DehydrocrenatidineDehydrocrenatidine
MedChemExpress (MCE)
HY-N3710
65236-62-6
Kumujian G
O-Methylpicrasidine I
98.0%
4°C, protect from light *In solvent : -80°C, 6 months
-20°C, 1 month (protect from light)
Room temperature in continental US
may vary elsewhere.
Dehydrocrenatidine, a natural alkaloid, is a specific JAK inhibitor. Dehydrocrenatidine inhibits voltage-gated sodium channels and ameliorates mechanic allodia in a rat model of neuropathic pain.
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].
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[1]. Jing Zhang, et al. Dehydrocrenatidine is a novel janus kinase inhibitor. Mol Pharmacol. 2015 Apr
87(4):572-81. [Content Brief]
[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. [Content Brief]