Quercimeritrin

Quercimeritrin is an orally active α-glucosidase inhibitor (with an IC₅₀ of 79.88 μM against the Saccharomyces cerevisiae enzyme) and a P-gp substrate, with anti-angiogenic and antioxidant activities. Quercimeritrin does not cross the blood-brain barrier and does not inhibit cytochrome P450 enzymes. Quercimeritrin precisely binds to and inhibits the active sites of c-Kit, MMP-2, Aurora-A kinases and α-glucosidase, thereby disrupting target functions. Quercimeritrin effectively regulates postprandial blood glucose and also exhibits significant anti-angiogenic activity, which inhibits endothelial cell proliferation and microvascular growth. Quercimeritrin can be used in the research of diabetes and breast cancer^[1][2][3]. In Vitro:Quercimeritrin has a high absorption rate in the human intestine, cannot cross the blood-brain barrier, and does not inhibit major CYPs. It is a substrate of P-gp, and fails to meet one of the Ghose rules due to its low lipophilicity^[1].
Quercimeritrin (3.91-500 μM; 10-20 min) potently inhibits α-glucosidase isolated from *Saccharomyces cerevisiae*, with an IC₅₀ of 79.88 μM, and exhibits a concentration-dependent inhibitory effect^[2].
Quercimeritrin (3.91-500 μM; 10-20 min) weakly inhibits porcine pancreas-derived α-amylase, with an IC₅₀ value greater than 250 μM^[2].
Quercimeritrin (15.6-500 μM) competitively inhibits α-glucosidase from *Saccharomyces cerevisiae* and α-amylase from porcine pancreas, and exhibits higher binding affinity for α-glucosidase^[2].
Quercimeritrin (10-100 μM; 72 h) inhibits the proliferation of human umbilical vein endothelial cells (HUVEC) in a dose-dependent manner, with a significant inhibitory effect observed at 100 μM^[3].
Quercimeritrin (100 μM; 12 h) cannot effectively inhibit tube formation in human umbilical vein endothelial cells (HUVECs), with an inhibition rate of less than 20%^[3].
Quercimeritrin (100 μM; 6 h) does not inhibit VEGF-induced HUVEC migration in Boyden chamber assays^[3]. In Vivo:Quercimeritrin (100-200 mg/kg; oral; single dose) significantly inhibits postprandial hyperglycemia in db/db mice, with the 200 mg/kg oral dose reducing glucose AUC_0-t by 24.5% and the 100 mg/kg dose reducing glucose AUC_0-t by 19.0%^[2].