune disease. In the Phase 1 portion of this trial, as of April 30, 2024, in the fourteen patients who were naïve to CAR-T, the overall response rate (ORR), which is the proportion of patients who have a partial response (PR) or CR, was 71%, including eight CRs (57%), and two PRs (14%), as determined by the Lugano 2014 criteria. The Lugano 2014 criteria is a widely accepted and published methodology used in clinical trials as well as in clinical practice for response assessment in lymphoma. The criteria recommend a combination of disease morphology assessment using computed tomography (CT) and lesion metabolic activity assessment on positron emission tomography (PET), with PET metabolic assessments being the driver for overall response assessment. For further description of the 2014 Lugano criteria, please see pages 131-132. Thirteen of these patients had aggressive forms of B-NHL, and the CR rate in this subset, as determined by the Lugano 2014 criteria, was 62%. As of the April 30, 2024, data cutoff date, six of the eight patients with a CR had an ongoing response (meaning continuation of the CR at all follow-up points), with five of these patients remaining progression free at six months or later. The longest responder remained progression free for at least 18 months after the start of treatment. We believe these data support that AlloNK in combination with B-cell targeted mAbs has the potential to provide deep B-cell depletion in common target tissues between B-NHL and autoimmune diseases and offer therapeutic potential, a differentiated safety profile and patient accessibility in numerous autoimmune diseases.

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Versatile mAb combination approach allows flexibility to tailor targeting approach to specific B-cell subpopulations. We believe combining AlloNK with approved B-cell targeted mAbs may offer therapeutic benefits in a broad range of B-cell-driven diseases. AlloNK, as a non-genetically modified, non-targeted NK cell, is designed to utilize a mAb for targeting. Therefore, we believe different mAbs could be used to target distinct B-cell populations based on the target cell’s antigen expression. Beyond rituximab and other anti-CD20 mAbs, we have already conducted numerous preclinical studies in which we have shown cytotoxic activity of AlloNK in combination with other approved B-cell targeted mAbs, such as anti-CD19 and anti-CD38 mAbs. Emerging evidence

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with auto-CAR-T targeting the plasma cell antigen BCMA, either alone or dual-targeted against CD19, has shown distinct therapeutic activity in several indications when compared with CD19-only auto-CAR-T, and we believe AlloNK in combination with approved anti-CD38 mAbs could target a similar plasma cell population. We have the opportunity to develop AlloNK in combination with approved B-cell targeted mAbs using a variety of targets, including the potential for dual targeting by treating in combination with two mAbs. We believe this versatility will enable us to pursue a wider range of indications than cell therapies engineered against specific targets.

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Proprietary manufacturing process allows for scalable and potentially cost effective AlloNK production. Our robust chemistry, manufacturing and controls (CMC) experience, ample capacity and limited overhead enable us to produce allogeneic, off-the-shelf, NK cell therapy candidates at scale. Utilizing our proprietary process we and GC Cell have manufactured over 50 clinical batches of AlloNK, producing thousands of AlloNK vials at one billion cells per vial, and have demonstrated both batch-to-batch and donor-to-donor consistency. Our manufacturing platform and scale-up process is rooted in over a decade of NK cell expansion experience by our strategic partner, GC Cell, and has been further improved upon by our team. In our San Diego headquarters, we have established a 9,000 square foot, purpose-built cell production center that is cGMP-compliant, and capable of producing enough vials to treat over 250 to 1,000 autoimmunity patients annually, depending on the cells per dose used. We are developing a 200-liter, commercial-scale process that we believe has the potential to efficiently supply many thousands of patients with a COGS below $1,000 per one billion-cell vial. Furthermore, assuming a range of one billion to four billion AlloNK cells per dose and three doses for a treatment regimen of an aggregate of three billion to twelve billion AlloNK cells total per patient with autoimmune disease, AlloNK COGS per patient would be below a range of $3,000 to $12,000, approximately an order of magnitude below the current COGS of auto-CAR-T. With this COGS, we could have the flexibility to reduce the price relative to auto-CAR-T while still maintaining a high margin.

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Non-genetically modified cell therapy has not shown integrating vector-induced secondary malignancies, which is a benefit in an autoimmunity setting. As of December 31, 2023, the FDA had received reports of 22 cases of secondary T-cell malignancies (including CAR+ lymphoma) in patients who received treatment with BCMA- or CD19-directed genetically modified auto-CAR-T therapy. Transgene insertion of CAR was detected in the malignant clone in each of the three cases for which genetic sequencing was performed. As a result, in January 2024, the FDA determined that boxed warning language addressing these malignancies should be included on the label for all BCMA- and CD19-directed genetically modified auto-CAR-Ts to alert patients and clinicians of the potential risk of developing secondary T-cell malignancies following treatment. Unlike CAR-T and any genetically modified cell therapy, AlloNK is a non-genetically modified NK cell therapy candidate and has not shown any secondary malignancies in our clinical trials as of April 8, 2024. We believe this will make our therapeutic candidate a preferable and differentiated treatment option for physicians and patients.

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AlloNK cell approach aims to broaden community access, drive improved patient experience, improve clinical recruitment timelines and expand commercial opportunity. In our clinical trials to date, AlloNK in combination with a B-cell targeted mAb was mostly administered and managed outside of a hospital setting. This is in contrast to auto-CAR-T cell therapies, which have been limited by the need for hospitalization due to the risks of ICANS and CRS, among other severe adverse events. Our product candidate is designed to enable rheumatologists to administer AlloNK in combination with a B-cell targeted mAb within their own outpatient infusion centers, potentially allowing patients to avoid the typically required hospitalization associated with CAR-T cell therapies. These limitations are also present for T-cell engaging bispecific antibodies. Approved T-cell engaging bispecific antibodies such as glofitamab, epcoritamab, and mosunetuzumab require hospitalization upon dosing due to the risk of CRS. We believe the potential to administer an off-the-shelf therapy in an outpatient setting could meaningfully reduce the patient’s treatment burden, translating to a potential competitive advantage in enrolling patients in our clinical trials and capturing market share, if approved.

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Strategic execution led to first-mover advantage in autoimmune disease. We have advanced AlloNK into clinical trials for autoimmune diseases, and we believe we have achieved multiple critical clinical and regulatory milestones ahead of other allogeneic, off-the-shelf NK cell therapy companies. Specifically, the FDA cleared our IND for AlloNK in combination with rituximab for our Phase 1/1b

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clinical trial in patients with class III or IV LN in August 2023, and we dosed the first patient in this trial in April 2024. We also amended the ongoing trial to broaden the patient population to include patients with SLE without LN. To our knowledge, this made AlloNK the first allogeneic, off-the-shelf NK cell therapy candidate to be administered to a patient with an autoimmune disease in a U.S. clinical trial and the first allogeneic, off-the-shelf NK cell therapy to receive Fast Track designation in an autoimmune indication. Further, in April 2024, the FDA cleared an IND submitted by IRIS, a large community practice rheumatology clinic in Florida, to conduct a basket IIT in multiple autoimmune indications. Treatment of the first patient in this basket IIT was initiated in August 2024. Through this IIT, to our knowledge, AlloNK is the first allogeneic NK cell therapy candidate in the United States to receive allowance to proceed with a basket study under an IND, and specifically the first to be evaluated in RA, PV and AAV, which we believe solidifies our potential leadership in multiple large-market diseases. We believe our established manufacturing capabilities empower us to capitalize on our first-mover advantage to efficiently develop and, if approved, potentially commercialize a wide range of indications relative to auto-CAR-Ts, which we believe are constrained due to the limitations associated with manufacturing autologous cell therapies. We believe all of these potential advantages, along with our expected competitive advantage in enrollment timing, will allow us to efficiently progress AlloNK through the clinic and position us to capitalize on the broad market opportunity of B-cell driven autoimmune diseases. Receiving IND clearance and any special designations, such as Fast Track designation, does not guarantee an accelerated review of AlloNK or increase the likelihood of approval of AlloNK by the FDA. Given our early stage of development, it will take several years before we complete clinical development and receive regulatory approval of AlloNK or any of our product candidates, if at all.

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Leading scientific advisors who guide our development strategy in autoimmune disease. With our focus on developing AlloNK in autoimmune diseases, we haverapidly assembled key opinion leaders from leading academic and medical institutions including UC San Diego, UCLA, NYU and OSU to serve as advisors and guide our development.

Our Strategy

Our strategy is to develop safe and effective NK cell-based therapies that patients and physicians can utilize in a community setting. We believe the compelling cell killing properties of NK cells, when combined with mAbs for targeting specific antigens, creates an opportunity to generate potentially transformative therapies. Key elements of our strategy include:

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Advance our lead product candidate, AlloNK, through clinical development and demonstrate the clinical potential of NK cell therapies in autoimmune diseases. We are advancing AlloNK through clinical development to address the significant unmet need in autoimmunity as well as patient and physician desire for a safe, accessible therapy. We believe data from our Phase 1/2 clinical trial of AlloNK in combination with rituximab in patients with relapsed or refractory B-NHL support the potential for AlloNK in combination with B-cell targeted mAbs to provide deep B-cell depletion in common target tissues between B-NHL and autoimmune diseases. The FDA cleared our IND for AlloNK in combination with rituximab for our Phase 1/1b clinical trial in patients with class III or class IV LN in August 2023, and we dosed the first patient in this trial in April 2024. We also amended the protocol for this trial to broaden the patient population to include patients with SLE without LN.

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Demonstrate the clinical potential of NK cell therapies to address limitations of auto-CAR-Ts. Auto-CAR-Ts have proven to be an effective therapeutic modality in cancer and have shown therapeutic clinical benefit in autoimmune disease. We believe this is the first step in an evolution where next generations of the technology will improve safety and expand access to the point where cell therapies truly are available to any patient in need. We have optimized an end-to-end NK cell manufacturing process to potentially deliver AlloNK on a large scale and at low cost, having leveraged more than a decade of NK cell manufacturing expertise and know-how. We believe AlloNK in combination with B-cell targeted mAbs represents the next-generation of B-cell depleting therapies because it aims to address important limitations of auto-CAR-T, including:

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Scalability: AlloNK is an allogeneic, off-the-shelf product candidate that can be manufactured at scale, cryopreserved, easily transported through cold-chain logistics and we believe can be made

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readily available for patients. In contrast, auto-CAR-T therapy requires a complex, costly, and lengthy manufacturing process that is individualized for each patient. The need for hospitalization further compounds the challenges of scalability and access, adding financial burden to the healthcare system. For example, toxicity and extended hospitalization from treatment with auto-CAR-T could add an incremental financial burden. According to a real-world study conducted in 2021 by Oregon Health & Science University and presented by Maziarz et al. the average cost of treatment, excluding the cost of auto-CAR-T itself, was $383,000 and could reach over $1 million per patient. The scalability of our process creates the potential to expand treatment access to the many autoimmune patients annually who currently live with the consequences of long-term steroid use.

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Safety: As a result of autologous and allogeneic CAR-Ts’ association with CRS, ICANS, and other severe adverse events, treatment is generally only available at advanced clinical centers capable of supporting these patients. Conversely, in our clinical trial of AlloNK in combination with rituximab in patients with relapsed or refractory B-NHL, as of April 8, 2024, more than two-thirds of the patients were not hospitalized at all within 30 days of dosing AlloNK. We believe this demonstrates the ability of AlloNK to be administered and managed in an outpatient setting, with limited risk of required hospitalization.

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Cost: Cost of goods to manufacture auto-CAR-Ts is estimated at over $100,000 per treatment course, limiting flexibility in therapy pricing. Assuming a range of one billion to four billion AlloNK cells per dose and three doses for a treatment regimen of an aggregate of three billion to twelve billion AlloNK cells total per patient with autoimmune disease, AlloNK COGS per patient would be below a range of $3,000 to $12,000, approximately an order of magnitude below the current COGS of auto-CAR-T. As auto-CAR-Ts move from their currently marketed indication of hematological malignancies towards chronic and more prevalent autoimmune diseases, AlloNK’s extremely competitive commercial COGS could allow for advantageous pricing flexibility and payor coverage, if approved.

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Expand AlloNK development across several autoimmune indications utilizing different mAbs. We are further exploring the potential of AlloNK in other indications and other antibody combinations through IITs and company-sponsored clinical trials. In April 2024, the FDA cleared an IND submitted by IRIS, a large community practice rheumatology clinic in Florida, to conduct a basket IIT under an IND testing the combination of AlloNK with rituximab in a study of four autoimmune diseases: RA; PV; GPA / MPA; and SLE.

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Continue to evaluate and pursue tailored strategies to advance our platform capabilities and maximize patient access to AlloNK. We have a disciplined strategy to evaluate partnerships that are designed to further our NK cell development and manufacturing efforts with the goal of delivering our product candidates to as many patients as stand to benefit. Our two main manufacturing and oncology program development partnerships with GC Cell and Affimed, respectively, are products of this strategy. We also plan to commercialize our product candidates and will look to make further investments at the appropriate time to maximize access and the commercial potential of our product candidates.

Introduction to Autoimmune Disease

Background

Many autoimmune diseases occur when autoreactive B-cells produce autoantibodies that target the body’s own healthy cells and tissues instead of foreign pathogens. In a healthy individual, these malfunctioning immune cells, such as B-cells and T-cells, are either eliminated before they fully develop or are kept in check by various regulatory mechanisms. However, in individuals with autoimmune diseases, these safety measures are compromised due to a mix of genetic factors and exposure to certain antigens from infections or environmental sources.

The prevalence of autoimmune diseases is both widespread and growing, with over 80 known autoimmune diseases. The persistent and severe nature of these diseases results in substantial medical expenses and a decline in quality of life, posing significant challenge for patients, their families and the healthcare system. Global sales for

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autoimmune disease, treatments for which in 2023 reached approximately $160.0 billion (including $65 billion for the top ten immunology and inflammation drugs focused on rheumatology) and represent the second-largest class of spending behind oncology, are expected to continue to grow. There is a significant unmet medical need in autoimmune diseases despite the number of approved therapies, given these treatments are often not curative and many patients do not achieve optimal outcomes.

B-Cell Driven Autoimmune Diseases

Autoimmune diseases encompass a broad range of diseases and symptoms, with the presence of autoantibodies—produced by autoreactive B-cells that mistakenly target the body’s healthy cells and tissues—being a common characteristic of many autoimmune diseases. While the specific autoantigen targeted and the primary affected tissue or organ may vary, the role of B-cells in producing these autoantibodies is generally consistent. Increasing evidence suggests that autoreactive B-cells also contribute to the pathology of many autoimmune diseases through their interaction with T-cells and cytokine production. This shared biological mechanism presents an opportunity to develop treatments targeting the production of autoantibodies by B-cells for a variety of autoimmune diseases.

The following table sets forth the estimated prevalence for select B-cell-driven autoimmune diseases in the United States and in Europe.

All figures for Europe are for geographic Europe, except δ: which is for the European Union.

Limitations of Current Therapies

Approved treatments for autoimmune diseases encompass various classes of therapies, including steroids, MMF, TNFa agents and IL inhibitors. These therapies largely provide general immunosuppression and manage symptoms of disease. For instance, steroids and MMF have broad anti-inflammatory and immune-suppressing effects, anti-TNFa therapies inhibit TNFa, a cytokine involved in systemic inflammation, and IL inhibitors target certain ILs that activate the immune system and cause inflammation, such as IL-1 and IL-6. Even though these therapies largely provide general immunosuppression and manage symptoms of disease, many patients suffer from disease progression, leading to worsening complications. Furthermore, chronic use of these therapies typically creates secondary complications for patients, including, but not limited to, increased risk of infections and cancer, cardiovascular disease, hypertension, Cushing’s disease, diabetes and osteoporosis. Monoclonal antibodies that

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target B-cell antigens have also received approval for treating various diseases involving pathological B-cells, including autoimmune diseases and blood cancers. Rituximab, a mAb targeting the B-cell antigen CD20, has demonstrated effectiveness in treating several autoimmune diseases, including RA, PV and AAV. However, rituximab alone does not typically induce complete B-cell depletion in all patients, which may account for incomplete and inconsistent clinical responses. For instance, a pivotal Phase 3 trial of rituximab for the treatment of LN failed to show statistical improvement in clinical outcomes with rituximab when added to the standard of care, MMF and steroids, as compared to MMF and steroids alone. However, in a post-hoc analysis of the same trial data, it was observed that achievement of complete peripheral B-cell depletion, as well as the rapidity and duration of complete peripheral depletion, were associated with complete renal responses. We believe these data support the notion that if a therapy induces deeper and more consistent B-cell depletion, it will achieve higher response rates.

Promise of Cell Therapy in Autoimmune Disease

The advancement of auto-CAR-T cell therapies in oncology has opened the door to applying B-cell targeting cellular therapies in B-cell driven autoimmune diseases. Auto-CAR-T cell therapy involves genetically modifying a patient’s own T-cells to produce and express a CAR, enabling the engineered T-cell to recognize and attack cancer cells more effectively. This personalized approach involves collecting the patient’s T-cells, genetically engineering them in a laboratory to target a specific cancer cell antigen, then re-infusing these enhanced cells back into the patient to seek out and destroy cancer cells. Since the first auto-CAR-T cell therapy, Kymriah, was approved by the FDA in 2017 for the treatment of B-cell acute lymphoblastic leukemia (B-ALL), additional auto-CAR-Ts have been approved and uses have expanded to treatment of other forms of cancer, including certain types of NHL and multiple myeloma.

Auto-CAR-T products targeting CD19 have been transformative in the treatment of B-cell driven hematological malignancies such as B-ALL and NHL. The first FDA-approved auto-CAR-T cell therapies were designed to target CD19, a B-cell specific antigen prevalent in B-cell malignancies. The use of auto-CAR-T cell therapy aims to deplete these malignant cells as well as other CD19-expressing cells, including healthy B-cells. The ultimate aim of CD19 auto-CAR-T is to deplete cancerous B-cells in the periphery and lymphatic tissue where cancerous lesions grow, and CRs, measured by PET imaging coupled with computed tomography (CT) imaging (PET/CT) provide evidence that auto-CAR-T can target and deeply deplete these cancerous B-cells. Given the significance of B-cells in multiple autoimmune diseases, we believe the depletion of these cells will have a therapeutic benefit in a wide range of B-cell driven autoimmune diseases.

Cell Therapy in Autoimmune Disease with Auto-CAR-T Cell Therapy

The success of auto-CAR-T cell therapies in treating B-cell hematologic malignancies has spurred interest in applying these mechanisms for the treatment of various autoimmune diseases. Given the role of autoantibodies produced by autoreactive B-cells, as well as evidence suggesting that autoreactive B-cells contribute to the pathology of many autoimmune diseases through their interaction with T-cells and cytokine production, the hypothesis is that deeply depleting B-cells with targeted cell therapy will lead to clinical responses in autoimmune diseases.

Third-party clinical studies have shown that treating autoimmune disease with B-cell targeted cell therapy in patients who were refractory to other therapies resulted in rapid responses and remissions as determined by the Definition of Remission in SLE criteria, with patients not receiving further immunosuppressive drugs or steroids (drug-free remission). In 2022, a study led by Dr. Georg Schett reported results from five SLE patients treated with a CD19 auto-CAR-T, published in 2022 by Mackensen et al. in Nature Medicine. We believe several important observations from this provided insight into the potential value of B-cell targeted cell therapy.

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Immune system reset. Auto-CAR-T cells were observed to expand in vivo following treatment, and B-cells were rapidly and deeply depleted upon initiation of treatment. However, auto-CAR-T cells were short-lived in circulation, and all five patients experienced B-cell reconstitution after an average time of 110 days with no relapse of SLE.

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Resolution of proteinuria. Rapid reduction in proteinuria in the four patients with underlying LN, from urine protein creatinine ratio (UPCR) levels of 2-8 g/g Cr to <0.5g/g by three months.

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Elimination of autoantibodies. Autoantibodies against common antigens in SLE, such as dsDNA, disappeared from the five patients, as well as autoantibodies against other antigens.

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Preservation of vaccination responses. No substantial decline in immune responses against common vaccines, including measles, rubella, mumps, varicella zoster, hepatitis B, tetanus, diphtheria and pneumococci, were detected compared to baseline.

In a follow-up study published in The New England Journal of Medicine by Muller et al. in 2024, reporting data from the five patients above and three additional SLE patients, long-term follow-up of up to 29 months showed that disease activity remained absent in all eight SLE patients. The therapy was also observed to be effective in idiopathic inflammatory myositis, where all three patients treated had an American College of Rheumatology–European League against Rheumatism major clinical response and normalization of creatine kinase levels after three months and maintained these responses for up to 12 months; and in systemic sclerosis, where all four patients treated showed reduced severity of skin and lung disease for up to three months (and for up to six months in three patients that continued follow-up).

Limitations of Autologous CAR-T Cell Therapy

While auto-CAR-T cell therapies have demonstrated the transformative potential of cell therapy, adoption has been limited since initial approvals due to several factors, including, but not limited, to safety, patient access and scalability, as summarized below.

Safety

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Adverse Events: Auto-CAR-T cell therapies have been associated with CRS and ICANS that could develop over a period of weeks. CRS in particular requires close observation, and any Grade 2 or higher case requires hospitalization and administration of tocilizumab. Auto-CAR-T products approved for use in NHL have shown that between 46% to over 90% of patients experience any grade CRS, with 4% to 13% experiencing serious Grade 3 or higher events. In practice, tocilizumab is often being utilized with Grade 1 CRS as well, possibly limiting the number of patients who escalate to Grade 2 and higher. For example, in a study by Schett of CD19 auto-CAR-T in autoimmune disease, 11 of 15 patients experienced CRS of any grade. Ten patients had Grade 1 CRS only, but tocilizumab was used in five of these patients. This early intervention and unpredictable time to onset requires that the patient remain within close proximity of a treatment facility that can manage CRS for a period of several weeks following the initial CAR-T infusion.

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Secondary T-Cell Malignancies: Cells that have been genetically modified could have the potential to become cancerous, resulting in secondary T-cell malignancies. As with all gene therapy products with integrating vectors (lentiviral or retroviral vectors), the potential risk of developing secondary malignancies is labeled as a class warning in the United States prescribing information for approved BCMA-directed and CD19-directed genetically modified auto-CAR-T cell therapies. In January 2024, the FDA recommended updated safety language be added across product labels for all CD19 and BCMA auto-CAR-T cell therapies to highlight the risk of secondary T-cell malignancy, including language in the box warning.

Patient Access

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Limited Availability: Treatment with auto-CAR-T cell therapies is generally only available at advanced clinical centers that can adequately support the complex logistics involved in the providing auto-CAR-T cell therapies and the patients that require extensive safety monitoring and potential need for hospitalization.

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High Cost Burden: COGS to manufacture auto-CAR-T cell therapies is estimated at over $100,000 per treatment course. This may limit pricing flexibility and could constrain the number of patients able to afford treatment.

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Manufacturing

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Complex Manufacturing: Because auto-CAR-T cell therapies are derived from a patient’s own cells, they are subject to numerous potential inefficiencies inherent to a patient-specific manufacturing process. Manufacturing auto-CAR-T cell therapies is an intricate process that begins with leukapheresis to obtain T-cells from the patient’s peripheral blood. These isolated T-cells are then shipped to a manufacturing site where CAR vectors are transduced and cells are expanded before being packaged as a drug product and returned to the clinical site for treatment. As many as 10% to 20% of patients may ultimately not receive product for treatment because of issues with either leukapheresis or the manufacturing process.

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Lengthy Lead Time: Because of such complexities, manufacturing processes for currently approved CAR-T cell therapies can take approximately three to five weeks following apheresis to be treated with their personalized auto-CAR-T cells.

Our Solution – AlloNK

AlloNK is an allogeneic, off-the-shelf, cryopreserved NK cell therapy candidate designed to enhance the ADCC effect of mAbs to drive B-cell depletion. In preliminary results from 29 B-NHL patients, as of March 26, 2024, AlloNK in combination with a B-cell targeted mAb has demonstrated deep depletion of peripheral B-cells and CRs in certain patients in clinical trials. Because in both B-NHL and autoimmune disease the potential therapeutic activity may be driven by B-cell depletion in the periphery and lymphoid tissues, we believe these preliminary data in B-NHL patients provide supporting evidence for our proposed mechanism of action in autoimmune disease. Using our cell therapy manufacturing platform, we have manufactured thousands of doses of cryopreserved, infusion-ready AlloNK cells from a single cord blood unit. We believe the design of AlloNK creates the potential for administration in the community setting and the scalability for broad commercialization, if approved.

NK Cell Background

NK cells are part of the innate immune system, which is the body’s first line of immune surveillance and defense. NK cells modulate their activity through a balance of activating and inhibiting receptors on their surface that engage with their environment including with target cells. This balance enables NK cells to recognize and kill abnormal cells while suppressing cytotoxic responses to normal tissue, thereby providing a population of immune effector cells that defend against cancer and virus-infected cells. NK cells naturally work in concert with antibodies. The antibody first binds to a target on a diseased cell, then to the NK cell via the cell-surface receptor CD16, also known as FcγRIII, which engages the antibody to mount an ADCC response. NK cells may have an advantage over other immune cells, such as the T-cells used in CAR-T cell therapy and other cell therapies, because they can be used as allogeneic therapies, meaning that NK cells from one donor can be administered to one or many patients without the requirement for gene editing or other genetic manipulations.

Schematic of NK Cell Receptor Interaction with

Target Cells. NK Cell Activation via ADCC Leads

to NK-mediated Cytotoxic Activity

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To produce AlloNK, we select cord blood units that have a variant of CD16 known as 158 V/V, which has been shown in preclinical studies to lead to increased ADCC activity. The CD16 158V/V point mutation variant encodes for a FcgRIII receptor that has been shown in preclinical studies to have higher affinity for immunoglobulin G mAbs. In a third-party clinical trial of rituximab, a significantly higher response rate was seen in follicular lymphoma patients with the CD16 genotype encoding the 158 V/V compared to those with other CD16 genotypes. As such, we believe NK cells sourced from donors with the CD16 158 V/V allele will have naturally higher affinity for therapeutic mAbs without the need for genetic engineering of the cell therapy product candidate.

AlloNK, as a non-genetically modified, non-targeted NK cell, is designed to utilize a mAb for targeting. Therefore, we believe different mAbs could be used to target distinct B-cell populations based on the target cell’s antigen expression. For instance, CD19 and CD20 are expressed on memory B-cells, whereas CD38 and BCMA are expressed on plasma cells. Therefore, we believe AlloNK could be combined with different mAbs to kill distinct B-cell populations.

B-NHL Readthrough to Autoimmune Disease

We believe the success of cell therapies such as auto-CAR-T in oncology has paved the way for the application of cellular therapies in autoimmune diseases. Auto-CAR-T’s clinical therapeutic benefit in autoimmune disease appears to be driven by a rapid and deep depletion of B-cells in the periphery and in the lymphoid tissues, followed by an immunological reset and B-cell reconstitution.

In the B-NHL setting, activity is also driven by deep depletion of B-cells, including cancerous B-cells in the periphery, and in the tissues where lesions are located, principally the lymphoid tissue. Peripheral B-cell levels can be measured in B-NHL patients, providing evidence of depletion of targeted cells in the periphery. CRs in B-NHL are assessed using the Lugano 2014 criteria which utilizes 18-fluorodeoxyglucose (FDG) PET/CT. CRs in B-NHL patients indicate disappearance of cancerous B-cells from lymphatic tissues, and therefore provide evidence that a therapy is targeting and eliminating cells of B-cell origin within tissues. An array of autoimmune diseases are driven by pathologic B-cells, and therefore, we believe observations of the pharmacodynamic response of a therapy or product candidate against cancerous B-cells in the periphery and in tissue in NHL patients can provide supporting evidence for the mechanism in autoimmune disease.

AlloNK Data in B-NHL

As of April 30, 2024, we had dosed 29 patients with AlloNK in combination with rituximab in our ongoing Phase 1/2 multicenter clinical trial in patients with relapsed or refractory B-NHL. The median age of the 29 patients dosed with AlloNK in combination with rituximab was 71 (range: 46 to 86), and patients had received a median of three prior lines of systemic treatment.

As part of this trial, we have assessed peripheral B-cell levels in patients before and after treatment with the combination of AlloNK and rituximab. In all 29 patients with samples analyzed, as of March 26, 2024, following the first cycle of treatment, all patients achieved non-quantifiable peripheral B-cell levels by Day 8 (except for one patient who achieved such B-cell depletion by Day 15) following the start of therapy, regardless of B-cell levels at baseline. Preliminary data, as of March 26, 2024, as described in further detail below, show peripheral B-cell depletion over the first cycle of treatment in all patients with detectable B-cells at baseline. We believe these preliminary data provide support for our proposed B-cell depleting mechanism of action.

AlloNK has also shown CRs in B-NHL patients, as measured using the Lugano 2014 criteria by imaging of tumor lesions, in our ongoing clinical trial. Because of the common tissues of interest, principally the lymphoid tissues, in B-NHL and autoimmune diseases, we believe data in these B-NHL patients may provide supporting evidence for our proposed mechanism of action in autoimmune disease.

As described further below, in the Phase 1 portion of this trial, as of April 30, 2024, in the fourteen patients who were naïve to CAR-T, the ORR was 71%, including eight CRs (57%) and two PRs (14%), as determined by the Lugano 2014 criteria. Thirteen of these patients had aggressive forms of B-NHL, and the CR rate in this subset, as determined by the Lugano 2014 Criteria, was 62%. As of the April 30, 2024 data cutoff date, six of the eight patients

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with a CR had an ongoing response (meaning continuation of the CR at all follow-up points), with five of these patients remaining progression free at six months or later. The longest responder remained progression free for at least 18 months after the start of treatment.

AlloNK Patient Journey

We believe AlloNK will improve the patient and physician experience when compared to the administrative complexity and management of potential toxicities associated with auto-CAR-T. This is in contrast to auto-CAR-T, which involves multiple steps that may materially delay time to treatment including a pre-treatment eligibility determination, apheresis within a specialized center, a wait period for auto-CAR-T manufacturing, infusion scheduling and finally receipt of cryopreserved auto-CAR-T in preparation for treatment. In addition, current Risk Evaluation and Mitigation Strategy programs for commercial auto-CAR-T requires patients to remain within two hours of the treatment center for four weeks following treatment (if healthcare providers require in-patient monitoring).

Illustrative Patient Journey on Auto-CAR-T Treatment

In contrast, AlloNK is an off-the-shelf cell therapy candidate that is cryopreserved with established end-to-end cold-chain logistics in place to enable a patient to start treatment without any prior steps. Further, AlloNK is logistically simple to administer and is in a format compatible with existing infusion center infrastructure. It is thawed at the bedside and administered in a 5-to-10 minute IV push without the need for any product formulation or processing.

In addition, AlloNK is designed to lend itself to an improved experience for the patient following treatment and we believe this will broaden access to the community setting. This is in contrast to auto-CAR-T, where mandatory hospitalization is often required in order to observe for side-effects such as CRS and ICANS. We believe AlloNK has the potential to enable rheumatologists to treat patients in their own infusion centers as opposed to having to refer patients to tertiary care centers. In preliminary data as of April 8, 2024, from our ongoing Phase 1/2 B-NHL trial, CRS was observed in four patients (9%) and of these patients, three patients experienced a Grade 1 CRS, one patient had a Grade 2 CRS, and no ICANS was observed.

The figure below shows the number of drug-related hospitalization days for the 30 days following dosing of AlloNK for all 45 B-NHL patients who received AlloNK in combination with rituximab in our Phase 1/2 clinical trial as of April 8, 2024. As shown in the figure below, 31 patients (69%) were treated entirely in the outpatient setting and were not hospitalized for adverse events during the first 30 days following administration of AlloNK in combination with rituximab dosing. Out of the 14 patients who were hospitalized, the median length of hospitalization was three days and the reasons for hospitalizations were related to fevers and infections. Further, these were heavily pre-treated elderly patients with a median age of 68 years and median four prior lines of therapy. Because of the advanced aged and frailty of this patient population, several hospital stays were extended to accommodate the next dose of AlloNK in combination with rituximab or in an abundance of caution. We believe these preliminary data support that AlloNK in combination with B-cell targeted mAbs has the potential to be

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administered and managed in the community setting, which, if approved for such use, has the potential to expand access to more patients and alleviate economic and logistical burden on the healthcare system.

Number of Hospitalization Days Due to Drug-related Adverse Events in 45 Patients Treated with AlloNK in Our Phase 1/2 B-NHL Trial

AlloNK Lends Itself to a Breadth of Targeting Approaches and Indications

AlloNK, as a non-genetically modified, non-targeted NK cell, utilizes a mAb for targeting. Therefore, different mAbs could be used to target distinct B-cell populations based on the target cell’s antigen expression. Beyond rituximab and other anti-CD20 mAbs, we have already conducted numerous preclinical studies in which we have shown cytotoxic activity of AlloNK in combination with other approved B-cell targeted mAb therapies, such as anti-CD19 and anti-CD38 mAbs. Emerging evidence with auto-CAR-T targeting the plasma cell antigen BCMA has shown therapeutic activity in several indications, and we believe AlloNK in combination with approved anti-CD38 mAbs could target a similar plasma cell population. We have the opportunity to develop AlloNK in combination with approved B-cell targeted mAbs using a variety of targets, including the potential for dual targeting by treating in combination with two mAbs. We believe this versatility will enable us to pursue a wider range of indications than cell therapies engineered against specific targets.

AlloNK Development in Autoimmune Diseases

AlloNK is an allogeneic, off-the-shelf, cryopreserved NK cell therapy candidate designed to enhance the ADCC effect of mAbs to drive B-cell depletion. AlloNK is designed to be administered in the community setting. Using our proprietary cell therapy manufacturing platform, we can generate thousands of doses of cryopreserved, infusion-ready AlloNK from a single cord blood unit.

We are currently evaluating AlloNK in combination with rituximab or obinutuzumab in a Phase 1/1b open-label multi-center clinical trial in patients with SLE with or without LN who previously failed treatment, for which the FDA has granted Fast Track designation to improve disease activity in patients with class III or class IV LN. In addition, in April 2024, the FDA cleared an IND submitted by IRIS, a large community practice rheumatology clinic in Florida, to conduct a basket IIT to assess the safety, tolerability and clinical activity of AlloNK in combination with rituximab in patients with RA, PV, GPA / MPA and SLE. Treatment of the first patient in the basket IIT was initiated in August 2024. We intend to pursue additional autoimmune diseases with AlloNK in combination with B-cell targeted mAbs.

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SLE and LN Background

SLE is an autoimmune disease characterized by autoantibody production and deposition of immune complexes with complement activation, resulting in inflammation and damage within the affected tissue, which contributes significantly to the disease’s morbidity and mortality rates. LN, a type of kidney disease, is a manifestation of SLE reported to affect approximately half of all patients with SLE. LN occurs when autoantibodies affect parts of the kidneys that filter out waste, which can result in swelling, weight gain from fluid retention, elevated blood pressure and urine that appears foamy from excessive protein loss. Diagnosis often reveals proteinuria, or the presence of excessive protein in the urine, blood in the urine, and lowered serum albumin levels.

The primary aim of managing LN involves preventing irreversible kidney damage, typically through anti-inflammatory and immunosuppressive therapies like steroids, MMF and cyclophosphamide to alleviate inflammation and blood pressure medications that protect the kidneys. Despite the availability of potent therapies, up to 10% of LN patients still progress to end-stage renal disease, requiring dialysis and eventually, a kidney transplant. There are an estimated 210,000 SLE patients with LN across the United States and Europe, and approximately 30% do not respond to currently available treatments. Furthermore, chronic use of these therapies typically creates secondary complications for patients, including, but not limited to, increased risk of infections and cancer, cardiovascular disease, hypertension, Cushing’s disease, diabetes and osteoporosis.

Rationale for AlloNK in SLE and LN

We are focusing on SLE and LN as the first target of our clinical development program in light of the clearly identifiable patient group, significant unmet need and presence of measurable clinical endpoints to facilitate regulatory approval submissions.

LN offers an objective clinical marker for tracking disease activity and renal impairment: proteinuria. This marker enables the use of the UPCR to assess renal function, making it a reliable and objective endpoint. The reduction of proteinuria, as determined by UPCR, is an important component of CRR, which has been historically used as a critical measure to evaluate a patient’s response to treatment for LN in clinical trials.

B-cells are recognized as key mediators of SLE pathogenesis and B-cell targeted mAbs direct B-cell killing via ADCC and induction of apoptosis. However, studies have shown that B-cell depletion is incomplete in the tissues of certain patients following rituximab treatment, leading to pathogenic B-cell escape and hindering effective reset of the immune system. NK cells from SLE patients have been shown to be reduced in number in peripheral blood, with reports of SLE patients having less than half as many CD16+ NK cells as healthy subjects. Further, the phenotype of NK cells in SLE patients can result in reduced cytotoxicity as well as defective ADCC, which could lead to incomplete B-cell depletion by rituximab. In several preclinical studies, AlloNK potentiated anti-CD20-mediated ADCC against CD20-expressing malignant B-lymphocytes in vitro and in vivo and was not negatively affected by steroids. Further, AlloNK induced B-cell apoptosis in combination with rituximab and obinutuzumab in peripheral blood mononuclear cells (PBMCs) isolated from SLE patients.

AlloNK Preclinical Results in SLE and LN

In vitro preclinical studies, we evaluated the cytotoxic activity of AlloNK in combination with rituximab or obinutuzumab mAbs against PBMCs isolated from SLE patients. PBMCs combined with thawed AlloNK were incubated with or without antibodies (0.0.01, 0.1.1 ug/mL) at different effector (AlloNK cell) to target (PBMCs) ratios (E:T ratios) for four hours. The E:T ratios tested were 0.2:1, 1:1, and 2:1 AlloNK to PBMCs. Apoptotic (caspase positive) B-cells in SLE PBMCs were quantified by flow cytometry.

ADCC against SLE B-cells was observed when AlloNK was combined with rituximab or obinutuzumab in an antibody concentration-dependent and an E:T ratio-dependent manner. Shown below is data from an E:T ratio of 1:1 at a single antibody concentration. The specificity of cell killing in the SLE PBMC sample was evaluated by examining the effects of the combination on SLE T-cells. Importantly, little to no off-target apoptosis was observed in this cell population in the presence of AlloNK and either of the antibodies tested. In addition to anti-CD20 mAbs, we have conducted in vitro preclinical studies of AlloNK in combination with tafasitamab, an anti-CD19 antibody, or daratumumab, an anti-CD38 antibody, which demonstrated specific killing of B-cells from SLE PBMCs.

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Data below shows fold change in B-cell killing when mAb (0.1μg/mL) was combined with AlloNK in a 1:1 ratio with SLE PBMCs (n=3–6 SLE PBMC donors). Increased B-cell apoptosis was observed when AlloNK was combined with B-cell targeting mAbs, which we believe demonstrates enhanced ADCC with the mAb combinations.

Fold Change in B-cell Killing when AlloNK was Added to mAb in SLE PBMCs. AlloNK was Added in a 1:1 ratio to PBMCs, with mAb at 0.1μg/mL (n=3–6 SLE PBMC donors)

AlloNK Clinical Development in SLE and LN

In April 2024, we began dosing patients in our Phase 1/1b open-label, multi-center clinical trial of AlloNK in combination with rituximab or obinutuzumab in patients with class III or class IV LN who previously failed treatment. We also amended the protocol for this trial to broaden the patient population to include patients with SLE without LN. The trial is designed as a two-stage trial. We plan to enroll up to six patients per cohort in dose escalation (stage 1) with a 3+3 design, and up to a total of 12 patients per cohort in the cohort expansion (stage 2), inclusive of those patients from the corresponding cohort in stage 1.

AlloNK dosing will start at one billion total cells per dose, and the rituximab cohort can enroll in parallel with the obinutuzumab cohort. The protocol allows dose escalation to four billion total cells per dose, with rituximab and obinutuzumab combination cohorts enrolling in parallel. Other than the first patient in each cohort, who will be hospitalized overnight following the first dose of AlloNK only, no other patients have any mandatory hospitalization requirement per the trial protocol.

The primary objective of the clinical trial is to assess the safety, tolerability and preliminary activity of AlloNK in combination with rituximab or obinutuzumab. The primary efficacy endpoint is the overall renal response rate (ORRR) defined as the proportion of subjects having either a complete renal response (CRR) or partial renal response (PRR) at 52 weeks. A CRR is defined as achieving a UPCR of less than 0.5 and normal renal function as determined by serum creatinine levels at or below the upper limit of normal without worsening of baseline serum creatinine by more than 15%. A PRR is defined as a 50% or more reduction in UPCR from baseline, to an absolute value of less than one, or to less than three if baseline UPCR was above three, and serum creatinine not increased by more than 15% from baseline. We will also collect global disease activity measurements using the SLEDAI-2K assessment, and translational biomarkers, including levels of autoantibodies, serum complement, serum immunoglobulins, and peripheral B-cell subsets.

In auto-CAR-T studies, an initial lymphodepletion regimen has been utilized consisting of cyclophosphamide and fludarabine, which depletes B-cells among other lymphocytes. Our clinical development approach in SLE and LN is to investigate our product candidate utilizing a similar initial lymphodepletion regimen followed by treatment with AlloNK in combination with a B-cell targeted mAb. We may explore ways to optimize and possibly remove the lymphodepletion regimen in future development.

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We utilize combination with rituximab to target CD20, an antigen present on B-cells in many of the same lineages that express CD19. In a clinical study of rituximab in SLE published by Vital et al. in 2011, when complete depletion of CD20-expressing B-cells was achieved, depletion of CD19-expressing, CD20-negative plasmablasts was also observed, suggesting that CD20 targeting can potentially deplete a broad range of B-cells, including plasmablasts. Further, in our B-NHL trial, AlloNK in combination with rituximab was observed to drive deep B-cell depletion in the periphery, as measured by CD19 expression, which we believe indicates that this regimen can potentially deplete CD19-expressing B-cell lineages. We believe this has the potential to mirror the approach of auto-CAR-T cell therapy in achieving an initial, generalized lymphodepletion before attacking the pathogenic B-cells, with the goal of achieving deep B-cell depletion. In the NOBILITY Phase 2 clinical study of obinutuzumab in LN, published by Furie et al. in 2022, obinutuzumab was superior to placebo for the achievement of CRR and ORR in patients with proliferative LN when added to mycophenolate (median 2g/day) and corticosteroids, indicating that obinutuzumab may be an attractive mAb to combine with AlloNK in order to achieve deep B-cell depletion. In a post-hoc analysis of the NOBILITY clinical study, presented by Vital et al. in 2024, the subset of patients with sustained B-cell depletion at weeks 24 and 52 achieved a 50% CRR at week 76, making these patients 72% more likely to achieve a CRR at week 76 than the subset of patients who had unsustained B-cell depletion.

The treatment schedule is outlined below. The lymphodepletion treatment regimen consists of three daily doses of 30 mg/m2 fludarabine and a single dose of 1000 mg/m2 cyclophosphamide, a very similar regimen as utilized in studies led by Schett. Rituximab or obinutuzumab is given in two doses of 1000 mg each, the same regimen used in autoimmune indications such as RA. AlloNK is given in three weekly doses at either one billion or four billion total cells per dose. All patients will receive at least one treatment cycle followed by scheduled assessments of overall health and response status. Patients who have not achieved a CRR are eligible for a second cycle, as described above, at six months. We dosed our first patient in this trial in April 2024, and the DLT assessment period has been cleared.

Treatment Regimen for AlloNK in Combination with B-cell Targeted mAbs in a Phase 1/1b Trial in SLE and LN

AlloNK Development in Additional Autoimmune Indications

We believe that AlloNK has the potential to impact multiple additional B-cell mediated autoimmune indications beyond SLE and LN. We are exploring the potential of AlloNK in these indications and other antibody combinations through company-sponsored clinical trials and by supporting IITs.

We believe supporting IITs, where we provide patient access to AlloNK by supplying AlloNK for use in IITs, allows us to prioritize patient needs while providing us insight that has the potential to support expansion of our development programs into additional indications where we believe AlloNK in combination with B-cell targeted mAbs has the potential to benefit patients who are refractory to existing therapies.

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B-cell depletion has a therapeutic activity in multiple additional autoimmune indications as evidenced by indications where mABs targeted against CD20 such as rituximab and ocrelizumab are approved, as well as data from the study led by Schett. These indications include RA, PV and GPA, formerly known as Wegener’s granulomatosis, MPA, IIM, SSc, MG and MS.

Rituximab is approved for certain RA, PV, and GPA / MPA indications. RA is a chronic inflammatory disorder that primarily affects joints, but can also have systemic effects, impacting various organs and tissues in the body. PV is a rare, chronic autoimmune disorder characterized by antibodies against desmogleins and the formation of blisters and erosions on the skin and mucous membranes, most commonly affecting the mouth, throat, nose, eyes, genitals and lungs. AAV is a group of rare autoimmune diseases of unknown cause characterized by anti-neutrophil cytoplasmic antibodies, and encompassing the subtypes GPA, which affects various organs, including the kidneys, lungs and upper respiratory tract, and MPA, which often involves the kidneys and lungs but can affect any organ system.

The Schett group developed clinical data, which we believe support the potential of B-cell depleting cell therapy in treating IIM and SSc. IIM is a group of autoimmune conditions characterized by inflammation of muscle (myositis) and other organ systems, resulting in widespread organ dysfunction. For patients with severe disease, symptoms can be debilitating, and can lead to mortality, especially when lungs are involved. SSc is a persistent, systemic autoimmune disease characterized by autoantibodies against transcriptional and translational components, including topoisomerase, centromeres and RNA polymerase, resulting in vascular damage and fibrosis. A significant portion of SSc patients develop interstitial lung disease (ILD), and for those who develop pulmonary hypertension, the three-year mortality rate exceeds 60%.

B-cell depletion has also shown therapeutic effects in neuroinflammatory diseases like MS and MG. MS is a long-term condition affecting the central nervous system, leading to neurodegeneration caused by inflammation. Ocrelizumab, a B-cell targeting anti-CD20 mAB, was approved in 2017 for treatment of relapsing MS and primary progressive MS, underscoring the role of B-cells in influencing relapse frequency and disease advancement in MS. MG is a chronic autoimmune disorder in which antibodies destroy the communication between nerves and muscle, resulting in weakness of the skeletal muscles, and case reports have shown an impact of B-cell-targeted auto-CAR-T.

In these other autoimmune and neuroinflammatory diseases, some patients with severe disease or who are refractory to prior therapies require continuous treatment with immunosuppressive regimens, including steroids, leading to long-term health consequences. We believe a therapy that could allow for a period of drug-free remission could therefore fill a significant unmet need for patients.

Investigator-Initiated Basket Trial

In April 2024, the FDA cleared an IND submitted by IRIS, a large community practice rheumatology clinic in Florida, to conduct a basket ITT to assess the safety, tolerability, and clinical activity of AlloNK in combination with rituximab. The IIT will initially enroll patients with RA, PV, GPA / MPA and SLE.

The IIT is a basket trial, which is a clinical trial that evaluates how well a therapy works in patients with different diseases that share a common characteristic, such as different autoimmune indications. The basket design utilizes an initial safety run-in stage of nine all-comers patients with any of the four included indications, followed by expansion cohorts to enroll a total of six patients per cohort for PV and GPA /MPA, and nine patients per cohort for RA and SLE. All patients will receive a single cycle of treatment, consisting of cyclophosphamide and fludarabine lymphodepletion, rituximab, and AlloNK. The dosing regimen leverages the standard of care dose and schedule of rituximab for each indication, with AlloNK given in three weekly doses of one billion total cells per dose. Other than the first patient in each cohort, who will be hospitalized overnight following the first dose of AlloNK only, no other patients have any mandatory hospitalization requirement per the trial protocol. The primary objective of the clinical trial is to assess the safety, tolerability and preliminary activity of AlloNK in combination with rituximab. Primary efficacy endpoints specific to each indication (RA, PV, GPA / MPA and SLE) will be used. We also anticipate assessing translational biomarkers, including levels of autoantibodies relevant in each indication, serum complement levels, serum immunoglobulin isotypes, peripheral B-cell subsets, and peripheral levels of AlloNK for pharmacokinetic analysis. Treatment of the first patient in the basket IIT was initiated in August 2024.

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Pursuant to an institution-initiated and sponsored clinical trial agreement with IRIS, we are providing support and supply AlloNK and funding for study-related expenses for the IIT, but unlike our sponsored clinical trials, IRIS is the regulatory sponsor of, and responsible for the conduct of the IIT. This IIT is not part of our clinical trials for AlloNK and data from this trial is reported by the relevant investigator. While we do not expect to be able to use the results from this IIT in our applications for marketing approval to the FDA or other comparable foreign regulatory agencies, we believe that this strategy may provide some competitive advantage as we will be able to acquire additional clinical insights beyond highly focused clinical trials in specific geographies and additional indications.

AlloNK Development in Non-Hodgkin Lymphoma

Non-Hodgkin Lymphoma Background

NHL is a neoplasm of the lymphoid tissues originating from B-cell precursors, mature B-cells, T-cell precursors and mature T-cells. Approximately 85% are B-cell malignancies. Currently available NHL treatments like auto-CAR-T products targeting CD19 have shown promise in aggressive lymphomas but we believe they are associated with life-threatening safety risks, have limited access and are slowly administered due to manufacturing inefficiencies.

AlloNK Clinical Development in B-NHL

We have tested AlloNK in combination with rituximab in 29 patients with relapsed or refractory B-NHL in our ongoing Phase 1/2 clinical trial with data, as of an April 30, 2024 cutoff date. The clinical trial also enrolled 16 patients in monotherapy cohorts, consisting of lymphodepletion and AlloNK without rituximab. The Phase 1 portion of the study is evaluating two AlloNK dose levels, four-weekly doses of either 1 billion cells or 4 billion cells per dose, as monotherapy or in combination with rituximab using the 3+3 dose escalation method. The primary objective of the clinical trial is to assess the safety and anti-tumor activity of AlloNK in combination with rituximab.

In our trials, clinical activity is primarily determined by responses as measured by the Lugano 2014 criteria using both modalities as described in the table below. The criteria classify clinical activity or treatment response as CR, PR, stable disease or progressive disease. The Lugano classification recommends the Deauville five-point scale for reporting response by FDG PET-CT. The Deauville five-point scale scores responses as follows (where 1 is best and 5 is the worst): (1) no uptake or no residual uptake (when used interim), (2) slight uptake, but equal to or below blood pool (mediastinum), (3) uptake above mediastinal, but below or equal to uptake in the liver, (4) uptake slightly to moderately higher than liver or (5) markedly increased uptake or any new lesion (on response evaluation). A summary of the Lugano 2014 criteria is described below.

CT-Based Response FDG PET-CT-Based Response

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CT-Based Response FDG PET-CT-Based Response

Lugano 2014 Criteria Table For Lymph Nodes and Extralymphatic Sites

All patients receive lymphodepleting chemotherapy for three days prior to treatment of AlloNK and low-dose subcutaneous IL-2 after each dose of AlloNK. Patients in the combination cohorts received up to two cycles of treatment with lymphodepletion, with the third and fourth cycle, if eligible, given without lymphodepletion. A third cohort was added to test a bi-weekly dosing schedule of AlloNK in combination with rituximab but without the administration of IL-2. Patients in this cohort received up to three cycles of treatment with lymphodepletion. Any patient experiencing clinical benefit (stable disease (SD), PR or CR, per the Lugano 2014 criteria) after one cycle of treatment with AlloNK and rituximab is eligible for additional cycles of AlloNK plus rituximab. The median age of the 29 patients dosed with AlloNK in combination with rituximab was 71 (range: 46 to 86), and patients had received a median of three prior lines of systemic treatment.

B-cell Depletion in B-NHL Patients

Blood samples were drawn at specified timepoints during the course of the trial. B-cell depletion was assessed in whole blood samples using the TBNK cells assay (BD Mulitest 6-color TBNK Reagent). In 29 patients treated with the combination of AlloNK and rituximab with samples analyzed, as of a March 26, 2024 cutoff date, we observed that all patients achieved non-quantifiable peripheral B-cell levels by Day 8 (except for one patient who achieved such B-cell depletion by Day 15) following the start of a single cycle of therapy, regardless of B-cell levels

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at baseline. Preliminary data below, as of March 26, 2024, demonstrates peripheral B-cell depletion over the first cycle of treatment in all patients with detectable B-cells at baseline.

Peripheral Depletion of CD19+ B-cells in NHL Patients Treated with AlloNK and Rituximab

Further, we assessed peripheral B-cell levels in patients treated in the monotherapy cohorts. Data, as of May 15, 2024, showed initial non-quantifiable peripheral B-cell depletion in seven monotherapy patients with detectable B-cells at baseline. This B-cell depletion was maintained in the majority of patients through approximately four weeks after the initial AlloNK dose. In contrast to the combination therapy cohorts, B-cell levels in the monotherapy patients began to increase approximately four to eight weeks after the initiation of treatment.

Peripheral Depletion of CD19+ B-cells in NHL Patients Treated in Monotherapy Cohorts (Lymphodepletion and AlloNK without Rituximab)

Clinical Responses in B-NHL Patients

Of the 29 patients treated with AlloNK in combination with rituximab, as of April 30, 2024, 14 patients (48%) were not exposed to prior CAR-T. In these patients, the ORR was 71%, including eight CRs (57%) and two PRs (14%). Thirteen of these 14 patients had aggressive forms of NHL, with one patient having indolent marginal zone lymphoma but having previously failed five prior lines of therapy. As of the April 30, 2024 data cutoff date, six of the eight patients with a CR had an ongoing response (meaning continuation of the CR at all follow-up points), with

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five of these patients remaining progression free at six months or later. The longest responder remained progression free for at least 18 months after the start of treatment.

Clinical Responses of AlloNK in Combination with Rituximab in All Patients Naïve to Prior CAR-T in Phase 1/2 B-NHL Trial

Fifteen patients (52%) treated with AlloNK in combination with rituximab received prior CAR-T, of which 13 (45%) received commercial auto-CAR-T-therapies. The ORR in the 15 patients exposed to prior cell therapies was observed to be 40% including four CRs and two PRs.

Preliminary Safety Data

As of April 8, 2024, a total of 45 patients were evaluated for safety across all cohorts in our Phase 1/2 B-NHL trial (16 monotherapy and 29 in combination with rituximab). The median age at enrollment was 68 years and patients had a median of four prior lines of systemic therapy. All, except for one monotherapy patient, received prior anti-CD20 mAb.

Only one dose-limiting toxicity (DLT) of an infusion-related reaction was observed across all combination cohorts. The maximum tolerated dose was not reached, and AlloNK at four billion cells per dose was deemed to be the maximum administered dose. CRS was observed in four of 45 patients (9%), with no Grade 3 or higher CRS reported. Three patients experienced a Grade 1 CRS and one patient had a Grade 2 CRS. Cytokine analysis of samples from 40 patients treated with AlloNK showed IL-6 concentrations below 100 pg/mL at all time points analyzed, including samples from the 4 patients where CRS was reported. These IL-6 levels were below the lower limit of the range typically associated with CAR-T-related CRS. No other cell therapy associated treatment emergent adverse effects were observed, including ICANS or graft-versus-host disease. Serious treatment emergent adverse events (TEAEs) occurred in almost half of the 45 patients treated across all cohorts, and the most common (experienced by two or more patients) were febrile neutropenia (11%), sepsis (9%), infusion-related reactions and malignant progression (7% each), and pneumonia and pyrexia (4% each). Serious TEAEs related to AlloNK were observed in seven out of 45 patients (16%) treated across all cohorts, and consisted of infusion-related reactions (7%), febrile neutropenia (4%), and CRS and pyrexia (2% each).

Among the 29 subjects treated with AlloNK in combination with rituximab, the most common severe (Grade ≥3) TEAEs reported were associated with hematological disorders, which we consider to be consistent with the usage of lymphodepletion in this patient population, and included leukopenia (86%), neutropenia (83%), lymphopenia (76%), anaemia (45%) and thrombocytopenia (28%). The only other TEAEs observed in ≥10% of the

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patients treated with AlloNK in combination with rituximab were febrile neutropenia (10%), sepsis (10%) and infusion-related reactions (10%).

Grade 3 or higher treatment emergent adverse events (TEAEs) observed in ≥10% of the patients treated with AlloNK in our Phase 1/2 clinical trial in B-NHL

Partnered Programs

AlloNK in HL

Our ongoing collaboration with Affimed involves investigating AlloNK in combination with acimtamig, a CD30-targeted NK cell engager, in HL and potentially other CD30+ cancers. Classical HL is a type of cancer that originates from lymphocytes, leading to the growth of abnormal cells in the lymphatic system. The disease is characterized by the presence of Reed-Sternberg cells which highly express the CD30 antigen, making CD30 a crucial target for certain therapies and a marker for diagnosing and monitoring the disease’s progression. Preclinical data showed in vitro cytotoxicity and in vivo anti-tumor activity with AlloNK, in combination with acimtamig, against a CD30+ T-cell lymphoma cell line.

In November 2022, we announced a strategic partnership to jointly develop, manufacture, and, if approved, commercialize a combination therapy comprising of acimtamig with AlloNK. Affimed chose us as a partner to commercialize the combination based on the preclinical and clinical evidence of activity of AlloNK observed in NHL to date and our manufacturing expertise to provide cryopreserved NK cells for a muti-center trial and the potential to produce a cryopreserved, off-the-shelf, commercially-viable product.

Under the agreement, Affimed will lead regulatory activities through clinical development and, if approved via the accelerated approval pathway, any confirmatory studies. Affimed will be responsible for funding clinical study costs, while we will be responsible for the costs of supplying AlloNK and IL-2 for such studies. If accelerated approval is obtained, we may continue in the collaboration and share confirmatory study costs on a 50/50 basis, and in return revenues from the combination will be shared in a proportion of 67%/33% (Affimed/Artiva). Affimed will be responsible for promotional activities and expenses of the combination therapy, if approved. We retain commercialization and distribution rights and books sales for AlloNK.

The Phase 2 LuminICE-203 trial is currently enrolling patients with relapsed or refractory HL, and Affimed presented initial data from the first 22 patients in December 2024. The initial run-in phase is evaluating four cohorts with two doses of acimtamig and two doses of AlloNK. In each cohort, patients are given an initial lymphodepletion regimen of cyclophosphamide and fludarabine, followed by six weekly treatments. The first three weekly treatments consist of acimtamig infusion, followed by infusion of AlloNK and IL-2. The last three weekly treatments consist of

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acimtamig infusion alone. Following the run-in portion, the trial will follow a Simon two-stage design, with up to two dose cohorts tested in Stage 1 and one-to-two cohorts in Stage 2. The trial will also include an exploratory cohort in peripheral T-Cell lymphoma (PTCL).

CAR-NK Programs

Our manufacturing platform also allows for the generation of CAR-targeted NK cells utilizing cord blood starting material with the same pre-selected characteristics and scale-up process as AlloNK. We own ex-APAC rights for AB-201, a HER2 targeting CAR-NK cell, and for AB-205, a CD5 directed CAR-NK.

Platform to Create Gene-Modified NK Cells

As an alternative to targeting NK cells to tumors by combining with mAb therapy or NK-engager bispecific technology, NK cells may be targeted directly through the addition of a CAR against a defined target antigen. This is accomplished through genetic modification of the NK cell and can also include the addition of cytokine transgenes to further enhance the activity and persistence of these CAR-NK cells. We believe these modifications can turn NK cells into the kind of flexible, potent and allogeneic therapy that CAR-T cells were intended to become. In particular, we believe that the potential therapeutic applications of NK cells can be expanded by two types of gene modifications:

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Addition of CAR constructs to direct NK cells to specific antigens: We introduce CAR constructs to our cord-blood derived NK cells via a lentiviral vector. This virus vector is manufactured under cGMP conditions in the United States prior to being transferred to the GC Cell manufacturing facility in Korea where it is combined with NK cells during the first expansion phase of our manufacturing process. Our CAR constructs have been designed to enhance the activity of our NK cell product candidates based on extensive empirical evaluation of costimulatory domains alone and in combination. In our preclinical studies, CAR-NK cells that contain the costimulatory domain OX40L used in our CAR construct exhibited greater cytotoxic potential than structures used in other T-cell and NK cell programs.

2.

Enhancement of viability and potency through overexpression of cytokines: IL-15 promotes NK cell viability, proliferation and function. Transduction of NK cells with gene constructs that lead to expression of IL-15 increased their cytotoxic potential in preclinical studies. Further, IL-15 expression has been associated with increased cell persistence in third-party human clinical studies. Expression of IL-15 in our CAR-NK cells has resulted in high viability in culture and our AB-201 product candidate expresses the IL-15 transgene. Our preclinical studies showed that the IL-15 co-expressed from the CAR lentivirus resulted in persistence of AB-201 cells in the circulation of mouse models beyond Day 30 and peak detection in lung and spleen tissues at Day 15. This was substantially longer than the persistence seen for cord blood-derived NK cells not expressing IL-15.

AB-201

AB-201 is an allogeneic anti-HER2 CAR-NK cell product candidate, containing a CAR with a proprietary HER2 antigen recognition domain and expressing soluble IL-15. HER2, also known as Human Epidermal Growth Factor Receptor 2 or ErbB2, is a receptor tyrosine kinase that is overexpressed on many solid tumors, such as breast, gastric and esophageal, and bladder cancers. AB-201 has shown specific cytotoxic activity against HER2+ tumor cells in vitro and anti-tumor activity and tumor infiltration in vivo. AB-201 is designed to bind to a region distinct from other HER2-targeting drugs, such as trastuzumab and pertuzumab. We have received orphan drug designation for AB-201 in the United States.

It is estimated that there are over 50,000 patients diagnosed annually in the United States with tumors having high expression of HER2, with overexpression found in approximately 10% to 15% of breast cancer cases and in over 10% of bladder and esophageal cancers. Many breast cancer patients with HER2+ localized disease experience pathologic complete responses when treated with HER2-directed therapies. However, for patients who relapse and for those who present initially with metastatic disease, current treatments can provide clinical responses but are not curative, and prognosis generally worsens with each subsequent line of therapy. HER2 is expressed in a subset of gastric, gastro-esophageal junction and esophageal cancers. Each year, over 5,000 patients in the United States begin various lines of treatment for HER2+ disease. Trastuzumab and fam-trastuzumab deruxtecan are approved for use in

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HER2+ gastric cancer, but a significant unmet medical need remains with only about half of patients responding to these therapies in first-line treatment and fewer than 30% of patients responding in third and later lines. HER2 is also expressed in a subset of bladder cancers. Each year, over 5,000 bladder cancer patients in the United States receive treatment for cancer that expresses HER2, but there are no approved HER2-directed therapies in bladder cancer.

AB-205

AB-205 is an allogeneic anti-CD5 CAR-NK cell product candidate, containing a CAR with a CD5 antigen recognition domain and expressing soluble IL-15. CD5 is a T-cell activation marker and negative regulator of TCR signaling expressed on tumor cells in the majority of cases of T-cell lymphoma and leukemia. Our partner, GC Cell, has observed specific cytotoxic activity against CD5+ T-cell leukemia cell lines, CCRF-CEM and RPMI-8402, with AB-205 in vitro and meaningful anti-tumor activity in vivo.

CD5 is expressed in a large number of cases of T-cell lymphoma (TCL) and T-cell Acute Lymphoblastic Leukemia (T-ALL). TCL accounts for 10-15% of all NHL cases and is categorized as cutaneous (CTCL) or more aggressive PTCL forms. PTCL, which accounts for approximately half of TCL cases, can be further subdivided into subtypes, with an estimated 80% of all cases expressing CD5. The CD30-targeted antibody drug conjugate Adcetris (brentuximab vedotin, BV) is used in PTCL, with the highest efficacy in the anaplastic large cell lymphoma (ALCL) subtype which uniformly expresses CD30. However, approximately 15% of ALCL patients are refractory or quickly progress following BV, while another 50% of ALCL patients initially respond, but ultimately progress after BV. Further, efficacy of BV and expression of CD30 in other PTCL subtypes is varied. There remains an unmet need for effective and safe therapies in these populations.

CAR-NKs may be an especially advantageous construct for targeting cancers of T-cell origin because of two limitations of CAR-T cells. First, autologous CAR-T products must be generated from T-cells isolated by leukapheresis, and using cells from a patient as starting material may risk generating CAR-T product from cancerous T-cells which could result in secondary malignancy. Second, since CD5 is expressed on normal, activated T-cells, CAR-T products, whether autologous or allogeneic, may need to be engineered to avoid fratricide of CAR-T cells against other CAR-T cells.

Manufacturing Capabilities and Industrialization of NK Cell Therapy

We have a manufacturing-first approach, referencing the fact that even before we were founded, our strategic partner GC Cell had already invested years pioneering the manufacturing process that we use today. Unlike most other companies in the NK field who started clinical development before establishing a scalable manufacturing process, we started clinical development with a mature and robust process in place. Our process is designed to allow us to produce off-the-shelf, allogeneic NK cell therapy candidates at scale, with the mission to make these therapies broadly accessible for patients with devastating autoimmune diseases and cancers. We leveraged our deep expertise in NK cell biology to establish an end-to-end proprietary process in collaboration with our strategic partner, GC Cell.

We believe the following features of our platform provide multiple key advantages:

Cord Blood as the Donor Source of our NK Cell Product Candidates

Cord blood is a recognized source of healthy donor cells for hematopoietic stem cell transplants and is readily available from multiple public banks in the United States and Europe. NK cells make up 5% to 15% of peripheral blood lymphocytes. Traditionally, peripheral blood has been used as the source for NK cells for therapeutic use. However, studies conducted by GC Cell have shown that NK cells derived from cord blood have a nearly ten-fold greater potential for expansion in our proprietary culture systems than those derived from peripheral blood, without premature exhaustion. The expression of receptors of interest on the surface of NK cells, such as those involved in the activation of NK cells on engagement of tumor cells, was seen to be more consistent donor-to-donor for cord blood NKs than peripheral-blood NK cells. Our manufacturing process activates the NK cells in cord blood in a donor-independent manner, resulting in a highly scaled, active and consistent NK cell product.

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Selection of Optimal Genetic Characteristics in the Donor Cord Blood Units

We pre-screen banked cord blood units for both the KIR-B haplotype and high-affinity variant of the CD16 receptor which are drivers of NK cell activity:

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KIR-B haplotype selection: We base our product candidates on cord blood units encoding KIR-B alleles of the KIR receptor family. It has been reported that KIR-B haplotype NK cells have more activating receptors than KIR-A. It has also been reported that acute myeloid leukemia patients receiving allogeneic transplants from homozygous KIR-B donors have significantly decreased relapse rates and increased disease-free survival than those receiving transplants from KIR-A donors.

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High-Affinity CD16 158V/V selection: We select cord blood units that have a variant of CD16 known as 158 V/V, which has been shown to lead to increased ADCC activity. In a clinical trial of rituximab, an anti-CD20 mAb, follicular lymphoma patients with the CD16 genotype encoding the 158 V/V allele had a significantly higher response rate compared to those with other CD16 genotypes.

Approximately 15% of cord blood units have the characteristics above. Following pre-selection, we ship the cord blood units to our manufacturing facility where they are held in cryostorage. We believe that the availability, quality, ability to prescreen and ease of logistics of cord blood make it the optimal donor cell source for our proprietary manufacturing process.

Established and Highly Scaled Proprietary Manufacturing Process

We are leveraging a manufacturing process designed to be cGMP-compliant and potentially optimized for highly scaled expansion of the NK cells from a cord blood unit using a proprietary culture system. The NK cells from selected cord blood units are expanded using a proprietary engineered feeder (eFeeder) cell culturing process. The eFeeder cells are engineered to express a combination of factors on their surface, which enhance the activation and expansion of NK cells from the cord blood unit. The eFeeder cells are manufactured in-house, irradiated and do not persist in the final product. This process has been developed to produce large numbers of mature and highly active NK and CAR-NK cells while avoiding overstimulation, which has been shown to lead to cellular senescence.

The NK cell expansion process consists of the following steps:

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MCB production: The cord blood unit is thawed and depleted of T-cells before culturing with the eFeeder cells, resulting in a significant expansion and enrichment of NK cells. For CAR-NK product candidates, a lentivirus vector encoding the specific CAR construct and IL-15 can be introduced at this stage. This results in the generation of cryopreserved MCB which is then stored in vials. MCB samples are assessed for quality against qualified release specifications before use in the second expansion stage. For AlloNK, we routinely produce 50-80 vials of MCB from each cord blood unit. We have produced multiple MCBs from different donor cord blood units for each product candidate.

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Drug product production: A single vial of MCB is used to seed a second expansion step. This takes place in a 50-liter, single-use bioreactor and results in highly activate, pure NK cells. The NK cells are harvested, vialed and cryopreserved. For AlloNK, we routinely produce >80 vials of one billion NK cells per vial for clinical use from each drug product batch. We have multiple bioreactors installed at both our San Diego facility and GC Cell and have capacity to produce up to 100 batches per year across both sites. Samples of drug product from each batch are tested using qualified assays prior to release for clinical use.

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Product characterization: Our highly scaled and reproducible process for generating cord blood-derived NK and CAR-NK cells has yielded drug product that has consistently been observed to meet release specifications across manufacturing runs. For AlloNK, we and GC Cell have produced over 50 batches of drug product which passed all of our release criteria including criteria for purity, identity and functional activity.

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Effective cryopreservation: The effective long-term storage of cells while retaining product viability and potency is an essential step in providing off-the-shelf NK and CAR-NK cell therapies. The final step in the manufacturing process is cryopreservation. We believe that the ability to effectively cryopreserve our NK and CAR-NK cell therapy product candidates is a key differentiator for our

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platform and is essential to providing off-the-shelf products that can be shipped around the world and be available on demand for single or repeat patient dosing. Historically, NK cells have been reported to be highly sensitive to the stresses of a freeze-thaw cycle, and cryopreservation of NK cells has therefore been more challenging than T-cells. Our proprietary cryopreservation process uses methods that have consistently demonstrated >90% viability of our NK cells upon thawing, with no significant differences in NK cell activity or expression of cytokines, such as interferon-g and TNFa.

For AlloNK, at the current scale, each cord blood unit is expanded to yield 50 to 80 cryopreserved MCB units. In turn, each MCB unit is further expanded to yield 80 to 100+ one billion-cell drug product vials. The demonstrated expansion from a single cord blood unit is therefore over 4,000 one billion-cell vials which are enough to treat over 250 to 1,000 autoimmune patients assuming one billion to four billion AlloNK cells per dose and three doses for a treatment regimen of an aggregate of three billion to twelve billion AlloNK cells total per patient with autoimmune disease. To date, we and GC Cell have produced over 50 clinical batches of AlloNK, producing thousands of AlloNK vials at one billion cells per vial, and have performed release testing on drug product derived from eight different donors. We have demonstrated both batch-to-batch and donor-to-donor consistency.

Our Manufacturing Process Can Generate Thousands of Doses of AlloNK from a Single Cord Blood Unit

We are conducting an ongoing product stability study to assess the shelf-life of our NK cell product candidates. We have tested each batch of AlloNK for cell viability, identity, purity, sterility and potency. To date, we have demonstrated stable results at 48 months. Our cryopreservation process was designed using an infusion-ready media not only to ensure that the thawed cells retain high and consistent activity, but also to enable a simple thawing process in which the drug product does not require any further processing before administration.

Our Facility

In addition to the research and manufacturing capabilities at GC Cell’s headquarters in Korea, we have established full development and manufacturing facilities in San Diego, California. We have built a new 52,000-square-foot corporate headquarters, which includes research and process development laboratories, and have recruited a team of cell therapy experts driving discovery research, preclinical development, translational science, process and analytical development, and cell therapy manufacturing Our headquarters also includes a 9,000 square-foot purpose-built cGMP manufacturing center to support NK and CAR-NK cell production for our pipeline development and clinical trial supply. This new facility capacity is in addition to on-going manufacturing in Korea.

Our scaled manufacturing process established at GC Cell over more than ten years has enabled us to design an efficient layout for our San Diego manufacturing center that is cGMP compliant. Our facility comprises multiple production suites, a MCB / virus suite and a suite devoted to product fill-finish and cryopreservation. Each of the three 50L bioreactor suites dedicated to drug product production have the capacity to run 20 batches per year. Given drug product batches can yield more than 80-100 AlloNK vials with one billion NK cells each, our facility has the capacity to generate over 5,000 one billion NK cell vials per year.

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Released finished product is stored off site at a third-party logistics vendor, as is currently the case for drug products manufactured for us by GC Cell. We intend to use our facility to enable new pipeline program research, development and manufacturing, to further optimize the AlloNK manufacturing process and produce AlloNK for current and future clinical trials and to supply any potential commercial launch.

Competition

The biopharmaceutical industry in general, and the cell therapy field in particular, is characterized by rapidly advancing and changing technologies, intense competition and a strong emphasis on intellectual property. We face substantial and increasing competition from large and specialty biopharmaceutical companies, as well as public and private medical research institutions and governmental agencies. Competitors may compete with us in hiring scientific and management personnel, establishing clinical study sites, recruiting patients to participate in clinical trials and acquiring technologies complementary to, or necessary for, our programs.

Our known biopharmaceutical competitors that are developing allogeneic CAR-NK or CAR-T cell therapies or T-cell engaging bispecific antibodies include, but may not be limited to, the following: Adicet Bio, Inc., Allogene Therapeutics, Inc., Amgen Inc., Autolus Therapeutics plc, Bristol-Myers Squibb Co, Cabaletta Bio, Inc., Candid Therapeutics, Inc., Caribou Biosciences, Inc., Cartesian Therapeutics, Inc., Century Therapeutics, Inc., Cullinan Therapeutics Inc., Fate Therapeutics, Inc., Galapagos NV, Gilead Sciences, Inc., Gracell Biopharmaceuticals, Inc. (acquired by AstraZeneca), GSK plc, iCell Gene Therapeutics Inc., ImmPACT Bio USA, Inc. (acquired by Lyell Immunopharma, Inc.), ITabMed Co., Ltd., Johnson & Johnson, Kyverna Therapeutics, Inc., Luminary Therapeutics, Inc., Merck & Co., Inc., Nkarta, Inc., Novartis AG, Regeneron Pharmaceuticals, Inc., Roche, Sana Biotechnology, Inc., Sanofi, Shoreline Biosciences Inc., Synthekine Inc., Takeda Pharmaceuticals Company Limited, Wugen, Inc. and Xencor, Inc.

Many of our current or potential competitors have significantly greater financial, technical and human resources, as well as more expertise in research and development, manufacturing, preclinical testing, conducting clinical studies and trials and commercializing and marketing approved products, than us. Mergers and acquisitions in the biopharmaceutical industry may result in even greater resource concentration among a smaller number of competitors. Smaller or early-stage companies may also prove to be significant competitors, either alone or through collaborative arrangements with large and established companies.

Our commercial opportunity could be reduced or eliminated if our competitors develop and commercialize products that are safer, more effective, have fewer or less severe side effects, are more convenient or are less expensive than any products that we may develop. Our competitors also may obtain FDA or other comparable foreign regulatory authority approval for their products more rapidly than us, which could result in our competitors establishing a strong market position before we are able to enter the market. Key competitive factors affecting the success of all of our programs are likely to be their efficacy, safety, convenience, price and degree of reimbursement.

Intellectual Property

Intellectual property is of vital importance in our field and in biotechnology generally. Our commercial success depends in part on our ability to obtain intellectual property that protects our product candidates and combinations of our product candidates with other therapeutics. We seek to protect and enhance proprietary technology, inventions and improvements that are commercially important to the development of our business by seeking, maintaining and defending U.S. and foreign patent rights, whether developed internally or licensed from third parties.

We are actively building our intellectual property portfolio around our product candidates and our discovery programs, based on our own intellectual property and licensed intellectual property. One important step in building our current portfolio was executing the Core Agreement, described below, with GC Cell. The Core Agreement grants us an exclusive, royalty-bearing license, with the right to sublicense through multiple tiers, to certain intellectual property and technology owned or controlled by GC Cell relating to non-genetically modified and genetically modified NK cells, and culturing, engineering, and manufacturing thereof, to research, develop, manufacture, and commercialize NK cell pharmaceutical products anywhere in the world except for Asia, Australia

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and New Zealand (the Artiva Territory). Applications to date have been filed in the United States, Europe, Canada and Israel. Further, we intend to file patent applications relating to new technologies we develop, either ourselves or with our strategic partners. We also intend to continue to identify and license patents that provide protection and serve as an optimal platform to enhance our intellectual property and technology base.

Our current intellectual property estate is designed to provide multiple layers of protection, including (1) patent rights directed to innovative manufacturing processes and methods for generating therapeutic NK cells; (2) patent rights covering constructs for use in our CAR-NK candidates; and (3) patent rights covering methods of treatment for therapeutic indications using NK cells.

Our current patent portfolio as of March 1, 2025, includes seven patent families licensed from GC Cell that primarily relate to innovative manufacturing processes and methods for generating therapeutic NK cells. These families disclose compositions and methods used in NK cell manufacturing processes, as well as resulting products and therapeutic compositions, along with methods of treating cancer using these products and therapeutic compositions.

Our current patent estate as of March 1, 2025, includes three patent families licensed from GC Cell, three patent families we co-own with GC Cell, and one patent family that we own covering constructs for use in our CAR-NK programs. Two of the families we license from GC Cell relate to particular CAR components. The first of these includes pending applications in the United States, Europe, and Canada, and any patents that issue from these pending applications are expected to expire in 2037, without accounting for potentially available patent term adjustment or extensions, and assuming payment of appropriate maintenance, renewal, annuity, or other fees; the second of these includes a pending application in the United States, and any patents that issue from this pending application are expected to expire in 2042, without accounting for potentially available patent term adjustment or extensions, and assuming payment of appropriate maintenance, renewal, annuity, or other fees. The third family we license from GC Cell relates to a novel anti-HER2 antibody or antigen-binding fragment and includes three issued U.S. patents and pending applications in the United States, Europe, Canada, and Israel. The issued U.S. patents are expected to expire in 2038, and any patents that issue from the pending patent applications in these licensed families are expected to expire between 2038 and 2041, without accounting for potentially available patent term adjustments or extensions and assuming payment of appropriate maintenance, renewal, annuity or other fees. Two of the families we co-own with GC Cell relate to cells and constructs encoding IL-15 and a CAR utilizing the novel anti-HER2 antigen binding fragment we license from GC Cell and methods of treatment using these cells and constructs. The first of these families includes pending applications in the United States, Europe, Israel, and Canada, and any patents that issue from these pending applications are expected to expire in 2042, without accounting for potentially available patent term adjustment or extensions, and assuming payment of appropriate maintenance, renewal, annuity, or other fees; the second of these families includes pending applications in the United States, Thailand, Singapore, Israel, Indonesia, Europe, China, Canada, and Australia, and any patents that issue from these pending applications are expected to expire in 2043, without accounting for potentially available patent term adjustment or extensions, and assuming payment of appropriate maintenance, renewal, annuity, or other fees. The third family we co-own with GC Cell relates to our anti-CD19 CAR-NK cell products and includes pending applications in the United States and Europe; any patents that issue from these pending applications are expected to expire in 2042, without accounting for potentially available patent term adjustment or extensions, and assuming payment of appropriate maintenance, renewal, annuity, or other fees. The patent family that we own relates to a novel antibody or antigen binding fragment and includes a pending PCT application. Although no patents have yet issued from this owned patent family, we expect the term of any patents that may issue from the pending patent applications in this family to extend to at least 2043, without accounting for potentially available patent term adjustments or extensions and assuming payment of appropriate maintenance, renewal, annuity or other governmental fees.

Our current patent estate as of March 1, 2025, includes twelve patent families related to NK cells and to methods of treatment using NK cells in addition to a therapeutic antibody. The first family, which is co-owned by GC Cell and Incyte Corporation, relates to pharmaceutical combinations for treating tumors comprised of anti-CD19 antibody and NK cells. This family includes pending applications in Canada, Europe, Israel, the United States, Eurasia, Mexico, Ukraine, and South Africa; any patents that issue from these pending applications are expected to expire in 2039, without accounting for potentially available patent term adjustment or extensions, and assuming payment of appropriate maintenance, renewal, annuity, or other fees. The second family, which we co-own with GC Cell, relates to the treatment of cancer with NK cells and a CD20 targeted antibody. This family includes pending applications in the United States and Europe; any patents that issue from these pending applications are expected to expire in 2041, without accounting for potentially available patent term adjustment or extensions, and assuming

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payment of appropriate maintenance, renewal, annuity, or other fees. The third and fourth families, which we own, relate to the treatment of autoimmune indications with NK cells and therapeutic antibodies and includes a pending PCT application and a pending U.S. provisional application; any patents that issue from these pending applications are expected to expire in 2044 and 2045, respectively, without accounting for potentially available patent term adjustment or extensions, and assuming payment of appropriate maintenance, renewal, annuity, or other fees. The fifth and sixth families, which we own, relate to methods of treatment using NK cells in combination with other therapeutics. The fourth family includes a pending U.S. provisional application; any patents that issue from applications that claim priority to this provisional application are expected to expire in 2044, without accounting for potentially available patent term adjustment or extensions, and assuming payment of appropriate maintenance, renewal, annuity, or other fees. The fifth family includes a pending PCT application; any patents that issue from this pending application are expected to expire in 2044, without accounting for potentially available patent term adjustment or extensions, and assuming payment of appropriate maintenance, renewal, annuity, or other fees. The seventh family, which we own, relates to engineered NK cells and methods of treatment and includes a pending U.S. provisional application; any patents that issue from applications that claim priority to this provisional application expected to expire in 2045, without accounting for potentially available patent term adjustment or extensions, and assuming payment of appropriate maintenance, renewal, annuity, or other fees. The other five patent families, which we co-own with GC Cell, relate to NK cells and to additional combinations of NK cells and therapeutic antibodies directed to various targets. Of these, the first family includes pending applications in the United States, Europe, Canada, and Israel; any patents that issue from these pending applications are expected to expire in 2041, without accounting for potentially available patent term adjustment or extensions, and assuming payment of appropriate maintenance, renewal, annuity, or other fees. The remaining families each include pending applications in the United States, Europe, Australia, China, Japan, and Korea; any patents that issue from these pending applications are expected to expire in 2042, without accounting for potentially available patent term adjustment or extensions, and assuming payment of appropriate maintenance, renewal, annuity, or other fees.

Our current patent estate as of March,1 2025, also includes a patent family co-owned by us, Affimed GmbH and GC Cell related to therapeutic compositions and methods of treating cancer using NK cells in combination with one of Affimed’s innate cell engagers. This family includes pending applications in the United States, Australia, Canada, China, Europe, Israel, India, Japan, and Korea. We expect the term of any patents that issue from the pending patent applications in this family to extend until at least 2042, without accounting for potentially available patent term adjustment or extension and assuming payment of appropriate maintenance, renewal, annuity or other governmental fees.

With respect to both licensed and company-owned intellectual property, we cannot be sure that patents will be granted with respect to any of our pending patent applications or with respect to any patent applications filed by us in the future, nor can we be sure that any of our existing patents or any patents that may be granted to us in the future will be commercially useful in protecting our commercial products and methods of manufacturing the same.

The term of individual patents depends upon the legal term of the patents in the countries in which they are obtained. In most countries in which we file, the patent term is 20 years from the date of filing of the first non-provisional application to which priority is claimed. In the United States, patent term may be lengthened by patent term adjustment, which compensates a patentee for administrative delays by the U.S. Patent and Trademark Office (USPTO) in granting a patent, or may be shortened if a patent is terminally disclaimed over an earlier-filed patent. In the United States, the term of a patent that covers an FDA-approved drug may also be eligible for a patent term extension of up to five years under the Drug Price Competition and Patent Term Restoration Act of 1984 (the Hatch-Waxman Act), which is designed to compensate for the patent term lost during the FDA regulatory review process. The length of the patent term extension is calculated based on the length of time it takes for regulatory review. A patent term extension under the Hatch-Waxman Act cannot extend the remaining term of a patent beyond a total of 14 years from the date of product approval and only one patent applicable to an approved drug may be extended. Moreover, a patent can only be extended once, and thus, if a single patent is applicable to multiple products, it can only be extended based on one product. Similar provisions are available in Europe and certain other foreign jurisdictions to extend the term of a patent that covers an approved drug. When possible, depending upon the length of clinical trials and other factors involved in the filing of a biologics license application (BLA), we expect to apply for patent term extensions for patents covering our product candidates and their methods of use.

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In addition to patent protection, we also seek to rely on regulatory protection and exclusivities. For instance, we intend to rely on the 12-year period for marketing exclusivity in the United States, and similar marketing exclusivities in other countries, to prevent competitors from obtaining regulatory approval for our products.

We also rely on trademarks, trade secrets, know-how, continuing technological innovation, confidentiality agreements, and invention assignment agreements to develop and maintain our proprietary position. The confidentiality agreements are designed to protect our proprietary information and the invention assignment agreements are designed to grant us ownership of technologies that are developed for us by our employees, consultants, or other third parties. We seek to preserve the integrity and confidentiality of our data and trade secrets by maintaining physical security of our premises and physical and electronic security of our information technology systems. While we have confidence in our agreements and security measures, either may be breached, and we may not have adequate remedies. In addition, our trade secrets may otherwise become known or independently discovered by competitors.

Our commercial success also depends in part on our ability to operate without infringing on the proprietary rights of others and to prevent others from infringing our proprietary rights.

Collaboration and License Agreements

GC Cell and Related Agreements

We have entered into several agreements with GC Cell and related entities concerning our platform NK cell technology and manufacturing of our core products, as described below.

Option and License Agreement with GC Cell

In September 2019, we entered into an option and license agreement with GC Cell, as amended in June 2020 and February 2022 (Core Agreement). Under the Core Agreement, GC Cell granted us an exclusive, royalty-bearing license, with the right to sublicense through multiple tiers, under certain intellectual property and technology owned or controlled by GC Cell relating to non-genetically modified and genetically modified NK cells, and culturing, engineering, manufacturing thereof, to research, develop, manufacture and commercialize NK cell pharmaceutical products in the Artiva Territory. GC Cell retained rights under the license to allow it and its affiliates to perform obligations under the Core Agreement and other agreements between us and them.

Under the Core Agreement, GC Cell agreed to conduct a discovery, research, preclinical development and manufacturing program under a plan approved by a Joint Research Steering Committee (JSC), to generate and identify product candidates for nomination as option candidates. GC Cell will bear all costs for its work under the R&D Plan, except that we will bear all costs for completing IND-enabling activities performed by GC Cell on behalf of us, other than certain efficacy studies.

For each product candidate determined by the JSC to be an option candidate, we have an exclusive option under the Core Agreement to obtain an exclusive, sublicensable license to research, develop, manufacture and commercialize such candidate in the Artiva Territory for any therapeutic, prophylactic or diagnostic uses in humans, on economic terms to be determined in good faith by the parties. GC Cell retains exclusive rights to the licensed technology in Asia, Australia and New Zealand, though we have the right to request, and GC Cell has agreed to consider in good faith, inclusion of Australia, New Zealand and/or specific countries in Asia in the Artiva Territory on a product-by-product basis. If we elect not to exercise the option with respect to a particular option candidate, GC Cell retains the right to continue development of such candidate. To-date, we have exercised our rights to license four option candidates, including AlloNK (AB-101), AB-201 and AB-205.

We have control over and will bear the costs of the development, regulatory, manufacturing and commercialization activities relating to the option candidates for which we have exercised our option, each a licensed product. Accordingly, we have certain diligence obligations and must use commercially reasonable efforts to develop and seek regulatory approval for each licensed product in at least one indication in the United States and the EU, and following regulatory approval in a country, to commercialize such licensed product in at least one indication in such country. The Core Agreement provides that we have the right to engage GC Cell or its appropriate

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affiliate to provide research and manufacturing services for the licensed products being developed by us in the Artiva Territory under separately executed service agreements.

Under the Core Agreement, we are obligated to pay a low single-digit percentage royalty on net sales of any licensed products, the manufacture, use or sale of which is claimed by or uses any Core IP. The royalty rate is subject to reduction under certain scenarios, and royalties are payable on a product-by-product and country-by-country basis, beginning with the first commercial sale of a licensed product and continuing until the later of (i) expiration of the last-to-expire claim of the licensed patents and jointly owned patents in the country of sale; (ii) expiration of any regulatory exclusivity for a licensed product in that country; and (iii) the tenth anniversary of the first commercial sale of a licensed product in that country. We also have the exclusive option to extend our license to the Core IP to be worldwide with respect to products originated from us in exchange for a specified increase in the applicable royalty. GC Cell is also obligated to pay us a royalty at a rate equal to 50% of the royalty payable by us for such product in the Artiva Territory on net sales outside the Artiva Territory of any licensed product, the manufacture, use or sale of which is claimed by or uses any jointly owned intellectual property.

The Core Agreement will remain in effect until the expiration of the last-to-expire royalty payment obligations. The last to expire patents (or any patents that issue from pending applications) underlying the royalty payment obligations under the Core Agreement are currently expected to expire by 2042, without accounting for potentially available patent term extensions or adjustments. We have the right to terminate the Core Agreement for any reason upon 90 days’ written notice. Either party may terminate the Core Agreement upon the other party’s uncured material breach, bankruptcy or insolvency. Upon termination of the Core Agreement for any reason other than uncured material breach by GC Cell, we must (i) assign and transfer all regulatory materials and approvals relating to any licensed product to GC Cell, and (ii) grant GC Cell a right of reference and use to all pre-clinical and clinical data relating to any licensed product, except that both (i) and (ii) only apply to licensed products that were developed at least in part by GC Cell, or were developed by a third party, and are claimed by or use licensed GC Cell technology. If the Core Agreement is terminated by GC Cell due to an uncured material breach, bankruptcy or insolvency, sublicensees may receive a direct license from GC Cell.

AB-101 Selected Product License Agreement

In November 2019, we entered into a license agreement with GC Cell for our AB-101 product candidate, as amended in February 2022 (the AB-101 Agreement). AB-101 is the first product for which we exercised our option under the Core Agreement. Under the AB-101 Agreement, GC Cell granted us an exclusive, royalty-bearing license in the Artiva Territory, with the right to sublicense through multiple tiers, under certain intellectual property and technology owned or controlled by GC Cell, to research, develop, manufacture and commercialize AB-101.

Under the AB-101 Agreement, we are obligated to pay tiered royalties in the low-mid to high single-digit percentage range on annual net sales of any licensed AB-101 products. The royalty rate is subject to reduction under certain scenarios, and royalties are payable on a product-by-product and country-by-country basis, beginning with the first commercial sale of a licensed AB-101 product and continuing until the later of (i) expiration of the last-to-expire claim of the licensed patents and jointly owned patents in the country of sale; (ii) expiration of any regulatory exclusivity for a licensed product in that country; and (iii) the tenth anniversary of the first commercial sale of a licensed product in that country. We are also obligated to make milestone payments to GC Cell of (i) up to $22.0 million upon the first achievement of certain development milestones, and (ii) up to $55.0 million upon the first achievement of certain sales milestones. GC Cell is also obligated to pay us a royalty at a rate equal to 50% of the royalty payable by us for such product in the Artiva Territory on net sales outside the Artiva Territory of any licensed AB-101 product, the manufacture, use or sale of which is claimed by or uses any jointly owned intellectual property.

The AB-101 Agreement will remain in effect until the expiration of the last-to-expire royalty payment obligations. The last to expire patents (or any patents that issue from pending applications) underlying the royalty payment obligations under the AB-101 Agreement for AB-101 are currently expected to expire by 2042, without accounting for potentially available patent term extensions or adjustments. We have the right to terminate the AB-101 Agreement for any reason upon 90 days’ written notice. Either party may terminate the AB-101 Agreement upon the other party’s uncured material breach, bankruptcy or insolvency. Upon termination of the AB-101 Agreement for any reason other than uncured material breach by GC Cell, we must (i) assign and transfer all

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regulatory materials and approvals relating to AB-101 to GC Cell, and (ii) grant GC Cell a right of reference and use to all pre-clinical and clinical data relating to AB-101.

AB-201 Selected Product License Agreement

In October 2020, we entered into a license agreement with GC Cell for our AB-201 product candidate, as amended in February 2022 and September 2023 (the AB-201 Agreement). AB-201 is the second product for which we exercised our option under the Core Agreement. Under the AB-201 Agreement, GC Cell granted us an exclusive, royalty-bearing license in the Artiva Territory, with the right to sublicense through multiple tiers, under certain intellectual property and technology owned or controlled by GC Cell, to research, develop, manufacture and commercialize AB-201.