SMARCA4-deficient cells have shown dependency on SMARCA2 for survival, suggesting SMARCA2 as a promising synthetic lethal target in SMARCA4-deficient cancers. Chinese researchers recently published data on a series of SMARCA2 PROTACs, among which compound [I] exerted good SMARCA2 degradation.
Xuanzhu Biopharmaceutical Co. Ltd. reported positive data from a local phase III study of dirozalkib (Xuan Fei Ning), an ALK inhibitor approved in China to treat patients with advanced non-small-cell lung cancer.
Xuanzhu Biopharmaceutical Co. Ltd. reported positive data from a local phase III study of dirozalkib (Xuan Fei Ning), an ALK inhibitor approved in China to treat patients with advanced non-small-cell lung cancer.
In a boon for licensee Bristol Myers Squibb Co., Systimmune Inc.’s next-generation cancer drug, izalontamab brengitecan (iza-bren), hit both progression-free survival and overall survival endpoints in a phase III trial of Chinese patients with advanced triple-negative breast cancer.
In a boon for licensee Bristol Myers Squibb Co., Systimmune Inc.’s next-generation cancer drug, izalontamab brengitecan (iza-bren), hit both progression-free survival and overall survival endpoints in a phase III trial of Chinese patients with advanced triple-negative breast cancer.
Oncology-focused Eikon Therapeutics Inc. set the terms of its IPO Jan. 28, selling 17.648 million shares at a price range between $16 to $18 per share. At the top of the range, the Millbrae, Calif.-based biopharma company would raise about $317.7 million.
Researchers from Lanzhou University and Southern Medical University (China) have presented the discovery of a structurally distinct pyrimidine-based chemotype for the inhibition of KRAS G12C.
GAS41, the chromatin-associated protein encoded by YEATS4, is frequently overexpressed in non-small-cell lung cancer (NSCLC). Beyond its association with epigenetic dysregulation, GAS41 plays an active role in modulating transcriptional programs that are essential for NSCLC pathogenesis, underscoring its suitability as a mechanistically well-supported therapeutic target.
METTL3, the enzyme that adds the m6A RNA modification, is a key regulator of RNA processing and protein synthesis. In cancer, METTL3 is often overexpressed, driving tumor growth, invasion and therapy resistance across multiple malignancies, including lung, pancreatic, ovarian, colorectal cancers and acute myeloid leukemia.
