IMMX US Equity☆

Item 1A. Risk Factors 51

Item 1B. Unresolved Staff Comments 78

Item 2. Properties 79

Item 3. Legal Proceedings 79

Item 4. Mine Safety Disclosures 79

Part II

Item 6. [Reserved] 80

Item 7A. Quantitative and Qualitative Disclosures about Market Risk 86

Item 8. Financial Statements and Supplementary Data F-1

Item 9A. Controls and Procedures 87

Item 9B. Other Information 87

Item 9C. Disclosure Regarding Foreign Jurisdictions that Prevent Inspections 88

Part III

Item 10. Directors, Executive Officers and Corporate Governance 88

Item 11. Executive Compensation 88

Item 14. Principal Accountant Fees and Services 88

Part IV

Item 15. Exhibits and Financial Statement Schedules 89

Signatures 91

CAUTIONARY

NOTE ON FORWARD-LOOKING STATEMENTS

This

Annual Report on Form 10-K contains forward-looking statements which are made pursuant to the safe harbor provisions of Section 27A of

the Securities Act of 1933, as amended (the “Securities Act”), and Section 21E of the Securities Exchange Act of 1934, as

amended (the “Exchange Act”). These statements may be identified by such forward-looking terminology as “may,”

“should,” “expects,” “intends,” “plans,” “anticipates,” “believes,”

“estimates,” “predicts,” “potential,” “continue” or the negative of these terms or other

comparable terminology. Our forward-looking statements are based on a series of expectations, assumptions, estimates and projections

about our company, are not guarantees of future results or performance and involve substantial risks and uncertainty. We may not actually

achieve the plans, intentions or expectations disclosed in these forward-looking statements. Actual results or events could differ materially

from the plans, intentions and expectations disclosed in these forward-looking statements. Our business and our forward-looking statements

involve substantial known and unknown risks and uncertainties, including the risks and uncertainties inherent in our statements regarding:

● our projected financial position and estimated cash burn rate;

● our estimates regarding expenses, future revenues and capital requirements;

● our ability to continue as a going concern;

● our need to raise substantial additional capital to fund our operations;

● the success, cost and timing of our clinical trials;

● our dependence on third parties in the conduct of our clinical trials;

● the results of market research conducted by us or others;

● our reliance on third-party suppliers and manufacturers;

● the success of competing therapies and products that are or become available;

All

of our forward-looking statements are as of the date of this Annual Report on Form 10-K only. In each case, actual results may differ

materially from such forward-looking information. We can give no assurance that such expectations or forward-looking statements will

prove to be correct. An occurrence of, or any material adverse change in, one or more of the risk factors or risks and uncertainties

referred to in this Annual Report on Form 10-K or included in our other public disclosures or our other periodic reports or other documents

or filings filed with or furnished to the U.S. Securities and Exchange Commission (the “SEC”) could materially and adversely

affect our business, prospects, financial condition and results of operations. Except as required by law, we do not undertake or plan

to update or revise any such forward-looking statements to reflect actual results, changes in plans, assumptions, estimates or projections

or other circumstances affecting such forward-looking statements occurring after the date of this Annual Report on Form 10-K, even if

such results, changes or circumstances make it clear that any forward-looking information will not be realized. Any public statements

or disclosures by us following this Annual Report on Form 10-K that modify or impact any of the forward-looking statements contained

in this Annual Report on Form 10-K will be deemed to modify or supersede such statements in this Annual Report on Form 10-K.

This

Annual Report on Form 10-K may include market data and certain industry data and forecasts, which we may obtain from internal company

surveys, market research, consultant surveys, publicly available information, reports of governmental agencies and industry publications,

articles and surveys. Industry surveys, publications, consultant surveys and forecasts generally state that the information contained

therein has been obtained from sources believed to be reliable, but the accuracy and completeness of such information is not guaranteed.

While we believe that such studies and publications are reliable, we have not independently verified market and industry data from third-party

sources.

RISK

FACTOR SUMMARY

Our

business is subject to significant risks and uncertainties that make an investment in us speculative and risky. Below we summarize what

we believe are the principal risk factors but these risks are not the only ones we face, and you should carefully review and consider

the full discussion of our risk factors in the section titled “Risk Factors,” together with the other information in this

Annual Report on Form 10-K. If any of the following risks actually occurs (or if any of those listed elsewhere in this Annual Report

on Form 10-K occur), our business, reputation, financial condition, results of operations, revenue, and future prospects could be seriously

harmed. Additional risks and uncertainties that we are unaware of, or that we currently believe are not material, may also become important

factors that adversely affect our business.

Risks

Relating to Our Financial Position and Capital Needs

Risks

Relating to the Development and Regulatory Approval of Our Product Candidates

Risks

Relating to our Business and Operations

Risks

Relating to our Intellectual Property

Risks Related to Owning our Common Stock

PART

I

Throughout

this Annual Report on Form 10-K, references to “we,” “our,” “us,” the “Company,” “Immix,”

or “Immix Biopharma” refer to Immix Biopharma, Inc., individually, or as the context requires, collectively with its subsidiary.

ITEM

1. BUSINESS

Overview

We

are a clinical-stage biopharmaceutical company developing a novel class of Tissue-Specific Therapeutics (“TSTx”)TM in

oncology and inflammation. Our lead asset, IMX-110, is currently in Phase 1b/2a clinical trials for solid tumors in the United States

and Australia. IMX-110 is a negatively-charged TSTx that simultaneously disables resistance pathways with a poly-kinase inhibitor (which

inhibits multiple kinases simultaneously) and induces tumor cell death with an apoptosis inducer (which activates apoptosis, a non-inflammatory

programmed cell death pathway), leveraging our TME NormalizationTM Technology, delivered deep into the tumor micro-environment

(“TME”). Our proprietary System Multi-Action RegulaTors SMARxT Tissue-SpecificTM Platform produces

drugs that accumulate at intended therapeutic sites at 3-5 times the rate of conventional medicines. Our TME NormalizationTM Technology

allows our drug candidates to circulate in the bloodstream, exit through tumor blood vessels and simultaneously attack all components

of the TME. To date, we have not generated any revenues. Since inception, we have devoted substantially all of our resources to developing

product and technology rights, conducting research and development, organizing and staffing our Company, business planning and raising

capital.

Pipeline

Our

SMARxT Tissue-SpecificTM Platform has produced 3 drug candidates which we believe derisks the clinical development

of each subsequent candidate due to shared design elements across tolerability, chemistry, manufacturing and controls, regulatory understanding,

and multi-target therapeutic approach, the first of which is IMX-110, currently in Phase 1b/2a oncology clinical trials.

Figure

3: ImmixBio SMARxT Tissue-SpecificTM Platform – Pipeline

Our

Lead Product Candidate

IMX-110,

currently in Phase 1b/2a clinical trials, is a Tissue-Specific TherapeuticTM with TME NormalizationTM, a technology

that we are developing initially for soft tissue sarcoma (“STS”). Tumor growth is sustained by hypoxia (low oxygen concentration)

and acidosis (an excessively acidic condition) which produce recurring waves of activation of multiple kinases that upregulate NF-κB,

STAT3 and other key transcriptional factors which cause recurrent inflammation. This inflammatory environment activates the TME to provide

metabolic and structural support to the tumor and to recruit Treg T-cells (immune cells suppressing immune response) to suppress anti-tumor

immune response. IMX-110’s poly-kinase inhibitor polyphenol curcuminoid complex (“PCC”) halts this fundamental tumor-sustaining

inflammation by blocking multiple kinases and interfering with NF-κB and STAT3 activation, interrupting the positive feedback loop

underlying the inflammatory cycle. With tumor-sustaining inflammation halted, IMX-110’s apoptosis inducer (Polyethylene glycol

– phosphatidylethanolamine (“PEG-PE”)-doxorubicin complex) is then able to induce tumor cell death where conventional

therapies have been hampered by resistance caused by NF-κB and STAT3 activation.

As

of March 2022, we have treated 14 patients in our ongoing Phase 1b/2a clinical trial in the United States and Australia. 100% of these

patients received between 3 and 13 lines of therapy prior to IMX-110. Zero drug-related serious adverse events and zero dose interruptions

due to toxicity have been observed in our 1b/2a clinical trial to-date. In our trial, we observed radiological progression-free-survival

of 6 months in 50% of our STS patients, with a 4-month median progression free survival (“mPFS”) across all STS patients.

mPFS is the time that patients live without their cancer progressing. The trial includes patients with leiomyosarcoma, carcinosarcoma,

poorly differentiated soft tissue sarcoma, cholangiocarcinoma, colorectal cancer, prostate cancer, pancreatic cancer, esophageal cancer,

breast cancer, and nasopharyngeal cancer.

In

August 2021, we entered into a Clinical Collaboration and Supply Agreement with BeiGene Ltd. (“BeiGene”) for a combination

Phase 1b clinical trial in solid tumors of IMX-110 and anti-PD-1 Tislelizumab (the subject of a collaboration and license agreement among

BeiGene and Novartis). In genetic mouse models of pancreatic cancer, IMX-110 has demonstrated an immunomodulation effect, turning “cold”

tumors “hot,” and, in combination with murine anti-PD-1, IMX-110 produced extended survival versus multi-drug combinations.

The goal of this study is to demonstrate the potential for TSTx to be an integral component of combination therapies for a wide range

of advanced solid tumors. Pursuant to the terms of the agreement, we and BeiGene shall form a committee made up of an equal number

of individuals, but not more than two representatives of each of our Company and BeiGene, which shall, among other things, coordinate

activities with respect to the trial; provided, however, we shall be entitled to receive, review or approve any budgets or other costs

relating to the trial. Pursuant to the terms of the agreement, we shall be responsible for all costs associated with the manufacturing

and supply of IMX-110 for the trial as well as all costs associated with conducting the trial and BeiGene shall be responsible for costs

associated with supplying Tislelizumab for the trial. Notwithstanding the foregoing, if the Tislelizumab supplied by BeiGene is lost,

damaged or destroyed or becomes unable to comply with applicable specifications while under our control, BeiGene shall not be required

to replace such Tislelizumab and in the event BeiGene replaces such Tislelizumab, it may charge us a reasonable replacement cost. The

agreement shall continue until the earlier of (i) the one year anniversary of the date upon which we provide BeiGene with the trial’s

final clinical study report and (ii) the date of termination of the trial. In addition, either party may terminate the agreement

(i) upon 30 days prior written notice to the other party if, in the case of our Company, we cease the development of IMX-110 or, in the

case of BeiGene, it ceases the development, marketing and sale of Tislelizumab, (ii) upon written notice to the other party if there

have been one or more serious adverse events indicating a patient safety issue with continuing the trial, (iii) upon written notice to

the other party if a regulatory authority withdraws approval of IMX-110 or Tislelizumab, as applicable, and/or the trial, (iv) upon 60

days notice to the other party with or without reason, (v) immediately upon written notice to the other party if such other party consummates

a Change of Control Transaction (as defined in the agreement) and/or (vi) upon written notice to the other party in the event such other

party is in material breach of the agreement and has not cured such breach within 60 days after receipt of notice from the non-breaching

party. As of the date hereof, we have not paid any amounts to BeiGene.

In

September 2021, the United States Food and Drug Administration (“FDA”) granted Orphan Drug Designation (“ODD”)

to IMX-110 for the treatment of soft tissue sarcoma. If a product that has ODD subsequently receives the first FDA approval for the disease

for which it has such designation, the product is entitled to orphan drug exclusive approval (or exclusivity), which means that the FDA

may not approve any other applications to market the same drug for the same indication for 7 years (except in limited circumstances,

such as a showing of clinical superiority to the product with orphan drug exclusivity).

Our

Other Product Candidates

IMX-111

is a Tissue-Specific BiologicTM built on our TME NormalizationTM Technology with proprietary GLUT1 antibody biomarker

targeting coupled with our poly-kinase inhibitor / apoptosis inducer. IMX-111 takes advantage of the fact that GLUT1 is an essential

cancer biomarker that is overexpressed on 92% of colorectal cancer cells and other tumor types. Furthermore, the degree of its overexpression

correlates with more advanced stages of tumor progression. Building on the well-tolerated profile of our lead candidate from our ongoing

clinical trial, we believe IMX-111 is the first cancer therapeutic to be developed that takes advantage of GLUT1 overexpression

in cancer.

IMX-120

is a Tissue-Specific BiologicTM built on our Immune Normalization TechnologyTM for inflammatory bowel disease with

proprietary GLUT1 antibody biomarker targeting coupled with polyphenol poly-kinase inhibitors. IMX-120 takes advantage of the fact that

overexpression and activation of GLUT1 on overactive immune cells has been shown to be widely present in patients with inflammatory bowel

diseases (“IBD”). Similar to tumor growth, the inflammatory processes active in IBD are caused by recurring waves of activation

of multiple kinases that upregulate NF-κB, STAT3 and other key transcriptional factors. IMX-120’s polyphenol poly-kinase

inhibitors block upstream kinase signal transduction systems that activate NF-κB and STAT3. GLUT1 presents an ideal targeting moiety

(component of a drug) for these overactive immune cells, allowing for tissue-specific delivery of IMX-120.

Other

than IMX-110, the FDA has not given any indication as to whether any of our other product candidates will receive ODD.

Figure

4: ImmixBio SMARxT Tissue-SpecificTM Platform – Summary Rendering

Our

Platform and Technologies

Our

SMARxT Tissue-Specific Platform consists of 3 pillars: first, System-Tissue Biology Model Development, which allows us to

develop robust mechanisms of action in complex pathologies; second, Purpose-Built Physical Biochemistry Engine, which allows us to generate

actionable drug candidates; and third, Predictive Valuation Framework, which allows us to conduct highly predictive IND-enabling activities.

Figure

5: SMARxT Tissue-SpecificTM Platform Overview

Specifically,

the 3 pillars of our platform are:

1)

System-Tissue Biology Model Development: Interplay of cellular elements define and drive disease states. Based on transcriptional

and epigenetic factors operating in key cell types, we have built a proprietary model of network motifs driving human pathologies such

as cancer and auto-immune/inflammatory diseases. We believe this model represents the most complete view of biologic interrelationships

on an organismal and tissue level. We apply this model in the early stages of our drug development to overcome systemic factors that

have prevented traditional “targeted” therapies’ effectiveness in complex pathologies such as cancer and inflammatory

bowel disease.

2)

Purpose-Built Physical Biochemistry Engine: Traditional drug development focuses on “one drug, one target” approach.

In contrast, our proprietary physical biochemistry engine is designed to incorporate wide-ranging elements into our drug design, encompassing

a diverse target profile, allowing our drugs to operate simultaneously in time and space to jointly combat disease at the tissue and

organismal level.

3)

Predictive Validation Framework: Using our unique relationships and our internal expertise, we have developed a proprietary framework

of high-efficiency, rapid development in vitro and in vivo animal models that have high relatability to human disease,

minimizing the traditional poor predictive value of animal models.

The

application of the SMARxT Tissue-Specific Platform in oncology is TME NormalizationTM Technology, and in inflammation

is Immune NormalizationTM Technology.

Figure

6: TME NormalizationTM Technology

The

TME is made up of a tightly packed mass of: 1) cancer associated fibroblasts (“CAFs”), 2) tumor-associated macrophages/immune

cells (“TAMs”), and 3) cancer itself. The TME’s unique biophysical properties include regions of varying degrees of

hypoxia, acidosis and an immunosuppressive milieu. As cancer cells outgrow their blood supply, the resulting hypoxia and acidosis shift

their metabolism towards glycolysis, lactate and lipids. This, in turn, shapes the responses of proximal fibroblasts and resident immune

cells. Fibroblasts begin to secrete lactate that is taken up by nearby cancer cells and consumed as fuel. Lactate in the TME reprograms

the macrophages toward the M2 “tolerant” pro-inflammatory phenotype that drives immunosuppression. At the same time, the

TME hypoxia produces increased levels of reactive oxygen species that enhance tumorigenicity (tendency to form tumors) and immunosuppressive

functions of Treg T-cells, as well as resistance to immune drugs such as PD-1/PD-L1 inhibitors. Our TME NormalizationTM Technology

reverses the hypoxia- and acidosis-activated genetic programs in every cellular component of the TME, “normalizing” the TME,

and reactivating apoptosis cell death pathways. This technology offers an attractive opportunity to reshape the pathological niche that

is the TME and overcome the critical factors that have hampered available treatments to date.

Figure

7: Representation of the TME composed of CAFs, TAMs, and cancer cells

Our

TME NormalizationTM Technology causes tumor apoptosis, a non-inflammatory tumor-cell death (instead of necroptosis, which

results in repeat reignition of the inflammatory cascade leading to tumor progression). Thus, when the inflammatory cascade is inhibited,

tumor resistance can be suppressed, enabling tumor cell apoptosis by ImmixBio therapies.

We

believe that our TME NormalizationTM Technology is a promising direction of research that may enable a new generation of high-therapeutic

index drugs (drugs that have high relative safety as defined by the ratio of toxic to effective dose), unlocking additional therapeutic

benefit without adding toxicity.

IMX-110

- Tissue-Specific TherapeuticTM with TME NormalizationTM Technology

IMX-110

Market Opportunity

The

first potential indication we intend to pursue for IMX-110 is STS. STSs are cancers that arise from muscle, fat, nerves, fibrous tissues,

blood vessels or deep skin tissues. Globally, there are roughly 116,000 new cases of soft tissue sarcomas each year, of which 21,500

are in the European Union and 40,500 are in China. According to American Cancer Society, there were roughly 13,000 new cases of soft

tissue sarcomas in the United States during 2020. Approximately 160,000 people live with soft tissue cancers in the United States. The

five-year survival rate for all stages of STS is 65.0% in the United States, but this falls to 16.0% for patients with late-stage metastatic

disease.

The

global soft tissue sarcoma market is estimated to reach approximately $6.5 billion by 2030 from the estimated $2.9 billion in 2019. Drugs

used to treat STS include conventional doxorubicin, eribulin (marketed as Halaven®, by Eisai Co, Ltd), pazopanib (marketed as Votrient®,

by Novartis), and trabectedin (marketed as Yondelis®, by Janssen/Johnson & Johnson).

$898

million is the total publicly disclosed combined

annual sales of eribulin (Halaven®), pazopanib (Votrient®), and trabectedin (Yondelis®) according to the most recent available

annual reports.

Objective

response rates are increasingly considered as poor surrogates of clinical activity in STS. Therefore, lack of progression, or progression

free survival (“PFS”), is used as the primary measure of treatment success in STS.

Conventional

doxorubicin, in three separate studies as a first-line therapy, produced a mPFS (meaning the time patients live without their cancer

progressing) in STS patients of 2.5 months, 4.6 months, and 2.7 months according to Lorigan et al., 2007, Judson et al., 2014 and Chawla

et al., 2015.

Eribulin

(Halaven®), was trialed in a study in which 50% of patients received three or more lines of previous chemotherapy prior to eribulin.

Eribulin produced a mPFS in STS patients of 2.6 months according to Schöffski et al., 2016.

Pazopanib

(Votrient®), was trialed in a study in which 21% of patients received three or more lines of treatment prior to pazopanib. Pazopanib

produced a mPFS in STS patients of 4.6 months according to van der Graaf et al., 2012.

Trabectedin

(Yondelis®) was trialed in a study in which 12% of patients received three or more lines of chemotherapy prior to trabectedin. Trabectedin

produced a mPFS in STS patients of 4.2 months according to Demetri et al., 2016.

IMX-110

Clinical Data

As

of March 2022, we have treated 14 patients in our ongoing Phase 1b/2a clinical trial in the United States and Australia, of which 8 patients

completed a tumor measurement after the enrollment measurement. Of those 8 patients, a range of late-stage STSs were represented, including:

leiomyosarcoma, cholangiocarcinoma, carcinosarcoma, and poorly differentiated sarcoma.

4

months was the mPFS observed in STS patients treated with IMX-110 in the United States in our ongoing Phase 1b/2a clinical trial.

100%

of these patients received between 3 and 13 lines of therapy prior to IMX-110.

Zero

drug-related serious adverse events and zero dose interruptions due to toxicity have been observed in our 1b/2a clinical trial to-date.

Figure

8: IMX-110 Soft Tissue Sarcoma median Progression Free Survival and level of pre-treatment

In

our ongoing IMX-110 clinical trial:

- 100% of STS patients had controlled disease at 2 months.

Figure

9: IMX-110 Phase 1b/2a Clinical Trial Interim Patient Data:

75%

of Heavily Pretreated Soft Tissue Sarcoma Patients Experienced Tumor Shrinkage

Soft

Tissue Sarcoma % Change in Target Lesion Size from Baseline (Left)

Soft

Tissue Sarcoma Best % Change from Baseline in Size of Target Lesions (Center)

Non-Sarcoma

Cancers % Change in Target Lesion Size from Baseline (Right)

(Source:

Immix Biopharma, Inc. ImmixBio has evaluable data for 8 patients as of March 2022 (out of n=14, the remaining 6 did not complete any

tumor measurements after enrollment scan). All 8 evaluable patients have discontinued treatment. “Heavily Pretreated” refers

to 3-13 lines of therapy. Dose expressed in mg/m2. Our employees were involved in the design of this study and the results

are unpublished.)

In

addition to IMX-110 STS data, a colorectal cancer patient originally considered for hospice was subsequently treated with IMX-110 for

10 months with zero serious drug-related adverse events. This patient experienced 4 month PFS on half of what we expect to be IMX-110’s

recommended Phase 2 therapeutic dose.

IMX-110

Development Strategy

Figure

10: IMX-110: Direct Path To 1st Line Therapy In Soft Tissue Sarcoma – Clinical Trial Plan

We

plan to treat an additional 30 STS patients in our Phase 2a trial with IMX-110 as a first-line therapy.

We

expect our Phase 2a trial to require around 24 months after the first patient is dosed in 2022. The basis for IMX-110 as a first-line

therapy in STS is threefold:

- interest from leading STS PIs.

Subsequently,

we plan to initiate an 80 patient Phase 2b/3 clinical trial.

IMX-110

Composition and Mechanism of Action

Figure

11: IMX-110 Tissue-Specific TherapeuticTM with TME NormalizationTM Technology

for

soft tissue sarcoma

IMX-110

is a negatively-charged Tissue-Specific TherapeuticTM built on our TME NormalizationTM Technology encapsulating

a synergistic 5:1 ratio of poly-kinase inhibitor (PCC) and apoptosis inducer (PEG-PE doxorubicin complex) delivered deep into the TME.

IMX-110

is the first clinical-stage drug built on our TME NormalizationTM Technology.

Figure

12: IMX-110 – the first oncology micelle to achieve “small molecule penetration”

(Intravital

multiphoton imaging of intravenous injection into a mouse bearing an Mu89 melanoma in a dorsal skinfold chamber with a mixture of nanoparticles

with diameters of 12 nm, 60 nm, and 125 nm. Adapted from Popovic, et al., 2010. We did not fund or sponsor this study, and we were not

involved in this study or its publication.)

IMX-110

is 14-16 nanometers in diameter, and is about the size of an Immunoglobulin G (“IgG”) antibody. Tumor blood vessels have

perforations of several hundred nanometers in diameter. Once IMX-110 has exited the bloodstream toward the tumor, it must traverse the

fibrous extracellular matrix, laid down by CAFs, that encases and scaffolds the tumor. IMX-110’s small size enables IMX-110 to

exit perforated tumor blood vessels and penetrate the fibrous extracellular matrix.

Figure

13: Representation of IMX-110 in the bloodstream, prior to exiting perforated tumor blood vessels

Figure

14: Representation of IMX-110 traversing the fibrous extracellular matrix toward the tumor

Figure

15: IMX-110 – negative charge facilitates selective tumor accumulation

(Concentration

in tumor after IV injection. C-labeled doxorubicin in micellular or free form was injected into the tail veins of C 26-bearing CDF1

female mice (7 weeks old) at a volume of 0.1 ml/10g body weight. After defined time periods (15 min, 1, 4, 24, and 48 h), mice

were anesthetized with diethylether and tumor samples were collected. Adapted from Yokoyama, et al., 1999. We did not fund or sponsor

this study, and we were not involved in this study or its publication.)

We

believe IMX-110’s negative charge enables it to be electrostatically attracted to the tumor, and accumulate at tumor sites at a

rate 4-9 times higher than the rate of existing standard of care chemotherapies such as conventional doxorubicin.

Figure

16: IMX-110 – 12x tumor killing vs. conventional doxorubicin

(See

below paragraph for study description. Adapted from Sarisozen, et al., 2016)

We

observed that IMX-110 of statistically significantly increased apoptosis in 3D spheroid U87MG glioblastoma model as measured by increase

in caspase 3/7 activity after 24 hours versus groups treated with: control group (empty micelles), 0.1 μM free doxorubicin (free DOX),

0.1 μM micellular doxorubicin (DOX micelles), 20 μM micellular curcumin (CUR micelles). The primary endpoint of the study was level

of apoptosis as measured by increase in caspase 3/7 activity after 24 hours of treatment. 3D Spheroid U87MG glioblastoma cells were treated

with 0.1 μM DOX and 20 μM CUR in micellar formulations for 24 h, followed by the Apo-ONE Homogeneous Caspase-3/7 Assay. Results

were normalized against the control group and presented as mean ± SD. Our employees were involved in the design of this study

and Ilya Rachman, our Chief Executive Officer and Chairman of our board of directors, was a co-author of the results published in 2016.

Results were generated in triplicate using 15 spheroids per treatment.

IMX-110’s

synergistic combination induces caspase 3/7 activity, a proxy for apoptosis/tumor cell killing, at a rate of 12 times higher than that

of conventional doxorubicin, and at a rate 5 times higher than micellular doxorubicin, confirming IMX-110’s potent tumor cell killing

activity.

Figure

17: Representation of IMX-110 effector molecules (orange and red) attacking multiple protein targets simultaneously

Figure

18: IMX-110 Tissue-Specific TherapeuticTM with TME NormalizationTM Technology

Intracellular

Mechanism of Action

Specifically,

IMX-110 induces potent tumor killing by blocking multiple tumor escape pathways targeted by FDA approved targeted agents and targeted

agents in development.

Leveraging

its multi-kinase inhibition capabilities, not only does IMX-110 block activation of NF-κB and STAT3, IMX-110 also simultaneously

blocks activation of other well-known cancer-related proteins such as COX2, BCL2, BCL-xL, Survivin, c-myc, Notch, and Hes1. With these

pathways shut down, IMX-110 is able to activate apoptosis through double-stranded DNA breaks caused by IMX-110’s apoptosis inducer

(PEG-PE doxorubicin complex).

Table

1: Select Drugs Targeting Same Targets That IMX-110 Targets

Company Name Target 2021 status

Venetoclax / Venclexta BCL2 Approved

Navitoclax BCL2, BCL-xL Phase II

ZN-d5 BCL2, BCL-xL IND Enabling

Celebrex/celecoxib COX2 Off patent

Brontictuzumab Notch1 Phase I

IMX-110

Pre-clinical Data

We

have funded and sponsored pre-clinical experiments to characterize the activity profile of IMX-110 in a range of solid tumor models,

including genetic KPC pancreatic mouse model, xenograft mouse models of various cancers, and in vitro with various cancer cell

lines.

We

observed that IMX-110 statistically significantly inhibited tumor growth in a pre-clinical study that we funded and was conducted on

an industry sponsored research basis in a HCT-116 colon cancer xenograft mouse model (which is poorly sensitive to doxorubicin). The

primary endpoint of the study was tumor growth inhibition as measured by tumor volume, with the secondary endpoint being overall survival.

Female nude (NU/NU) mice bearing 250mm3 HCT-116 tumors were treated every 2 days starting at day 0 (7 total tail vein injections,

arrows correspond to injection days) at a dose of 4 mg/kg CUR and 0.4 mg/kg DOX (six mice per dosing group). Survival was determined

when the tumor reached 1000mm3. Our employees were involved in the design of this study and Ilya Rachman, our Chief Executive

Officer and Chairman of our board of directors, was a co-author of the results published in 2013. No adverse side effects of IMX-110

were observed as measured by lack of weight loss.

Figure

19: IMX-110 Tissue-Specific TherapeuticTM with TME NormalizationTM Technology Statistically Significantly Inhibited

Tumor Growth in HCT-116 Pre-clinical Xenograft Model

(See

above paragraph for study description. Adapted from Abouzeid et al., 2013)

In

this pre-clinical study of IMX-110 in the HCT-116 colorectal cancer xenograft mouse model, at day 24, 80% of mice treated with 1 cycle

of low-dose IMX-110 were alive while all control animals were dead.

We

observed that IMX-110 monotherapy statistically significantly inhibited tumor growth in a pre-clinical study that we funded and was conducted

in a genetic pancreatic cancer (KPC) mouse model. The primary endpoint of the study was tumor growth inhibition as measured by tumor

volume and weight. Transgenic mice (Pdx1-Cre) were treated every day starting at day 0 (5 total tail vein injections, arrows correspond

to injection days) at a dose of 6 mg/kg CUR and 1.4 mg/kg DOX (at least six mice per dosing group). Survival was determined when the

tumor reached 1500mm3. Surviving animals were euthanized after the last blood collection prior to Day 30, tumors were excised,

measured, weighted, photographed and sectioned for histological analysis. Our employees were involved in the design of this study and

the results are unpublished. No adverse side effects of IMX-110 were observed as measured by lack of weight loss.

Figure

20: IMX-110 Tissue-Specific TherapeuticTM with TME NormalizationTM Technology Monotherapy Statistically Significantly

Inhibited Tumor Growth in Genetic (KPC) Pancreatic Cancer Pre-clinical Model

(See

above paragraph for study description. ImmixBio unpublished results.)

In

this pre-clinical study of IMX-110 monotherapy in the genetic KPC pancreatic cancer mouse model, one cycle of low-dose IMX-110 produced

an average 43% reduction in tumor volume and weight at sacrifice vs. tumor volume and weight in untreated controls.

IMX-110

Immunomodulation Effects

In

this pre-clinical study of IMX-110 monotherapy in the genetic KPC pancreatic mouse cancer model, our histological analysis showed that

IMX-110 has the potential to transform “cold” tumors into “hot” tumors by eliminating immunosuppressive T-regulatory

immune cells (top), enabling cytotoxic T-lymphocytes to enter the tumor (middle), and eliminating tumor vascularization (bottom).

Figure

21: IMX-110 Tissue-Specific TherapeuticTM with TME NormalizationTM Technology

Monotherapy

Turns “Cold” Tumors “Hot” in Genetic (KPC) Pancreatic Cancer Pre-clinical Model

(See

above paragraph for study description. ImmixBio unpublished results.)

IMX-110

+ Anti-PD-1

In

published literature, the effect of a combination of murine anti-PD-1, gemcitabine, nab-paclitaxel, and murine anti-CD40 was studied

in a genetically engineered mouse model of pancreatic ductal adenocarcinoma (KPC), and produced median survival of 42 days.

The

primary endpoint of the study was tumor growth inhibition as measured by tumor volume and weight. Mice were treated intraperitoneally

(i.p.) with murine anti-PD-1 (RMP1-14; BioXcell; 200 mg/dose) on days 0, 3, 6, 9, 12, 15, 18, and 21 (after enrollment), with chemotherapy

(gemcitabine + nab-paclitaxel) injected i.p. at 120 mg/kg (for each chemotherapeutic) on day 1, and agonistic anti-CD40 (FGK45; BioXcell;

100 mg injected on day 3. For isotype controls, rat IgG2a (2A3; BioXcell; 100 mg) and rat IgG2b (LTF-2; BioXcell; 200 mg/dose) were used

(6-8 mice per group). Duration of survival was studied. We did not fund or sponsor this study, and we were not involved in this study

or its publication.

Figure

22: 4 Drug Combination (anti-PD-1, anti-CD40, gemcitabine, nab-paclitaxel) produced

median

42 day survival in Genetic (KPC) Pancreatic Cancer Pre-clinical Model

(See

above paragraph for study description. Adapted from Winograd et al., 2015)

A

combination of IMX-110 + murine anti-PD-1 in a pre-clinical study in a genetic pancreatic cancer (KPC) mouse model that we funded produced

extended median survival of 63 days.

The

primary endpoint of the study was tumor growth inhibition as measured by tumor volume and weight. Transgenic mice (Pdx1-Cre) were treated

every day starting at day 0 (5 total tail vein injections) at a dose of 6 mg/kg CUR and 1.5 mg/kg DOX, and treated on days 5, 8, and

11 with murine anti-PD-1 (RMP1-14; BioXcell) 100μg/dose (three mice). This treatment was repeated started on day 21 and day 25. Duration

of survival was studied. Tumors were periodically visualized using an in vivo luciferase assay. Our employees were involved in

the design of this study and the results are unpublished. No adverse side effects of IMX-110 were observed as measured by lack of weight

loss.

Figure

23: IMX-110 + murine anti-PD-1 Produced Extended Survival produced median 63 day survival

in

Genetic (KPC) Pancreatic Cancer Pre-clinical Model

(See

above paragraph for study description. ImmixBio unpublished results.)

In

our genetic pancreatic cancer (KPC) mouse model study, luciferase assay visually demonstrated tumor shrinkage in the IMX-110 + anti-PD-1

combination group throughout the study.

(See

above paragraph for study description. ImmixBio unpublished results.)

We

believe there exists significant potential for TSTx IMX-110 to be an integral component of combination therapies for a wide range of

advanced solid tumors.

IMX-111

Tissue-Specific BiologicTM with TME NormalizationTM Technology

IMX-111

Market Opportunity

The

first potential indication we intend to pursue for IMX-111 is colorectal cancer (“CRC”). CRCs are cancers that arise from

the colon, rectum and anus. According to American Cancer Society, there were roughly 149,500 new cases of colorectal cancer in the United

States. Globally, there are roughly 1,930,000 new cases of colorectal cancer each year, of which 519,500 are in Europe, 148,500 are in

Japan, 20,500 are in Australia and New Zealand, and 555,000 are in China. The five-year survival rate in the United States for all stages

of CRC is 64.7%, but this falls to 14.7% for patients with late-stage metastatic disease.

The

colorectal cancer market is estimated to reach approximately $31.2 billion by 2025 from the estimated $26.3 billion in 2019. Drugs used

to treat CRC include conventional irinotecan, oxaliplatin, 5-fluorouracil, pembrolizumab (marketed as Keytruda®, by Merck & Co.),

nivolumab (marketed as Opdivo®, by Bristol Meyers Squibb), bevacizumab (marketed as Avastin®, by Roche), and ramucirumab (marketed

as Cyramza®, by Eli Lilly).

$33.38

billion is the total publicly disclosed combined

annual sales of pembrolizumab (Keytruda®, Merck & Co.), nivolumab (Opdivo®), bevacizumab (Avastin®), and ramucirumab

(Cyramza®) according to the most recent available annual reports.

However,

these therapies are either approved in combination with chemotherapies, or in a small subset of colorectal cancer patients.

Table

2: Select Drugs Used To Treat Advanced Colorectal Cancer

Drug Comments

We

intend to pursue IMX-111 for treatment of advanced colorectal cancer (“aCRC”), which includes all CRC diagnosed with regional,

distant, and other staging, and includes approximately 63% of all patients newly diagnosed with CRC annually. Treatment of aCRC typically

involves removal of sections of the colon (colectomy) or rerouting of the intestine by colostomy. Radiotherapy and chemotherapy, including

the above drugs, are also used to treat aCRC patients.

IMX-111

Pre-clinical Data

We

have funded and sponsored pre-clinical experiments to characterize the activity profile of IMX-111 in a range of solid tumor models,

xenograft mouse models of various cancers, and in vitro with various cancer cell lines.

We

observed that IMX-111 statistically significantly inhibited tumor growth in a pre-clinical study that we funded and was conducted on

an industry sponsored research basis in a HCT-116 colon cancer xenograft mouse model (which is poorly sensitive to doxorubicin). The

primary endpoint of the study was tumor growth inhibition as measured by tumor volume, with the secondary endpoint being overall survival.

Female nude (NU/NU) mice bearing 250mm3 HCT-116 tumors were treated every 2 days starting at day 0 (7 total tail vein injections,

arrows correspond to injection days) at a dose of 4 mg/kg CUR and 0.4 mg/kg DOX (six mice per dosing group). Survival was determined

when the tumor reached 1000mm3. Our employees were involved in the design of this study and Ilya Rachman, our Chief Executive

Officer and Chairman of our board of directors, was a co-author of the results published in 2013. No adverse side effects of IMX-111

were observed as measured by lack of weight loss.

Figure

24: IMX-111 Tissue-Specific BiologicTM with TME NormalizationTM Technology Statistically Significantly Inhibited

Tumor Growth in HCT-116 Colorectal Cancer Pre-clinical Xenograft Model

(See

above paragraph for study description. Adapted from Abouzeid et al., 2013)

In

this pre-clinical study of IMX-111 in the HCT-116 colorectal cancer xenograft mouse model, at day 24, 100% of mice treated with 1 cycle

of low-dose IMX-111 were alive while all control animals were dead.

We

observed that IMX-111 statistically significantly inhibited tumor growth in a pre-clinical study that we funded and was conducted on

an industry sponsored research basis in a MDA-MB-231 triple-negative breast cancer xenograft mouse model (which is poorly sensitive to

doxorubicin). The primary endpoint of the study was tumor growth inhibition as measured by tumor volume, with the secondary endpoint

being overall survival. Female nude (NU/NU) mice bearing 150mm3 MDA-MB-231 tumors were treated every 2 days starting at day

20 except last injection administered at day 33 (7 total IV injections) at a dose of 6 mg/kg CUR and 1 mg/kg DOX (at least six mice per

dosing group). Survival was determined when the tumor reached 1000mm3. Our employees were involved in the design of this study

and Ilya Rachman, our Chief Executive Officer and Chairman of our board of directors, was a co-author of the results published in 2014.

No adverse side effects of IMX-111 were observed as measured by lack of weight loss.

Figure

25: IMX-111 Tissue-Specific BiologicTM with TME NormalizationTM Technology Statistically Significantly Inhibited

Tumor Growth in MDA-MB-231 Triple-Negative Breast Cancer Xenograft Model

(See

above paragraph for study description. Adapted from Abouzeid et al., 2014)

In

this pre-clinical study of IMX-111 in the MDA-MB-231 triple-negative breast cancer xenograft mouse model, treatment with one cycle of

low-dose IMX-111 resulted in 50% reduction in tumor mass, versus 33% growth in controls. The IMX-111 treatment effect lasted throughout

the 52 day experiment duration.

IMX-111

Composition and Mechanism of Action

Figure

26: IMX-111 Tissue-Specific BiologicTM with TME NormalizationTM Technology

for

CRC

IMX-111

is a Tissue-Specific BiologicTM built on our TME NormalizationTM Technology with proprietary GLUT1 antibody biomarker

targeting facilitating preferential accumulation in glucose-consuming cancer cells such as CRC. IMX-111 takes advantage of the fact that

GLUT1 is an essential cancer biomarker that is overexpressed on 92% of colorectal cancer tumor cells and other tumor types. Furthermore,

the degree of its overexpression correlates with more advanced stage of tumor progression. IMX-111 is the first cancer therapeutic to

take advantage of this fact by coupling anti-GLUT1 antibody to our poly-kinase inhibitor / apoptosis inducer.

IMX-111

is 17-23 nanometers in diameter, which is just larger than the size of an IgG antibody.

Figure

27: IMX-111’s target GLUT1 is overexpressed on colorectal and other cancers

(Adapted

from a review paper by Amann, et al., 2009. We did not fund or sponsor this study, and we were not involved in this study or its publication.)

GLUT1

is a glucose transporter which is overexpressed on 92% of CRC, making GLUT1 a prime biomarker for IMX-111 targeting in CRC.

Figure

28: IMX-111’s target GLUT1 overexpression is associated with a poor prognosis

(Adapted

from Shen, et al., 2011 and Haber, et al., 1998. Shen, et al.: Expression of GLUT1 in 163 primary patient colorectal cancer tumors was

examined using real-time PCR. Haber, et al.: GLUT1 glucose transporter immunostaining was studied in normal colon and benign colon adenomas

and in 112 colorectal carcinomas from patients with known clinical outcomes. We did not fund or sponsor these studies, and we were not

involved in these studies or their publication.)

GLUT1

overexpression in CRC correlates with advanced, later stage (stage III-IV) disease. Heavy GLUT1 staining is observed in cancerous colorectal

tissue versus healthy normal colon.

Figure

29: IMX-111 Tissue-Specific BiologicTM with TME NormalizationTM Technology

Intracellular

Mechanism of Action

Once

IMX-111 enters the TME, consisting of: 1) CAFs, 2) TAMs/immune cells, and 3) cancer itself, it binds to its GLUT1 biomarker target and

empties its poly-kinase inhibitor / apoptosis inducer payload into these cells, causing tumor apoptosis. Specifically, IMX-111 induces

potent tumor killing by blocking multiple tumor escape pathways targeted by FDA approved targeted agents and targeted agents in development

(see Table 1).

IMX-111

Development Strategy

We

plan to conduct IND-enabling studies for IMX-111 by mid-2022, pursuing advanced colorectal cancer as the initial indication. We anticipate

filing an IND for IMX-111 in 2023. We plan to initiate a Phase 1b/2a study with IMX-111 in solid tumors in the United States and Australia,

with the first patient anticipated to be dosed in 2023. We plan for IMX-111 to pursue advanced colorectal cancer as its initial indication.

IMX-120

Tissue-Specific BiologicTM with Immune Normalization TechnologyTM for inflammatory bowel disease

IMX-120

Market Opportunity