JSPR US Equity☆

UNITED

STATES

SECURITIES

AND EXCHANGE COMMISSION

Washington,

D.C. 20549

FORM

10-K

(Mark

One)

☒ANNUAL REPORT PURSUANT TO SECTION 13 OR 15(d) OF THE SECURITIES EXCHANGE ACT OF 1934

For

the fiscal year ended December 31, 2025

OR

☐TRANSITION REPORT PURSUANT TO SECTION 13 OR 15(d) OF THE SECURITIES EXCHANGE ACT OF 1934

For

the transition period from ______________ to ______________

Commission

File Number: 001-39138

JASPER

THERAPEUTICS, INC.

(Exact

name of registrant as specified in its charter)

(Address of principal executive offices) (Zip Code)

(Registrant’s telephone number, including area code)

Securities

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

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

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 Section 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, a 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 Act). Yes ☐ No ☒

The

aggregate market value of the voting and non-voting common equity held by non-affiliates of the registrant as of June 30, 2025 (the last

business day of the registrant’s most recently completed second fiscal quarter) was approximately $74.8 million based on the closing

price of the registrant’s common stock on June 30, 2025 of $5.55 per share, as reported by the Nasdaq Capital Market.

As of March 25, 2026, the number of shares of the

registrant’s common stock outstanding was 27,996,819 shares of voting common stock, $0.0001 par value per share, and no shares of

non-voting common stock, $0.0001 par value per share.

DOCUMENTS

INCORPORATED BY REFERENCE

None.

TABLE

OF CONTENTS

PART I

Item 1. Business 1

Item 1A. Risk Factors 30

Item 1B. Unresolved Staff Comments 97

Item 1C. Cybersecurity 97

Item 2. Properties 98

Item 3. Legal Proceedings 98

Item 4. Mine Safety Disclosures 98

PART II

Item 6. [Reserved] 99

Item 7A. Quantitative and Qualitative Disclosures About Market Risk 117

Item 8. Financial Statements and Supplementary Data F-1

Item 9A. Controls and Procedures 118

Item 9B. Other Information 118

Item 9C. Disclosure Regarding Foreign Jurisdictions that Prevent Inspections 118

PART III

Item 10. Directors, Executive Officers and Corporate Governance 119

Item 11. Executive Compensation 119

PART IV

Item 14. Principal Accountant Fees and Services 120

Item 15. Exhibit and Financial Statement Schedules 120

i

JASPER

THERAPEUTICS, INC.

As

used in this Annual Report on Form 10-K, unless the context requires otherwise, references to the “Company”, “Jasper”,

“we”, “us”, “our”, and similar terms refer to Jasper Therapeutics, Inc., a Delaware corporation formerly

known as Amplitude Healthcare Acquisition Corporation (“AMHC”), and its consolidated subsidiary.

Unless

otherwise noted or the context requires otherwise, references to our “common stock” refer to our voting common stock, par

value $0.0001 per share. In addition, except as otherwise indicated, all information in this Annual Report on Form 10-K gives effect

to the 1-for-10 reverse stock split of the common stock that was effected on January 4, 2024.

CAUTIONARY

NOTE REGARDING FORWARD-LOOKING STATEMENTS

Certain

statements contained in this Annual Report on Form 10-K may constitute “forward-looking statements” for purposes of federal

securities laws. Such statements can be identified by the fact that they do not relate strictly to historical or current facts. In addition,

any statements that refer to projections, forecasts or other characterizations of future events or circumstances, including any underlying

assumptions, are forward-looking statements. The words “anticipate,” “believe,” “contemplate,”

“continue,” “could,” “estimate,” “expect,” “intends,”

“may,” “might,” “plan,” “possible,” “potential,”

“predict,” “project,” “should,” “will,” “would”

and similar expressions (including the negative of any of the foregoing) may identify forward-looking statements, but the absence of

these words does not mean that a statement is not forward-looking.

Forward-looking

statements in this Annual Report on Form 10-K may include, for example, but are not limited to, statements about:

● our ability to research, discover and develop additional product candidates;

● our public securities’ potential liquidity and trading;

● our ability to grow and manage growth profitably;

ii

● our ability to identify, in-license or acquire additional technology;

● our ability to continue as a going concern; and

● the volatility of the trading price of our common stock.

These

forward-looking statements are based on current expectations and beliefs concerning future developments and their potential effects.

There can be no assurance that future developments affecting us will be those that we have anticipated. These forward-looking statements

involve a number of risks, uncertainties (some of which are beyond our control) or other assumptions that may cause actual results or

performance to be materially different from those expressed or implied by these forward-looking statements. These risks and uncertainties

include, but are not limited to, those factors described under the heading “Risk Factors” in this Annual Report on Form 10-K.

Should one or more of these risks or uncertainties materialize, or should any of our assumptions prove incorrect, actual results may

vary in material respects from those projected in these forward-looking statements. Some of these risks and uncertainties may in the

future be amplified, and there may be additional risks that we consider immaterial or which are unknown. It is not possible to predict

or identify all such risks. Readers are cautioned not to place undue reliance on forward-looking statements because of the risks and

uncertainties related to them and to the risk factors. We do not undertake any obligation to update or revise any forward-looking statements,

whether as a result of new information, future events or otherwise, except as may be required under applicable securities laws.

iii

PART

I

ITEM

1. BUSINESS

Overview

We

are a clinical-stage biotechnology company focused on developing therapeutics targeting mast cell driven diseases such as Chronic Spontaneous

Urticaria (“CSU”), Chronic Inducible Urticaria (“CIndU”) and asthma and we continue to consider additional indications

in mast cell driven diseases for potential future development. We have also historically explored development programs in diseases where

targeting diseased hemopoietic stem cells can provide benefits, such as stem cell transplant conditioning regimens, but those programs

have been discontinued and we are exclusively focused on mast cell driven diseases.

Our lead product candidate, briquilimab, is a monoclonal

antibody designed to block stem cell factor (“SCF”) from binding to and signaling through the CD117 (“KIT”) receptor

on mast and stem cells. The SCF/KIT pathway is a survival signal for mast cells and we believe that blocking this pathway may lead to

depletion of these cells throughout the body, including in the lungs and in the skin, which could lead to significant clinical benefit

for patients with mast-cell driven diseases such as asthma and chronic urticarias. To that end, we are focusing on advancing a portfolio

of clinical programs in mast cell driven diseases. Development highlights include:

CSU

- BEACON Study

We

commenced the Phase 1b/2a BEACON study in CSU in late 2023. The BEACON study is a randomized, double-blind, and placebo-controlled Phase

1b/2a trial evaluating multiple ascending doses of briquilimab both as a single dose (“SD”) (240mg & 360mg) as well as

with repeat dosing (multiple dose levels from 10mg Q8W up to 240mg Q8W) as a therapy for adult patients with moderate to severe CSU.

We reported positive preliminary data from the first 8 dosing cohorts (10mg, 40mg, 80mg Q8W, 120mg Q8W & Q12W, 180mg Q8W & Q12W

and 240mg SD), in January 2025. We also reported preliminary data from 3 additional cohorts (360mg SD, 240mg Q8W and 240mg/180mg Q8W)

in July 2025, and reported additional positive preliminary data from new patients enrolled in the 240mg/180mg Q8W cohort in January 2026.

In general, data generated in the BEACON study has been positive with strong efficacy and a favorable safety profile observed in CSU

patients. Highlights of the BEACON study data presented in those updates were as follows:

● Briquilimab was well-tolerated and demonstrated a favorable safety profile:

o KIT-related adverse events (“AEs”) were generally transient, low-grade events;

1

While the data generated to date in the BEACON

study has generally been positive, in the July 2025 data update, results from the 240mg Q8W and the 240mg/180mg Q8W dose cohorts demonstrated

an atypical absence of UAS7 reduction in 11 of the 13 patients enrolled, and as a result, we launched an investigation into those two

cohorts. Factors examined included clinical site conduct, site dosing procedures, patient selection criteria, as well as potential product

lot variability in one lot of drug product first introduced into the BEACON study in those two cohorts. We also provided new clinical

drug supply from a different lot for ongoing dosing of existing patients and subsequently enrolled an additional 10 patients in aggregate

across those two cohorts. Based on the work conducted during the investigation, we concluded the anomalous efficacy results in these two

cohorts was not the result of any issues with the investigational product used, or from drug substance (“DS”) or drug product

(“DP”) manufacturing or distribution processes, but rather appeared to be an issue resulting from patient selection process/criteria

at certain clinical sites participating in the study. The conclusions reached as a result of the investigation were supported by expert

panels comprised of key opinion leaders in clinical development and antibody manufacturing that reviewed the findings and provided feedback

and recommendations on patient enrollment processes that are being integrated into the planned Phase 2b/3 CSU study to increase the likelihood

that CSU patients enrolled in the study would be more likely to have mast cell driven disease. These recommendations were incorporated

into enrollment of the additional patients in the 240mg Q8W and 240mg/180mg Q8W cohorts. Given the additional data reported in January

2026 for 6 patients dosed with briquilimab in the 240mg/180mgQ8W cohort showed deep and meaningful clinical responses with UAS7 reductions

of as much as 29 points observed and 4 of 6 participants (67%) reporting a complete response at 12 weeks, we believe these recommendations

have been effective and we are integrating them into our planned Phase 2b/3 CSU study.

CIndU

– SPOTLIGHT Study

In

early 2024, we commenced the Phase 1b/2a SPOTLIGHT study in CIndU. The SPOTLIGHT study is a Phase 1b/2a open label clinical trial evaluating

single doses of subcutaneous briquilimab in adult participants with cold urticaria or symptomatic dermographism, the two most prevalent

sub types of CIndU, who are refractory to antihistamines. The study enrolled 27 participants across three single dose cohorts of 40mg,

120mg, and 180mg. In October 2024, we presented positive preliminary data on the 40mg and 120mg cohorts from the study for a 6-week preliminary

analysis period following dosing, and in June 2025, we reported positive preliminary data from the 180mg single dose cohort at the 8-week

preliminary analysis period. Highlights of the data presented were as follows:

Open

Label Extension (OLE) Study

In

2025, we commenced an Open Label Extension study (the “OLE”) in which patients in the BEACON study in CSU and the SPOTLIGHT

study in CIndU were eligible to roll over to once they either completed their initial safety follow up period or experienced a return

of disease during the safety follow up period. All patients rolling over to the OLE study were treated with a 180mg Q8W dosing regimen.

In January 2026, we reported preliminary data from the OLE study in both CSU and CIndU patients.

2

Highlights

of the clinical efficacy observed in CSU and CIndU participants for the OLE study released in January 2026 were as follows:

Across

both CSU and CIndU participants in the OLE study, briquilimab continued to demonstrate a favorable safety profile:

● KIT-related AEs were generally transient, low-grade events;

Asthma

– ETESIAN Study

In

late 2024, we commenced a Phase 1b study in asthma, the “ETESIAN” study, which is a single dose double-blind, placebo-controlled

challenge study seeking to demonstrate proof-of-concept in asthma utilizing a potential therapeutic dose to inform future trials in the

broader asthma population. The study was conducted utilizing a single 180mg dose of subcutaneous briquilimab and key assessments included

measuring improvements in Forced Expiratory Volume in 1 second (“FEV1”) in both Early Asthmatic Response (“EAR”),

and Late Asthmatic Response (“LAR”) measured at 6 and 12 weeks, changes in airway hyperresponsiveness, mast cell depletion

and recovery, and safety.

In December 2025, we reported preliminary results

from the ETESIAN study in 14 participants (7 receiving a single dose of 180mg briquilimab and 7 receiving placebo) who completed at least

the 6 week allergen challenge assessment following dosing with investigational product or placebo. Highlights of the clinical response

observed in ETESIAN participants reported in December 2025 were as follows:

3

The positive proof of concept

data generated in the ETESIAN study supports further development in the broader asthma population, however, advancing any future clinical

studies in asthma would be based on an evaluation of the competitive landscape, the potential for strategic partnerships and capital availability.

Historically,

we have also evaluated briquilimab as a one-time conditioning therapy for severe combined immunodeficiency (“SCID”) patients

undergoing a second stem cell transplant for which we conducted a Phase 1/2 clinical trial as well as via Investigator Sponsored Trials

(“ISTs”) in several other stem cell transplant indications. In July 2025, we re-focused resources on our mast cell disease

development programs.

We

intend to become a fully integrated discovery, development and commercial company in the field of mast cell therapeutics. We are developing

our product candidates to be used individually or, in some cases, in combination with other therapeutics. Our goal is to advance our

product candidates through regulatory approval and bring them to the commercial market based on the data from our clinical trials and

communications with regulatory agencies and payor communities. We expect to continue to broaden our pipeline with additional mast cell

indications.

We

have an exclusive license agreement with Amgen Inc. (“Amgen”) for the development and commercialization of the briquilimab

monoclonal antibody in all indications and territories worldwide. We also have an exclusive license agreement with Stanford University

for the right to use briquilimab in the clearance of diseased stem cells prior to the transplantation of hematopoietic stem cells (“HSCs”).

Briquilimab

We believe briquilimab is a unique, humanized,

monoclonal antibody that targets the underlying biology of mast cell survival to potentially serve as a therapeutic to prevent mast cell

driven diseases. In addition, we believe briquilimab targets a key differentiation pathway for HSCs and may be developed to improve the

efficacy and safety of hematopoietic stem cell transplantation. Briquilimab binds to human KIT, the receptor for SCF, which is expressed

on the surface of various cells, including mast cells. The interaction of SCF and KIT is required for mast cells to survive. By blocking

SCF from binding to KIT and disrupting these critical signals, briquilimab leads to the depletion of mast cells in the skin. Briquilimab

is designed to bind to KIT with a greater affinity than SCF.

The monoclonal antibody isotype and other modifications

of briquilimab were chosen carefully to retain high affinity binding to the KIT receptor and SCF signal blockade without recruiting other

immune cells that could lead to receptor activation, mast cell degranulation or other off-target toxicities. For example, designing briquilimab

as an IgG1 isotype instead of an IgG2 isotype results in more potent inhibition of KIT, potentially increasing the effect on mast cell

depletion. Briquilimab was also designed to be aglycosylated in order to eliminate the recruitment of other immune effector cells that

may bring unwanted effects to any cell that expresses KIT. This finding and other data demonstrate that not all anti-KIT antibodies behave

equally or have the same mechanism of action.

We

are focused on advancing Briquilimab in development as a chronic therapy in mast cell driven diseases such as CSU, CIndU, asthma and

other mast cell driven indications currently under evaluation.

Briquilimab

as a Primary Therapeutic for Disorders of Mast Cells

Mast

cells are primary cells of the immune system derived from HSCs in the bone marrow. Mast cells store a number of different chemical mediators

such as tryptase, histamine, interleukins and heparin in granules found throughout the cell. When a mast cell is triggered, such as by

an allergen specific to membrane-bound Immunoglobulin E (“IgE”) antibodies, the mast cell is activated and releases the content

of the granules into the surrounding tissue. These chemical mediators attract other immune cells to help with any response as well as

produce a local allergic reaction consisting of inflammation, swelling, contraction of smooth muscle and increased mucus secretion. Mast

cells are usually long-lived and found at boundaries to the external environment such as the skin, mucosal surfaces of the gut and lungs

and eye.

4

Dysfunctional

regulation and activation of mast cells is thought to be a significant driver of multiple diseases, including urticarias, asthma, prurigo

nodularis, allergic eye disease and others. Each of these diseases has been shown to have local concentrations of mast cells, cellular

response consistent with mast cell degranulation and disease modification with use of antihistamines. Unfortunately, currently approved

agents targeting mast cells in these diseases are ineffective in many patients, leading to continued high disease burden.

Briquilimab blocks signaling on the KIT receptor

by inhibiting the binding of SCF, the ligand for the KIT receptor. The interaction of SCF/KIT on mast cells is critical for development,

proliferation and survival. Without continued signaling through KIT, mast cells will undergo apoptosis and die. We have shown that a single

subcutaneous dose of briquilimab leads to depletion of mast cells in the skin of healthy human volunteers for at least 29 days. We believe

that depletion of mast cells in the skin of patients with chronic urticaria or other mast cell driven diseases has the potential to lead

to improved disease control for those patients without adequate response to current therapies.

Figure

1 – Healthy volunteers administered single doses of briquilimab 42 mg to 280 mg subcutaneously received punch skin biopsies to

evaluate the decreases in mast cells at 4 weeks after briquilimab was administered compared to the baseline.

(1) Jasper internal data (Phase 1a, healthy volunteer study).

Briquilimab

in Chronic Urticaria

Mast

cells are immune cells that play a key role in the inflammatory response to pathogens or injury and are typically found in the skin,

lungs, digestive track, conjunctiva of the eye and the mucosal linings of the mouth and nose. Typically, mast cells are triggered by

a specific antigen or antibody interaction to release histamine, a variety of cytokines and other chemical mediators in order fight

a potential infection and to recruit additional types of immune cells to aid in the body’s response. However, with certain

diseases, such as CSU, CIndU, allergic asthma, prurigo nodularis and eosinophilic esophagitis, the mast cell response is

dysregulated and may lead to unwanted responses such as hives, itching, airway constriction or conjunctivitis. Current therapeutic

approaches to controlling mast cell response include antihistamines to counteract the release of histamine by activated mast cells,

anti-IgE antibody therapy to try to eliminate the antibodies responsible for a trigger of mast cell activation and inhibition of

other signaling pathways such as Bruton’s Tyrosine Kinase (“BTK”) or IL4/IL13 that may suppress mast cell

activation. We believe that new chronic therapies that target mast cells could be beneficial in treating many diseases that are a

function of mast cell dysfunction.

5

In late 2023, we commenced a Phase 1b/2a clinical

trial in patients with CSU. CSU is a disorder of mast cells in the skin in which patients experience swelling, redness and itching of

the skin that lasts at least six weeks due to either an unknown cause, Type I autoimmunity with IgE against self or Type IIb autoimmunity

with activating antibodies directed at mast cells. CSU is thought to affect over five million patients in the United States, France, Germany,

Italy, Spain, and the United Kingdom. The U.S. Food and Drug Administration (the “FDA”)-approved drug therapy for CSU

includes second generation H1-antihistamines for first line use followed by consideration for use of omalizumab, a monoclonal antibody

directed at circulating IgE; dupilumab, a monoclonal antibody directed at the IL-4 and IL-13 signaling pathways; and remibrutinib, a small

molecule inhibitor of BTK. The biologic rationale for these therapies is based on modulating mast cell response. Antihistamines work to

counteract the effects of histamine that is released from activated mast cells and the other agents are thought to remove or suppress

signaling pathways that trigger mast cell activation. Based on human healthy volunteer clinical data showing that briquilimab can deplete

mast cells from the skin and from data in a study of CSU patients showing that an anti-KIT antibody can control disease symptoms, we believe

that briquilimab could be effective therapy for CSU patients. The Phase 1b/2a study is a monotherapy study being conducted in CSU patients

who are refractory to antihistamine therapy and who have had an inadequate response to omalizumab. The study design has three parts. The

first part is an open-label 3+3 dose escalation with two dose cohorts (10mg and 40mg). The second part consists of seven dose cohorts

(80mg Q8W, 120mg Q8W, 120mg Q12W, 180mg Q8W, 180mg Q12W, 240mg Q8W and 240mg/180mg Q8W) in a double-blind placebo controlled format. The

final part is a single dose cohort with two dose levels being explored (240mg single-dose and 360mg single-dose) in a double-blind placebo

controlled format.

Figure

2 – Study design for the Phase 1b/2a BEACON study in CSU.

In

January 2025, we presented positive preliminary data from the first 8 dosing cohorts in this study (10mg, 40mg, 80mg Q8W, 120mg Q8W,

120mg Q12W, 180mg Q8W, 180mg Q12W, and 240mg single-dose). Average patient duration on study as of the cutoff date for the data presented

was approximately 28 weeks. Highlights of the data presented were as follows:

6

● Briquilimab was well-tolerated and demonstrated a favorable safety profile:

o KIT-related AEs were generally transient, low-grade events;

In

July 2025, we reported updated data from the Phase 1b/2a BEACON study in CSU with updates on the 240mg and 360mg single dose cohorts

as well as the 240mg Q8W and the 240mg/180mg Q8W cohorts. Highlights of the data update presented were as follows:

In

December 2025, we reported the completion of the investigation into the confounded efficacy results reported in July 2025 from the 240mg

Q8W and the 240mg/180mg Q8W cohorts of the BEACON study in CSU. Based on the work conducted, we concluded the anomalous efficacy results

in these two cohorts was not the result of any issues with the investigational product used, or from DS or DP manufacturing or distribution

processes, but rather appeared to be an issue resulting from patient selection process/criteria at certain clinical sites participating

in the study. This conclusion reflects, among other factors:

● a comprehensive review of manufacturing and distribution records;

7

● review of patient selection and enrollment processes;

● review of additional patient- and site-level data.

The conclusions reached as a result of the investigation were supported

by expert panels comprised of key opinion leaders in clinical development and antibody manufacturing that reviewed the findings and provided

feedback and recommendations that are being integrated into the planned Phase 2b/3 CSU study to increase the likelihood that CSU patients

enrolled in the study would be more likely to have mast cell driven disease.

In

January 2026, we reported updated data from the Phase 1b/2a BEACON study in CSU with updates on an additional 8 patients enrolled in

the 240mg/180mg Q8W cohort (6 on briquilimab and 2 on placebo). Highlights of the data update were as follows:

o KIT-related AEs were generally transient, low-grade events;

8

We

are also conducting a Phase 1b/2a clinical trial in patients with CIndU. Similar to CSU, CIndU is a disorder of mast cells in the skin

in which patients experience swelling, redness and itching of the skin that lasts at least six weeks, but CIndU is induced by specific

physical or environmental stimuli, including cold, heat, exercise, pressure, sunlight and others. CIndU includes physical urticarias,

such as symptomatic dermographism and cold urticaria, as well as non-physical urticarias caused by exposure to specific stimuli, such

as cholinergic urticaria and aquagenic urticaria.

The

FDA-approved drug therapy for CIndU consists solely of second generation H1-antihistamines. The biologic rationale for this therapy is

based on modulating mast cell response. Antihistamines work to counteract the effects of histamine that is released from activated mast

cells. CIndU is thought to affect over two million patients in the United States, France, Germany, Italy, Spain and the United Kingdom.

Approximately 40% of these patients’ CIndU is not controlled by first line antihistamines and these patients could be eligible

for biologic therapy depending on disease severity. Based on preclinical and human healthy volunteer clinical data showing that briquilimab

can deplete mast cells from the skin, we believe that briquilimab could be an effective therapeutic for CIndU patients. The Phase 1b/2a

study is a monotherapy study being conducted in CIndU patients who are refractory to antihistamine therapy. The study design contains

a single dose in three dosing cohorts (40mg, 120mg and 180mg) with a provocation test measured at various timepoints through 12 weeks

post-dosing.

Figure

3 – Study Design for the Phase 1b/2a SPOTLIGHT Study in CIndU

In

early 2024, we commenced the Phase 1b/2a SPOTLIGHT study in CIndU. In October 2024, we presented positive preliminary data on the 40mg

and 120mg cohorts from the study showing the following for the 6-week preliminary analysis period following dosing, as follows:

9

In

late 2024, we added a 180mg single dose cohort to the SPOTLIGHT study in CIndU. In June 2025, we reported positive preliminary data from

the 180mg single dose cohort, the highlights of which were as follows:

In

addition to the BEACON and SPOTLIGHT studies, we also commenced an Open Label Extension study (the “OLE”) in which patients

in the BEACON study in CSU and the SPOTLIGHT study in CIndU are eligible to roll over to once they have completed their initial safety

follow up period or experienced return of disease during the safety follow up period. All patients rolling over to the OLE study are

treated with a 180mg Q8W dosing regimen.

Figure

4 – Study Design for the OLE Study in CSU and CIndU

In January 2026, we reported preliminary

data from the OLE study in both CSU and CIndU patients. Highlights of the clinical efficacy observed in CSU and CIndU participants for

the OLE study released in January 2026 were as follows:

10

Across

both CSU and CIndU participants in the OLE study, briquilimab continued to demonstrate a favorable safety profile:

● KIT-related AEs were generally transient, low-grade events;

Briquilimab

in Asthma

Allergic

asthma is a form of asthma triggered by specific allergens that leads to constriction of smooth muscles in the airways, cellular infiltration

of various immune mediators and excess production of mucus. Patients with allergic asthma may have an increased number of mast cells

in the bronchi and mast cells are believed to not only be a direct driver of inflammation the asthmatic response, but to also be recruiters

of other cell types that contribute to that inflammation. Given these factors, we believe that asthma may be responsive to agents that

modulate mast cell response, including antihistamines and anti-IgE monoclonal antibody therapy.

In

late 2024, we commenced a Phase 1b clinical trial in patients with allergic asthma (the ETESIAN study). The Phase 1b study is a double-blind

placebo controlled single-dose monotherapy allergen challenge study being conducted in allergic asthma patients. Patients enrolled in

the study will either receive placebo, or a single 180mg dose of briquilimab. Endpoints evaluated will include both early and late asthmatic

response, as measured by % decrease in FEV1 relative to baseline, and change in airway hyperresponsiveness from baseline,

and both will be measured at 6 weeks post-dose and 12 weeks post-dose.

Figure

5 – Study Design for the Phase 1b ETESIAN study in Asthma

In December 2025, we reported preliminary results from the ETESIAN

study in 14 participants (7 receiving a single dose of 180mg briquilimab and 7 receiving placebo) who completed at least 6 weeks of allergen

challenge testing following dosing with investigational product. Highlights of the clinical response observed in ETESIAN participants

reported in December 2025 were as follows:

11

Figure

6 – Change in FEV1 observed in ETESIAN study

Figure

7 –Reduced eosinophil levels observed in participants receiving briquilimab in the ETESIAN study

The positive proof of concept

data generated in the ETESIAN study supports further development in the broader asthma population, however, advancing any future clinical

studies in asthma would be based on an evaluation of the competitive landscape, the potential for strategic partnerships and capital availability.

12

Briquilimab

in Other Mast Cell Disorders

Mast cells may also be the key cellular target

for a number of other inflammatory or autoimmune diseases outside of the chronic urticarias and asthma, such as atopic dermatitis, prurigo

nodularis and food allergies.

Atopic

dermatitis is a chronic disease that causes inflammation, redness, and irritation of the skin. It is a common condition that usually

begins in childhood; however, anyone can get the disease at any age. Atopic dermatitis causes the skin to become extremely itchy. In

most cases, there are periods of time when the disease is worse, called flares, followed by periods when the skin improves or clears

up entirely, called remissions. Treatments include moisturizers, topical steroids, immunomodulators (tacrolimus and pimecrolimus) and

biologic therapies (dupilumab). Mast cells may play an important role in the disease and agents that modulate mast cells may provide

benefit to patients.

Prurigo

Nodularis is also a disease that manifests in the skin. Patients develop severe itch and firm bumps on the skin, called nodules, that

may lead to loss of sleep and bleeding due to scratching. Degranulation of mast cells in the skin is thought to trigger peripheral sensory

neurons in the skin leading to itch. Various medications are used to treat Prurigo Nodularis including anti-itch creams and topical steroids.

For cases that remain uncontrolled physicians may prescribe antihistamines or biologics such as dupilumab.

Food

allergy is an immune-mediated disease characterized by an IgE-mediated response to specific dietary antigens, which leads to

allergic hypersensitivity reactions. In IgE-mediated food allergies, allergic reactions from exposure to the food result from receptor-bound

allergen-specific IgE antibodies binding to the food proteins, leading to the cross-linking of IgE receptors on mast cells and subsequently

mast cell activation and degranulation; resulting in the release of chemical mediators of inflammation. Symptoms of food allergy

can range from mild symptoms, such as hives and itching to potentially fatal systemic allergic reactions including anaphylaxis. Treatments

include antihistamines and steroids for mild to moderate reactions, epinephrine for severe reactions and anaphylaxis, as well as preventative

therapies such as oral immunotherapy or biologic therapies (omalizumab).

We

have performed pre-clinical evaluation of briquilimab as a potential therapeutic in these and a number of other mast cell driven diseases

and expect to continue to expand our portfolio of mast cell indications in clinical development in the future.

Briquilimab

in Non-Mast Cell Driven Disorders

Briquilimab

as a Conditioning Agent for SCID Patients Undergoing Re-Transplantation

We

historically funded a program developing briquilimab as a conditioning agent for SCID patients undergoing a stem cell re-transplantation.

Due to genetic errors at birth, SCID patients do not possess fully functional immune systems, which results in chronic infections, failure

to thrive and significantly decreased lifespans. If available, these patients are typically given a transplant from a close relative

with the goal of allowing healthy donor stem cells to establish in the patient’s bone marrow, leading to production of normal immune

cells. However, stem cell transplants are not universally successful. SCID patients with poor transplant outcomes are typically dependent

on external therapies such as intravenous immunoglobin (“IVIG”) and often have poor immunity, leading to chronic infections

and decreased lifespans. SCID patients who fail transplant are not usually given a second transplant due to their fragile health and

the significant toxicities of current conditioning agents.

We

conducted a Phase 1/2 dose escalation open label clinical trial to evaluate briquilimab as the sole conditioning agent to achieve HSC

engraftment in SCID patients undergoing stem cell re-transplantation. The primary endpoint in Phase 1 was to assess the safety and tolerability

of briquilimab as a conditioning agent in SCID patients. The two primary efficacy endpoints defined in the Phase 2 study are

the proportion of patients achieving adequate donor HSC engraftment and the proportion of patients achieving naïve CD4+ T cell production

greater than or equal to 85 cells/uL, a level expected to provide immune reconstitution, during weeks 36 to 104 post-transplant. Secondary

endpoints include durability of naïve T cell production, incidence and severity of GvHD, hematopoietic recovery and pharmacokinetic

properties of briquilimab. Patients received a single intravenous infusion of briquilimab on study day 0 in one of four dose cohorts:

0.1 mg/kg, 0.3 mg/kg, 0.6mg/kg or 1.0 mg/kg. Patients were to potentially be followed for up to five years following transplant.

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We

believe briquilimab has enabled immune reconstitution for patients based on naïve CD4+ T-cell levels and has shown clinical benefit

in T-B-SCID patients in a re-transplant setting. Patients have shown resolution of chronic infections, independence from or reduction

of IVIG therapy and antibody response to vaccine challenge. Through December 31, 2024, in this open label clinical trial, eleven T-B-SCID

re-transplant patients have been treated in the ongoing SCID Phase 1/2 study. Seven of the eleven transplanted patients with 1-

5 years of follow-up have shown engraftment of donor cells and production of functional immune cells. No briquilimab treatment-related

“SAEs” have been reported through December 31, 2023 in this clinical trial. In July 2025, the SCID program was discontinued

to focus resources exclusively on our mast cell disease development programs.

The

FDA has granted rare pediatric disease designation to briquilimab as a conditioning treatment for patients with SCID. In addition, both

the FDA and the European Medicines Agency (“EMA”) have granted orphan drug designation to briquilimab for conditioning treatment

prior to hematopoietic stem cell transplantation.

Stem

Cell Transplant Indications

We

have historically evaluated briquilimab in a number of stem cell transplant indications, including patients with Fanconi Anemia (“FA”),

Sickle Cell Disease (“SCD”), Chronic Granulomatous Disease (“CGD”), GATA-2 MDS and others through ISTs run by

partners including the National Institute of Health (“NIH”), the National Heart, Lung, and Blood Institute, the National

Institute of Allergy and Infectious Diseases, the National Cancer Institute and Stanford University.

While

promising data has been generated to date in FA, SCD, CGD and GATA-2 MDS, given our corporate focus on mast cell driven diseases, we

have discontinued these ISTs and we have no plans to pursue additional clinical development in these indications.

Our

Strategy

Our

goal is to develop and commercialize briquilimab as a safe and efficacious therapeutic to address the significant unmet medical need

for patients suffering from mast cell driven diseases such as CSU, CIndU and asthma. As part of our strategy, we aim to:

Build

a leading biotechnology company to enable cures via immune modulation. We are bringing together a team of biotech veterans, leading

academic institutions and a strong syndicate of healthcare-focused investors to achieve our vision of developing and commercializing

therapeutics with a focus on mast cell driven diseases.

Advance the development of briquilimab as

a chronic therapeutic in mast cell driven diseases. We are focused on developing briquilimab as a repeat dose therapy for disorders

of mast cells, such as CSU, CIndU, asthma and additional potential mast cell driven indications.

Commercialize

our product candidates to expand the use of effective and safe mast cell therapies for patients and physicians in our target markets.

If approved, we plan to bring our product candidates to the American, European and Japanese markets, focusing on the top physicians

who administer the majority of mast cell therapies.

Form

and strengthen strategic collaborations with leading industry and academic organizations to further develop our pipeline, unlock the

commercial potential of our portfolio and provide enabling technologies for collaborators. We intend to continue collaborations

with our existing partners and enter new strategic partnerships to develop additional candidates, generate evidence, and commercialize

new products in the field of mast cell therapies.

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Agreements

with Amgen

In November 2019, we entered into a worldwide exclusive

license agreement with Amgen for briquilimab (formerly AMG-191 and JSP191) in all indications and territories worldwide, which also includes

translational science and materials from Stanford University. We were assigned and accepted Amgen’s rights and obligations, effective

November 21, 2019, for the Investigator Sponsored Research Agreement (“ISRA”), entered into in June 2013, between Amgen

and The Board of Trustees of the Leland Stanford Junior University (“Stanford”) and Quality Agreement between Amgen and Stanford,

effective as of October 7, 2015. Under the ISRA, we received an option to negotiate a definitive license with Stanford for rights to certain

Stanford intellectual property related to the study of briquilimab in exchange for an option exercise fee of $1.0 million, payable over

a two-year period (the “Option”). We exercised the Option to Stanford docket S06-265 “Antibody-based clearance of endogenous

stem cell niches prior to transplantation of bone marrow or HSCs (KIT)” granted by Stanford under the ISRA on June 2, 2020. As a

result, we have worldwide exclusive rights to develop and commercialize briquilimab in all indications, including stem cell transplants.

The issued U.S. patents would be expected to expire in 2027, absent any applicable patent term extensions.

License

Agreement with Stanford

In

March 2021, we entered into an exclusive license agreement with respect to the use of briquilimab from the Stanford Office of Technology

Licensing to license U.S. Patent Application Serial Number 60/856,435, filed Nov. 3, 2006, and U.S. Patent Application Serial Number

12/447,634 (publication number US 2010/0226927 Al) and know-how for the purpose of depleting endogenous blood stem cells in patients

for whom hematopoietic cell transplantation is indicated.

Intellectual

Property

Our

success depends in part on our ability to obtain and maintain proprietary protection for our product candidates and other discoveries,

inventions, trade secrets and know-how that are critical to our business operations. It also depends in part on our ability to operate

without infringing the proprietary rights of others, and in part, on our ability to prevent others from infringing our proprietary rights.

We have a series of in-licensed patents outlined below with an additional pending patent application in the United States.

In-licensed

Amgen Portfolio

We have exclusively licensed a patent family from

Amgen applicable to our clinical development programs that contains patents and applications directed to a humanized KIT antibody. As

of March 25, 2026, this patent portfolio includes three issued U.S. patents and one European patent, as well as granted patents in Australia,

Canada, Japan, and Mexico, and pending patent applications in Europe and Hong Kong. The issued U.S. and European patents would be expected

to expire in 2027, absent any applicable patent term extensions.

In-licensed

Stanford Portfolio

We have an exclusive license in the field of use

of briquilimab for the purpose of depleting endogenous blood stem cells in patients for whom hematopoietic cell transplantation is indicated

to a patent family from Stanford University applicable to targeted conditioning that contains patents and applications directed to immunodepletion

of endogenous stem cell niche prior to hematopoietic stem cell transplantation. As of March 25, 2026, this patent portfolio includes two

issued U.S. patents and one European patent, as well as pending European and Hong Kong patent applications. The issued U.S. and European

patents would be expected to expire in 2027, absent any applicable patent term extensions.

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Jasper

Portfolio

As of March 25, 2026, we own two patent families

directed to compositions and/or methods for hematopoietic stem cell transplantation, one patent family directed to other methods of treating

certain hematopoietic malignancies, three patent families directed to treating mast cell-driven disease, and one patent family directed

to therapeutic efficacy testing models. These patent families include one pending U.S. provisional applications, three pending U.S. utility

applications, two pending Patent Cooperation Treaty applications, and applications pending certain other jurisdictions. Any patents that

grant from these applications would be expected to expire in 2042 to 2046, absent any applicable patent term extensions.

Additional

Intellectual Property

We

also rely on trade secrets, including know-how, confidential information, unpatented technologies and other proprietary information,

to strengthen or enhance our competitive position, and prevent competitors from reverse engineering or copying our technologies. We maintain,

as trade secrets, information relating our product candidates currently in development, as well as information related to our business

strategy and business methods. However, trade secrets and confidential know-how are difficult to protect. To avoid inadvertent and improper

disclosure of trade secrets, and to avoid the risks of former employees using these trade secrets to gain future employment, it is our

policy to require employees, consultants and independent contractors to assign to us all rights to intellectual property they develop

in connection with their employment with or services for us. We also protect our existing and developing intellectual property expressly

through confidentiality provisions in agreements with third parties. There can be no assurance, however, that these agreements will be

self-executing or otherwise provide meaningful protection for our trade secrets or other intellectual property or proprietary information,

or adequate remedies in the event of unauthorized use or disclosure of such trade secrets or other intellectual property or proprietary

information. We also seek to preserve the integrity and confidentiality of our trade secrets and other confidential information by maintaining

physical security of our premises and physical and electronic security of our information technology systems. While we have confidence

in the measures we take to protect and preserve our trade secrets, such measures can be breached, and we may not have adequate remedies

for any such breach. In addition, our trade secrets may otherwise become known or be independently discovered by competitors.

We

intend to pursue additional intellectual property protection to the extent we believe it would advance our business objectives, which

may include objectives within and outside the United States. Despite our efforts to protect our intellectual property rights these rights

may not be respected in the future or may be circumvented or challenged (and potentially invalidated) in a legal proceeding in any jurisdiction

where we have intellectual property rights. In addition, the laws of various foreign countries may not afford the same protections or

assurances to the same extent as the laws in the United States. See the section titled “Risk Factors — Risks Related to Our

Intellectual Property” for additional information regarding these and other risks related to intellectual property.

Competition

The

industry we operate in is highly competitive and dynamic, subject to rapid technological change. We have competition in the market for

both our product candidates and may face competition from large pharmaceutical and biotechnology companies, smaller pharmaceutical and

biotechnology companies, specialty pharmaceutical companies, generic drug companies, academic institutions, government agencies, research

institutions and others.

We

believe that our intellectual property, proprietary scientific knowledge, development experience and partnerships will provide us with

competitive advantages in the market we operate in.

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We