Phytochemical Name : Ellagic acid

Properties Information
PhytoCAT-ID PhytoCAT-1489
Phytochemical name or plant extracts Ellagic acid
PMID 28718725
Literature evidence It is suggested that EA may be a potential drug adjuvant for improving cancer radiotherapy by increasing tumor toxicity and reducing the normal cell damage caused by irradiation.
IUPAC name 6,7,13,14-tetrahydroxy-2,9-dioxatetracyclo[6.6.2.04,16.011,15]hexadeca-1(15),4,6,8(16),11,13-hexaene-3,10-dione
Phytochemicals’ class or type of plant extracts Polyphenolic compound
Source of phytochemicals or plant Extracts Rubus idaeus
Geographical availability Alaska, Albania, Altay, Amur, Arizona, Austria, Baltic States, Belarus, Belgium, British Columbia, Bulgaria, Buryatiya, California, Central European Russia, China North-Central, China South-Central, Chita, Colorado, Connecticut, Corse, Czechoslovakia, Delaware, Denmark, District of Columbia, East European Russia, Finland, France, Germany, Great Britain, Greece, Hungary, Idaho, Illinois, Indiana, Inner Mongolia, Iowa, Ireland, Irkutsk, Italy, Japan, Kazakhstan, Khabarovsk, Kirgizstan, Korea, Krasnoyarsk, Krym, Labrador, Magadan, Maine, Manchuria, Manitoba, Maryland, Massachusetts, Mexico Gulf, Mexico Northeast, Mexico Northwest, Michigan, Minnesota, Missouri, Mongolia, Montana, Nebraska, Netherlands, Nevada, New Brunswick, New Hampshire, New Jersey, New Mexico, New York, Newfoundland, North Carolina, North Caucasus, North Dakota, North European Russia, Northwest European Russia, Northwest Territorie, Norway, Nova Scotia, Nunavut, Ohio, Oklahoma, Ontario, Oregon, Pennsylvania, Poland, Primorye, Prince Edward I., Qinghai, Québec, Rhode I., Romania, Sakhalin, Saskatchewan, Sicilia, South Dakota, South European Russia, Spain, Sweden, Switzerland, Tennessee, Transcaucasus, Turkey, Turkey-in-Europe, Turkmenistan, Tuva, Ukraine, Utah, Vermont, Virginia, Washington, West Siberia, West Virginia, Wisconsin, Wyoming, Xinjiang, Yakutskiya, Yugoslavia, Yukon
Plant parts Fruits
Other cancers Breast cancer, Bladder cancer, Prostate cancer, Colorectal cancer, Lung cancer
Target gene or protein CDK6, ACTN4, AKT/mTOR
Gene or Protein evidence EA inhibited breast cancer growth and metastasis via directly targeting ACTN4 in vitro and in vivo, and was accompanied by a limited CSC population, the expression of CDK6 has been downregulated in EA-treated human breast cancer cell lines. Furthermore, we found that EA promoted apoptosis and further reduced AKT/mTOR activation in GDC-0941- treated breast cancer cells.
Target pathways TGF-beta/Smads signaling pathway VEGFR-2 signaling pathway Phosphatidylinositol 3 kinase (PI3K) signaling pathway
IC50 Fluorescence binding studies revealed that EA binds to the CDK6 with a binding constant of K = 107 M-1 and subsequently inhibits its enzyme activity with an IC50 value of 3.053 µM.
Potency Together, our data suggest that EA may be a safe and effective agent to boost the efficacy of PI3K-directed breast cancer therapy and that such drug combination may merit further clinical investigation.
Cell line/ mice model MCF-7, HeLa, HUVEC, HEL 299, Caco-2, Hs 578T, DU 145, C32, A375
Additional information  A 6.2-fold decrease in the mitochondrial membrane potential was observed in the combined treatment of EA and IR that facilitated the upregulation of pro-apopttotic Bax and downregulation of Bcl-2, pushing the MCF-7 cells to undergo an apoptotic cell death. It is suggested that EA may be a potential drug adjuvant for improving cancer radiotherapy by increasing tumor toxicity and reducing the normal cell damage caused by irradiation.
PubChem ID 5281855
Additional PMIDs 25647396 32429317 25941816 28718725
Additional sources of information https://powo.science.kew.org/taxon/urn:lsid:ipni.org:names:298089-2
Safety NA