4′-O-Methylglabridin is an apoptosis inducer with antioxidant, cell cycle-disrupting and anticancer cytotoxic activities. 4′-O-Methylglabridin inhibits various cancer cell lines including liver cancer, breast cancer and colorectal cancer cell lines. By reducing the expression levels of phosphorylated Rb (Ser807/811) and p21 proteins, 4′-O-Methylglabridin promotes cell accumulation at the subG1 and G2/M phases, and triggers caspase-dependent apoptosis via cytochrome C release and caspase-9 activation. 4′-O-Methylglabridin also exerts antioxidant effects by inhibiting lipid peroxide levels and reducing β-carotene consumption, thereby blocking LDL oxidation. 4′-O-Methylglabridin can be used in the research of various cancers and atherosclerotic diseases [1] [2].
In Vitro, 4′-O-Methylglabridin (2.5-40 μM; 72 h) inhibits proliferation of Huh7, MCF7, and HCT116 cancer cell lines in vitro, with the strongest activity against Huh7 cells (IC50=9.6 μM)[1]. 4′-O-Methylglabridin (IC50 concentration; 24 h, 48 h, 72 h) inhibits proliferation of Huh7 cells in a time-dependent manner, with IC50 values increasing from 7.31 μM at 24 h to 11.4 μM at 72 h[1]. 4′-O-Methylglabridin (10 μM; 48 h) induces apoptotic nuclear changes in Huh7 cells after 48 h of treatment[1]. 4′-O-Methylglabridin (10 μM; 48 h) induces caspase-dependent apoptosis in Huh7 cells after 48 h of treatment by increasing cytochrome C release and cleaved caspase-9 levels, while also reducing phospho-Rb, p53, Mdm2, and p21 levels to disrupt cell cycle regulation[1]. 4′-O-Methylglabridin (50 μM; 90 min at 50°C) inhibits β-carotene consumption by 78% in a cell-free β-carotene-linoleate assay[2]. 4′-O-Methylglabridin (30 μM; 2 h at 37°C) potently inhibits AAPH-induced oxidation of ex vivo human LDL[2].
References:
[1]. Cevik D, et al. Bioactivity-guided isolation of cytotoxic secondary metabolites from the roots of Glycyrrhiza glabra and elucidation of their mechanisms of action[J]. Industrial Crops and Products, 2018, 124: 389-396.
[2]. Vaya J, et al. Antioxidant constituents from licorice roots: isolation, structure elucidation and antioxidative capacity toward LDL oxidation. Free Radic Biol Med. 1997;23(2):302-313.
In Vitro, 4′-O-Methylglabridin (2.5-40 μM; 72 h) inhibits proliferation of Huh7, MCF7, and HCT116 cancer cell lines in vitro, with the strongest activity against Huh7 cells (IC50=9.6 μM)[1]. 4′-O-Methylglabridin (IC50 concentration; 24 h, 48 h, 72 h) inhibits proliferation of Huh7 cells in a time-dependent manner, with IC50 values increasing from 7.31 μM at 24 h to 11.4 μM at 72 h[1]. 4′-O-Methylglabridin (10 μM; 48 h) induces apoptotic nuclear changes in Huh7 cells after 48 h of treatment[1]. 4′-O-Methylglabridin (10 μM; 48 h) induces caspase-dependent apoptosis in Huh7 cells after 48 h of treatment by increasing cytochrome C release and cleaved caspase-9 levels, while also reducing phospho-Rb, p53, Mdm2, and p21 levels to disrupt cell cycle regulation[1]. 4′-O-Methylglabridin (50 μM; 90 min at 50°C) inhibits β-carotene consumption by 78% in a cell-free β-carotene-linoleate assay[2]. 4′-O-Methylglabridin (30 μM; 2 h at 37°C) potently inhibits AAPH-induced oxidation of ex vivo human LDL[2].
References:
[1]. Cevik D, et al. Bioactivity-guided isolation of cytotoxic secondary metabolites from the roots of Glycyrrhiza glabra and elucidation of their mechanisms of action[J]. Industrial Crops and Products, 2018, 124: 389-396.
[2]. Vaya J, et al. Antioxidant constituents from licorice roots: isolation, structure elucidation and antioxidative capacity toward LDL oxidation. Free Radic Biol Med. 1997;23(2):302-313.