Acrivon Therapeutics Inc. has developed a new WEE1/PKMYT1 inhibitor, ACR-2316, to overcome the limitations observed with previous WEE1 and PKMYT1 inhibitors in the treatment of cancer.
Accutar Biotechnology Inc. recently presented preclinical data on AC-4847, a first-in-class PI3Kα-targeting degrader-antibody conjugate (DAC) designed for selective treatment of PI3Kα-driven cancers.
Researchers at Crossbridge Bio Inc. have conducted preclinical evaluation of CBB-120, a novel TROP2-directed dual-payload ADC designed to combine TOP1i and ATR inhibitor (ATRi) mechanisms for enhanced therapeutic efficacy.
Changchung Genescience Pharmaceutical Co. Ltd., reported effects of the bispecific antibody-drug conjugate (ADC) of Gensci-143, is in metastatic castration-resistant prostate cancer (mCRPC) and other solid tumors.
Advanced gastric cancer continues to pose a significant medical challenge because of the scarcity of effective treatments and the frequent development of resistance to available drugs.
ADAM9 (a disintegrin and metalloproteinase 9) is overexpressed in several gastrointestinal cancers, with expression levels correlating with suppressive tumor microenvironment, metastasis and poor prognosis. DB-1317, under development at Duality Biologics (Suzhou) Co. Ltd., is an ADAM9-targeting antibody-drug conjugate including a topoisomerase inhibitor payload P1003 at a drug-antibody ratio of 8.
Alterations in HER2 are known oncogenic drivers in several solid tumors, including breast, lung and gastric cancers, among others. VRN-101099 is an oral and HER2-selective tyrosine kinase inhibitor developed by Voronoi Inc. that had demonstrated brain permeability and preclinical safety.
KIF18A is a kinesin motor protein that moves toward the plus-end of spindle microtubules during mitosis. Inhibition of KIF18A disrupts spindle microtubule dynamics and chromosome alignment, selectively inducing mitotic catastrophe in chromosomally unstable cancer cells while sparing normal cells.
KRAS acts as a key molecular switch in cell signaling, activated by the guanine nucleotide exchange factor SOS1. Mutant KRAS drives many cancers, yet has been difficult to target directly. SOS/pan-KRAS modulators represent a new approach that blocks the SOS1-KRAS interaction, preventing KRAS activation and suppressing oncogenic signaling across multiple KRAS variants.
