Kairos Pharma, Ltd. · AMEX:KAPA
Kairos Pharma — Technical Presentation (November 2026)
22 slides from Kairos Pharma's technical presentation, Nov 3, 2026
Slide 1: Targeting metabolism and tumor dormancy in prostate and lung cancer patients
Targeting metabolism and tumor dormancy in prostate and lung cancer patients. Neil Bhowmick
Slide 2: Forward Looking Statements
FORWARD LOOKING STATEMENTS KAIROS PHARMA This presentation may contain “forward-looking statements” regarding the current expectations and projections about future events of Kairos Pharma, Lid. (“Kairos Pharma” or the “Company”). “Forward-looking statements” (statements as to matters other than hist
Slide 3: Resistance develops for even blockbuster drugs
Resistance develops for even blockbuster drugs oNOaR WD . Tumors are heterogeneous before treatment . Cancer evolves under drug pressure . Signaling networks are redundant . Cancer cells can change phenotype without changing genotype The tumor microenvironment protects tumor cells . Resistance can b
Slide 4: Mechanisms of resistance to cancer therapies
Prostate Lung Cancer Cancer — ~ £6 development ¢ AR Splice Variants of resistance (CD105) e Receptor Mutations TGFR Page e BMPS © Small Cell = H = H Car TBRII||||ALKS, Differntiation | “um ALKA metastasis survival de-differentiation Mechanisms of resistance to cancer therapies Anti-androgen drugs EG
Slide 5: Androgen Receptor Signaling Inhibition Resistance
Androgen Receptor Signaling Inhibition Resistance DD AR antagonist AR alterations (e.g., apalutamide) (e.g., mutations, splice variants) (ar? Lar ) Increased AR expression (ar ) (AR amplification/overexpression) Car) Compensatory signaling (e.g., PI3K/AKT, MAPK) Li lasticit AR signaling (ele —> a, I
Slide 6: Radiographic PFS points of reference
Radiographic PFS points of reference CARD Trial ARPI-switch median PFS = 3.7 months Cabaxitaxel median PFS = 8 months Dd< PSMAfore trial ARPI-switch median PFS = 5.6 months 177Lu-PSMA median PFS = 11.6 months N=255 N= 468 = SMA 100 — "tw PsMaox7 a — anPlchange ss 80 80. £E 7 33 z 60 ze ° ot SE 50: ‘
Slide 7: BMP signaling contributes to AR inhibitor resistance
BMP signaling contributes to AR inhibitor resistance nih —® Vehicle © BMP9 -* Carotuximab — -™ Carotuximab + BMP9 ENV105 100] @—~a = (carotuximab) Apalutamide NS cc 3 cc 05) é 50: TGFR, as BMPS x = ao . TSRII||IALKS — gypRuillll ALKt 0.01 0.1 1 10 100 Apalutamide (uM) BMP provides pro-survival and d
Slide 8: ENV105 restores sensitivity to hormone therapy
ENV105 restores sensitivity to hormone therapy nih ENV105 kills cancer cells resistant to AR Tx (H&E stain in PDX model) More differentiated smaller tumors ee pre y i, 5 ENV105 inhibits the creation of the AR splice : | variant which has resistance to AR Tx CD105§BMP AR splice variant ENV105= AR-ful
Slide 9: CD105 (ENG) downregulates CHOP and promotes fatty acid oxidation
CD105 (ENG) downregulates CHOP and promotes fatty acid oxidation paid ° Pp coefficient (toENG) i) iD Pp coefficient (toENG) ALDH1L: 22Rv1 C4-2BMOvR —control - + = + - + = + —si Ser + carotuximab —siCHOP + carotuximab Apalutamide Carotuximab IRE1a CHOP phos-PERK ATF4 Actin 0 01 +14 10 100 apalutamide
Slide 10: ENV-105 causes fat to shuttle to the peroxisomes to promote terminal ER stress
Jan ENV-105 causes fat to shuttle to the peroxisomes to promote terminal ER stress a Carotuximab - + Apalutamide - = siACOX2 + - ATF6) ATF4|« CHOP vehicle Survivin] x 8-actin te carotuximab apalutamide a MR. combination % Did Nucleus @ sopiPy @ Peroxisome
Slide 11: ENV105 in prostate cancer patients
ENV105 pid IN PROSTATE CANCER PATIENTS RANDOMIZED PHASE 2 TRIAL: NCT03418324 Apalutamide with or without ENV105 lupron ee ensination thetee @-@ apalutamide single agent Snzalotamids fe @-© apalutamide + ENV105 abiraterone Prostate : N=10 — Cancer darolutamide Safety lead-in we lupron @... nA enzalut
Slide 12: Phase II Patient Summary NCT05534646
Phase 2 Patient Summary NCT05534646 DD Apalutamide and ENV105 for the Treatment of Metastatic Castration-Resistant Prostate Cancer Age at revious therapies GEESE NANTES enrollment PSA @ week 16 001 68 7.59 Abiraterone Stable disease 002 76 278.55 Enzalutamide, Lu-PSMA Not assessable (unrelated strok
Slide 13: Progression Free Survival NCT05534646
Progression Free Survival NCT05534646 nid > still on trial @w) Unrelated withdrawal Median PFS = 17.7 months* *Based on patients 1-10 (} Apalutamide + ENv-105 .) Apalutamide 0 4 8 12 16 20 24 28 Months
Slide 14: Change in PSA
Change in PSA pid NCT05534646 20 Comparing baseline pre- treatment PSA to nadir PSA values 35% mean PSA decrease Percent (%) change in PSA -100 —
Slide 15: Protocol Modification: AR-105
Protocol Modification: AR-105 Dade NCT05534646 Phase II Study of AR suppression with Carotuximab in Metastatic, Castration-Resistant Prostate Cancer CRPC with PD through prior ARSI exposure ] 3 Enzalutamide naive Enzalutamide exposed 5 z 3 100 Part |: Safety Lead-In Part Il: 3 30 (N=10) ization (1:
Slide 16: CD105 is upregulated by EGFR inhibition
CD105 is upregulated by EGFR inhibition ETP. « 45,000 EGFR driven NSCLC diagnosed last year * Tagrisso is the standard of care for EGFR driven NSCLC, yet 80% of patients have only a partial response EGFR Inhibitor A go, Parental Resistant 4g, Parental Resistant i carotuximab Ae (cD105) TOFS ooo BMPo
Slide 17: EGFR inhibition promotes tumor dormancy in a BMP-dependent manner
EGFR inhibition promotes tumor dormancy EP in a BMP-dependent manner Slow-cycling population Parental Resistant UMAP 2 o restored proliferative state by blocking CD105 4 a “a oe ens a a NDRG: @ 4 0 a 4 0 a p27 Ir Drug Res Updates (2025) 81: 101237 qa
Slide 18: Tumor volume with osimertinib and carotuximab
Norm. tumor val. (mm?) 0 é 8 o H1957R © Osimertinity e Osirnertinib + tums P= 0.0008 1 70°15 20 25 30 35 40 45 Days of Treatment HCcaZiR Days of Treatment Survivin Drug Res Updates (2025) 81:101237 {
Slide 19: ENV105 in lung cancer: NCT05401110
ENV105 IN LUNG CANCER: NCT05401110 PHASE 1 TRIAL FOR EGFR-DRIVEN LUNG CANCER: Osimertinib (Tagrisso) + ENV105 Patients that have become Lung resistant to Tagrisso Cancer N=9-20 Patients that are incompletely treated Ale Safety lead-in with Tagrisso CO Bayesian design N=20 (persistent ctDNA) PRIMARY
Slide 20: Patient characteristics: NCT05401110
Patient characteristics: NCT05401110 Patient Characteristic Safety population All data shown as n (%) unless otherwise n=11 specified Age, median (range), years 72 (56-87) Female 11 (64%) Race White 6 (55%) Asian 4 (36%) Black/AA 1 (9%)
Slide 21: Efficacy: NCT05401110
Efficacy: NCT05401110 Best Response Efficacy population (n=8) PR 0 sD 5 (63%) PD 3 (37%)
Slide 22: Summary
Summary AR antagonist EGFR antagonist (e.g., apalutamide) (e.g., osimertinib) Androgen Receptor Epidermal Growth (AR) Factor Receptor (EGFR) Compensatory signaling (e.g., CD105/BMP) Therapy resistance Fatty acid oxidation a Tumor dormancy fatty-acid oxidation and tumor-cell dormancy/persistence can
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