NXP900 targets the SRC family of kinases (SFKs)—proteins that are normally quiet in healthy tissues but become highly active in tumor cells, driving cancer growth, invasion, and survival.

What makes NXP900 unique is its type 1.5 binding mechanism, which locks SRC and YES1 kinases into a closed, inactive form. This not only blocks their enzyme activity but also disrupts their ability to assist cancer-promoting signaling networks—something traditional SFK inhibitors struggle to achieve. Importantly, NXP900 is highly selective for SFKs, minimizing the risk of off-target effects.

For prostate cancer patients, the most exciting finding comes from preclinical studies suggesting that NXP900, especially when combined with osimertinib and enzalutamide, could reverse acquired resistance in mCRPC models. Treatment resistance is one of the greatest hurdles in advanced prostate cancer, and a therapy capable of restoring sensitivity could fill a critical gap.

Currently, NXP900 is being tested in a Phase 1 clinical trial for patients with advanced solid tumors (including prostate). Early results show that it is biologically active and has a manageable safety profile, with mainly mild side effects like fatigue and nausea. Pharmacodynamic studies confirmed that NXP900 effectively inhibits its intended target in the body.

Source.

Clinical trial.