Investor Presentation (05/18/2026 00: 00

Published: 2026-05-18 10:02:05 ET KAPA

Published on 05/18/2026 at 10:02 am EDT

INVESTOR PRESENTATION

NYSE American: KAPA

kairospharma.com

Kairos Pharma is dedicated to advancing therapies to overcome critical challenges in cancer drug resistance and immune suppression.

KAIROS HIGHLIGHTS

The Problem:

INNOVATIVE CANCER THERAPEUTICS

New technologies reverse key mechanisms of drug resistance and immune suppression of cancer.

Drug Resistance develops for

even blockbuster drugs, reducing their effectiveness over time

CD105 is elevated with resistance.

Kairos' lead candidate ENV 105 reverses resistance for hormone therapy and EGFR targeted therapy for prostate and lung cancer.

KAIROS INVESTMENT HIGHLIGHTS

Three clinical programs already in progress

INNOVATIVE CANCER THERAPEUTICS

New technologies reverse key mechanisms of drug resistance and immune suppression of cancer.

ENV 105

Phase 2 trial treating castrate resistant prostate cancer

Phase 1 trial treating EGFR-driven Lung Cancer

KROS 201

immunotherapy cleared IND for glioblastoma

New clinical programs to be initiated

KROS 741 (cMET antagonist) initiating

Phase 1 trial treating biomarker driven lung and esophageal-gastric cancers

Experienced Team and Cedars Sinai to drive enrollment and grant funding has created non-dilutive value grounded by science

PORTFOLIO OF INNOVATIVE DRUGS

DRUG CANDIDATE

MODALITY/ MOA

ENV-105

Antibody targeting CD105 to reverse resistance to anti-androgen drugs

Antibody targeting CD105 to reverse resistance to EGFR targeted drugs

KROS-201

Activated

T cell therapy

LEAD INDICATION

Prostate cancer

EGFR-driven lung cancer

Glioblastoma

LEAD IDENTIFICAITON

IND enabling studies

PHASE 1 CLINICAL TRIALS

PHASE 2 CLINICAL TRIALS

PHASE 3 CLINICAL TRIALS

US Market

$6.5B

$2B

$3.6B

KROS-741

Small molecule cMET

antagonist

KROS-101

Small molecule increasing T cell # and function

Lung and Gastric cancers

Solid tumors

$1.5B

Pre-clinical assets

KROS-301

Small molecule targeting cancer growth and immune evasion

KROS-102

Small molecule decreasing T cell # and function

Antibody targeting secreted mtDNA reverse muscle wasting

KROS-401

ENV-205

Peptide that makes pro-tumor macrophages into anti-tumor macrophages

ENV105

OVERCOMING CANCER DRUG RESISTANCE

Anti-androgen drugs (enzalutamide, abiraterone, apalutamide)

EGFR drugs (osimertinib, erlotinib, gefitinib)

THE PROBLEM: Resistance

As cancers become resistant to standard of care, their cancer cells make CD105 on the surface, that mediates tumor cell survival and therapy resistance.

CD105 is elevated in in resistant cancer cells that recur or are incompletely treated.

THE SOLUTION: Block CD105

ENV105 blocks CD105 to restore sensitivity to the entire class of hormone therapies for prostate cancer patients(eg. enzalutamide, abiraterone and apalutamide) and EGFR-targeted therapies for lung cancer patients (e.g. Osimertinib)

Broadly applicable to reverse resistance in cancer: Although prostate and lung cancer are the first indications for ENV 105, this drug has been shown to be effective in models of colon, breast cancers, and head & neck cancers in the resistance developed against radiation and chemotherapy.

ENV105 restores sensitivity to hormone therapy

Targets CD105-mediated PROSTATE CANCER castrate resistance

ENV105 kills cancer cells resistant to AR Tx (H&E stain in PDX model)

More differentiated smaller tumors

ENV105 inhibits the creation of the AR splice variant which has resistance to AR Tx

Enzalutamide Enzalutamide+ ENV105

ENV105 + AR Tx reduces tumor volume more than AR Tx alone

AR splice variant AR-full length

AR-V7

ENV105=

Castration

ENV105

Basis for clinical trials: NCT03418324 and NCT05534646

ENV105

Mol Therapy (2023) 31:78

Oncogene (2019) 38:716 8

ENV105

IN PROSTATE CANCER

PRESENT RANDOMIZED PHASE 2 TRIAL: NCT03418324

2 mos.

Apalutamide with or without ENV105

2 mos.

Tanya Dorff

darolutamide

Edwin Posadas

darolutamide

Accruing

PRIMARY ENDPOINT: Progression free survival based on RECIST 1.1 and PCWG 3 criteria

SECONDARY ENDPOINT: Companion biomarker validation

Umang Swami

Apalutamide and ENV105 for the Treatment of Metastatic Castration-Resistant Prostate Cancer

Patient

Age at

enrollment

Pre-treatment

PSA

Previous therapies

RECIST/PWCG

@ week 16

001

7.59

Abiraterone

Stable disease

002

278.55

Enzalutamide, Lu-PSMA

Not assessable (unrelated stroke)

003

32.35

Enzalutamide

Stable disease

004

59.03

Enzalutamide, Abiraterone

Stable disease

005

4.49

Apalutamide

Stable disease

006

278.43

Abiraterone, Enzalutamide

Stable disease

007

5.63

Enzalutamide

Stable disease

008

3.37

Abiraterone

Stable disease

009

20.59

Abiraterone

clinical PD at 3 months

010

0.82

Enzalutamide, Darolutamide, Lu-PSMA

Stable disease

CARD Trial

ARPI-switch median PFS = 3.7 months

Cabaxitaxel median PFS = 8 months N = 255

NEJM (2019) 318:2506

PSMAfore trial

ARPI-switch median PFS = 5.6 months 177Lu-PSMA median PFS = 11.6 months N = 468

Lancet (2024) 404:1227

Weeks

Median PFS = 13.7 months*

(59 weeks)

* Patients continue to be evaluated

Partnering ENV105 for synergy

ENV-105 and radiation combination shows increased efficacy in a metastatic mouse model

Preclinical collaboration

Combining ENV-105 and alpha-emitting isotope

in animal models of bone metastatic prostate cancer

Endo Rel Can 202C

Supporting a Phase 2 Clinical Trial

ENV-105 and alpha-emitting isotope combination in metastatic prostate cancer patients

ENV105

SUPPORTING EGFR-DRIVEN LUNG CANCER PATIENTS - In Phase I

NON-SMALL CELL LUNG CANCER BECOMES RESISTANT TO OSIMERTINIB (TAGRISSO)

OSIMERTINIB RESISTANCE IS DEPENDENT ON CD105

Drug Res Updates (2025) 81:101237

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

ENV105 in EGFR-Driven Lung Cancer

AstraZeneca's EGFR inhibitor Tagrisso ($7B in 2024 sales) offers only a partial response in 80% of patients

CD105 is elevated with Tagrisso treatment

Preclinical models show ENV105 can overcome resistance and shrink tumors

ENV105 could not only reverse resistance but make Tagrisso work better to enable complete responses

Accruing Phase I study of patients resistant to Tagrisso or partial responders with persistent circulating tumor cell DNA

Drug Res Updates (2025) 81:101237

ENV105 IN LUNG CANCER: NCT05401110

PHASE 1 TRIAL FOR EGFR-DRIVEN LUNG CANCER: Osimertinib (Tagrisso) + ENV105

Patients that are incompletely treated with Tagrisso (persistent ctDNA)

Patients that have become resistant to Tagrisso

Accruing

PRIMARY ENDPOINT: Determine safety and effective dose of ENV105 in patients with EGFR lung cancer

SECONDARY ENDPOINT: Identify biomarkers for patients most responsive to ENV105

Cedars-Sinai Medical Center

Mayo Clinic Stanford Vanderbilt Rutgers

Cleveland Clinic

Extend The Reach Of Innovative Therapies To Patients Across Diverse Communities

CRO consortium leveraging the the efficiencies of each institute to achieve 40 day clinical trial activation (June 1, 2026)

Centralized regulatory oversight and institutional investigator-initiated trials are subsidized

$3.2M (NCI)

$2.4M (Donor)

$1.8M (DOD)

$0.6M (DOD)

ENV105 prostate cancer companion biomarker validation

ENV105 lung cancer preclinical and phase 1 trial

ENV105 lung cancer companion biomarker identification

ENV205 cachexia preclinical studies

$8M in non-dilutive funding for the preclinical and clinical assets

EGFR-family receptors and MET converge on PI3K-AKT, MAPK, and STAT pathways. Inhibition of one axis often leads to compensatory signaling through the other.

KROS-741

MET amplification or HGF-driven activation is a common acquired resistance mechanism following EGFR blockade, particularly in NSCLC. MET-mediated HER3 transactivation can restore PI3K signaling despite EGFR inhibition.

Small molecule cMET antagonist

Stronger more defensible positioning both differentiation and pricing via biomarker defined patients Better controlled resistance narrative - pre-empt vs react

Dotmatics: GeoM value from Kyinno BaF3-TPR-MET CTG assay.

Clin Pharmacokinet (2017) 56:477-491

Cancer science (2020) 111:536-547.

Clinical Cancer Research (2020) 26: 1237-1246. Result is from 500 mg daily dose.

Clinical Cancer Research (2019) 25: 4924-4932.

Projected for 100 mg BID human daily dose to reach TGI80. DL1 or DL2 pending on GLP.

Kinase MET

% inhibition at 100nM

≤75

76-90

≥90

Capmatinib

Tepotinib

Cabozantinib

KROS-741

Plasma Free Fraction

0.2%

Total plasma concentration needed

to cover c-Met WT EC50

40 ng/mL

(3.2 nM)1

525 ng/mL

(19.2 nM)1

26,600 ng/mL

(53.3 nM)2

230 ng/mL

(13.6 nM)1

Clinical daily dose

400 mg X 2

450 mg

60 mg

100 mg X 26

Clinical plasma Cave at SS

~1800 ng/mL3

~1100 ng/mL4

~1000

ng/mL5

250 ng/mL6

Clinical plasma Cave over c-Met

WT EC50

45x

70-130x

ORR

44%-67%

45%

10%

PFS

9.7 - 12.3 mo

8.5 mo

3.5 mo

MET_D1228A MET_D1228G MET_D1228H MET_D1228N MET_D1228V MET_D1228Y MET_F1200I MET_G1163R MET_H1094L MET_H1094Y MET_K1244R MET_L1195F MET_L1195V MET_M1250I MET_M1250T MET_P991S MET_T1173I MET_T992I MET_V1092I MET_Y1230A MET_Y1230C MET_Y1230D MET_Y1230H MET_Y1230S MET_Y1235D

MET-KIF5B (Kex24Mex14)

MET-TFG

Cabozantinib 98

<50

KROS-741 106

100

Disclaimer

Kairos Pharma Ltd. published this content on May 18, 2026, and is solely responsible for the information contained herein. Distributed via Public Technologies (PUBT), unedited and unaltered, on May 18, 2026 at 14:01 UTC.