| Bioactivity | Takinib (EDHS-206) is an orally active and selective TAK1 inhibitor (IC50=9.5 nM), more than 1.5 log more potent than the second and third ranked targets, IRAK4 (120 nM) and IRAK1 (390 nM), respectively. Takinib is an inhibitor of autophosphorylated TAK1 that non-competitively binds within the ATP binding pocket. Takinib induces apoptosis following TNFα stimulation in cell models of rheumatoid arthritis and metastatic breast cancer. Takinib is also a P. falciparum protein kinase 9 (PfPK9) inhibitor (KD(app) of 0.46 μM)[1][2][3]. | ||||||||||||
| Invitro | Takinib (10-10000 nM; 24 hours) induces apoptosis following TNF-α stimulation in MDA-MB-231 cells[1].Takinib (10 μM; 0-1 hours) reduces phosphorylation of IKK and p65[1].Takinib serves as a chemical starting point for the development of PfPK9 (KD(app) of 0.46 μM) inhibitors for malaria[3].Takinib (2 hours; 0.1-20 µM; human RASFs) induces phosphorylation of TAK1Thr184/187, STAT3Tyr705 and STAT3Ser727 in IL-1β-treated (10 ng/mL; 30 min) RASFs[4]. Western Blot Analysis[1] Cell Line: | ||||||||||||
| Name | Takinib | ||||||||||||
| CAS | 1111556-37-6 | ||||||||||||
| Formula | C18H18N4O2 | ||||||||||||
| Molar Mass | 322.36 | ||||||||||||
| Transport | Room temperature in continental US; may vary elsewhere. | ||||||||||||
| Storage |
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