| Properties | Information | |
|---|---|---|
| PhytoCAT-ID | PhytoCAT-952 | |
| Phytochemical name or plant extracts | Panaxydol | |
| PMID | 26421996 | |
| Literature evidence | In MCF-7 cells, EGFR was activated immediately after exposure to panaxydol, and this activation was necessary for induction of apoptosis, suggesting that panaxydol might be a promising anticancer candidate, especially for EGFR-addicted cancer. | |
| IUPAC name | (3R)-8-[(2R,3S)-3-heptyloxiran-2-yl]oct-1-en-4,6-diyn-3-ol | |
| Phytochemicals’ class or type of plant extracts | Sesquiterpenoid | |
| Source of phytochemicals or plant Extracts | Panax ginseng | |
| Geographical availability | Khabarovsk, Korea, Manchuria, Primorye | |
| Plant parts | Root | |
| Other cancers | Breast cancer, Prostate cancer, Renal cancer | |
| Target gene or protein | EGFR | |
| Gene or Protein evidence | In summary, we identified roles of EGFR, the CAMKII-TAK1-p38/JNK pathway, and ER stress in panaxydol-induced apoptosis and demonstrated the in vivo anticancer effect of panaxydol. | |
| Target pathways | CAMKII-TAK1-p38/JNK pathway | |
| IC50 | NA | |
| Potency | Among the three signaling branches of the unfolded protein response, protein kinase R-like ER kinase (PERK), but not inositol-requiring enzyme 1 or activating transcription factor 6, played a role in transmitting the apoptosis signal. PERK induced C/EBP homologous protein (CHOP), and CHOP elevated Bim expression, initiating mitochondrial Ca(2+) uptake and apoptosis. | |
| Cell line/ mice model | MCF-7 , PC3 and Renca mouse renal cancer cells | |
| Additional information | In summary, these data indicate that panaxydol induces apoptosis preferentially in cancer cells, and the signaling mechanisms involve a [Ca(2+)](i) increase, JNK and p38 MAPK activation, and ROS generation through NADPH oxidase and mitochondria. | |
| PubChem ID | 126312 | |
| Additional PMIDs | 21190085 | |
| Additional sources of information | https://powo.science.kew.org/taxon/urn:lsid:ipni.org:names:91472-1 | |
| Safety | NA |