BTK inhibitor 17 is a potent and orally active irreversible BTK inhibitor with an IC 50 of 2.1 nM. BTK inhibitor 17 can be used for rheumatoid arthritis research In Vitro BTK inhibitor 17 (compound 8) could covalently bind to Cys481 and formed an HB network with hinge key residues Met477, Glu475, and gatekeeper Thr474. MCE has not independently confirmed the accuracy of these methods. They are for reference only. In Vivo BTK inhibitor 17 (compound 8; 3-10 mg/kg; oral gavage; daily; for 28 days) treatment inhibits the significant progression of the disease and exhibits a clear dose-dependent reduction per paw clinical scores, and no significant body weight loss is observed for all different dosages . BTK inhibitor 17 (compound 8) shows >95% plasma protein binding across three species of human, rat, and mouse. After an intravenous injection, the half-life (rat, 0.32 h; mice, 0.42 h), clearance (rat, 54.6 mL/min/kg; mice, 31.3 mL/min/kg), volume of distribution (rat, 1.55 L/kg; mice, 0.82 L/kg), and AUC exposure (rat, 604 ng.h/mL; mice, 576 ng.h/mL) are observed in two species. After oral administration, BTK inhibitor 17 exhibits higher C max (rat, 466 ng/mL; mice, 252 ng/mL) and plasma exposure (rat, 642 ng.h/mL; mice, 128 ng.h/mL) with a favorable oral bioavailability (rat, 23.7%; mice, 11.2%) . MCE has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: Male Balb/C mice injected with collagen Dosage: 3 mg/kg or 10 mg/kg Administration: Oral gavage; daily; for 28 days Result: Inhibited the significant progression of the disease and exhibited a clear dose-dependent reduction per paw clinical scores. Form:Solid IC50& Target:IC50: 2.1 nM (BTK)