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Item 1. Business

2024-03-29 compared with 2023-03-27 · 513 added, 1101 removed, 712 unchanged (69% of the section changed)

Biopharma, Inc.

has the following two business units:

ImmixBio is focused on developing Tissue Specific Therapeutics targeting solid tumors and immune-dysregulated diseases.

As of February

2023, 19 patients with advanced solid tumors were treated with IMX-110, ImmixBio’s lead candidate.

Our majority-owned subsidiary, Nexcella, Inc.

(formerly known as Immix Biopharma Cell Therapy, Inc.), is engaged in the discovery and development of novel cell therapies for hematologic

malignancies (blood cancers) and other indications.

As of February 2023, 42 patients with relapsed/refractory multiple myeloma (90%

overall response rate at therapeutic dose) and 5 relapsed/refractory light chain (AL) amyloidosis patients (100% organ response,

100% complete response rate) have been treated with next-generation CAR-T NXC-201.

– TISSUE SPECIFIC THERAPEUTICS FOR SOLID TUMORS

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 Normalization TM Technology, delivered deep into the tumor micro-environment

Our proprietary System Multi-Action RegulaTors SMAR x T Tissue-Specific TM Platform produces

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

Our TME Normalization™ Technology

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

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

SMAR x T Tissue-Specific TM 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.

ImmixBio SMAR x T Tissue-Specific TM Platform – Pipeline

Lead Product Candidate

currently in Phase 1b/2a clinical trials, is a Tissue-Specific Therapeutic TM with TME Normalization TM , 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.

of February 2023, we have treated the first 2 patients in our ongoing Phase 1b/2a clinical trial of IMX-110 + Novartis/BeiGene anti-PD-1

Tislelizumab.

of February 2023, we have treated 17 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.

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.

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

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

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).

January 2022, the FDA granted Rare Pediatric Disease Designation (“RPDD”) to IMX-110 for the treatment of rhabdomyosarcoma,

a life-threatening pediatric cancer in children.

RPDD qualifies us to receive fast track review and a priority review voucher (“PRV”)

at the time of marketing approval of IMX-110.

Other Product Candidates

is a Tissue-Specific Biologic TM built on our TME Normalization TM 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.

is a Tissue-Specific Biologic TM built on our Immune Normalization Technology TM 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.

ImmixBio SMAR x T Tissue-Specific TM Platform – Summary Rendering

Immix Biopharma, Inc.

is a clinical-stage biopharmaceutical company focused

on the application of chimeric antigen receptor cell therapy (“CAR-T”) in light chain (AL) Amyloidosis and autoimmune disease.

Our lead cell therapy candidate is U.S.

Food and Drug Administration (“FDA”) investigational new drug (“IND”)

cleared CAR-T NXC-201, currently being evaluated in our ongoing Phase 1b/2a NEXICART-1 (NCT04720313) clinical trial.

Based on early clinical

data, we believe NXC-201 has the potential to be the world’s first “Single-Day Cytokine Release Syndrome”, or “Single-Day

CRS” CAR-T (CRS median onset day 1, median duration 1 day), enabling the potential for a faster return home for patients.

has been awarded Orphan Drug Designation (“ODD”) by the FDA in both AL Amyloidosis and multiple myeloma, and ODD by the European

Commission (“EMA”) in AL Amyloidosis.

strategy is to:

● Develop our lead candidate CAR-T NXC-201 in AL Amyloidosis and other autoimmune

● Pursue development of NXC-201 and additional cell therapy candidates in

other applicable indications where CAR-T is not an approved therapy today

mission is to harness the immune system through innovative cell therapies and other modalities to deliver widely accessible cures in

autoimmune and other indications, as we believe patients are waiting.

Select ImmixBio Possible Autoimmune Target Indications

N-GENIUS platform has produced our clinical-stage lead candidate NXC-201, a next-generation CAR-T for AL Amyloidosis and autoimmune disease,

complemented by emerging programs.

ImmixBio Pipeline

is in clinical trials to treat relapsed/refractory AL Amyloidosis.

of February 2024, we have treated 73 patients in our ongoing Phase 1b/2a NEXICART-1 (NCT04720313), of which 63 were relapsed/refractory

multiple myeloma patients, and 10 were relapsed/refractory AL Amyloidosis patients.

September 2023, the FDA granted ODD to NXC-201 for the treatment of AL Amyloidosis.

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).

November 2023, the U.S.

FDA cleared an IND application for NXC-201 to enroll U.S.

patients into NXC-201 clinical trials.

December 2023, NXC-201 clinical data in relapsed/refractory AL Amyloidosis was presented in an oral presentation at the 65 th

annual American Society of Hematology (“ASH”) meeting, covering 10 relapsed/refractory AL Amyloidosis patients treated with

NXC-201, indicating an overall response rate of 100% (10/10) and a complete response rate of 70% (7/10).

February 2024, the European Commission (“EC”) granted orphan drug designation to NXC-201 for the treatment of AL Amyloidosis.

of European ODD include:

10 years of market exclusivity once authorized in the EU;

Access to the EU centralized authorization procedure;

and reduced fees for EU protocol assistance, marketing authorization applications, inspections before authorization, applications for

changes to marketing authorizations made after approval, and reduced annual fees.

Other Programs

other programs include NXC-201 for autoimmune diseases, a $25 billion combined annual market size according to Grand View Research and

Fortune Business Insights;

NXC-201 for relapsed/refractory multiple myeloma, a $14 billion market size growing to $27 billion

according to Wilcock, et al, Nature Reviews;

IMX-110 for soft tissue sarcoma, a $3 billion market size according to Medgadget,

and in combination with anti-PD-1 for colorectal cancer, a $27 billion market size according to IndustryARC.

Platform and Technologies

SMAR x T 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.

SMARxT Tissue-Specific TM Platform Overview

Specifically,

the 3 pillars of our platform are:

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.

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.

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.

application of the SMAR x T Tissue-Specific Platform in oncology is TME Normalization TM Technology, and in inflammation

is Immune Normalization TM Technology.

TME Normalization TM Technology

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

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 Normalization TM 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.

Representation of the TME Composed of CAFs, TAMs, and Cancer Cells

TME Normalization TM 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.

believe that our TME Normalization TM 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.

- Tissue-Specific Therapeutic TM with TME Normalization TM Technology

believe our N-GENIUS platform has broad potential utility in hematologic and autoimmune diseases.

N-GENIUS platform, which has produced NXC-201, consists of three key elements:

(1) Purpose-Built Cell Therapy Evidence Capture

Engine + Relational Database, which relates ImmixBio internal data to external to accelerate therapy design, manufacture, and

(2) proprietary EXPAND technology, which is applied to multiple cell therapy indications, already utilized to create

and (3) Atomized, Novel Binding Scaffold Generation Engine, which allows for optimal molecule binding.

We believe key

characteristics of NXC-201 may apply to other products candidates produced by the N-GENIUS Platform.

Those 3 key characteristics

(a) high transduction efficiency (supporting efficient manufacturing), (b) low tonic signaling (lower off-target toxicity may

lead to lower toxicity), and (c) anti-exhaustion capability (increased persistence may lead to activity over an extended period of

Our Lead Program:

NXC-201 in relapsed/refractory AL Amyloidosis

Market Opportunity

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 and about 13,400 new cases of soft tissue sarcomas in the United States are anticipated

first indication we intend to pursue for NXC-201 is relapsed/refractory AL Amyloidosis.

AL amyloidosis is a life-threatening immunological disorder in which an

abnormal protein called amyloid builds up in tissues and organs.

This abnormal protein is produced by long-lived plasma cells (“LLPCs”),

a type of immune B-cell.

The signs and symptoms of AL amyloidosis vary among patients because build-up may occur in the heart (most frequent

cause of mortality), liver, kidneys, intestines, muscles, joints, nerves, or spleen, according to the National Institutes of Health (“NIH”).

Diagnosis is frequently delayed, due to varied and non-specific symptoms including:

fatigue, weight loss, shortness of breath, dizziness,

and numbness in hands and feet.

Upon diagnosis, many patients already have late-stage disease, and are not aware of available treatment

options and clinical trials.

observed prevalence of relapsed/refractory AL Amyloidosis is growing 12% per year according to Staron, et

al Blood Cancer Journal, estimated to reach 29,712 patients in 2023.

AL amyloidosis has a one-year mortality rate

of 47 percent, 76 percent of which is caused by cardiac amyloidosis, according to Alexion.

The current market size for amyloidosis therapies is

$3.6 billion, expected to reach $6 billion in 2027, according to Grand View Research.

of February 2024, there are no FDA approved drugs for AL Amyloidosis.

NXC-201 “Blue Ocean Opportunity” in AL Amyloidosis

Composition and Mechanism of Action

is a next-generation CAR-T targeting B-cell maturation antigen (“BCMA”).

CAR-T cell therapy is a type of immunotherapy that

uses the patient’s own immune cells, modified with our proprietary technology, to create NXC-201, which is then introduced into

the patient’s body.

Then the patient’s modified NXC-201 CAR-T cells are able to recognize and eliminate diseased cells.

What is CAR-T Cell Therapy?

Our N-GENIUS cell engineering platform with EXPAND technology has already

produced clinical-stage CAR-T NXC-201, targeting BCMA, which we believe is the first and only autologous CAR-T being developed to treat

light-chain (AL) Amyloidosis.

NXC-201 is currently being evaluated in our ongoing Phase 1b/2a NEXICART-1 (NCT04720313) clinical trial.

First CAR-T Generated by the N-GENIUS Platform

3 key characteristics of NXC-201 are:

(a) high transduction efficiency (supporting efficient manufacturing), (b) low tonic signaling

(lower off-target toxicity may lead to lower toxicity), and (c) anti-exhaustion capability (increased persistence may lead to activity

over an extended period of time).

Key Characteristics

NXC-201 has been designed with a proprietary, optimized C3ζγ

for enhanced signal transduction, proprietary, optimized modified-stiffness CD8 hinge, and proprietary, optimized COBRA binder for enhanced

signal binding.

We believe the combination of these modifications has the potential to allow for NXC-201 to deliver “digital”

intracellular signaling, potentially eliminating neurotoxicity and reducing CRS duration to 1 day.

N-GENIUS Platform – EXPAND Technology + COBRA Binder

NXC-201 was designed for high activity against disease-causing AL Amyloidosis

LLPCs, which are also the source of autoimmune antibodies in a variety of autoimmune disorders.

Pre-clinical Data

AL Amyloidosis, we believe there are two primary challenges with CAR-T patient dosing:

Uneven BCMA expression across disease-causing LLPCs;

b) frail patient due to pre-existing organ (heart) damage.

in Clinical Cancer Research in 2022, NXC-201 was tested preclinical and clinically in AL Amyloidosis.

In AL Amyloidosis, BCMA expression is at a low-to-medium level

Clinical Cancer Research, Kfir-Erenfeld,et al, 2022

testing demonstrated low-to-medium expression of BCMA in 18 AL Amyloidosis patient samples.

High Activity Level of NXC-201 in AL Amyloidosis

Clinical Cancer Research, Kfir-Erenfeld,et al, 2022

demonstrated high activity in the presence of AL Amyloidosis diseased plasma cells.

NXC-201 Targets Diseased AL Amyloidosis LLPCs in Patient Bone Marrow

Clinical Cancer Research, Kfir-Erenfeld,et al, 2022

Near-complete

elimination of diseased AL Amyloidosis LLPCs was observed in relapsed/refractory AL Amyloidosis patients treated with NXC-201.

Clinical Data – Relapsed/refractory AL Amyloidosis

December 2023, NXC-201 clinical data in relapsed/refractory AL Amyloidosis was presented in an oral presentation at the 65 th

annual ASH meeting, covering 10 relapsed/refractory AL Amyloidosis patients treated with NXC-201.

These data represent the largest cohort

of AL patients treated with CAR T-based therapy reported in the literature thus far.

AL amyloidosis patients presented with organ involvement and were heavily pretreated with prior lines of therapy (median 6, range 3-10).

All patients had refractory, progressive disease.

No patients received bridging therapy.

was administered at cell doses of either 150 × 10 6 , 450 × 10 6 , and 800 × 10 6 per patient.

characteristics:

(9/10) had high-risk cytogenetics

(8/10) had cardiac involvement

(5/10) had New York Heart Association (“NYHA”) stage 3 or 4 heart failure (3 stage 4, 2 stage 3)

(4/10) had Mayo stage 3 (1 stage 3b, 3 stage 3a) AL amyloidosis disease

(4/10) had t(11;14) translocation

Relapsed/refractory

to a median 6 lines of prior therapy (range:

response rate of 100% (10/10)

response + very good partial response rate of 90% (9/10)

response rate of 70% (7/10) (6 out of 7 were minimum residual disease (“MRD”) 10 -5 )

response rate of 60% (6/10)

responder had a duration of response of 23.7 months as of December 10, 2023, with response ongoing

were no immune effector cell-associated neurotoxicity syndrome (ICANS) events

Median CRS duration was 1 day (range:

grade 4 CRS events

experienced no CRS;

2 experienced grade 1 CRS;

4 Experienced grade 2 CRS;

2 experienced grade 3 CRS

the 8 patients with cardiac involvement:

response rate of 100% (8/8)

response rate of 63% (5/8) (4 out of 5 were MRD 10 -5 )

response rate of 63% (5/8)

the 4 patients with t(11;14) disease:

response rate of 100% (4/4)

response rate of 75% (3/4) (MRD 10 -5 )

response rate of 50% (2/4)

Vitro Studies

has demonstrated efficient eradication of plasma cells from patients with AL amyloidosis (Kfir-Erenfeld et al.

Co-cultures of

plasma cells from AL amyloidosis patients and NXC-201 resulted in an almost complete eradication of the plasma cells.

A control of AL

amyloidosis plasma cells with non-transduced (“NT”) cells, in contrast, did not result in a similar elimination of the plasma

Elimination of Plasma Cells After Co-culture with NXC-201 Compared to NT Cells

Abbreviations:

amyloid light chain;

non-transduced;

HBI0101 = NXC-201.

(Kfir-Erenfeld et al.

data suggest that NXC-201 cells were able to recognize the AL amyloidosis plasma cells and exert specific BCMA-directed antitumoral effect,

as further evidenced by the fact that following co-culture with AL amyloidosis plasma cells, NXC-201 cells underwent significant activation,

demonstrated by upregulation of the 4-1BB cell marker and increased secreted levels of inflammatory cytokines (interferon gamma:

tumour necrosis factor alpha:

TFNα), which was not seen in NT cells.

Furthermore, non-tumour bone marrow derived mononuclear

cells were not affected by co-culture with NXC-201, demonstrating the targeted effect of this therapy.

NXC-201 Activation Following Overnight Co-culture with Amyloid Light Chain Amyloidosis Plasma Cells

65 th ASH NXC-201 presentation:

Rapid elimination of disease-causing amyloid chains by NXC-201 within ~30 days was

in Relapsed/refractory multiple myeloma

of February 2024, 63 patients with triple-refractory relapsed/refractory multiple myeloma with median 4 lines of prior therapy (range:

3-13) have been treated with NXC-201.

A 95% overall response rate to NXC-201 treatment was observed in relapsed/refractory multiple myeloma

patients not previously treated with BCMA-targeted therapy (98% overall response rate observed in relapsed/refractory multiple myeloma

patients without extra-medullary disease).

“Single-Day CRS” was demonstrated – median duration of CRS of 1 day, median

Multiple myeloma is a $14 billion market size growing to $27 billion according to Wilcock, et al, Nature Reviews.

Development Strategy

In our lead program, NXC-201 for relapsed/refractory AL Amyloidosis, we

plan to enroll 40 patients in our open label, single-arm clinical trial, and then submit a biologics license application (“BLA”)

for FDA approval.

NXC-201 Clinical Development Plan Through

FDA BLA Submissions

primary objectives in relapsed/refractory AL Amyloidosis are to study the safety and efficacy of NXC-201.

The efficacy endpoints are

to evaluate response rates according to consensus recommendations for AL amyloidosis treatment response criteria in AL (Palladini et

The expected primary endpoints

are complete response rate and overall response rate in our NXC-201 relapsed/refractory AL Amyloidosis clinical trial.

Our strategy is to pursue orphan

drug indications in which open-label, single-arm clinical trials may lead to possible BLA submissions, or indications with large populations

with remaining unmet medical need.

– Tissue-Specific Therapeutic TM with tissue micro environment

(“TME”) Normalization TM Technology

in Colorectal Cancer

first potential indication we intend to pursue for IMX-110 (in combination with anti-PD-1 antibody) is relapsed/refractory colorectal

cancer (“CRC”).

CRCs are cancers that arise from the colon and rectum.

According to American Cancer Society, there were roughly

153,020 new cases of colorectal cancer in the United States in 2023.

The five-year survival rate in the United States for all stages

of CRC is 65.1%, but this falls to 15.1% for patients with late-stage metastatic disease according to the National Cancer Institute (“NCI”).

CRC market is estimated to reach approximately $31.2 billion by 2025 from the estimated $26.3 billion in 2019 according to IndustryARC.

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), ramucirumab

(marketed as Cyramza®, by Eli Lilly), and regorafenib (marketed as Stivarga® by Bayer).

$41.11 billion is the total publicly

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

and ramucirumab (Cyramza®) according to 2023 available annual reports.

In relapsed/refractory proficient mismatch repair (pMMR) (microsatellite-stable

- MSS) relapsed/refractory mCRC, regorafenib (marketed as Stivarga® by Bayer) produced a median progression free survival (“mPFS”)

of 2.0 months according to the FDA approval label.

of February 2024, we continue to dose escalate IMX-110 + BeiGene anti-PD-1 Tislelizumab in our IMMINENT-01 (NCT05840835) study.

2023, we reported the following clinical data for IMX-110 + Tislelizumab in proficient mismatch repair (“pMMR”, or microsatellite-stable

– “MSS”) relapsed/refractory mCRC in IMMINENT-01:

Out of 4 relapsed/refractory metastatic colorectal cancer patients

treated with IMX-110 + tislelizumab:

3 out of 4 (75%) patients experienced tumor shrinkage at 2 months;

1 out of 4 (25%) patients experienced

tumor control at 2 months;

1 out of 4 patients remain on IMX-110 + tislelizumab therapy as of July 7, 2023;

Median progression-free survival

and overall survival not yet reached;

Patients received a median of 8 earlier anti-cancer treatments that failed to halt cancer growth

(lines of therapy) prior to receiving IMX-110 + tislelizumab.

in Soft Tissue Sarcoma (“STS”)

second potential indication we intend to pursue for IMX-110 is relapsed/refractory STS.

STSs are cancers that arise from muscle, fat,

nerves, fibrous tissues, blood vessels or deep skin tissues.

According to American Cancer Society, there were roughly 13,000 new cases

of soft tissue sarcomas in the United States during 2020 and about 13,400 new cases of soft tissue sarcomas in the United States are

anticipated in 2023.

Approximately 160,000 people live with soft tissue cancers in the United States.

The five-year survival rate for all stages

of STS is 65.4% in the United States, but this falls to 17.1% for patients with late-stage metastatic disease.

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

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).

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.

The five-year survival rate for

all stages of STS is 65.4% in the United States, but this falls to 17.1% for patients with late-stage metastatic disease according the

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

2019 according to Medgadget.

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).

response rates are increasingly considered as poor surrogates of clinical activity in STS.

1 unchanged sentence

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

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.

(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.

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

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

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

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

Clinical Data

of March 2023, we have treated 17 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.

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

Pazopanib (Votrient®),

was trialed in a study producing a mPFS in STS patients of 4.6 months according to van der Graaf et al., 2012.

Trabectedin (Yondelis®)

was trialed in a study producing a mPFS in STS patients of 4.2 months according to Demetri et al., 2016.

of February 2024, we have treated 21 patients in our ongoing IMX-110 Phase 1b/2a clinical trial in the United States and Australia, of

which clinical analysis has been completed for the initial 14 patients.

Of those 14 patients, 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.

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

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.

6 months of radiological PFS was observed in 50% of our STS patients treated with IMX-110.

100% of these patients received between 3 and 13 lines of therapy prior to IMX-110.

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

IMX-110 Soft Tissue Sarcoma Median Progression Free Survival and Level of Pre-treatment

our ongoing IMX-110 clinical trial:

of STS patients had controlled disease at 2 months.

of STS patients experienced tumor shrinkage.

The range of the best percentage change from baseline in size of target lesions was

between -10% and -18%.

59 year old male STS patient experienced 6 month PFS, despite having 13 prior lines of therapy and the largest tumor burden at the

time of enrollment (312mm diameter across 5 target lesions).

77 year old male STS patient with 8 lines of prior therapy experienced 4 month PFS.

27 year old female STS patient with 3 lines of prior therapy experienced 4 month clinical PFS and 6 month radiological PFS.

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

of Heavily Pretreated Soft Tissue Sarcoma Patients Experienced Tumor Shrinkage

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

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

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

Immix Biopharma, Inc.

ImmixBio has evaluable data for 8 patients as of March 2022 (out of n=17, the remaining 9 did not complete any

tumor measurements after enrollment scan, of which 2 due to being dosed in December 2022).

All 8 evaluable patients have discontinued

“Heavily Pretreated” refers to 3-13 lines of therapy.

Dose expressed in mg/m 2 .

Our employees were involved

in the design of this study and the results are unpublished.)

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.

Development Strategy

Direct Path To 1 st Line Therapy In Soft Tissue Sarcoma – Clinical Trial Plan

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

expect our Phase 2a trial to require around 24 months after the first patient is dosed in 2023.

The basis for IMX-110 as a first-line

therapy in STS is threefold:

clinical trial mPFS (4 month mPFS) data and tolerability data in our IMX-110 Phase 1b dose escalation trial;

have identified precedent FDA clinical trial design for a first-line treatment;

from leading STS PIs.

Subsequently,

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

Zero drug-related serious adverse events and zero

dose interruptions due to toxicity have been observed in our 1b/2a clinical trial to-date.

Composition and Mechanism of Action

IMX-110 Tissue-Specific Therapeutic TM with TME Normalization TM Technology

Soft Tissue Sarcoma

is a negatively-charged Tissue-Specific Therapeutic TM built on our TME Normalization TM Technology encapsulating

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

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

IMX-110 – the First Oncology Micelle to Achieve “Small Molecule Penetration”

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.)

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.

Representation of IMX-110 in the Bloodstream, Prior to Exiting Perforated Tumor Blood Vessels

Representation of IMX-110 Traversing the Fibrous Extracellular Matrix Toward the Tumor

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 CDF 1

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.)

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.

IMX-110 – 12x Tumor Killing vs.

Conventional Doxorubicin

below paragraph for study description.

Adapted from Sarisozen, et al., 2016)

observed that IMX-110 has 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.

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.

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

Representation of IMX-110 Effector Molecules (Orange and Red) Attacking Multiple Protein Targets Simultaneously

IMX-110 Tissue-Specific Therapeutic TM with TME Normalization TM 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.

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.

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).

Select Drugs Targeting Same Targets That IMX-110 Targets

Celebrex/celecoxib

Brontictuzumab

Pre-clinical Data

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

observed that IMX-110 has 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 250mm 3 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 1000mm 3 .

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

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

IMX-110 Tissue-Specific Therapeutic TM with TME Normalization TM Technology Statistically Significantly Inhibited

Tumor Growth in HCT-116 Pre-clinical Xenograft Model

above paragraph for study description.

Adapted from Abouzeid et al., 2013)

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.

observed that IMX-110 monotherapy has 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 1500mm 3 .

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.

IMX-110 Tissue-Specific Therapeutic TM with TME Normalization TM Technology Monotherapy Statistically Significantly

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

above paragraph for study description.

ImmixBio unpublished results.)

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, currently in Phase 1b/2a clinical trials, is a Tissue-Specific

Therapeutic TM with TME Normalization TM , a technology that we are developing initially for mCRC and STS.

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.

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.

IMX-110 Induces Apoptosis while Blocking Multiple Escape Pathways

Immunomodulation Effects

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

this pre-clinical study of IMX-110 monotherapy in the genetic Kras, p53, and Cre (“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

4 unchanged sentences

ImmixBio unpublished results.)

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.

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;

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;

100 mg injected on day 3.

For isotype controls, rat IgG2a (2A3;

100 mg) and rat IgG2b (LTF-2;

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.

4 Drug Combination (Anti-PD-1, Anti-CD40, Gemcitabine, Nab-paclitaxel) Produced

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

above paragraph for study description.

Adapted from Winograd et al., 2015)

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.

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.

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

IMX-110 + Murine Anti-PD-1 Produced Extended Survival Produced Median 63 Day Survival

Genetic (KPC) Pancreatic Cancer Pre-clinical Model

above paragraph for study description.

ImmixBio unpublished results.)

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.

above paragraph for study description.

ImmixBio unpublished results.)

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.

Tissue-Specific Biologic TM with TME Normalization TM Technology

Market Opportunity

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 153,020 new cases of colorectal cancer in the United

States in 2023.

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 65.1%, but this falls to 15.1% for patients with late-stage metastatic disease.

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

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).

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.

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

Select Drugs Used To Treat Advanced Colorectal Cancer

in combination with 5-FU or 5-FY/LV chemotherapy

in combination with FOLFIRI chemotherapy

pembrolizumab

Unresectable/metastatic

MSI-H or mismatch repair deficient metastatic CRC that have progressed following prior treatment and have no alternative options

/ MSI-H or dMMR CRC (<10% of metastatic CRC)

Bristol Meyers Squibb)

MSI-H/dMMR CRC who have progressed following treatment with fluoropyrimidine, oxaliplatin and irinotecan (<10% of metastatic CRC)

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.

Pre-clinical Data

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.

observed that IMX-111 has 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 250mm 3 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 1000mm 3 .

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

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

IMX-111 Tissue-Specific Biologic TM with TME Normalization TM Technology Statistically Significantly Inhibited

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

above paragraph for study description.

Adapted from Abouzeid et al., 2013)

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.

observed that IMX-111 has 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 150mm 3 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 1000mm 3 .

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

IMX-111 Tissue-Specific Biologic TM with TME Normalization TM Technology Statistically Significantly Inhibited

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

above paragraph for study description.

Adapted from Abouzeid et al., 2014)

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.

Composition and Mechanism of Action

IMX-111 Tissue-Specific Biologic TM with TME Normalization TM Technology

is a Tissue-Specific Biologic TM built on our TME Normalization TM 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.

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.

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

IMX-111’s Target GLUT1 is Overexpressed on Colorectal and Other Cancers

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.)

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

IMX-111’s Target GLUT1 Overexpression is Associated with a Poor Prognosis

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.)

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.

IMX-111 Tissue-Specific Biologic TM with TME Normalization TM Technology

Intracellular

Mechanism of Action

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).

Development Strategy

plan to conduct IND-enabling studies for IMX-111 in 2023 (completing in in the first half 2024), pursuing advanced colorectal cancer

as the initial indication.

We anticipate filing an IND for IMX-111 in in the first half 2024.

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 2024.

IMX-111 to pursue advanced colorectal cancer as its initial indication.

Tissue-Specific Biologic TM with Immune Normalization Technology TM for inflammatory bowel disease

Market Opportunity

first potential indications we intend to pursue for IMX-120 are ulcerative colitis (“UC”) and severe Crohn’s disease

(“CD”), which are both forms of inflammatory bowel disease (“IBD”).

IBD is estimated to affect over 2,000,000

people in the United States and over 5,000,000 people globally.

IBD is a complex gastrointestinal disease caused primarily by a dysregulated

immune system.

used to treat IBD include adalimumab (marketed as Humira®, by Abbvie), ustekinumab (marketed as Stelara®, by Janssen/Johnson

& Johnson), and vedolizumab (marketed as Entyvio®, by Takeda).

billion is the total publicly disclosed combined annual sales of adalimumab (Humira®), ustekinumab (Stelara®), and vedolizumab

(Entyvio®, Takeda) according to the most recent available annual reports.

for clinical trials in IBD are measured in terms of remission rates at 4-8 weeks post treatment.

adalimumab (Humira®), in a study of moderate-to-severe UC who received concurrent treatment with oral corticosteroids or immunosuppressants,

overall rates of clinical remission at week 8 were 16.5% on adalimumab and 9.3% on placebo, according to Sandborn et al., 2012.

ustekinumab (Stelara®), in a study of moderate-to-severe UC, overall rates of clinical remission at week 8 were 15.6% on 130mg intravenous

ustekinumab and 5.3% on placebo, according to Sands et al., 2019.

vedolizumab (Entyvio®), in a study of moderately to severely active UC, overall rates of clinical remission at week 6 were 17% on

vedolizumab and 5% on placebo, according to the FDA Entyvio® Prescribing Label.

and CD are two of the most common forms of IBD.

Both UC and CD are chronic, relapsing, remitting, inflammatory conditions of the gastrointestinal

tract that begin most commonly during adolescence and young adulthood.

UC involves the innermost lining of the large intestine, and symptoms

include abdominal pain and diarrhea, frequently with blood and mucus.

CD can affect the entire thickness of the bowel wall and all parts

of the gastrointestinal tract from mouth to anus.

CD symptoms include abdominal pain, diarrhea, and other more systemic symptoms such

as weight loss, nutritional deficiencies, and fever.

current standard of care for the treatment of patients with moderate-to-severe IBD is typically anti-inflammatory agents.

of IBD patients do not respond to first-line anti-tumor necrosis factor agents.

The approvals of the first anti-tumor necrosis factor

agent for the treatment of CD in 1998 and newer biological agents, including anti-integrin and anti-IL12/23, have improved the care of

moderate-to-severe IBD.

these subsequently approved therapies in UC have generally failed to demonstrate a clinical remission effect size of more than 15% relative

Moreover, among those patients who do respond to therapy, up to 50% will lose response over time.

Additionally, the markets

for UC and CD represent a high unmet need patient population.

Only 2 out of 5 UC patients are on advanced therapy.

Composition and Mechanism of Action

IMX-120 Tissue-Specific Biologic TM with Immune Normalization Technology TM for Inflammatory Bowel Disease

built on our SMAR x T Tissue-Specific TM Platform with shared CMC and design elements with our other drug candidates,

is a Tissue-Specific Biologic TM with proprietary GLUT1/confidential target antibody encapsulating polyphenol poly-kinase inhibitors

selectively silencing disease-causing inflammatory bowel immune cells.

inflammatory bowel disease are the interactions between 3 components of the immune synapse:

1) gut-lining enterocytes, 2) gut microbes,

and 3) gut-resident immune cells.

Cellular contacts and signaling molecules exchanged between these components activate abnormal inflammatory

responses in immune cells driving a self-sustaining feed-forward loop of pathological inflammation in gastrointestinal tissues.

simultaneous repression of pathological inflammatory signaling in all of these components at the same time, Immune Normalization TM

Technology halts this self-sustaining feed-forward loop propagated among these 3 components, addressing the root cause of inflammatory

is caused by a dysregulated, chronic, pathological immune response by bowel immune cells to the microbiome and other components of the

gastrointestinal cellular environment.

In the process of becoming dysregulated, cytotoxic T-cells and macrophages secrete signaling cytokines,

resulting in a self-sustaining feed-forward loop of inflammation.

Similar to tumor growth, these 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.

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 IBD.

IMX-120’s polyphenol poly-kinase inhibitors block upstream kinase signal transduction systems that activate

NF-κB and STAT3, thus shutting down the self-sustaining feed-forward loop of inflammation.

GLUT1 presents an ideal targeting moiety

for these overactive immune cells, allowing for tissue-specific delivery of IMX-120.

polyphenols have been generally well-tolerated in multiple clinical trials, two of which are summarized below.

a randomized, multi-center placebo-controlled, double-blind study of 50 mesalamine-treated patients with active mild-to-moderate ulcerative

colitis (UC) (defined by the Simple Clinical Colitis Activity Index, or SCCAI) who did not respond to an additional 2 weeks of the maximum

dose of mesalamine oral and topical therapy, patients were randomly assigned to groups who were given curcumin capsules (3 g/day, n =

26) or an identical placebo (n = 24) for 1 month, with continued mesalamine.

The primary endpoint was the rate of clinical remission

(SCCAI <=2) at week 4.

Clinical and endoscopic responses were also recorded.

The incidence of adverse effects was not significantly

different between the 2 arms.

The primary results of the trial at 4 weeks are outlined in the figure below (left hand side).

a randomized, double-blinded study performed at 5 independent medical centers in Japan, curcuminoid Theracurmin (360 mg/day, 20 patients)

or placebo (10 patients) was administered to patients with active mild-to-moderate Crohn’s disease (CD) for 12 weeks.

clinical activity was assessed by evaluating clinical and endoscopic remission, healing of anal lesions, and blood levels of inflammatory

The primary endpoint was the difference in Crohn’s disease activity index, or CDAI, improvement between the Theracurmin

and placebo groups when comparing week 12 to week 0.

No serious adverse events were observed in either group throughout the study.

primary results of the trial at 4 weeks are outlined in the figure below (right hand side).

both studies, because of the lack of previous data on the subject, a formal power analysis calculation of sample size was not performed.

Also for both studies, P < 0.05 was considered statistically significant.

For all results below, p values of differences between placebo

and treatment group was < 0.05.

We did not fund or sponsor these studies, and we were not involved in these studies or their publications.

Polyphenols have Shown Promise in Both Ulcerative Colitis and Crohn’s

from Lang, et al., 2015 and Sugimoto et al., 2020.

See above paragraphs for study descriptions)

an almost complete lack of bioavailability in oral form, a polyphenol (curcumin) showed signs of clinical activity in a 50 patient UC

study, with >50% remission rate in the treatment arm at week 4 compared to a 0-13% remission rate in a control group at week 4.

a 30 patient CD study, a polyphenol (theracurmin) produced a 35% clinical remission rate in the treatment arm at week 4 compared to 0%

in a control group at week 4.

IMX-120’s proprietary GLUT1 targeting, we believe the potential for IMX-120 in IBD is favorable.

GLUT1 Targeting Significantly Reduces IBD Inflammation in in vitro Models

from Macintyre et al., 2014 and Renaudin et al., 2020.

See below paragraph for study descriptions.

We did not fund or sponsor these studies,

and we were not involved in these studies or their publications.)

inflammatory bowel disease in mice, GLUT1 appears to be required for metabolic reprogramming of CD4 T cells into T effector cells that

are critical for induction of disease-causing inflammation (above figure left hand side graphical abstract).

In mice, GLUT1 inhibition

results in the reduction of global tissue inflammatory score observed by hematoxylin and eosin (HE) staining (above figure right hand

IMX-120 Silences Disease Causing Inflammatory Bowel Immune Cells

(Illustrative

figure adapted from Alzahrani, et al., 2019.

We did not fund or sponsor this study, and we were not involved in this study or its publication.)

targets GLUT1 and a second proprietary target that were described in the literature as key activators of overactive immune response,

that are expected to allow IMX-120 to selectively silence disease-causing, overactive inflammatory bowel immune cells with its polyphenol

poly-kinase inhibitors.

Development Strategy

plan to conduct IND-enabling studies for IMX-120 in 2023 (completing in the first half of 2024), pursuing ulcerative colitis and severe

Crohn’s disease indications.

We anticipate filing an IND for IMX-120 in the first half of 2024.

We plan to initiate a Phase 1b/2a

study with IMX-120 in IBD in the United States and Australia with the first patient anticipated to be dosed in 2024.

We plan for IMX-120

to pursue UC and severe CD indications.

– CELL THERAPIES FOR HEMATOLOGIC MALIGNANCIES

Inc, our majority-owned subsidiary, is a clinical-stage biopharmaceutical company engaged in the discovery and development of novel cell

therapies for oncology and other indications.

We believe cell therapies are one of the forward pillars of medicine, and our mission is

to harness the power of cell therapies to rapidly engineer safe, effective, accessible treatments to improve patient outcomes in oncology

and other indications.

Our N-GENIUS cell engineering platform with EXPAND technology has already produced clinical-stage NXC-201, which

we believe is the first outpatient autologous chimeric antigen receptor T-cell therapy (“CAR-T”).

Autologous cells refer

to the patient’s own cells (versus allogeneic, which refers to another person’s cells).

NXC-201 targets B-cell maturation

antigen (“BCMA”) for multiple myeloma (“MM”) and AL amyloidosis (“ALA”).

Though CAR-T cell therapies

have shown benefits to date, they have historically faced barriers to adoption due to prolonged hospitalization with frequent intensive

care unit (“ICU”) stays due to unpredictable onset and duration of immune effector cell-associated neurotoxicity syndrome

(“ICANS”) neurotoxicity and grade 3 and 4 cytokine release syndrome (“CRS”), leading to a 15-day median hospital

stay for CAR-T treatments today.

NXC-201 has already demonstrated class-leading 90% overall response rates, 59% complete response rates,

and favorable tolerability in MM (exemplified by no ICANS neurotoxicity over 42 multiple myeloma patients).

According to the National

Cancer Institute, “overall response” refers to “the percentage of patients whose cancer shrinks or disappears after

treatment” and “complete response” refers to “the disappearance of all signs of cancer in response to treatment.”

Additionally, 8 ALA patients have also been treated by NXC-201 to-date with a 100% hematologic complete response rate, of which 5 published patients demonstrated 100% hematologic complete response

rate and 100% cardiac,

liver, and renal organ system response rate.

Based on NXC-201 short (median onset day 1, median duration 2 day) low-grade CRS, we believe

NXC-201 could require only a 2-3 day hospital stay, potentially reducing hospital stay costs by 80-87% and make NXC-201 the first and

only potential outpatient CAR-T in development.

Additionally, outpatient treatment could create a much larger accessible market/wider

access for NXC-201 (99% of CAR-T today is administered in large academic medical centers, which account for only 5% of medical centers

by count today in the US).

estimate the current market size for multiple myeloma therapies is $18 billion, expected to reach $29 billion in 2027, according to Wilcock,

Nature Reviews .

The Amyloidosis market was $3.6 billion in 2017, expected to reach $6 billion in 2025.

We believe our N-GENIUS platform with EXPAND

technology will allow us to treat additional BCMA-positive indications such as chronic lymphocytic leukemia (“CLL”), follicular

lymphoma (“FL”), Waldenstrom’s macroglobulinemia, and B-cell lymphoma with NXC-201.

We believe our platform will also

accelerate the development of CAR-T NXC-301 for acute lymphoblastic leukemia (“ALL”), large B-Cell lymphoma (“LBCL”)

and mantle cell lymphoma (“MCL”), as well as NXC-401 for Acute myeloid leukemia (“AML”).

We plan to treat oncology

and other indications.

Lead Product Candidate (Nexcella)

currently in Phase 1b/2a clinical trials for relapsed or refractory (“r/r”) MM and relapsed or refractory (r/r) ALA, is a next generation

autologous CAR-T targeting BCMA.

BCMA is a highly expressed protein in a number of hematologic malignancies including MM.

When an antigen

such as BCMA is expressed on cancer cells, NXC-201 is able to target and kill those cancer cells, sparing healthy tissue.

BCMA has been

shown to be over-expressed on MM, LBCL, CLL, ALA and other plasma cell dyscrasia diseased cells.

Multiple Myeloma Clinical Data To-Date

in Haematologica in 2022 and presented at the 5th European CAR T-cell Meeting, we recently announced positive interim results

for the 42 patients enrolled in our ongoing NEXTIVATE-1 (NCT04720313) Phase 1b/2a clinical trial of NXC-201, our lead product candidate,

for the treatment of patients with relapsed or refractory (r/r) MM.

As of the October 23, 2022 data cutoff date, based on median follow-up

of 146 days (range, 18-314), clinical data is presented below.

These data comprised the dose escalation cohorts for the first dose level

(DL1) (150 million CAR+ T cells, n=6), the second dose level (DL2) (450 million CAR+ T cells, n=7), and the third, therapeutic dose level

(DL3) (800 million CAR+ T cells, n=29).

highlights from the MM data presented are as follows:

overall response rate (“ORR”) was observed in 29 multiple myeloma patients receiving

the therapeutic dose of NXC-201

of 29 (59%) of patients receiving the therapeutic dose reached complete response (“CR”)

or stringent complete response (“sCR”)

was manageable and no neurotoxicity was observed

therapeutic dose of NXC-201 (800 million CAR+T cells) has been established as the recommended

Phase 2 dose (“RP2D”)

supports investigating NXC-201 as the first potential outpatient CAR-T cell therapy

patients in the clinical trial experienced Grade 4 CRS

1 patient in the clinical trial experienced Grade 3 CRS

longest response in the clinical trial so far was over 11 months

42 patients treated as of the October 23, 2022 were triple-class refractory (to at least 1 immunomodulatory drug, 1 proteasome

inhibitor and 1 anti-CD38 antibody).

AL Amyloidosis Clinical Data To-Date

ALA patients have been treated by NXC-201 to-date with a 100% hematologic complete response rate, of which, 4 were Published in Clinical

Cancer Research in 2022 and presented at the 5th European CAR T-cell Meeting.

We recently published positive interim results for the

first 5 patients enrolled in our ongoing clinical trial of NXC-201, our lead product candidate, for the treatment of patients with ALA.

of the October 23, 2022 cutoff for 5 patients treated with NXC-201 with r/r ALA:

100% organ response rate:

organ response rate (cardiac)

organ response rate (renal)

organ response rate (kidney)

100% complete responses (MRD negativity 10 -5 ) were produced by NXC-201.

data comprised the dose escalation cohorts for the first dose level (DL1) (150 million CAR+ T cells, n=1), the second dose level (DL2)

(450 million CAR+ T cells, n=2), and the third, therapeutic dose level (DL3) (800 million CAR+ T cells, n=2).

information is available in our Clinical Cancer Research publication for the first 4 ALA patients treated with NXC-201.

the February 26, 2022 publication date, based on median follow-up of 5.2 months, key highlights are as follows:

100% organ response rate:

organ response rate (cardiac)

organ response rate (renal)

organ response rate (kidney)

100% achieved CR (MRD negativity 10 -5 )

2-stage improvement in New York Heart Association (“NYHA”) Heart Failure Stage was observed with NXC-201

Mean 65% reduction (2,656pg/mL) in NT-proBNP from baseline

No patients experienced ICANS neurotoxicity

No patients experienced Grade 4 CRS

the 4 patients in the ongoing AL amyloidosis clinical trial as of the February 26, 2022 publication date, of the patients with NYHA stage

> 2, 1 was stage 4, and 2 were stage 3.

After treatment with NXC-201, the stage 4 patient improved to stage 2, and both of the stage

3 patients also improved to stage 2.

Pre-treatment

Post-treatment

NXC-201 Treatment Effect

NYHA Stage Reduction

the ongoing AL amyloidosis clinical trial, N-terminal (NT)-pro hormone BNP (NT proBNP) (pg/mL) levels were reported.

the Cleveland Clinic, for patients above 50 years of age, >900 NT proBNP (pg/mL) could mean heart function is unstable.

patients in the ongoing AL amyloidosis ALA clinical trial as of the February 26, 2022 publication date, 3 had pre-treatment NT

proBNP levels of 7,500, 2,800 and 2,773, respectively, which were reduced to 2,700 (4,800 point reduction), 1,505 (1,295 point

reduction) and 901 (1,872 point reduction) (units:

pg/mL), respectively, after treatment with NXC-201.

Pre-treatment

ProBNP (pg/mL)

Post-treatment

ProBNP (pg/mL)

Treatment Effect

ProBNP absolute reduction (pg/mL)

Treatment Effect

ProBNP percentage reduction (pg/mL)

our ongoing AL amyloidosis clinical trial, N-terminal (NT)-pro hormone BNP (NT proBNP) (pg/mL) levels were reported.

According to the

Cleveland Clinic, for patients above 50 years of age, NT proBNP >900 (pg/mL) could mean heart function is unstable.

Of the 4 patients

in the ongoing AL amyloidosis clinical trial as of the February 26, 2022 publication date, 3 had pre-treatment NT proBNP levels of 7,500,

2,800 and 2,773, respectively, which were reduced to 2,700 (4,800 point reduction), 1,505 (1,295 point reduction) and 901 (1,872 point

reduction) (units:

pg/mL), respectively, after treatment with NXC-201.

Potentially The First Outpatient CAR-T

believe NXC-201 is the first and only potential next-generation CAR-T treatment that could be delivered as an outpatient

Outpatient therapy may enable NXC-201

to address a much larger accessible market/wider access to NXC-201 CAR-T therapy (99% of CAR-T today is administered in large academic

medical centers, which account for only 5% of medical centers by count today in the US).

Additionally, NXC-201 treatment may result in

an 80-87% reduction in hospital stay costs (2-3 day hospital stay NXC-201 vs.

15-day CAR-T standard).

multiple myeloma, as of the October 23, 2022 data cutoff, low-grade CRS duration of median 2 days at therapeutic dose (range:

(n=42) points to NXC-201 potentially becoming the first and only out-patient CAR-T for Multiple Myeloma and other BCMA-positive malignancies.

AL amyloidosis, as of the October 23, 2022 publication date, no grade 4 CRS was observed, and CRS duration of median 4 days at therapeutic

1-5 days) (n=5) points to NXC-201 potentially becoming the first and only out-patient CAR-T for AL Amyloidosis.

Market Opportunity (Nexcella)

hematologic cancer market size is $60 billion today, growing to $120 billion in 2028.

– Multiple Myeloma

estimate the current market size for multiple myeloma therapies is $18 billion, expected to reach $29 billion in 2027, according to Wilcock,

Nature Reviews .

myeloma (“MM”) is an incurable blood cancer of plasma cells that starts in the bone marrow and is characterized by an excessive

proliferation of these cells.

Despite initial remission, unfortunately, most patients are likely to relapse.

There are 34,470 patients

in the United States diagnosed with MM each year.

Prognosis for patients who do not respond to or relapse after treatment with standard

therapies, including protease inhibitors and immunomodulatory agents remains poor.

is the third most common hematological malignancy in the United States and Europe, representing approximately 10% of all hematological

cancer cases, 20% of deaths due to hematological malignancies and impacting over 100,000 patients globally each year.

The Surveillance,

Epidemiology, and End Results (“SEER”) Program database projects that approximately 35,000 new cases of MM in the United States and over

35,000 new cases in six select markets within Europe and Asia.

2021, the FDA approved idecabtagene vicleucel (marketed as ABECMA® by Bristol Myers Squibb), at the time the only BCMA-targeted CAR-T

for multiple myeloma.

ABECMA® was approved based on a 100-patient, open-label MM study which resulted in a complete response rate

of 28% and >= Grade 3 neurotoxicity of 8% at the therapeutic dose, according to the ABECMA® FDA approval label.

December 2022, Gilead paid $225 million upfront and invested $100 million in Arcellx, Inc.

in exchange to equally share profits of CART-ddBCMA,

a BCMA-targeted CAR-T for multiple myeloma.

CART-ddBCMA was evaluated in a clinical trial in which 19 patients were treated at the therapeutic

dose, which resulted in a complete response rate of 71%, and >= Grade 3 neurotoxicity of 4%, according to Arcellx, Inc.

– AL amyloidosis

estimate the current market size for amyloidosis therapies is $3.6 billion, expected to reach $6 billion in 2027.

is a rare systemic disorder caused by an abnormality of plasma cells in the bone marrow.

Misfolded amyloid proteins produced by plasma

cells cause buildup in and around tissues, nerves and organs, gradually affecting their function.

This can cause progressive and widespread

organ damage, and high mortality rates.

affects roughly 30,000 – 40,000 patients in total throughout the U.S.

and Europe, and it is estimated that there are approximately

3,000 – 4,000 new cases of AL amyloidosis annually in the U.S., though actual incidence is likely higher as a result of under-diagnosis.

Amyloidosis has a one-year mortality rate of 47 percent, 76 percent of which is caused by cardiac amyloidosis.

ALA remains a high unmet need disease with just one FDA approved therapy

in the last two decades - daratumumab.

2021, the FDA approved daratumumab (marketed as DARZALEX® by Janssen/Johnson & Johnson), which is the only FDA approved therapy

for AL amyloidosis.

Daratumumab (DARZALEX®) was trialed in an ALA study where daratumumab was combined with cyclophosphamide + bortezomib

+ dexamethasone in a 4-drug combination, which produced a 53% hematologic complete response rate with a 42% organ response rate (cardiac)

according to Kastritis, et al., 2021.

● We are leveraging market CAR-T experience so far—manufacturing consistency,

automation technology, efficacy, tolerability.

for MM CAR-Ts continues to exceed supply – there are currently only 2 MM CAR-Ts on

common with approved CAR-Ts:

High grade Cytokine Release Syndrome (> grade 3) and neurotoxicity

side-effects.

● Bi-specifics/Allogeneic

CAR-Ts still work in progress.

Pipeline (Nexcella)

are building a broad and scalable pipeline that has positioned us to capitalize on the potential of our proprietary platform technologies

and achieve long-term growth and sustainability within the field of cell therapy.

We believe our N-GENIUS platform and EXPAND technology

will enable us to target a range of hematologic malignancies.

have worldwide rights to all of our programs and have summarized our preclinical and clinical programs in the pipeline chart below:

are in the process of extending our ongoing NEXICART-I (NCT04720313) Phase 1b/2a clinical trial to the United States, which could cause

NEXICART-I to be a registrational clinical trial, generating clinical data that could be included in a Biologics License Application

(BLA) to the U.S.

Food and Drug Administration (FDA).

Based on our current regulatory pathway, we believe that results from our NEXICART-I

trial, if positive, together with clinical results from our United States studies could be sufficient to support the filing of a BLA.

Platform and Technologies (Nexcella)

N-GENIUS platform has broad potential utility in hematologic and autoimmune disease.

Our N-GENIUS platform, which has produced NXC-201, consists three key elements:

(1) Purpose-Built Cell Therapy Evidence Capture Engine + Relational Database, which relates Nexcella internal data to external to accelerate

therapy design, manufacture, and preclinical;

(2) proprietary EXPAND technology, which is applied to multiple cell therapy indications,

already utilized to create NXC-201, to potentially increase efficacy and tolerability;

and (3) Atomized, Novel Binding Scaffold Generation

Engine, which allows us to make the correct binding for every molecule.

We believe key characteristics of NXC-201 may apply to other products

candidates produced by the N-GENIUS Platform.

Those 3 key characteristics are:

(a) high transduction efficiency (lower dose may lead to

lower toxicity), (b) low tonic signaling (lower off-target toxicity may lead to lower toxicity), and (c) anti-exhaustion capability (increased

persistence may lead to efficacy over an extended period of time).

Clinical Development Plan and Milestones (Nexcella)

are in the process of extending our ongoing NEXICART-I (NCT04720313) Phase 1b/2a clinical trial to the United States, which could cause

NEXICART-I to be a registrational clinical trial, generating clinical data that could be included in a Biologics License Application

(BLA) to the U.S.

Food and Drug Administration (FDA).

We also intend to rapidly pursue clinical development of NXC-201 in AL Amyloidosis,

in earlier lines of multiple myeloma therapy, and other BCMA-positive hematologic malignancies on an outpatient basis.

MM, we plan to enroll approximately 100 patients in our ongoing open-label study at the recommended phase 2 dose, then submit a BLA for

approval to the FDA.

ALA, we plan to enroll approximately 30-40 patients in an open-label study at the recommended phase 2 dose, then submit a BLA for approval

2023, we plan to continue to report interim data results from our ongoing phase 1b/2a NXC-201 clinical trial, complete a pre-IND meeting

with the FDA, file an IND for US phase 2 trial for NXC-201, and open a US clinical trial for NXC-201.

plan to submit our first NXC-201 BLA to the FDA in the first half of 2025.

believe that the foundation of our competitive advantage is our proprietary technology, clinical evidence, track record of execution,

manufacturing success, and assembly of a proven management team.

We believe these advantages may position us to achieve significant market

share in a large and attractive market and to ultimately transform the cell therapy market, contributing to a significant advancement

Other Programs

We are also pursuing development of NXC-201 in autoimmune diseases, a $25

billion combined annual market size according to Grand View Research and Fortune Business Insights.

Manufacturing

have already established a track record of producing 7 batches of our TSTx according to current Good Manufacturing Practice (“cGMP”),

and have treated 17 patients so-far in our ongoing Phase 1b/2a clinical trial as of February 2023.

have a strong track record of successful manufacturing.

We have already established a track record of producing NXC-201 for patient

dosing and testing in the U.S.

(73 patients dosed to-date).

In addition, we have already developed a scalable, reliable

manufacturing process for our TSTx according to current Good Manufacturing Practice (“cGMP”).

will continue to leverage our established technical, manufacturing, analytical, quality, cGMP, project management expertise and existing

relationships to contract with appropriate CMOs to manufacture our TSTx TM moving forward.

currently do not own or operate any manufacturing facilities.

To date, we have obtained active pharmaceutical ingredients (“API”)

and drug product for our product candidates from several third party contract manufacturers.

We are in the process of developing our

supply chain for each of our product candidates and have entered into agreements pursuant to which third-party contract manufacturers

will provide us with necessary quantities of API and drug product on a project-by-project basis based upon our needs.

We rely, and expect

to continue to rely for the foreseeable future, on FDA, EMA, or other jurisdiction-registered third-party contract manufacturing organizations

to produce our product candidates for pre-clinical and clinical testing, as well as for commercial manufacture if our product candidates

receive marketing approval.

As part of the manufacture and design process for our product candidates, we rely on internal, scientific

and manufacturing know-how and trade secrets and the know-how and trade secrets of third-party manufacturers.

We also contract with additional

third parties for the filling, labeling, packaging, storage and distribution of investigational drug products.

We believe that this strategy

allows us to maintain a more efficient infrastructure by eliminating the need for us to invest in our own manufacturing facilities, equipment

and personnel while also enabling us to focus our expertise and resources on the development of our product candidates.

We maintain agreements

with our manufacturers that include confidentiality and intellectual property, and quality provisions to protect our proprietary rights

related to our product candidates and satisfy regulatory requirements.

relationships to contract with appropriate CMOs to manufacture our cell therapies and TSTx moving forward.

January 2024, the Company entered into a long-term operating lease agreement for biopharmaceutical manufacturing space located in

To date, we have obtained active pharmaceutical ingredients (“API”) and drug product for our product

candidates from several third party contract manufacturers.

We are in the process of developing our supply chain for each of our

product candidates and have entered into agreements pursuant to which third-party contract manufacturers will provide us with

necessary quantities of API and drug product on a project-by-project basis based upon our needs.

We rely, and expect to continue to

rely for the foreseeable future, on FDA, EMA, or other jurisdiction-registered third-party contract manufacturing organizations to

produce our product candidates for pre-clinical and clinical testing, as well as for commercial manufacture if our product

candidates receive marketing approval.

As part of the manufacture and design process for our product candidates, we rely on

internal, scientific and manufacturing know-how and trade secrets and the know-how and trade secrets of third-party manufacturers.

We also contract with additional third parties for the filling, labeling, packaging, storage and distribution of investigational

drug products.

We believe that this strategy allows us to maintain a more efficient infrastructure by eliminating the need for us to

invest in our own manufacturing facilities, equipment and personnel while also enabling us to focus our expertise and resources on

the development of our product candidates.

We maintain agreements with our manufacturers that include confidentiality and

intellectual property, and quality provisions to protect our proprietary rights related to our product candidates and satisfy

regulatory requirements.

biotechnology industry is extremely competitive in the race to develop new products.

While we believe we have significant competitive

advantages with our years of expertise in systems biology drug design, pharmacology and drug delivery, and clinical depth, trials and

expertise, and intellectual property position, we currently face and will continue to face competition for our development programs from

groups that are developing therapies for oncology and inflammation.

The competition is likely to come from multiple sources, including

larger pharmaceutical companies, biotechnology companies, and academic institutions.

developing therapies for both oncology and inflammation include, but are not limited to, Kymera Therapeutics Inc., Morphic Holding Inc.,

and RAPT Therapeutics Inc.

Companies developing therapies for IBD (including UC and CD) include, but are not limited to, Arena Pharmaceuticals

Inc., Landos Biopharma Inc., and Seres Therapeutics Inc.

developing CAR-Ts targeting multiple myeloma include, but are not limited to, Janssen/Johnson & Johnson, Bristol Myers Squibb, and

Arcellx, Inc.

Companies developing therapies for AL amyloidosis include, but are not limited to, Prothena Corp, Caelum Biosciences (Now

Alexion/AstraZeneca), and Janssen/Johnson & Johnson.

– Soft Tissue Sarcoma

in trials to treat STS include nivolumab (marketed as Opdivo®, by Bristol Meyers Squibb), ipilimumab (marketed as Yervoy®, by

Merck & Co), and pembrolizumab (marketed as Keytruda®, by Merck & Co).

(Opdivo®), was trialed in a study in which 61% of patients had received at least three previous lines of chemotherapy prior to nivolumab.

Nivolumab monotherapy produced a mPFS in sarcoma of 1.7 months, according to D’Angelo et al., 2018.

(Opdivo®) and ipilimumab (Yervoy®), were trialed in a study in which 61% of patients had received at least three previous lines

of chemotherapy prior to a combination of nivolumab + ipilimumab.

Nivolumab + ipilimumab combination therapy produced a mPFS in sarcoma

of 4.1 months, according to D’Angelo et al., 2018.

Pembrolizumab

(Keytruda®, Merck & Co), was trialed in a study in which 42% of patients had received at least three previous lines of chemotherapy

prior to pembrolizumab.

Pembrolizumab monotherapy produced a mPFS in sarcoma of 4.2 months, according to Tawbi et al., 2017.

addition to the above, companies with approved therapies and that are developing therapies for soft tissue sarcoma include, but are

not limited to, BioAtla Inc., Epizyme Inc., Nanobiotix SA, C4 Therapeutics, Inc., Adaptimmune Therapeutics plc, Eisai, Novartis,

Mirati Therapeutics, Inc., and Janssen/Johnson & Johnson.

We currently face and will continue to face

competition for our development programs from groups that are developing therapies for oncology and inflammation.

The competition is

likely to come from multiple sources, including larger pharmaceutical companies, biotechnology companies, and academic

institutions.

developing therapies for AL amyloidosis include, but are not limited to, Prothena Corp, Caelum Biosciences (Now Alexion/AstraZeneca),

and Janssen/Johnson & Johnson.

developing or intend to develop cell therapies for autoimmune indications include, but are not limited to:

Kyverna Therapeutics, Inc.;

Cabaletta Bio, Inc.;

Fate Therapeutics Inc.;

and Arcellx, Inc.

success depends in part on our ability to obtain and maintain proprietary protection for our product candidates, technology and know-how,

13 unchanged sentences

and foreign patent

applications, 2 pending international (PCT) patent applications, and 1 pending U.S.

provisional patent application related to our

technology platform and our product candidates.

Of those, 1 patent has been granted in the U.S.

and 10 patents have been granted in

the following countries:

France, Germany, Ireland, Switzerland, and the United Kingdom.

One non-provisional patent application is

currently pending in the U.S.

and 2 foreign patent applications are currently pending before the European Patent Office and Hong Kong.

applications, 2 pending international (PCT) patent applications related to our technology platform and our product candidates.

those, 2 patents has been granted in the U.S.

and 10 patents have been granted in the following countries:

France, Germany, Ireland,

Switzerland, and the United Kingdom.

Two non-provisional patent applications are currently pending in the U.S.

and 9 foreign patent

applications are currently pending in Australia, Brazil, Canada, Europe, Hong Kong, Japan and Mexico.

Certain platform patents are expected to remain in force until 2036.

Other patents directed to platform

technology are expected to remain in force until 2036.

below patents and patent applications comprise our patent portfolio.

All of the patents and patent applications listed below are owned

Expected Expiration Date

Type of Patent Protection

United States

Cancer therapeutics

Methods of treatment

United States

Methods and related compositions for the treatment of cancer

Compositions and methods of treatment

United States

Nanoparticles for the treatment of inflammatory diseases

Compositions and methods of treatment

PCT/US2022/036419

Nanoparticles for cancer treatment

Compositions and methods of treatment

PCT/US22/44948

Nanoparticles for cancer treatment

Compositions and methods of treatment

Micelles ciblant le Glut-1 et comprenant de la curcumine (Glut-1 targeted and curcumin loaded micelles)

Glut-1 zielgerichtete und mit Kurkumin beladene Mizellen (Glut-1 targeted and curcumin loaded micelles)

Glut-1 targeted and curcumin loaded micelles

Glut-1 zielgerichtete und mit Kurkumin beladene Mizellen (Glut-1 targeted and curcumin loaded micelles)

United Kingdom

Glut-1 targeted and curcumin loaded micelles

European Patent Office

Micelle comprising an inhibitor of NF-KB

Expiration Date

of Patent Protection

AND RELATED COMPOSITIONS FOR THE TREATMENT OF CANCER

and methods of treatment

AND RELATED COMPOSITIONS FOR THE TREATMENT OF CANCER

and methods of treatment

COMPRISING AN INHIBITOR OF NF-KB

and methods of treatment

42021037058.1

Micelle comprising an inhibitor of NF-kB

et compositions associées pour le traitement du cancer (methods and related compositions for the treatment of cancer)

und verwandte zusammensetzungen zur behandlung von krebs (methods and related compositions for the treatment of cancer)

COMPRISING AN INHIBITOR OF NF-KB

and methods of treatment

ZIELGERICHTETE UND MIT KURKUMIN BELADENE MIZELLEN

TARGETED AND CURCUMIN LOADED MICELLES

UND VERWANDTE ZUSAMMENSETZUNGEN ZUR BEHANDLUNG VON KREBS

ET COMPOSITIONS ASSOCIÉES POUR LE TRAITEMENT DU CANCER

AND RELATED COMPOSITIONS FOR THE TREATMENT OF CANCER

und verwandte zusammensetzungen zur behandlung von krebs (methods and related compositions for the treatment of cancer)

AND RELATED COMPOSITIONS FOR THE TREATMENT OF CANCER

MX/a/2024/000302

NANOPARTICLES

FOR CANCER TREATMENT

and methods of treatment

NANOPARTICLES

FOR CANCER TREATMENT

and methods of treatment

NANOPARTICLES

FOR CANCER TREATMENT

and methods of treatment

NANOPARTICLES

FOR CANCER TREATMENT

and methods of treatment

2024 000075 3

NANOPARTICLES

FOR CANCER TREATMENT

and methods of treatment

NANOPARTICLES

FOR CANCER TREATMENT

and methods of treatment

NANOPARTICLES

FOR CANCER TREATMENT

and methods of treatment

PCT/US2022/044948

NANOPARTICLES

FOR CANCER TREATMENT

and methods of treatment

NANOPARTICLES

FOR CANCER TREATMENT

and methods of treatment

PCT/US2023/69537

NANOPARTICLES

FOR THE TREATMENT OF INFLAMMATORY DISEASES

Provided all maintenance and renewal fees are timely paid.

Any resulting patents in this family are expected to expire in 2042 (not including any patent term adjustment and patent term extension

in the United States and equivalents in foreign countries).

Additionally,

as of March 17, 2022, Nexcella, Inc.

has global exclusive rights to patents #63/308,277, #63/368,002, PCT/IL2023/050142 which are directed to our N-GENIUS platform,

EXPAND technology, and to our product candidates, including NXC-201.

The patents include one pending PCT application (PCT

Application No.

PCT/IL2023/050142), filed in 2023.

The application relates to a chimeric antigen receptor (CAR) molecule specific

for B cell maturation antigen (BCMA), compositions and methods thereof for the treatment of immune-related disorders.

enter the national phase of the PCT application in multiple countries.

Any resulting patents in this family are expected to expire

in 2043 (not including any patent term adjustment and patent term extension in the United States and equivalents in foreign

as of March 15, 2024, our subsidiary Nexcella, Inc.

has global exclusive rights to PCT Application No.

PCT/IL2023/050142 filed in 20023 and claiming priority

Provisional Patent Application Nos.

63/308,277 and 63/368,002.

The application is directed to our N-GENIUS platform, EXPAND technology,

and to our product candidates, including NXC-201.

The application relates to a chimeric antigen receptor

(CAR) molecule specific for B cell maturation antigen (BCMA), compositions and methods thereof for the treatment of immune-related disorders.

We plan to enter the national phase of the PCT application in multiple countries.

Any resulting patents in this family are expected to

expire in 2043 (not including any patent term adjustment and patent term extension in the United States and equivalents in foreign countries).

generally pursue multilayered patent protection covering the composition of matter including the formulations of the product candidates,

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and License Agreement with Hadasit and BIRAD

December 8, 2022, Nexcella entered into a Research and License Agreement (the “Agreement”) with Hadasit Medical Research Services

& Development, Ltd.

December 8, 2022, our subsidiary Nexcella entered into a Research and License Agreement (the “Agreement”) with Hadasit Medical

Research Services & Development, Ltd.

and BIRAD – Research and Development Company Ltd.

(collectively, the “Licensors”) pursuant to

which the Licensors granted to Nexcella an exclusive, worldwide, royalty-bearing license throughout the world, except Israel, Cyprus and

other countries in the Middle East (the “Territory”), to an invention entitled “Anti-BCMA CAR-T cells to target plasma

cell” to develop, manufacture, have manufactured, use, market, offer for sale, sell, have sold, export and import the Licensed Product

(as defined in the Agreement).

Pursuant to the Agreement, Nexcella shall paid the

Licensors an upfront fee of $1,500,000 in December 2022 .

Additional quarterly payments totaling approximately $13.0 million are due through September 2026 along with an annual license fee of

Nexcella has agreed to pay royalties to the Licensors equal to 5% of based on Net Sales (as defined in the Agreement) during

the Royalty Period.

(collectively, the “Licensors”)

pursuant to which the Licensors granted to Nexcella an exclusive, worldwide, royalty-bearing license throughout the world, except Israel,

Cyprus and other countries in the Middle East (the “Territory”), to an invention entitled “Anti-BCMA CAR-T cells to

target plasma cell” to develop, manufacture, have manufactured, use, market, offer for sale, sell, have sold, export and import

the Licensed Product (as defined in the Agreement).

Pursuant to the Agreement, Nexcella paid the Licensors an upfront fee of $1,500,000

in December 2022.

Additional quarterly payments totaling approximately $13.0 million are due through September 2026 along with an annual

license fee of $50,000.

Nexcella has agreed to pay royalties to the Licensors equal to 5% of based on Net Sales (as defined in the Agreement)

during the Royalty Period.

“Royalty Period” means for each Licensed Product, on a country-to-country basis, the period commencing

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Product or (c) 15 years from the date of First Commercial Sale (as defined in the Agreement) of a Licensed Product in such country.

Nexcella shall pay milestone payments of up to $20 million upon the achievement of certain Net Sales as set forth in the Agreement and

Nexcella has committed to funding NXC-201 clinical trials in Israel over 4 years for an estimated total cost of approximately $13 million,

spread on a quarterly basis over that period, which Nexcella believes will generate clinical trial data owned by Nexcella.

the Agreement commenced on December 8, 2022 and, unless earlier terminated pursuant to the terms thereof, shall continue in full force

and effect until the later of the expiration of the last Valid Claim under a Licensed Patent or a Joint Patent (as defined in the Agreement)

or Exclusivity Right covering a Licensed Product or the expiration of a continuous period of 15 years during which there shall not have

been a First Commercial Sale of any Licensed Product in any country in the world.

Licensors may terminate the Agreement immediately if

Nexcella or its affiliates or sublicensees commences an action in which it challenges the validity, enforceability or scope of any of

the Licensed Patents or Joint Patents.

In addition, either party may terminate the Agreement if the other party materially breaches the

Agreement and fails to cure such breach within 30 days.

addition, Nexcella shall pay milestone payments of up to $20 million upon the achievement of certain Net Sales as set forth in the Agreement

and Nexcella has committed to funding NXC-201 clinical trials in Israel over 4 years for an estimated total cost of approximately $13

million, spread on a quarterly basis over that period, which Nexcella believes will generate clinical trial data owned by Nexcella.

term of the Agreement commenced on December 8, 2022 and, unless earlier terminated pursuant to the terms thereof, shall continue in full

force and effect until the later of the expiration of the last Valid Claim under a Licensed Patent or a Joint Patent (as defined in the

Agreement) or Exclusivity Right covering a Licensed Product or the expiration of a continuous period of 15 years during which there shall

not have been a First Commercial Sale of any Licensed Product in any country in the world.

Licensors may terminate the Agreement immediately

if Nexcella or its affiliates or sublicensees commences an action in which it challenges the validity, enforceability or scope of any

of the Licensed Patents or Joint Patents.

In addition, either party may terminate the Agreement if the other party materially breaches

the Agreement and fails to cure such breach within 30 days.

Additionally, Licensors may terminate the Agreement if Nexcella becomes insolvent

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with Nexcella

December 8, 2022, we entered a Founders Agreement with Nexcella (the “Nexcella Founders Agreement”).

Pursuant to the Nexcella

Founders Agreement, in consideration for the time and capital expended in the formation of Nexcella and the identification of specific

assets, the acquisition of which benefit Nexcella, we received 250,000 shares of Nexcella’s Class A Preferred Stock, 1,000,000

December 8, 2022, we entered a Founders Agreement with our subsidiary Nexcella (the “Nexcella Founders Agreement”).

to the Nexcella Founders Agreement, in consideration for the time and capital expended in the formation of Nexcella and the identification

of specific assets, the acquisition of which benefit Nexcella, we received 250,000 shares of Nexcella’s Class A Preferred Stock,

1,000,000 shares of Nexcella’s Class A Common Stock, and 5,000,000 shares of Nexcella’s common stock.

In addition, pursuant to the

Nexcella Founders Agreement, prior to a Qualified IPO (as defined in Nexcella’s Amended and Restated Certificate of Incorporation,

In addition, pursuant

to the Nexcella Founders Agreement, prior to a Qualified IPO (as defined in Nexcella’s Amended and Restated Certificate of Incorporation,

as amended (the “Nexcella COI”)) or Qualified Change in Control (as defined in the Nexcella COI), we shall provide funds

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solely for cash, then $5,000,000 in cash).

We shall be entitled to cast such number of votes equal to the number of whole shares

of Nexcella common stock into which our Class A Common Stock are convertible as of the record date for determining stockholders entitled

to vote on matters presented to the stockholders of Nexcella.

We shall be entitled to cast such number of votes equal to the number of whole shares of Nexcella

common stock into which our Class A Common Stock are convertible as of the record date for determining stockholders entitled to vote

on matters presented to the stockholders of Nexcella.

addition to the foregoing, we shall be entitled to one vote for each share of Nexcella common stock held by us.

Except as provided by

law or by the Nexcella COI, holders of Nexcella Class A Common Stock and Class A Preferred Stock shall vote together with the

holders of Nexcella common stock, as a single class.

law or by the Nexcella COI, holders of Nexcella Class A Common Stock and Class A Preferred Stock shall vote together with the holders

of Nexcella common stock, as a single class.

additional consideration under the Nexcella Founders Agreement, Nexcella will also:

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Services Agreement

as of December 8, 2022, we entered into a Management Services Agreement (the “Nexcella MSA”) with Nexcella.

Pursuant to the

terms of the Nexcella MSA, we will render management, advisory and consulting services to Nexcella.

Services provided under the Nexcella

MSA may include, without limitation, (i) advice and assistance concerning any and all aspects of Nexcella’s operations, clinical

trials, financial planning and strategic transactions and financings and (ii) conducting relations on behalf of Nexcella with accountants,

attorneys, financial advisors and other professionals (collectively, the “Services”).

At our request, Nexcella shall utilize

clinical research services, medical education, communication and marketing services and investor relations/public relation services of

companies or individuals designated by us, provided those services are offered at market prices.

In consideration for the Services, Nexcella

will pay us an annual base management and consulting fee of $500,000 (the “Annual Consulting Fee”), payable in advance in

equal quarterly installments;

provided, however, that such Annual Consulting Fee shall be increased to $1.0 million for each calendar

year in which Nexcella has Net Assets (as defined in the Nexcella MSA) in excess of $100 million at the beginning of the calendar year.

Notwithstanding the foregoing, the first Annual Consulting Fee payment shall be made on the first business day of the calendar quarter

immediately following the completion of the first equity financing for Nexcella that is in excess of $10 million in gross proceeds.

first payment shall include all amounts in arrears from the effective date of the Nexcella MSA through such payment as well as the amounts

in advance for such first quarterly payment.

Actual and direct out-of-pocket expenses reasonably incurred by us in performing the Services

shall be reimbursed to us by Nexcella.

The Nexcella MSA shall continue for a period of five years from the effective date thereof and

shall be automatically extended for additional five year periods unless we and Nexcella provide written notice to not extend the term

at least 90 days prior to the end of the term, unless the Nexcella MSA is terminated earlier by mutual agreement between us and Nexcella.

On December 8, 2022,

we issued an aggregate of 350,000 shares of Nexcella restricted common stock to our officers for services to be performed, which shares

vest in 48 equal monthly installments.

12, 2023, Nexcella entered into share purchase agreements with certain accredited investors for their purchase of an aggregate 100,152

shares of Nexcella’s common stock at a purchase price of $6.49 per share, for gross proceeds of approximately $650,000.

our Chief Executive Officer and Chief Financial Officer collectively purchased 23,112 shares of Nexcella’s common stock for an aggregate

purchase price of $150,000.

As a result of the foregoing offering, as of January 12, 2023, we owned 98% of Nexcella.

22, 2023, we entered into an ATM Sales Agreement (the “Sales Agreement”) with ThinkEquity LLC (the “Sales Agent”),

pursuant to which we may offer and sell, from time to time, through the Sales Agent, shares of our common stock having an aggregate offering

price of up to $5,000,000, subject to the terms and conditions set forth in the Sales Agreement.

We will pay the Sales Agent a fixed commission

rate of 3.75% of the aggregate gross proceeds from the sale of the shares of our common stock pursuant to the Sales Agreement.

paid an expense deposit of $15,000 to the Sales Agent, which will be applied against the actual out-of-pocket accountable expenses.

have agreed to reimburse the Sales Agent for all expenses related to the offering including, without limitation, the fees and expenses

of the Sales Agent’s legal counsel up to $50,000, and shall reimburse the Sales Agent, upon request, for such costs, fees and expenses

in an amount not to exceed $7,500 on a quarterly basis for the first three fiscal quarters of each year and $10,000 for the fiscal fourth

quarter of each year.

The offering pursuant to the Sales Agreement will terminate upon the earlier of (i) the sale of all of the shares

of common stock subject to the Sales Agreement, and (ii) termination of the Sales Agreement as permitted therein.

We may terminate

the Sales Agreement in our sole discretion at any time by giving ten days’ prior notice to the Sales Agent.

The Sales Agent may

terminate the Sales Agreement under the circumstances specified in the Sales Agreement and in its sole discretion at any time by giving

ten days’ prior notice to us.

In addition, the Sales Agreement may be terminated upon mutual agreement by us and the Sales Agent.

as of December 8, 2022, we entered into a Management Services Agreement (the “Nexcella MSA”) with our subsidiary Nexcella.

Pursuant to the terms of the Nexcella MSA, we will render management, advisory and consulting services to Nexcella.

Services provided

under the Nexcella MSA may include, without limitation, (i) advice and assistance concerning any and all aspects of Nexcella’s

operations, clinical trials, financial planning and strategic transactions and financings and (ii) conducting relations on behalf of

Nexcella with accountants, attorneys, financial advisors and other professionals (collectively, the “Services”).

At our request,

Nexcella shall utilize clinical research services, medical education, communication and marketing services and investor relations/public

relation services of companies or individuals designated by us, provided those services are offered at market prices.

In consideration

for the Services, Nexcella will pay us an annual base management and consulting fee of $500,000 (the “Annual Consulting Fee”),

payable in advance in equal quarterly installments;

provided, however, that such Annual Consulting Fee shall be increased to $1.0 million

for each calendar year in which Nexcella has Net Assets (as defined in the Nexcella MSA) in excess of $100 million at the beginning of

the calendar year.

Notwithstanding the foregoing, the first Annual Consulting Fee payment shall be made on the first business day of

the calendar quarter immediately following the completion of the first equity financing for Nexcella that is in excess of $10 million

in gross proceeds.

The first payment shall include all amounts in arrears from the effective date of the Nexcella MSA through such payment

as well as the amounts in advance for such first quarterly payment.

Actual and direct out-of-pocket expenses reasonably incurred by us

in performing the Services shall be reimbursed to us by Nexcella.

The Nexcella MSA shall continue for a period of five years from the

effective date thereof and shall be automatically extended for additional five year periods unless we and Nexcella provide written notice

to not extend the term at least 90 days prior to the end of the term, unless the Nexcella MSA is terminated earlier by mutual agreement

between us and Nexcella.

February 2024, we conducted an underwritten public offering of 5,535,055 shares of common stock at the public offering price is $2.71

per shares, for the net proceeds, after underwriter discounts and offering expenses, of $13,566,697.

Pursuant to the underwriting

agreement, we granted the underwriter a 30-day over-allotment option to purchase up to an additional 783,970 shares of our common stock,

which was exercised in full on March 1, 2024 for the net proceeds, after underwiring discounts and offering expenses, of $1,954,594.

February 2024, the European Commission (EC) granted orphan drug designation to NXC-201 for the treatment of AL Amyloidosis.

of European ODD include:

10 years of market exclusivity once authorized in the EU;

Access to the EU centralized authorization procedure;

and reduced fees for EU protocol assistance, marketing authorization applications, inspections before authorization, applications for

changes to marketing authorizations made after approval, and reduced annual fees.

States Regulation of Drugs and Biologics

expect that IMX-110 will be regulated by the FDA as a complex non-biologic by submitting a New Drug Application (“NDA”).

We expect that IMX-111 and IMX-120 will be regulated by the FDA as a biological product, or biologic, by submitting a Biologics License

Application (“BLA”) to the FDA.

We expect to pursue United States and global regulatory designations, vouchers, conditional

approvals and accelerated approvals where appropriate.

expect that NXC-201 will be regulated by the FDA as a biologic by submitting a Biologic License Application (“BLA”).

that IMX-110 will be regulated by the FDA as a complex non-biologic by submitting a New Drug Application (“NDA”).

to pursue United States and global regulatory designations, vouchers, conditional approvals and accelerated approvals where appropriate.

business activities are subject to various laws, rules and regulations of the United States as well as of foreign governments.

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Development and Review Programs

Fast Track Designation

Track Designation

FDA offers several expedited development and review programs for qualifying product candidates.

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required user fees upon submission of the first section of the NDA or BLA.

Breakthrough Therapy Designation

Therapy Designation

product intended to treat a serious or life-threatening disease or condition may also be eligible for breakthrough therapy designation

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development and review of the product, including involvement of senior managers.

Priority Review

product is eligible for priority review if it has the potential to provide a significant improvement in the treatment, diagnosis or prevention

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Medicine Advanced Therapy Designation

passage of the Cures Act in December 2016, Congress authorized the FDA to accelerate review and approval of products designated as

regenerative medicine advanced therapies.

A product is eligible for RMAT designation if it is a regenerative medicine therapy that

is intended to treat, modify, reverse or cure a serious or life-threatening disease or condition and preliminary clinical evidence

indicates that the product has the potential to address unmet medical needs for such disease or condition.

Regenerative medicine

therapies include cell therapy, therapeutic tissue engineering product, human cell and tissue products and combination products that

use such products.

The benefits of a regenerative medicine advanced therapy designation include early interactions with FDA to

expedite development and review, benefits available to breakthrough therapies, potential eligibility for priority review, and

accelerated approval based on surrogate or intermediate endpoints.

RMAT designation may be rescinded if a product no longer meets

the qualifying criteria.

passage of the Cures Act in December 2016, Congress authorized the FDA to accelerate review and approval of products designated as regenerative

medicine advanced therapies.

A product is eligible for RMAT designation if it is a regenerative medicine therapy that is intended to

treat, modify, reverse or cure a serious or life-threatening disease or condition and preliminary clinical evidence indicates that the

product has the potential to address unmet medical needs for such disease or condition.

Regenerative medicine therapies include cell

therapy, therapeutic tissue engineering product, human cell and tissue products and combination products that use such products.

benefits of a regenerative medicine advanced therapy designation include early interactions with FDA to expedite development and review,

benefits available to breakthrough therapies, potential eligibility for priority review, and accelerated approval based on surrogate

or intermediate endpoints.

RMAT designation may be rescinded if a product no longer meets the qualifying criteria.

Pediatric Disease Priority Review Voucher Program

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and (b) rare disease or conditions within the meaning of the Orphan Drug Act.

A sponsor may

choose to request RPDD, but the designation process is entirely voluntary;

requesting designation is not a prerequisite to requesting

or receiving a priority review voucher.

In addition, sponsors who choose not to submit a RPDD request may nonetheless receive a

priority review voucher if they request such a voucher in their original marketing application and meet all of the eligibility criteria.

The Rare Pediatric Disease Priority Review Voucher Program was extended as part of the 2021 Coronavirus Response and Relief Supplemental

Consolidated Appropriations Act in December 2020.

As part of this extension, after September 30, 2024, the FDA may only award a voucher

for an approved rare pediatric disease product application if the sponsor has a RPDD for the drug that was granted by September 30, 2024.

After September 30, 2026, the FDA may not award any additional rare pediatric disease priority review vouchers.

A sponsor may choose

to request RPDD, but the designation process is entirely voluntary;

requesting designation is not a prerequisite to requesting or receiving

a priority review voucher.

In addition, sponsors who choose not to submit a RPDD request may nonetheless receive a priority review voucher

if they request such a voucher in their original marketing application and meet all of the eligibility criteria.

The Rare Pediatric Disease

Priority Review Voucher Program was extended as part of the 2021 Coronavirus Response and Relief Supplemental Consolidated Appropriations

Act in December 2020.

As part of this extension, after September 30, 2024, the FDA may only award a voucher for an approved rare pediatric

disease product application if the sponsor has a RPDD for the drug that was granted by September 30, 2024.

After September 30, 2026,

the FDA may not award any additional rare pediatric disease priority review vouchers.

Drug Designation

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provides for the imposition of civil penalties.

the Omnibus Budget Reconciliation Act of 1993 (42 U.S.C.

(the “Stark Law”) prohibit referrals by a physician of “designated health services” which are payable, in whole

or in part, by Medicare or Medicaid, to an entity in which the physician or the physician’s immediate family member has an investment

interest or other financial relationship, subject to several exceptions.

The Stark Law also prohibits billing for services rendered pursuant

to a prohibited referral.

Several states have enacted laws similar to the Stark Law.

These state laws may cover all (not just Medicare

and Medicaid) patients.

We consider the Stark Law in planning our products, marketing and other activities, and believe that our operations

are in compliance with the Stark Law.

Omnibus Budget Reconciliation Act of 1993 (42 U.S.C.

§ 1395nn) (the “Stark Law”) prohibit referrals by a physician

of “designated health services” which are payable, in whole or in part, by Medicare or Medicaid, to an entity in which

the physician or the physician’s immediate family member has an investment interest or other financial relationship, subject

to several exceptions.

The Stark Law also prohibits billing for services rendered pursuant to a prohibited referral.

Several states

have enacted laws similar to the Stark Law.

These state laws may cover all (not just Medicare and Medicaid) patients.

the Stark Law in planning our products, marketing and other activities, and believe that our operations are in compliance with the

If we violate the Stark Law, our financial results and operations could be adversely affected.

for violations include denial of payment for the services, significant civil monetary penalties, and exclusion from the Medicare and Medicaid

Penalties for violations

include denial of payment for the services, significant civil monetary penalties, and exclusion from the Medicare and Medicaid programs.

false claims and false statement laws, including the federal civil False Claims Act, prohibits, among other things, any person or

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of March 15, 2024, we had 17 employees, 14 of which are full-time employees.

Of such employees, 7 are engaged in research and development.

None of our employees are represented by a labor union or covered by a collective bargaining agreement, nor have we experienced work

Of such employees, 8 are engaged in research and

None of our employees are represented by a labor union or covered by a collective bargaining agreement, nor have we

experienced work stoppages.

We believe that relations with our employees are good.

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ImmixBio currently

owns 98% of Nexcella.

owns 95% of outstanding common stock on a fully diluted basis of Nexcella.

website address is www.immixbio.com .

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Compared sentence by sentence after normalising whitespace, quotation marks, case and digits, so re-formatting and restated figures do not read as changed language. Wording changes appear as one removal and one addition. The current filing and the prior one are authoritative.

What changed 10-K

Item 1. Business