Description |
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[1][2].
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In Vitro |
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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In Vivo |
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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Density | 1.3±0.1 g/cm3 |
Boiling Point | 491.8±40.0 °C at 760 mmHg |
Flash Point | 174.9±17.6 °C |
Exact Mass | 254.105530 |
PSA | 47.14000 |
LogP | 3.70 |
Vapour Pressure | 0.0±1.2 mmHg at 25°C |