GQ-16

GQ-16 is an orally active PPARγ partial agonist with an IC₅₀ of 1.84 μM and a K_i of 160 nM against human PPARγ. GQ-16 inhibits Cdk5-mediated Ser-273 phosphorylation. GQ-16 improves insulin sensitivity and glucose tolerance in obese and diabetic mice. GQ-16 also exhibits certain cytotoxicity against tumor cells. GQ-16 can be used in research related to obesity, diabetes and cancer^[1][2][3]. In Vitro:GQ-16 (7 days) promotes the differentiation of 3T3-L1 preadipocytes and upregulates the expression of adipogenic genes, but its efficacy is lower than that of Rosiglitazone (HY-17386)^[1].
GQ-16 (10 nM-10 μM; 24 h) weakly activates the expression of PPARγ target genes acca1b and fgf21, and inhibits the expression of vcam1 and dcn in mature 3T3-L1 adipocytes^[1].
GQ-16 (10 μM; 6-48 h) weakly and transiently upregulates the expression of OLR1 in mature 3T3-L1 adipocytes, with its activity peak occurring at 10 h post-treatment^[1].
GQ-16 (10 μM; 4 days) exhibits reduced adipogenic potential in C3H10T1/2 and NIH-3T3L1 cells, with less intracellular lipid accumulation and lower aP2 expression levels compared to Rosiglitazone (HY-17386)^[2].
GQ-16 (10 nM-100 μM; 24-48 h) reduces the viability of MCF-7 cells^[3]. In Vivo:GQ-16 (20 mg/kg; p.o.; 10-15 days) improves insulin sensitivity and glucose tolerance in mice with diet-induced insulin resistance^[2].