Changchun Genescience Pharmaceuticals Co. Ltd. has reported GSC-000829, a novel and selective FGFR2/FGFR3 inhibitor being developed for the potential treatment of cancer.
Hangzhou Synrx Therapeutics Biomedical Technology Co. Ltd. recently presented the development and characterization of a novel PARG inhibitor, SYN-608, for the potential treatment of tumors with/without homologous recombination deficiency (HRD).
Tumor cell survival is dependent on phosphate homeostasis, which requires high amounts of energy. Researchers have demonstrated that the silencing of xenotropic and polytropic retrovirus receptor 1 (XPR1) led to reduced tumor growth in an ovarian cancer cell line xenograft, and similar vulnerability was found in lung cancer.
MBT-C101 is a selective, potentially first-in-class potent HSP90 chaperone-mediated degrader of PI3Kα, for the treatment of breast cancer. It was developed by Magicbullet Therapeutics Inc. using the company’s Chaperone-mediated Degrader (CM-Degrader) platform.
Genetic alterations in FAT1, YAP1 or WWTR1 genes are commonly seen in head and neck squamous cell carcinoma (HNSCC) patients. Targeting Hippo and MAPK pathways in combination has proven effective in preclinical models of HNSCC.
The next-generation farnesyl transferase inhibitor KO-2806 is currently in phase I clinical development at Kura Oncology Inc. for the treatment of patients with solid tumors, including non-small-cell lung cancer (NSCLC) and colorectal cancer (CRC).
Gain-of-function mutations and overexpression of the EZH2 gene lead to H3K27Me3 accumulation, which in turn initiates tumorigenesis and tumor progression, thus making it a promising target for therapy.
Activin receptor-like kinase 5 (ALK5) is a member of the transforming growth factor-β (TGF-β) family associated with tumor development and progression that impacts cancer immune response within the tumor microenvironment.
Nonselective poly(ADP-ribose) polymerase (PARP) inhibitors have shown antitumoral activity, but they are tied to hematotoxicity, most probably due to PARP2 inhibition. Instead, selective PARP inhibitors retain antitumoral activity without risking PARP2-related toxicity.
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