| Properties | Information | |
|---|---|---|
| PhytoCAT-ID | PhytoCAT-858 | |
| Phytochemical name or plant extracts | Picrasidine G | |
| PMID | 28427809 | |
| Literature evidence | In the present study, a natural compound library was screened to identify molecules that target TNBCs that overexpress EGFR. | |
| IUPAC name | NA | |
| Phytochemicals’ class or type of plant extracts | Alkaloid | |
| Source of phytochemicals or plant Extracts | Picrasma quassioides | |
| Geographical availability | Assam, China North-Central, China South-Central, China Southeast, East Himalaya, Hainan, Japan, Korea, Manchuria, Nansei-shoto, Nepal, Taiwan, Tibet, West Himalaya | |
| Plant parts | NA | |
| Other cancers | Breast cancer | |
| Target gene or protein | Caspase 3, PARP, STAT-3, EGFR, Survivin | |
| Gene or Protein evidence | PG treatment increased markers of apoptosis, including chromatin condensation, sub-G1 population, cleavage of caspase 3 and cleavage of poly (ADP-ribose) polymerase (PARP). PG inhibited the phosphorylation of signal transducer and activator of transcription 3 (STAT3) and inhibited transcription of the STAT3-target gene encoding survivin. Picrasidine G decreases viability of MDA-MB 468 EGFR-overexpressing triple-negative breast cancer cells through inhibition of EGFR/STAT3 signaling pathway | |
| Target pathways | EGFR/STAT3 signaling pathway | |
| IC50 | NA | |
| Potency | These results suggest that PG may contribute to the development of targeted therapy of patients with EGFR-overexpressing TNBC. | |
| Cell line/ mice model | MDA-MB-468 | |
| Additional information | Further, PG inhibited EGF-induced STAT3 phosphorylation but not interleukin-6 (IL-6)-induced STAT3 phosphorylation. | |
| PubChem ID | NA | |
| Additional PMIDs | NA | |
| Additional sources of information | https://powo.science.kew.org/taxon/urn:lsid:ipni.org:names:813963-1 | |
| Safety | NA |