Cancer Research

EGCG

(-)Epigallocatechin Gallate

Prod. No. E4143 – Minimum 95%
Prod. No. E4268 – Minimum 80%

Anti-oxidant that preferentially induces apoptosis in neoplastic cells

Epigallocatechin Gallate (EGCG) is an anti-oxidant polyphenol flavonoid isolated from green tea. Its possible benefit as a nutritional chemopreventive agent for cancer, atherosclerosis, and neurodegenerative diseases is generating increased scientific interest. EGCG has demonstrated chemopreventive and chemotherapeutic actions in cellular and animal models of cancer.1,2


  • EGCG selectively induces apoptosis in human carcinoma cell lines.1-3
  • It inhibits MAP kinase mediated signaling pathways.2,4
  • EGCG blocks the activation of EGF receptors and HER-2 receptors which are over-expressed or constitutively active in many human malignancies.4,5
  • It interferes with angiogenesis by suppressing VEGF activity, VE-cadherin phosphorylation and matrix metalloproteinase activity.6-8
  • EGCG inhibits telomerase and DNA methyltransferase, two enzymes involved in cancer gene expression and cellular immortality.9-12
  • EGCG's anti-oxidant action protects cells from lipid peroxidation and DNA damage induced by reactive free radicals.13-16

Sigma® is pleased to make this important compound available to cancer researchers.

  1. Borska, S., et al., Induction of apoptosis by EGCG in selected tumour cell lines in vitro. Folia Histochem. Cytobiol. 41, 229-32 (2003).
  2. Lambert, J.D., et al., Mechanisms of cancer prevention by tea constituents. J. Nutr. 133, 3262S-3267S (2003).
  3. Gupta, S. et al., Essential role of caspases in epigallocatechin-3-gallate-mediated inhibition of nuclear factor κB and induction of apoptosis. Oncogene 23, 2507-2522 (2004).
  4. Sah, J.F., et al., Epigallocatechin-3-gallate inhibits epidermal growth factor receptor signaling pathway. Evidence for direct inhibition of ERK1/2 and Akt kinases. J. Biol. Chem. 279, 12755-12762 (2004).
  5. Masuda M, et al., Epigallocatechin-3-gallate inhibits activation of HER-2/neu and downstream signaling pathways in human head and neck and breast carcinoma cells. Clin. Cancer Res. 9, 3486-3491 (2003).
  6. Tang, F.Y. et al., Green tea catechins inhibit VEGF-induced angiogenesis in vitro through suppression of VE-cadherin phosphorylation and inactivation of Akt molecule. Int. J. Cancer 106, 871-878 (2003).
  7. Lee, Y.K., et al., VEGF receptor phosphorylation status and apoptosis is modulated by a green tea component, epigallocatechin-3-gallate (EGCG) in B cell chronic lymphocytic Leukemia. Blood. Mar 2, 2004 [Epub ahead of print]
  8. Tosetti, F., et al., Angioprevention: angiogenesis is a common and key target for cancer chemopreventive agents. FASEB J. 16, 2-14 (2002).
  9. Yokoyama, M. et al., The tea polyphenol, (-)-epigallocatechin gallate effects on growth, apoptosis, and telomerase activity in cervical cell lines. Gynecol Oncol. 92, 197-204 (2004).
  10. Didiano, D., et al.,Telomere maintenance in childhood primitive neuroectodermal brain tumors. Neuro-oncol. 6, 1-8 (2004).
  11. Mittal, A., et al.,EGCG down-regulates telomerase in human breast carcinoma MCF-7 cells, leading to suppression of cell viability and induction of apoptosis. Int. J. Oncol. 24, 703-710 (2004).
  12. Fang, M.Z., et al., Tea polyphenol (-)-epigallocatechin-3-gallate inhibits DNA methyltransferase and reactivates methylation-silenced genes in cancer cell lines. Cancer Res. 63, 7563-7570 (2003)
  13. Saffari, Y. and Sadrzadeh, S.M., Green tea metabolite EGCG protects membranes against oxidative damage in vitro. Life Sci. 74, 1513-1518 (2004).
  14. Peng, I.W. and Kuo, S.M., Flavonoid structure affects the inhibition of lipid peroxidation in Caco-2 intestinal cells at physiological concentrations. J. Nutr. 133, 2184-2187 (2003).
  15. Lee, S.R., et al., Protective effect of green tea polyphenol (-)-epigallocatechin gallate and other antioxidants on lipid peroxidation in gerbil brain homogenates. Phytother. Res. 17, 206-209 (2003)
  16. Sugisawa, A., et al., Anti-genotoxic effects of tea catechins against reactive oxygen species in human lymphoblastoid cells. Mutat. Res. 559, 97-103 (2004).

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