Phytochemical Name : AG36

Properties Information
PhytoCAT-ID PhytoCAT-627
Phytochemical name or plant extracts AG36
PMID 32643027
Literature evidence The results indicated that AG36 could significantly inhibit the proliferation, migration and invasion of human umbilical vein endothelial cells (HUVEC).
IUPAC name NA
Phytochemicals’ class or type of plant extracts Triterpenoid saponin
Source of phytochemicals or plant Extracts Ardisia gigantifolia
Geographical availability China South-Central, China Southeast, Hainan, Laos, Thailand, Vietnam
Plant parts Rhizome
Other cancers Breast cancer
Target gene or protein Cyclin B1, Cyclin D1, FAK, AKT, VEGF, VEGFR2, Caspase 3, Caspase 8, Bax, Bcl-2, Fas, FasL, TNFR1, DR5, cyt-c
Gene or Protein evidence Moreover, AG36 decreased the protein expression of cycle regulatory proteins cyclin B1 or cyclin D1. Further antiangiogenic molecular mechanism investigation showed that AG36 significantly suppressed phosphorylated FAK and AKT, and downregulated the expressions of vascular endothelial growth factor (VEGF) and vascular endothelial growth factor receptor 2 (VEGFR2) in HUVECs. In addition, AG36 inhibited the tumor growth in xenograft model and expressions of p-VEGFR2 and p-Akt in vivo. Moreover, AG36 decreased the protein expression of cycle regulatory proteins cyclin B1 or cyclin D1. In MCF-7 and MDA-MB-231 cells, AG36 strongly increased the cleaved caspase-3 and -8 protein expressions, while in SK-BR-3 cells, AG36 only increased the protein expression of cleaved caspase-3. In all the three breast cancer cells, the ratio of Bax/Bcl-2 and cytosolic cytochrome c content increased significantly compared with control group. The death receptor-related proteins Fas/FasL, TNFR1, and DR5 were detected by Western blot, it showed that different breast cancer cells activated the death receptor-mediated extrinsic caspase-8 pathway through different receptors.
Target pathways NA
IC50 At 48h: 0.73 μM against MCF-7 18.1 μM against MDA-MB-231 3.4 μM against SKBR-3
Potency Our recent studies proved that AG36 displayed prominent cytotoxicity against breast cancer cells both in vitro and in vivo. In conclusion, AG36 inhibited MCF-7, MDA-MB-231, and SK-BR-3 cells proliferation by the intrinsic mitochondrial and the extrinsic death receptor pathways and AG36 might be a potential breast cancer therapeutic agent.
Cell line/ mice model MCF-7, MDA-MB-231, SKBR-3, BALB/c nude mice
Additional information  NA
PubChem ID NA
Additional PMIDs 28184196 32643027
Additional sources of information https://powo.science.kew.org/taxon/urn:lsid:ipni.org:names:587033-1
Safety NA