ATP Synthase Modulator

BMS-199264 hydrochloride is an inhibitor of F1F0 ATP hydrolase (IC₅₀=0.5 μM) without inhibitory effect on F1F0 ATP synthase. BMS-199264 hydrochloride selectively inhibits ATP decline during ischemia to reduces cardiac necrosis. BMS-199264 hydrochloride also enhances the recovery of contractile function following reperfusion.

KI-DX-014 is a DDX21 inhibitor with high RNA-binding inhibitory activity (IC₅₀ of 3.31 μM). KI-DX-014 targets DDX21’s intrinsically disordered C-terminal domain, inhibits DDX21-structured RNA interaction, modulates DDX21’s RNA-dependent ATPase activity, and disrupts DDX21 biomolecular condensate formation. KI-DX-014 attenuates in vitro P-TEFb release from the 7SK snRNP complex, suppresses P-TEFb-dependent RNA polymerase II CTD phosphorylation, and induces developmental defects in zebrafish embryos. KI-DX-014 acts as a chemical probe for dissecting DDX21 functions in normal physiology and disease states. KI-DX-014 can be used for cancers and neurodegenerative disorders research.

BMS-199264 is an inhibitor of F1F0 ATP hydrolase (IC₅₀=0.5 μM) without inhibitory effect on F1F0 ATP synthase. BMS-199264 selectively inhibits ATP decline during ischemia to reduces cardiac necrosis. BMS-199264 also enhances the recovery of contractile function following reperfusion.