Ibrutinib

Description	Ibrutinib shows the potent and irreversible inhibitory effect and selectivity for Btk enzymatic activity. In BCR pathway-activated DOHH2 cell line, Ibrutinib inhibits autophosphorylation of Btk, phosphorylation of Btk's physiological substrate PLCγ, and phosphorylation of further downstream kinase, ERK with IC50 of 11 nM, 29 nM and 13 nM, respectively.Ibrutinib exhibits a significant dose-dependent and time-dependent induction of cytotoxicity in chronic lymphocytic leukemia (CLL) cells. In addition, Ibrutinib induces cell death depending on caspase pathway activation and antagonizes the ability of CLL cells to proliferate after TLR signaling. A recent study shows that Ibrutinib inhibits BCR-activated primary B cell proliferation with IC50 of 8 nM and results in inhibition of TNFα, IL-1β and IL-6 production in primary monocytes with IC50 of 2.6 nM, 0.5 nM and 3.9 nM, respectively.
Pathways	Angiogenesis/Protein Tyrosine Kinase
Targets	BTK

Bruton's tyrosine kinase is essential for NLRP3 inflammasome activation and contributes to ischaemic brain injury Publications Citing of Biochempartner's Ibrutinib(CAS:936563-96-1)

Publications Citing of Biochempartner's Ibrutinib(CAS:936563-96-1)

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