Rosiglitazone (5 mg/kg, orally) reduces serum glucose levels in diabetic rats, decreases levels of IL-6, TNF-α, and VCAM-1 in the diabetic group, and when combined with losartan, increases glucose levels compared to groups treated only with diabetes or losartan. It significantly improves endothelial dysfunction, demonstrated by reduced contractile responses to PE and Ang II and enhanced ACh-induced relaxation in aortas from diabetic rats^[5].

Rosiglitazone maleate, a potent and selective activator of PPARγ, exhibits EC50 values of 30 nM and 100 nM for PPARγ1 and PPARγ2, respectively, and a Kd of approximately 40 nM for PPARγ. Rosiglitazone (BRL49653) at concentrations of 0.1, 1, 10 μM, promotes the differentiation of C3H10T1/2 stem cells into adipocytes^[1].

Rosiglitazone activates PPARγ with an EC50 of 60 nM^[2].

Rosiglitazone (1 μM) activates PPARγ, which binds to the NF-α1 promoter, enhancing gene transcription in neurons. Additionally, Rosiglitazone (1 μM) protects Neuro2A cells and hippocampal neurons against oxidative stress and upregulates BCL-2 expression in an NF-α1-dependent manner^[3].

Rosiglitazone effectively blocks TRPM3 channels with IC50 values of 9.5 μM and 4.6 μM against nifedipine- and PregS-evoked activities, respectively, through mechanisms not involving PPARγ. It also inhibits TRPM2 channels at a higher concentration, with an IC50 of approximately 22.5 μM. Additionally, Rosiglitazone acts as a potent activator of TRPC5 channels, with an EC50 of about 30 μM^[4].