LOS ANGELES -- Kairos Pharma, Ltd. (NYSE American: KAPA), a clinical-stage biopharmaceutical company focused on innovative cancer therapeutics, announces the signing of a term sheet for a strategic asset acquisition with Celyn Therapeutics, Inc., a privately held biotechnology company backed by OrbiMed and Torrey Pines Investment. Under the proposed terms of the agreement, Kairos Pharma will acquire worldwide rights to two highly differentiated, clinical-stage oncology assets targeting non-small cell lung cancer (NSCLC): CL-273, a pre-IND, reversible, wild-type-sparing pan-EGFR inhibitor, and CL-741, a Phase 1-ready, orally available type IIb c-MET kinase inhibitor.

John Yu, M.D., Kairos Pharma Chief Executive Officer, commented: "We anticipate this acquisition will significantly expand our oncology pipeline with late-preclinical and Phase 1-ready assets in a multi-billion dollar market with substantial unmet medical needs. With this acquisition, if completed, we will strengthen our armamentarium to reverse oncology drug resistance - by implementing therapeutics that specifically target resistance mutations that arise from targeting the EGFR receptor. Importantly, our established clinical consortia on the West Coast, anchored at Cedars-Sinai Medical Center in Los Angeles, provides us with the clinical infrastructure and expertise to rapidly initiate and execute Phase 1 and Phase 2 studies for both compounds.”

Kairos Pharma believes the scientific rationale for combining a pan-EGFR inhibitor with a c-MET inhibitor in non-small cell lung cancer as demonstrated with these two assets is compelling and well-validated clinically. MET amplification represents one of the most important resistance mechanisms in EGFR-mutant NSCLC, and the ability to address both pathways with highly selective, brain-penetrant molecules represents a significant therapeutic advance. The Company anticipates that CL-273‘s wild-type-sparing profile and broad coverage of EGFR mutations, combined with CL-741’s potent and selective c-MET inhibition, upon acquisition, will position it to develop best-in-class monotherapies as well as a differentiated combination regimen. Mechanistically, dual inhibition of EGFR and MET pathways can overcome compensatory signaling that drives resistance, deepens tumor responses, and extends progression-free survival in this difficult-to-treat patient population.

Kinase inhibitors for cancer treatment were estimated to be valued at $60.7B in 2025. Of these, EGFR inhibitors represented 32.5% of the market in 2025 (Future Market Insights).

CL-273, developed using a proprietary AI-driven drug discovery platform, targets the EGFR mutated lung cancer treatment, a market valued at $16.2B in 2026 (Future Market Insights). EGFR mutations are present in approximately 10-15% of NSCLC cases in Western populations and up to 50% in Asian populations (CoherentMI), creating a substantial addressable patient population for targeted therapies.

CL-741 addresses the cMet inhibitor market which is experiencing rapid growth, valued at more than $2B and projected to reach over $10B by 2030 with a CAGR in excess of 17% (Biospace). The c-MET metastatic NSCLC market represents a high-value niche with significant unmet medical needs, with c-MET amplification being a critical resistance mechanism for EGFR-targeted therapies. C-MET alterations, including MET exon 14 skipping mutations and MET amplification, is a driver of multiple cancer types inclusive of gastric, liver, and renal cancer.

“Our proprietary AI-driven drug design platform has enabled the discovery of a highly efficacious, wild-type-sparing, pan-mutant EGFR inhibitor. This molecule offers a 4-to-5-fold broader safety margin than current competitive inhibitors,” stated Nikolay Savchuk, Ph.D., CEO of Celyn Therapeutics. “By partnering with Kairos Pharma and leveraging their clinical consortia at Cedars-Sinai Medical Center, we are positioned to rapidly advance CL-273 and CL-741. This collaboration combines Kairos’s operational expertise with our innovative pipeline to create an optimal pathway for patients fighting EGFR-mutant and c-MET-driven lung cancers.”

Clinical studies have demonstrated that combination treatment with EGFR and MET inhibitors for EGFR-mutant, MET-amplified NSCLC patients is able to achieve progression-free survival of approximately 7 months, representing a significant advance over single-agent therapy (SAVANNAH trial).

CL-273 is an investigational, reversible, wild-type-sparing pan-EGFR small-molecule inhibitor specifically engineered for EGFR-mutant non-small cell lung cancer (NSCLC). Preclinical data demonstrate that CL-273 maintains broad-spectrum activity against classical EGFR mutations including Exon 19 and 21 deletions and Exon 20 insertions, atypical mutations, and resistance-associated variants that bypass currently approved tyrosine kinase inhibitors (TKIs).

A defining feature of CL-273 is its exceptional selectivity index. By sparing wild-type EGFR, studies to date have shown CL-273 offers a 4-5 fold wider therapeutic window, suggesting significantly improved safety and tolerability over existing therapies. Designed for high brain and lung permeability to address metastatic disease, CL-273 possesses favorable ADME properties and has successfully completed GLP toxicology studies. The program is currently pre-IND, with first-in-human clinical trials projected to commence in 2026.

CL-741 is an orally available, small-molecule, type IIb c-MET kinase inhibitor designed to be highly selective for c-MET with broad coverage of activating and acquired resistance mutations in solid tumors. The compound was discovered as a drug-like lead with potent activity across multiple c-MET resistance mutants and is being developed for c-MET-driven advanced solid tumors, with a primary focus on non-small cell lung cancers harboring MET exon 14 skipping alterations and MET amplification.

The acquisition of both CL-273 and CL-741, if the acquisition is successfully completed, are anticipated to enable Kairos Pharma to pursue a differentiated dual-target strategy addressing both primary EGFR mutations and MET-mediated resistance mechanisms. MET amplification is one of the most common mechanisms of acquired resistance to EGFR TKIs.

Developing CL-273 and CL-741 together provides a rational combination therapy approach for EGFR-mutant NSCLC patients who either harbor baseline MET amplification/overexpression or acquire MET-driven resistance on EGFR-TKI therapy. Combined EGFR and MET inhibition has already demonstrated meaningful clinical response rates and survival benefit with other agents in this setting. Pairing CL-273 with CL-741 could deepen and prolong responses, reduce outgrowth of MET-mediated escape clones, and potentially expand the addressable population of MET-dependent, EGFR-mutant tumors.