Dehydrocrenatidine
Dehydrocrenatidine is a JAK-specific inhibitor, can inhibit JAK-STAT3-dependent DU145 and MDA-MB-468 cell survival and induce cell apoptosis.
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Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to
24 months(2-8C).
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
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The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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Mol Pharmacol. 2015 Apr;87(4):572-81.
Dehydrocrenatidine is a novel janus kinase inhibitor.[Pubmed:
25583084]
Janus kinase (JAK) 2 plays a pivotal role in the tumorigenesis of signal transducers and activators of transcription (STAT) 3 constitutively activated solid tumors. JAK2 mutations are involved in the pathogenesis of various types of hematopoietic disorders, such as myeloproliferative disorders, polycythemia vera, essential thrombocythemia, and primary myelofibrosis. Thus, small-molecular inhibitors targeting JAK2 are potent for therapy of these diseases.
METHODS AND RESULTS:
In this study, we screened 1,062,608 drug-like molecules from the ZINC database and 2080 natural product chemicals. We identified a novel JAK family kinase inhibitor, Dehydrocrenatidine, that inhibits JAK-STAT3-dependent DU145 and MDA-MB-468 cell survival and induces cell apoptosis. Dehydrocrenatidine represses constitutively activated JAK2 and STAT3, as well as interleukin-6-, interferon-α-, and interferon-γ-stimulated JAK activity, and STAT phosphorylation, and suppresses STAT3 and STAT1 downstream gene expression. Dehydrocrenatidine inhibits JAKs-JH1 domain overexpression-induced STAT3 and STAT1 phosphorylation. In addition, Dehydrocrenatidine inhibits JAK2-JH1 kinase activity in vitro. Importantly, Dehydrocrenatidine does not show significant effect on Src overexpression and epidermal growth factor-induced STAT3 activation.
CONCLUSIONS:
Our results indicate that Dehydrocrenatidine is a JAK-specific inhibitor.
