JS25 is a selective and covalent inhibitor ofBTKthat inactivatesBTKwith anIC₅₀value of 5.8 nM by chelating Tyr551. JS25 inhibitscancercells proliferation, pronounces cell death, and promotes murine xenograft model of Burkitt’s lymphoma. JS25 effectively crosses the blood-brain barrier^[1].

IC50: 5.8 nM (BTK), 49.0 nM (BMX), 440 nM (ITK), 190 nM (TXK), 220 nM (TEC), 2.60 μM (BLK)^[1]

JS25 (0-50 μM; 72 h) inhibits the proliferation of myeloid and lymphoid B-cell cancer cell lines. JS25 shows inhibitory capability against BTK, BMX, ITK, TXK, TEC, and BLK with IC₅₀s of 28.5 nM, 49.0 nM, 0.44 μM, 0.19 μM, 0.22 μM, and 2.60 μM, respectively; shows little inhibition against other BTK pathway-related proteins (EGFR, ERBB2, and JAK3), with IC₅₀>3 μM. JS25 presents a more favorable selectivity profile thanIbrutinib(HY-10997) andAcalabrutinib(HY-17600)^[1].
JS25 (10 μM; 0, 4, 15 h) degrades BTK and inhibits both the catalytic activity and the expression of BTK in tumor cells^[1].
JS25 (10 μM; 72 h) inhibits the tumor growth of Burkitt’s lymphoma and induces selective ex vivo cytotoxicity in primary diffuse large B-cell lymphoma (DLBCL) samples^[1].

JS25 (10 mg/kg and 20 mg/kg; i.p.; every 2 days, for 14 d) inhibits tumor growth and results a significant reduction in their secondary tumor formation in murine xenograft model of Burkitt’s lymphoma^[1].
JS25 (1, 2.5, and 5 μM; injection; every day for 2 days) decreases tumor burden in zebrafish patient-derived xenografts of chronic lymphocytic leukemia, wich efficacy is better thanIbrutinib(HY-10997)^[1].

524.59

C₂₉H₂₄N₄O₄S

2411771-95-2

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.