On April 17, 2026 Cogent Biosciences, Inc. (Nasdaq: COGT), a biotechnology company focused on developing precision therapies for genetically defined diseases, reported that preclinical data from the Company’s KRAS and ErbB2 pipeline programs will be presented during poster sessions at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) Annual Meeting 2026 taking place in April 17-22 in San Diego, CA.

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"As we prepare for the potential launch of bezuclastinib later this year, we are excited to share updates from two of our pipeline programs this weekend at the 2026 annual AACR (Free AACR Whitepaper) meeting," said Andrew Robbins, Cogent’s President and Chief Executive Officer. "First, we are presenting data on CGT1263, our novel pan-KRAS(ON) inhibitor, which shows best-in-class cellular potency along with evidence that its kinase selectivity advantage over multi-RAS inhibitors could drive clinical differentiation with regards to skin toxicity, a current liability of advanced clinical programs. Separately, we provide an update on CGT4255, our novel, selective ErbB2 inhibitor that was specifically designed for its best-in-class CNS penetrant properties to address a significant unmet need for HER2+ patients with brain metastases. This presentation also includes preclinical data in combination with a HER2 ADC suggesting potential synergistic activity leading to improved duration of therapy as well as re-sensitization of patients following HER2 ADC resistance. With multiple potential blockbuster programs advancing in our pipeline, we believe these new data underscore the long-term potential of Cogent Biosciences."

Poster Details

Title: Characterization of CGT1263, a KRAS (ON/OFF) inhibitor clinical candidate with selectivity for mutant KRAS over HRAS and NRAS
Session Category: Experimental and Molecular Therapeutics
Session Title: Novel Antitumor Agents 1
Session Date and Time: April 19, 2026 – 2:00 PM – 5:00 PM PT (5:00 PM – 8:00 PM ET)
Location: Poster Section 17
Poster Board Number: 13
Poster Number: 410

Mutations in KRAS are among the most prevalent mutations found in cancer, occurring most often in colorectal cancer, non-small cell lung cancer and pancreatic cancer. The preclinical poster highlights Cogent’s internally developed pan-KRAS(ON) inhibitor with >500x selectivity for KRAS over HRAS and NRAS. Plasma exposure following oral administration across species resulted in sustained pERK inhibition and robust antitumor activity. Tumor pERK inhibition was also achieved with limited skin suppression, supporting the potential of a larger therapeutic window for CGT1263 when compared to multi-RAS inhibitors currently in clinical development. This aligns with historical data implicating the RAS-MAPK-ERK pathway as essential for skin development given its role in regulation of keratinocyte proliferation, differentiation, and survival; combined suppression of multiple targets within this pathway is thought to be the driver of frequent rash observed in patients treated with multi-RAS inhibitors. Overall, these findings suggest CGT1263 could provide an advantage for patients, enabling higher dosing designed to elicit a more profound molecular response. Investigational New Drug (IND) enabling studies are ongoing with an IND submission expected later this year.

Title: Preclinical characterization of CGT4255, an EGFR sparing, pan-mutant HER2 clinical development candidate with potential best-in-class brain penetration
Session Category: Experimental and Molecular Therapeutics
Session Title: Tyrosine Kinase, Phosphatase, and Other Inhibitors
Session Date and Time: April 21, 2026 – 2:00 PM – 5:00 PM PT (5:00 PM – 8:00 PM ET)
Location: Poster Section 18
Poster Board Number: 7
Poster Number: 5869

Cogent’s EGFR-sparing, brain-penetrant ErbB2 inhibitor includes potent coverage of key mutations (YVMA, S310F, V842I, L755S) inadequately addressed by currently approved therapies. Activating mutations in the ErbB2 gene have been identified in multiple cancers and demonstrate a tumorigenic role similar to that of ErbB2 amplification. New data presented describe CGT4255’s >100-fold selectivity over EGFR while robustly engaging HER2 amplification, insertion and mutant lines in addition to reinforcing best-in-class potential CNS performance relative to other agents in development. Additional mechanistic studies presented suggest CGT4255 may have synergistic effects on efficacy and durability when combined with HER2 targeted ADCs. Preclinical evidence demonstrates that concurrent treatment of CGT4255 and T-DXd enhances receptor internalization and cancer cell apoptosis, suggesting the potential for a synergistic combination that could improve patient outcomes. The Phase 1 study of CGT4255 is ongoing.

Posters will be available on the ‘Posters and Publications’ page of Cogent’s website.

(Press release, Cogent Biosciences, APR 17, 2026, View Source [SID1234664468])