| Properties | Information | |
|---|---|---|
| PhytoCAT-ID | PhytoCAT-753 | |
| Phytochemical name or plant extracts | Dichamanetin | |
| PMID | 31362371 | |
| Literature evidence | Our findings demonstrate the potential applicability of C. kirkii as a source of antimalarial and anticancer agents. | |
| IUPAC name | (2S)-5,7-dihydroxy-6,8-bis[(2-hydroxyphenyl)methyl]-2-phenyl-2,3-dihydrochromen-4-one | |
| Phytochemicals’ class or type of plant extracts | Flavonoid | |
| Source of phytochemicals or plant Extracts | Cleistochlamys kirkii | |
| Geographical availability | Malawi, Mozambique, Tanzania, Zambia, Zimbabwe | |
| Plant parts | Root | |
| Other cancers | Breast cancer, Colon cancer, Prostate cancer | |
| Target gene or protein | PARP1 | |
| Gene or Protein evidence | Triple–negative cells have been reported to be highly sensitive to PARP-1 inhibition and the cytotoxic data correlated with the fact that the triple-negative MDA-MB-231 breast cancer cells had lower IC50 values in the XTT assay. | |
| Target pathways | Dichamanetin inhibits cancer cell growth by affecting ROS-related signaling components through mitochondrial-mediated apoptosis. | |
| IC50 | 9.6 µM against MDA-MB-231 | |
| Potency | This indicates the potential applicability of C. kirkii as a source of antimalarial, and even more likely of anticancer agents. | |
| Cell line/ mice model | MDA-MB-231, HT-29, DU145, | |
| Additional information | Dichamanetin significantly reduced the cell viability of various types of human cancer cells (HT-29 colon, DU145 prostate, and MDA-MB-231 breast cancer) in a concentration- and time-dependent manner and induced G1 arrest of the cell cycle.. . Dichamanetin was shown to arrest cells at the G1 and G2/M phases in this study. Furthermore, dichamanetin induced loss of MMP as an evidence of cellular apoptosis. | |
| PubChem ID | 181193 | |
| Additional PMIDs | 24324069 | |
| Additional sources of information | https://powo.science.kew.org/taxon/urn:lsid:ipni.org:names:72604-1 | |
| Safety | NA |