| Properties | Information | |
|---|---|---|
| PhytoCAT-ID | PhytoCAT-1999 | |
| Phytochemical name or plant extracts | 3-Deoxy-2β,16-dihydroxynagilactone E (B6) | |
| PMID | 31201357 | |
| Literature evidence | Epub 2019 Jun 14. 3-Deoxy-2β,16-dihydroxynagilactone E, a natural compound from Podocarpus nagi, preferentially inhibits JAK2/STAT3 signaling by allosterically interacting with the regulatory domain of JAK2 and induces apoptosis of cancer cells. | |
| IUPAC name | NA | |
| Phytochemicals’ class or type of plant extracts | Nagilactone | |
| Source of phytochemicals or plant Extracts | Podocarpus nagi | |
| Geographical availability | China Southeast, Hainan, Japan, Nansei-shoto, Taiwan | |
| Plant parts | Leaves | |
| Other cancers | Breast cancer | |
| Target gene or protein | JAK-2, IL-6, STAT-3 | |
| Gene or Protein evidence | B6 preferentially inhibited the phosphorylation of STAT3 by interacting with and inactivating JAK2, the main upstream kinase of STAT3. B6 dose-dependently inhibited IL-6-induced STAT3 signaling with an IC50 of 0.2 μM. In contrast to other JAK2 inhibitors, B6 did not interact with the catalytic domain but instead with the FERM-SH2 domain of JAK2. | |
| Target pathways | JAK2/STAT3 signaling | |
| IC50 | B6 dose-dependently inhibited IL-6-induced STAT3 signaling with an IC50 of 0.2 μM. | |
| Potency | Furthermore, B6 potently inhibited the growth and induced apoptosis of MDA-MB-231 and MDA-MB-468 breast cancer cells with overactivated STAT3. | |
| Cell line/ mice model | MDA-MB-231, MDA-MB-468 | |
| Additional information | Taken together, our study uncovers a novel compound and a novel mechanism for the regulation of JAK2 and offers a new therapeutic approach for the treatment of cancers with overactivated JAK2/STAT3. | |
| PubChem ID | NA | |
| Additional PMIDs | NA | |
| Additional sources of information | https://powo.science.kew.org/taxon/urn:lsid:ipni.org:names:263543-1 | |
| Safety | NA |