Acute myeloid leukemia (AML) is a hematological cancer with limited treatment options and characterized by frequent relapse and poor prognosis. The only approved antibody-drug conjugate for AML is gemtuzumab ozogamicin, which targets CD33.
Receptor-interacting protein kinase 1 (RIPK1) helps promote the survival of cancer cells, and degrading it can sensitize tumors to immunotherapy against PD-1. Degrading the entire protein seems to be essential: merely blocking its kinase activity does not sensitize tumors.
Triple-negative breast cancer (TNBC) is a highly aggressive subtype affecting 15%-20% of breast cancer patients. TNBC patients harboring breast cancer susceptibility gene 1/2 (BRCA1/2) mutations have shown improved therapeutic response to poly(ADP-ribose) polymerase (PARP) inhibitors (PARPi).
In an effort to develop more effective estrogen receptor α (ERα) inhibitors, researchers at Nanjing University of Chinese Medicine and collaborators aimed to develop a proteolysis targeting chimera (PROTAC) against the receptor.
FGFR3 genomic alterations, including S249C as the most common, are recognized oncogenic drivers in 10%-60% of bladder cancers depending on the disease stage. Onco3r Therapeutics BV recently reported the identification of a novel series of highly potent, isoform-selective small-molecule FGFR3 inhibitors.
Researchers from Eilean Therapeutics LLC and collaborators presented the discovery and characterization of a new, selective CDK2 inhibitor showing potent in vitro and in vivo activity at the 2025 AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics.
At the AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics, researchers from Onco3r Therapeutics BV presented a novel series of selective SMARCA2 small-molecule inhibitors with a best-in-class potency and selectivity profile.
Although tricomplex pan-RAS (ON) inhibitors, such as RMC-6236, constitute a promising class of therapeutics against RAS-driven cancers, their on-target, off-tumor toxicities challenge the dosing strategy and the safety of drug combinations.
Inactivation of the tumor suppressor p53 occurs in approximately half of human cancer cases. In particular, the Y220C point mutation, which induces p53 misfolding and inactivation, is found in about 1% of solid tumors. Previous research identified a unique, druggable pocket on the p53 surface created by this mutation that constitutes a promising cancer therapeutic target.
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