Abbisko presented the following posters at the 2025 AACR:

Title 1: Preclinical Evaluation of ABSK112, a Selective and CNS-penetrant Compound with Strong HER2 Inhibitory Activity for Treating HER2-Driven Solid Tumors

Session Category: Late-Breaking Research: Experimental and Molecular Therapeutics 2

Session Date and Time: April 28, 2025, 2:00 PM - 5:00 PM (CDT)

Location: Poster Section 54

Poster Board Number: 14

Poster Number: LB240

Conclusion: Our findings establish ABSK112 as a potent, selective and CNS-penetrant HER2 inhibitor, warranting further clinical evaluation of it as a monotherapy or in combination with HER2-targeted ADCs for the treatment of HER2+ cancers with brain metastases.

Title 2: Loss-of-Function (LoF) of KEAP1 promotes cell survival through multiple mechanisms, leading to resistance to KRAS G12C inhibitors

Session Title: Late-Breaking Research: Experimental and Molecular Therapeutics 3

Session Date and Time: April 29, 2025 9: 00AM – 12: 00 PM (CDT)

Location: Poster Section 52

Poster Board Number: 1

Poster Number: LB278

Conclusion: KEAP1 LoF mutant NSCLCs develop resistance to KRAS G12C inhibitors through reduced drug-induced ROS accumulation, metabolic adaptation, and sustained activation of MAPK and AKT signaling. Combination therapies targeting glutamine metabolism (e.g., GLS1 inhibitors), MAPK (e.g., MEK inhibitors), and PI3K-AKT-mTOR pathways (e.g., BEZ235) reverse resistance and improve therapeutic efficacy in KEAP1-mutant cell lines. These strategies may restore sensitivity to KRAS G12C inhibitors and enhance clinical outcomes.

Title 3: The MTA-Cooperative PRMT5 Inhibitor ABSK131 Exhibits Potent Activity and Broad Synergistic Potential in MTAP-Deleted Cancer Models

Session Category: Late-Breaking Research: Experimental and Molecular Therapeutics 4

Session Date and Time: April 30, 2025 9:00 AM - 12:00 PM (CDT)

Location: Poster Section 51

Poster Board Number: 9

Poster Number: LB427

Conclusion: ABSK131 exhibits strong anti-tumor activity in MTAP-deleted lung and pancreatic cancer models and synergizes effectively with multiple therapeutic agents. These findings support the continued clinical development of ABSK131 as both a monotherapy and in combination regimens for MTAP-deleted cancers.

Title 4: Discovery and characterization of a highly potent and orally available small-molecule inhibitor for diverse KRAS mutations 

Session Category: Late-Breaking Research: Experimental and Molecular Therapeutics 4

Session Date and Time: April 30, 2025 9:00 AM - 12:00 PM (CDT) 

Location: Poster Section 51

Poster Board Number: 13

Poster Number: LB431

Conclusion: Taken together, ABK-KRAS-1 exhibits broad in vitro activity against different KRAS mutations and induces dose-dependent tumor regression in KRAS mutated xenograft models. Moreover, ABK-KRAS-1 possesses favorable drug-like properties. Here, ABK-KRAS-1 is presented as a promising therapeutic candidate for the treatment of cancers harboring KRAS mutations.