In This Article:
SHANGHAI, April 27, 2025 /PRNewswire/ -- Abbisko Therapeutics Co., Ltd. (Abbisko Therapeutics 02256.HK) today announced that it has presented four late-breaking pre-clinical research posters at the 2025 AACR conference held in Chicago, Illinois (USA) from April 25 to April 30. 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.
Abbisko presented the following posters at the 2025 AACR:
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.