TAK-715是一种p38 MAPK抑制剂，作用于p38α，IC50为7.1 nM，作用于p38α比作用于p38β选择性高28倍多，对p38γ/δ， JNK1， ERK1， IKKβ， MEKK1和TAK1没有抑制作用。TAK 715抑制LPS刺激的TNF-α从THP-1释放，IC50为48 nM。 TAK 715 (10 μM)作用于U2OS-EFC细胞，抑制Wnt-3a诱导的hDvl2磷酸化和hDvl2转变。 TAK715的酰胺NH通过氢键结合到p38α的Met109的主链羰基上。

>98%

Store at -20℃ for one year（Powder）；Store at 2-4℃ for two weeks；Store at -20℃ for six months after dissolution.

N-(4-(2-乙基-4-(3-甲基苯基)噻唑-5-基)吡啶-2-基)苯甲酰胺

白色固体

Ethanol ：20 mg/mL (50 mM)

DMSO ：40 mg/mL (100 mM)

p38α ,p38β

TAK 715 inhibits LPS-stimulated release of TNF-alpha from THP-1 with IC50 of 48 nM. TAK 715 (10 μM) inhibits Wnt-3a-induced hDvl2 phosphorylation and the hDvl2 shift in U2OS-EFC cells. The amide NH of TAK 715 is hydrogen bonded to the main-chain carbonyl of Met109 of p38 alpha. TAK 715 binds relatively high in the ATP pocket, occupying the hydrophobic back pocket, the adenine region and the front pocket of p38 as well as extending to most of the length of the Gly-rich loop.

TAK 715 (10 mg/kg, po) inhibits LPS-induced TNF-alpha production in mice with 87.6% inhibition. TAK 715 has a modest mouse bioavailability of 18.4% and a slightly improved rat bioavailability of 21.1%. TAK 715 has a modest mouse bioavailability of 18.4% and a slightly improved rat bioavailability of 21.1%. TAK 715 results in Cmax of 0.19 μg/mL and AUC(0-24 hours) of 1.16 μg·h/mL in rats. TAK 715 (30 mg/kg, po) significantly reduces the secondary paw volume with 25 % inhibition in a rat adjuvant-induced arthritis (AA) model.