HX531

HX531 is an orally active RXR antagonist with an IC₅₀ of 18 nM. HX531 upregulates the p53-p21Cip1 pathway. HX531 abrogates the anti-apoptotic effect of t-RA. HX531 exerts anti-obesity, anti-diabetic and anti-melanoma activities^[1][2][3]. In Vitro:HX531 (2.5 μM, 30 min) eliminates the anti-apoptotic effect of t-RA^[1].
HX531 (0-10 μM, 24 h) has no significant effect on transcriptional activation induced by PPARα/RXR agonists and molecular expression induced by PPARγ agonists^[2].
HX531 (2.5 μM, 0-10 days) upregulates the p53-p21Cip1 pathway, inducing G0/G1 cell cycle arrest and inhibiting the differentiation of human visceral preadipocytes HPV^[3].
HX531 (2.5 μM, 0-10 days) reverses high glucose-induced G0/G1 cell cycle arrest to normal glucose levels in normal human mesangial cells (NHMCs)^[3].
HX531 delays resistance to melanoma and prevents M2 macrophage polarization in the tumor microenvironment^[4]. In Vivo:HX531 (0.1% and 0.3% food additive, oral, for two weeks) prevents weight gain in mice on a high-fat diet and stops high blood sugar and high insulin levels induced by the high-fat diet, while increasing leptin levels^[2].
HX531 (0.1% and 0.3% food additive, oral, for two weeks) blocks the enlargement of fat cells and alleviates insulin resistance^[2].
HX531 (0.1% and 0.3% food additive, oral, for two weeks) directly antagonizes PPARγ/RXR, reducing molecules involved in fatty acid influx and fat formation in skeletal muscle, while increasing molecules involved in energy expenditure^[2].
HX531 (0.1% and 0.3% food additive, oral, for 3-4 weeks) leads to a rebound in high blood sugar and insulin resistance associated with fat atrophy^[2].
HX531 (10mg/kg, oral, daily, for 30 weeks) reduces body weight in rats, inhibits fat cell enlargement, and induces G0/G1 cell cycle arrest in fat cells^[3].