Dehydrocrenatidine inhibits JAK-STAT3 dependent DU145 and MDA-MB-468 cell survival and induces cell apoptosis. Dehydrocrenatidine inhibits JAKs-JH1 domain over-expression induced STAT3 and STAT1 phosphorylations[1].
Dehydrocrenatidine diminishes IL-6, IFNα and IFNγ stimulated STAT3 phosphorylation as well as constitutive STAT3 phosphorylation[1].
DHCT suppresses both tetrodotoxin-resistant (TTX-R) and sensitive (TTX-S) voltage-gated sodium channel (VGSC) currents with IC50 values of 12.36 µM and 4.87 µM, respectively[2].
Dehydrocrenatidine inhibits JAK-STAT3 dependent DU145 and MDA-MB-468 cell survival and induces cell apoptosis. Dehydrocrenatidine inhibits JAKs-JH1 domain over-expression induced STAT3 and STAT1 phosphorylations[1].
Dehydrocrenatidine diminishes IL-6, IFNα and IFNγ stimulated STAT3 phosphorylation as well as constitutive STAT3 phosphorylation[1].
DHCT suppresses both tetrodotoxin-resistant (TTX-R) and sensitive (TTX-S) voltage-gated sodium channel (VGSC) currents with IC50 values of 12.36 µM and 4.87 µM, respectively[2].
References:
[1]. Jing Zhang, et al. Dehydrocrenatidine is a novel janus kinase inhibitor. Mol Pharmacol. 2015 Apr;87(4):572-81.
[2]. Fang Zhao, et al. Dehydrocrenatidine Inhibits Voltage-Gated Sodium Channels and Ameliorates Mechanic Allodia in a Rat Model of Neuropathic Pain. Toxins (Basel). 2019 Apr 18;11(4):229.
















