On April 27, 2025 Abbisko Therapeutics Co., Ltd. (Abbisko Therapeutics 02256.HK) reported that it has presented four late-breaking pre-clinical research posters at the 2025 AACR (Free AACR Whitepaper) conference held in Chicago, Illinois (USA) from April 25 to April 30 (Press release, Abbisko Therapeutics, APR 27, 2025, View Source;abbisko-therapeutics-presents-late-breaking-pre-clinical-research-results-on-absk112-egfr-exon20ins-absk131-prmt5mta-and-abk-kras-1-302439218.html [SID1234652204]). Results were shared for ABSK112 (EGFR exon20ins inhibitor), ABSK131 (PRMT5*MTA inhibitor), and ABK-KRAS-1 (pan-KRAS inhibitor), as well as results from a study investigating potential resistance mechanisms to KRAS G12C inhibitors.

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Abbisko presented the following posters at the 2025 AACR (Free AACR Whitepaper):

Title1: 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.