Phytochemical Name : Caffeic acid phenethyl ester (CAPE)

Properties Information
PhytoCAT-ID PhytoCAT-1730
Phytochemical name or plant extracts Caffeic acid phenethyl ester (CAPE)
PMID 19394397
Literature evidence Also, TAM treatment resulted in inhibition of hepatic activity of glutathione reductase (GR), glutathione peroxidase (GPx), superoxide dismutase (SOD) and catalase (CAT).
IUPAC name 2-phenylethyl 3-(3,4-dihydroxyphenyl)prop-2-enoate
Phytochemicals’ class or type of plant extracts Polyphenol
Source of phytochemicals or plant Extracts Propolis, Euonymus alatus
Geographical availability E. Asia - Japan
Plant parts NA
Other cancers Breast cancer
Target gene or protein TLR4, MyD88, IRAK4, TRIF, NF-κB p65
Gene or Protein evidence CONCLUSIONS: These findings indicated that EECP and its major constituent - CAPE inhibited breast cancer MDA-MB-231 cells proliferation in inflammatory microenvironment through activating apoptosis, autophagy and inhibiting TLR4 signaling pathway., TLR4 signaling pathway molecules such as TLR4, MyD88, IRAK4, TRIF and NF-κB p65 were all down-regulated after EECP and CAPE treatment in LPS-stimulated MDA-MB-231 cells.
Target pathways Ethanol extract of propolis and its constituent caffeic acid phenethyl ester inhibit breast cancer cells proliferation in inflammatory microenvironment by inhibiting TLR4 signal pathway and inducing apoptosis and autophagy.
IC50 14.08 µM against MDA-MB-231
Potency CAPE may markedly affect the viability of breast cancer cells, suggesting the potential role of bioactive compounds in chemoprevention/chemotherapy by potentiating the action of standard anti-cancer drugs.
Cell line/ mice model MDA-MB-231, MCF-7, Hs578T, HaCaT
Additional information  Caffeic acid phenethyl ester protects against tamoxifen-induced hepatotoxicity in rats.
PubChem ID 5281787
Additional PMIDs 28950845 26007182 33014153 2450776
Additional sources of information NA
Safety NA