In vitro activity: (-)-Epigallocatechin gallate functions as a powerful antioxidant, preventing oxidative damage in healthy cells, but also as an antiangiogenic and antitumor agent and as a modulator of tumor cell response to chemotherapy. (-)-Epigallocatechin gallate shows multiple anticancer effects, such as anti-proliferation, anti-angiogenesis, transformation prevention of various cancer cells, cancer cell cycle arrest and inhibition of tumor metastasis. (-)-Epigallocatechin gallate exerts multi-anticancer effects through regulating several cancer-related cell signal pathways (regulated the function or the expression of key signal proteins, such as nuclear factor-κB, MAPKs and activator protein-1, EGFR, IGF, COX-2 signaling pathway, and so on.), effecting methylation of cancer genes and combination of ligand with membrane receptors. (-)-Epigallocatechin gallate also shows an immunomodulating effects. Several types of immune cells in both the innate and adaptive immune systems are known to be affected in varying degrees by (-)-Epigallocatechin gallate. Among them, the dramatic effect on T cell functions has been repeatedly demonstrated, including T cell activation, proliferation, differentiation, and production of cytokines. Studies using animal models of autoimmune diseases have reported disease improvement in animals treated with green tea/EGCG. (-)-Epigallocatechin gallate displays anti-infective properties. Antiviral activities of (-)-Epigallocatechin gallate with different modes of action have been demonstrated on diverse families of viruses, such as Retroviridae, Orthomyxoviridae and Flaviviridae and include important human pathogens like human immunodeficiency virus, influenza A virus and the hepatitis C virus.

Cell Assay: (-)-Epigallocatechin Gallate (EGCG) altered human and rat NPC development in vitro. EGCG affected migration distance, migration pattern and nuclear density of NPCs growing as neurospheres. EGCG exerted these functional impairments by binding to the extracellular matrix (ECM) glycoprotein laminin, preventing its binding to β1-integrin subunits, thereby prohibiting cell adhesion and resulting in altered glia alignment and decreased number of migrating young neurons.

Cancer Res. 2006 Mar 1;66(5):2500-5; Food Funct. 2013 Sep;4(9):1287-303; Br J Pharmacol. 2013 Mar;168(5):1059-73.