JS25 is a selective, covalent BTK inhibitor that deactivates BTK by chelating Tyr551, exhibiting an IC50 of 5.8 nM. It suppresses cancer cell proliferation, induces pronounced cell death, and enhances Burkitt's lymphoma murine xenograft model outcomes. Importantly, JS25 efficiently penetrates the blood-brain barrier.

The 3-Hydroxybutyric acid medium can interact with lipids (using DPPC monolayer modeling) and alter phase behavior at clinical concentrations. The 3-Hydroxybutyric acid solid also reduces the interfacial viscosity of the DPPC monolayer.[1]