Licoflavone A

Licoflavone A is an orally active PTP1B/VEGFR-2 inhibitor, with an IC₅₀ of 54.5 μM against PTP1B, an IC₅₀ of 14.36 μM and a K_d of 142.38 nM against human VEGFR-2. Licoflavone A blocks the PI3K/AKT and MEK/ERK signaling pathways. Licoflavone A induces G1 phase cell cycle arrest, apoptosis via the intrinsic mitochondrial pathway (apoptosis), and inhibits migration, invasion and epithelial-mesenchymal transition (EMT) of gastric cancer cells. Licoflavone A inhibits the proliferation of gastric cancer cells in vitro and in xenograft models. Licoflavone A reduces the expression levels of HIF-1α, GLUT1, LDHA, PKM2 and HK2 in hypoxic gastric cancer cells, decreases glucose uptake and suppresses glycolysis. Licoflavone A can be used in research related to gastric cancer, type 2 diabetes and obesity^[1][2][3]. IC50 & Target:IC50: 54.5 μM (PTP1B)^[1] In Vitro:Licoflavone A (6.25-100 μM; 24-72 h) inhibits the proliferation of human gastric cancer SGC-7901, MKN-45, MGC-803 cells and normal GES-1 cells in a dose- and time-dependent manner. Among these cell lines, it exhibits the strongest activity against MKN-45 cells (72 h IC₅₀ = 12.19 μM) and the weakest activity against GES-1 cells^[1].
Licoflavone A (25-100 μM; 14 days) dose-dependently inhibits colony formation of human gastric cancer MKN-45 cells stimulated by VEGF^[1].
Licoflavone A (25-100 μM; 0-96 h) inhibits VEGF-stimulated 3D spheroid formation in human gastric cancer MKN-45 cells in a dose-dependent manner^[1].
Licoflavone A (25-100 μM; 24-48 h) inhibits the proliferation of hypoxic human gastric cancer AGS cells in a time- and concentration-dependent manner^[3].
Licoflavone A (25-100 μM; 10-14 d) reduces the colony-forming ability of human gastric cancer AGS cells under hypoxic conditions in a dose-dependent manner, and the 100 μM concentration decreases the colony formation rate to 38.78%^[3].
Licoflavone A (25-100 μM; 24-48 h) potently and dose-dependently inhibits the migration of human gastric cancer AGS cells under hypoxic conditions, and the 100 μM concentration reduces the 48 h scratch wound healing rate to 14.31%^[3].
Licoflavone A (25-100 μM; 72 h) arrests VEGF-stimulated human gastric cancer MKN-45 cells at the G0 phase of the cell cycle in a dose-dependent manner by downregulating cyclin D1 and c-Myc^[1].
Licoflavone A (25-100 μM; 72 h) dose-dependently induces apoptosis in VEGF-stimulated human gastric cancer MKN-45 cells via the mitochondrial intrinsic pathway, which involves an increased Bax/Bcl-2 ratio, cytochrome c release, and caspase activation^[1].
Licoflavone A (25-100 μM; 48 h) dose-dependently inhibits the migration and invasion abilities of VEGF-stimulated human gastric cancer MKN-45 cells^[1].
Licoflavone A (25-100 μM; 72 h) inhibits epithelial-mesenchymal transition (EMT) in VEGF-stimulated human gastric cancer MKN-45 cells in a dose-dependent manner by regulating EMT-related proteins^[1].
Licoflavone A (25-100 μM; 72 h) blocks the PI3K/AKT and MEK/ERK signaling pathways in VEGF-stimulated human gastric cancer MKN-45 cells in a dose-dependent manner by downregulating PI3K/AKT transcription and inhibiting MEK/ERK phosphorylation^[1].
Licoflavone A (25-100 μM; 48 h) downregulates the mRNA expression of key glycolytic genes in human gastric cancer AGS cells under hypoxic conditions, and the 100 μM concentration significantly inhibits the mRNA expression of GLUT1, LDHA, PKM2 and HK2^[3].
Licoflavone A (25-100 μM; 48 h) significantly downregulates the expression of HIF-1α and key glycolysis-related proteins in hypoxic human gastric cancer AGS cells at the concentration of 100 μM^[3].
Licoflavone A (25-100 μM; 48 h) inhibits glucose uptake and HK activity in hypoxic human gastric cancer AGS cells at the concentration of 100 μM^[3]. In Vivo:Licoflavone A (50 mg/kg; p.o.; daily; 14 days) significantly reduces tumor volume and weight in a BALB/c-nude mouse gastric cancer xenograft model, with no observed impact on body weight^[1].