Bioxytran, Inc. · OTC:BIXT

Bioxytran — Investor Presentation (2025)

57 slides from Bioxytran's investor presentation, Jan 6, 2025

Slide 1: Galectin Antagonists in Cancer
Galectin Antagonists in Cancer
Slide 2: Forward Looking Statement
Forward Looking Statement This Descriptive Presentation (the “Presentation") has been prepared by Bioxytran, Inc (the “Company”) and recipients are not entitled to rely on the accuracy or completeness of the Presentation. Statistical information contained in this Presentation is based on information
Slide 4: Outline
Outline ! Competent Immune System is capable of curing cancer ! Cancer Tricks the immune system in various ways ! The current tools to fight cancer / shortcomings -Radiation, Immunotherapy, ADC, CAR-T, Chemotherapy ! Galectin Universal Cancer Target ! Clinical Trial Results – Galectin Antagonists Co
Slide 5: Metastasis Kills - Not the Primary Tumor
Metastasis Kills - Not the Primary Tumor The majority of deaths (about 90%) associated with cancer are due to the metastasis of the original tumor1 In the past the focus of therapy was reduction of the primary tumor. With so many tools like Surgery, Radiation, Chemo, CAR-T, ADC’s, and Immunotherapy
Slide 6: Galectins Linked to many Chronic Diseases
Galectins Linked to many Chronic Diseases !"#$%&'(#)* '%(%&'+, -.%'#/0"12#3)4'5&6# &'78+6%(#)5#9&6%+785( :#;&5+%' 9&6%+785(#&'%#&#<%$# =8)>&'<%'#)*#85*6&>>&7)'$ ?8(%&(% @)#&AA').%?#9&6%+785# 85,8=87)'#B CDE !"#$%&'()*)+),'+"--./&'+)0),'1/"22"#&'()3),'+456&'7)8)'14-.9:"#%'4%'+6-.9;-4/'<4/$.:%'26/'<=.
Slide 7: The human immune system is designed to detect and eliminate abnormal cells
The human immune system is efficiently designed to detect & eliminate abnormal cells w/ the potential to become cancerous The human body is capable of Curing Cancer and does so multiple times in a lifetime. Copyright © Bioxytran 2025. All rights. Version 2.01.01 &
Slide 8: Competent Immune Systems Stop Cancer
Competent Immune Systems Stop Cancer Immune Cells Prevent Cancer Body’s Neverending Fight Against Cancer Formation Surveillance & Elimination (T-Cell) Natural Killer (NK) Cells Tumor Infiltrating Lymphocytes (TIL’s) Copyright © Bioxytran 2025. All rights. Version 2.01.01 '
Slide 9: Cancer Tricks The Immune System
Cancer Tricks The Immune System Deactivates T-Cells Altering Genes Galectin Effect Mutations from carcinogens Oncogenes spur Growth (ie HER2, EGFR, KRAS, NMYC) Defense Mechanisms of Cancer Suppression of Creates Hypoxia Immune Response Tumor Growth w/o blood Stimulating Regulatory flow Suppressor Ce
Slide 10: T-Cell Deactivation / Cloaking
Tumors Are Like Insurgent Outposts T-Cell Deactivation / Cloaking Primary Defensive Tactics of Tumors Stuns Attacking T-Cell Army Reduces the effectiveness of T-Cells ! T-Cell Anergy ! Downregulates T-Cell Receptors Cloaks itself from the Immune System (Suppressor Cells) Barbed wire represents the d
Slide 11: Cancer's Primary Defense Mechanism (Gal-3)
Cancer’s Primary Defense Mechanism (Gal (Gal-3) 3) Killer T-Cells Must Have Good Adhesion to Kill Impact of Galectin-3 Surrounding Tumor Impact of Gal-3 within the TME. Gal-3 is secreted by the tumor cells as monomers, which can form Galectins are guardians of the pentamers and bind substrates. The
Slide 12: Galectin Effect (T-Cell Anergy)
Galectin Effect (T-Cell Anergy) Galectins are responsible for T-Cell Anergy and prevent the LFA-1 lectins (depicted in blue) from coalescing at the target cell and developing good adhesion in order to destroy it with cytotoxins. !"#"$%&'()*(+,-"''(./"$01 van der Bruggen, P. (2017). (rep.). T Lymphoc
Slide 13: Galectin-3 Upregulated T-Cell Anergy
Galectin-3 Upregulated T-Cell Anergy linked to Cancer, Viral Infection, and Fibrosis Virally infected cells upregulate Gal-3 which is used in the budding process of virion. When cells burst after the nuclear material is used up it goes into the inflammatory environment. Effect of Elevated - Galectin
Slide 14: Reduction in T-Cell Receptors
Reduction in T-Cell Cell Receptors Expansion theory is that Gal-3 downregulates the number of T-Cell Receptors (TCR’s) on the surface of the T-Cell making it harder to sniff out cancer cells. Less Receptor Density Means its harder to find target cancer cell – (Less hooks on a Velcro Ball) Fewer Canc
Slide 15: Killer T-Cell Suppression
Killer T-Cell Suppression CD4+ cells known as regulatory T-Cells (Tregs) are attracted by the Gal-3 secretions in the Tumor Microenvironment (TME) Once positioned, they too will secrete Gal-3 thereby attracting more Tregs & Macrophages that further limit the population of the CD8+ T-Cells designed t
Slide 17: How Cancer Spreads
How Cancer Spreads Metastasis Angiogenesis Tumor Escape – Intravasation Adhesion - Extravasation Stimulating VEGF to create blood flow to tumor Offensive Mechanisms of Cancer Hypoxic Conditions Tumor Growth w/o blood flow – Low pH Sigamani A, Ruthra M, Sudhishma, Shetty S, Madhavi, Chugani A, et al.
Slide 18: Cancer's Offensive Capability - Metastasis
Cancer’s Offensive Capability - Metastasis Metastasis Linked to Galectin-3 Gal-3 adhesion molecules play a part in every facet of cancer metastasis. Tumor cells upregulate & secrete Gal-3 which interacts with cell surface glycans on endothelial cells (veins) like MUC-1 and integrins which play a cru
Slide 19: Galectin-3 Makes Tumor Cells Sticky
Galectin-3 Makes Tumor Cells “Sticky” Mechanism of Metastasis A.Tumor Escape B.Intravasation of tumor cells squeezing into blood stream C.MUC-1 prevents adhesion allowing it to travel D.Extracellular Gal-3 attaches to MUC-1 making the cell “Sticky” allowing it to adhere to the endothelial cells E.Tu
Slide 20: Cancer's Offensive Capability - Angiogenesis
Cancer’s Offensive Capability - Angiogenesis Galectins are key modulators of the Vasculature ! Activation ! Migration ! Proliferation ! Sprouting ! Permeability ! Tube Formation Gal-1 & Gal-3 are common modulators of endothelial cell function during all phases of angiogenesis. In general they are st
Slide 21: Immune Modulation & Angiogenesis
Immune Modulation & Angiogenesis Gal-1 Immuno Regulation/Suppression/Angiogenesis Gal-1 binds to sugars located on the cell surface of T-Cells & Circulatory cells creating an immunosuppressive tumor microenvironment (TME) ! Destroys T-Cells ! Creates Tolerogenic Dendritic Cells producing suppressor
Slide 22: Reprogramming Tumor, Vasculature, Immune Landscape
Reprogramming Tumor, Vasculature, Immune Landscape Galectins in Cancer Gaby Rabinovich summarizes the downstream impact of Galectins and how they reprogram their environment permitting cancer to thrive. Mariño, K.V., Cagnoni, A.J., Croci, D.O. et al. Targeting galectin-driven regulatory circuits in
Slide 23: Cancer's Offensive Capability - Hypoxia
Cancer’s Offensive Capability – Hypoxia Tumor cells grow very fast and the vasculature can’t keep up with the growth creating an Intratumoral hypoxia increases ROS production. ROS environment where the tumor cells are not getting inhibits prolyl and asparginyl hydoxylases resulting in enough oxygen
Slide 26: Surgery
Surgery ! Surgery is the first line of defense against cancer especially in the early stages ! Surgical removal of the tumor Drawbacks of Surgery remains the most ideal and most ! Bleeding frequently used treatment ! Blood clots method ! Damage to nearby tissues ! Drug reactions ! Typically, surgery
Slide 27: Chemotherapy
Chemotherapy Side Effects ! Chemo drugs act like poison to target fast replicating Nausea, fatigue, hair loss, and some cells – specifically cell division and growth chemotherapies are deleterious to the immune mechanisms. system Side effects come from the targeting of healthy fast replicating cells
Slide 28: Targeted Therapy
Targeted Therapy ! Targeted therapy takes advantage of Side Effects a specific marker or protein Fewer than chemo, but associated with cancer or cancer still significant growth Dependent upon the specific medication & ! Includes antibodies, antibody drug target conjugates (ADC), hormone therapy, Tar
Slide 29: Targeted Therapy: Kinase Inhibitors
Targeted Therapy: Kinase Inhibitors ! Kinase inhibitors interfere with kinase enzyme functions. Kinases use ATP to turn on or off certain proteins and cellular pathway; for oncology, typically for cell division and growth mechanisms. ! Kinase inhibitors target cancer cells and generally spare health
Slide 30: Targeted Therapy: Hormone Therapy
Targeted Therapy: Hormone Therapy Hormone therapies stop the growth of hormone Side effects include: dependent cancers by depriving them of the hormones they need to grow. hot flashes, decreased sexual desire, erectile dysfunction, bone, Hormone therapies work by either: fatigue, weight, muscle loss
Slide 31: Targeted Therapy: Monoclonal Antibodies
Targeted Therapy: Monoclonal Antibodies (mABs) Monoclonal antibodies are lab-created antibodies that work like naturally-created antibodies, but are designed to interact with specific targets on cancer cells Antibodies can directly kill cancer cells, block tumor blood vessels from growing, help the
Slide 32: Antibody-Drug Conjugates (ADCs)
Antibody-Drug Conjugates (ADCs) ADCs are a class of oncology treatment that combine a monoclonal antibody with a cytotoxic agent, such as traditional chemotherapy. ADCs are designed to target tumor cells with localized chemotherapy and antibodies while minimizing damage to normal cells. Similar Side
Slide 33: CCR5 Antagonists – Antimetastatic
CCR5 Antagonists – Antimetastatic !CCR5 is upregulated in many tumor types w/ poor outcomes !CCR5 expression on tumor cells create a suppressive TME leading to metastasis (proliferation, invasion, migration) !Leronlimab (CCR5 Antagonist - mAB) binds to CCR5 in multiple breast cancer lines !Xenograph
Slide 34: Radiation
Radiation ! Radiation is used in conjunction with other therapies Side effects ! Radiation destroys the DNA of cells Skin irritation, hair loss, inflammation near the tumor, pain, dry mouth, weight loss, fertility issues, fatigue, memory or concentration problems, nausea and vomiting, headache, ! It
Slide 35: Immunotherapy
Immunotherapy ! Immunotherapy aims to improve the endogenous immune system response towards cancer cells ! Checkpoint inhibitors either take the “brakes” off immune cells, and other immunotherapies stimulate the immune system to attack the tumor ! Stimulatory (Activation)/Inhibitory T-Cell Receptors
Slide 36: Checkpoint Inhibitors Only Increase Counts
Checkpoint Inhibitors Only Increase Counts !"#$%&'()*+,)"(-(*'./+012 No Immune System Activation Despite Higher Counts Checkpoint Inhibitors result in higher CD-8+ counts which means there are more T-Cells capable of destroying the cancer cells. Why do these higher T-Cell counts not translate into 1
Slide 37: Theory Explains Poor Checkpoint Response Rates
Theory Explains Poor Checkpoint Response Rates Theory: Successful Immunotherapy Galectin-3 interferes with immune system function. It favors cancer on multiple pathways Requires an Activated Immune System that include cancer growth, metastasis, and survival. It also negatively interfers with immune
Slide 38: Immunotherapy: Vaccines
Immunotherapy: Vaccines Cancer vaccines are used to prevent or treat cancer by sensitizing the immune system to certain cancer antigens. Cancer vaccines being developed can be gene related or virus related, or created in a personalized manner based on a patient’s own cancer antigens The mechanism is
Slide 39: Cell Therapy
Cell Therapy ! Currently approved cell therapies work like monoclonal antibodies but the antibodies Side effects already have cells, typically T cells, attached Cytokine release syndrome (CRS), nervous system effects, nausea, vomiting, diarrhea, muscle and joint pain, rapid heartbeat, low blood pres
Slide 40: Stem Cell Transplantation
Stem Cell Transplantation ! Stem cell transplantation is a procedure that replaces a patient's blood stem cells with healthy ones to treat a variety of diseases, including some types of cancer. ! The patient’s own immune system is often reduced before transplantation to allow for grafting. Side effe
Slide 41: Siglec Targeting Therapies
Siglec Targeting Therapies ! SIGLECs (sialic acid-binding immunoglobulin-like lectins) GlycoImmune Checkpoint Therapy ! SIGLECs play a major role in suppressing innate immune response to cancer. ! Cancer cells overexpress SILGECs (hypersialylation) and use them to evade immune response. Cloaking Mec
Slide 42: Evolution of Cancer Treatment
Evolution of Cancer Treatment Timeline of Groundbreaking Treatment Options Evolving Clinical !"#$%&'()*(+','&-./ Endpoints: !"#$%&'( "(&"*+(',&, ,&+- %"(%$. /$&",&",',0 -.+#'1$."&'+(0 "(2 "(*'+*$($,', 1) Reducing Primary Tumor !"!# 2) Progression Free Survival 3) Stopping Metastasis Falzone, L., Sal
Slide 43: Treatment Summary - Targeting the Primary Tumor is Not the Solution
Treatment Summary - Targeting the Primary Tumor is Not the Solution Cancer Metastasis Remains a Large Unmet Medical Need There are many ways to treat cancer tumors, and many are effective with mild side effects, but there are few solutions to treat cancer metastasis which is the leading cause of dea
Slide 45: Galectin Cancer Targets
Galectin Cancer Targets The ultimate cancer target spans multiple cancer indications, multiple disease stages, and is relevant for all combination therapies. ! Galectins 1, 2, 3, 4, 8, 7, 9, and 12 are implicated in solid tumor cancers ! Galectins are responsible for proliferation, growth, migration
Slide 46: Galectins Are The Missing Link In Cancer
Galectins Are The Missing Link In Cancer Galectin Science Remains in the Shadows ! 4029 medical journal articles written on Galectins and roles in cancer in the past 30+ years, yet no approved drug ! Only 10 Galectin Antagonists have been developed (DAVANAT, Belapectin, GB0139, GB1211, GCS-100, Upro
Slide 47: Resistance in Cancer Treatment
Resistance in Cancer Treatment !"#$%&'#()%$#)#**#+,'-#) ./,)01,)(/**'+'#0, "#$%&'(&) +,(-+&.+ /01 2+,+03+- '/0' )03+.'(& +452+11($& (& '%6$2 '(11%+ %&-+2)$+1 6$-%30'($& (& 2+15$&1+ '$ !"#$%&"#'()* 7+,-./89 '/(1 $:1+2,0'($& 1%))+1'1 0 2$3+ ;$2 '/+1+ 52$'+(&1 (& 2+1(1'0&.+ '$ 0&'(.0&.+2 '/+205(+1 70(1
Slide 48: Cancer Targets
Cancer Targets Galectins are implicated in all these druggable targets Gal 1, 3, 9 Gal 3 Gal 3 Gal 3 References: Seguin L, Camargo, et al. Galectin-3, a Druggable Vulnerability for KRAS-Addicted Cancers. Cancer Discov. 2017 Dec;7(12):1464-1479. doi: 10.1158/2159-8290.CD-17-0539. Epub 2017 Sep 11. PM
Slide 49: Galectins Essential to Tumor Survival
Galectins Essential to Tumor Survival Galectins provide the essential elements for a tumor to flourish. From cancer’s perspective, taking them away is like a person living without food, water, and shelter. Shimada C, Xu R, Al-Alem L, Stasenko M, Spriggs DR, Rueda BR. Galectins and Ovarian Cancer. Ca
Slide 50: Galectin Signature Changes with Progression
Galectin Signature Changes with Progression 5$1(,%,#)6%0+#$)6%(#)7,/89 The galectin disease signature, expressed by classification & percentage of galectin type, is prevalent during all stages of disease and it can vary from stage to stage. A diagnostic test could utilize the different ratio of gale
Slide 51: Galectins Impair the Immune System
Galectins Impair the Immune System When Galectin-1 starts to elevate it impairs the cancer patients immune system. Cancer patients with less impairment have a better chance of survival. #$" !" Low Stromal Gal-1 Expression is Associated with Long Term Survival Fig 1. Immune system evasion using Gal-1
Slide 53: High Galectin Expression Leads to Bad Outcomes
High Galectin Expression Leads to Bad Outcomes Study of NSCLC Patients Categorized by Biopsy Galectin Expression Despite all patients testing positive for PD-1 ! Galectin-3 expression was extremely accurate in predicting bad outcomes What if Galectin-3 expression on various cancers plays an oncogeni
Slide 54: Cancer Trial Results – Gal-3 Antagonist
Cancer Trial Results – Gal-3 Antagonist Belapectin in Cohort 2 had a 100% ORR in advanced Melanoma for a 85 day trial using PET Scan Before and After optimal dosage. of Melanoma patient is the Complete Response in 1 in 5 had a Complete Response Cohort 2 (All Tumors Resolved) 50% had ORR in Melanoma
Slide 55: Cancer Trial Results – Gal-3 Antagonist
Cancer Trial Results – Gal-3 Antagonist GB1211 in NSCLC w/Atezolizumab (ATZ) 4/10 (40%) achieved a Partial Response Cohort1 (100 mg) 3/5 (60%) achieved a Partial Response Cohort2 (200 mg) Gal-3 Serum levels decreased in responders !"#$%&'$()*+,-..,'/,01232,445 678 Curti, B. D., et al. (2021). Enhanc
Slide 56: Ongoing Gal-3 Antagonist Clinical Trials
Ongoing Gal-3 Antagonist Clinical Trials Company Area of Indication Gal-3 Antagonist Drug Name Phase Interest Therapeutic Class Galectin Hepatology MASH Cirrhosis Complex Polysaccharide Belapectin 2b/3 Therapeutics (GR-MD-02) Galecto Biotech Oncology NSCLC, HNSCC, MM Small Molecule GB1211 2 TrueBind

Bioxytran — Investor Presentation (2025) on 6ix

Bioxytran — Investor Presentation (2025)

Slide 1: Galectin Antagonists in Cancer

Slide 2: Forward Looking Statement

Slide 3: Cancer Metastasis

Slide 4: Outline

Slide 5: Metastasis Kills - Not the Primary Tumor

Slide 6: Galectins Linked to many Chronic Diseases

Slide 7: The human immune system is designed to detect and eliminate abnormal cells

Slide 8: Competent Immune Systems Stop Cancer

Slide 9: Cancer Tricks The Immune System

Slide 10: T-Cell Deactivation / Cloaking

Slide 11: Cancer's Primary Defense Mechanism (Gal-3)

Slide 12: Galectin Effect (T-Cell Anergy)

Slide 13: Galectin-3 Upregulated T-Cell Anergy

Slide 14: Reduction in T-Cell Receptors

Slide 15: Killer T-Cell Suppression

Slide 16: Galectins Are Protein Receptors That Recognize Sugar Molecules

Slide 17: How Cancer Spreads

Slide 18: Cancer's Offensive Capability - Metastasis

Slide 19: Galectin-3 Makes Tumor Cells Sticky

Slide 20: Cancer's Offensive Capability - Angiogenesis

Slide 21: Immune Modulation & Angiogenesis

Slide 22: Reprogramming Tumor, Vasculature, Immune Landscape

Slide 23: Cancer's Offensive Capability - Hypoxia

Slide 24: Cancer Treatments

Slide 25: Existing Treatment Options

Slide 26: Surgery

Slide 27: Chemotherapy

Slide 28: Targeted Therapy

Slide 29: Targeted Therapy: Kinase Inhibitors

Slide 30: Targeted Therapy: Hormone Therapy

Slide 31: Targeted Therapy: Monoclonal Antibodies

Slide 32: Antibody-Drug Conjugates (ADCs)

Slide 33: CCR5 Antagonists – Antimetastatic

Slide 34: Radiation

Slide 35: Immunotherapy

Slide 36: Checkpoint Inhibitors Only Increase Counts

Slide 37: Theory Explains Poor Checkpoint Response Rates

Slide 38: Immunotherapy: Vaccines

Slide 39: Cell Therapy

Slide 40: Stem Cell Transplantation

Slide 41: Siglec Targeting Therapies

Slide 42: Evolution of Cancer Treatment

Slide 43: Treatment Summary - Targeting the Primary Tumor is Not the Solution

Slide 44: Universal Cancer Target

Slide 45: Galectin Cancer Targets

Slide 46: Galectins Are The Missing Link In Cancer

Slide 47: Resistance in Cancer Treatment

Slide 48: Cancer Targets

Slide 49: Galectins Essential to Tumor Survival

Slide 50: Galectin Signature Changes with Progression

Slide 51: Galectins Impair the Immune System

Slide 52: Clinical Trial Results

Slide 53: High Galectin Expression Leads to Bad Outcomes

Slide 54: Cancer Trial Results – Gal-3 Antagonist

Slide 55: Cancer Trial Results – Gal-3 Antagonist

Slide 56: Ongoing Gal-3 Antagonist Clinical Trials

Slide 57: BioXyTran, Inc.