Rosiglitazone sodium is an effective and selective PPARγ activator, with EC50 values of 30 nM for PPARγ1, 100 nM for PPARγ2, and 60 nM for PPARγ. It also has an approximate Kd of 40 nM for PPARγ. Additionally, Rosiglitazone sodium acts as a regulator of TRP channels, inhibiting the activities of TRPM2 and TRPM3, while activating TRPC5.

PPARγ1:30 nM (EC50), PPARγ2:100 nM (EC50)

Rosiglitazone sodium serves as a potent and selective activator of PPARγ, demonstrating EC50 values of 30 nM and 100 nM for PPARγ1 and PPARγ2 respectively, along with a Kd of approximately 40 nM. Rosiglitazone (BRL49653; 0.1, 1,10 μM) induces the differentiation of C3H10T1/2 stem cells into adipocytes and shows activity in Neuro2A cells and hippocampal neurons by protecting against oxidative stress, up-regulating BCL-2 expression dependent on NF-α1. Further, it completely inhibits TRPM3 channels with IC50 values of 9.5 μM and 4.6 μM for nifedipine- and PregS-evoked activities respectively, without involvement of PPARγ activity. At higher concentrations, Rosiglitazone inhibits TRPM2 with an IC50 of approximately 22.5 μM and robustly stimulates TRPC5 channels with an EC50 of about 30 μM.

Administered at a dosage of 5 mg/kg orally, rosiglitazone effectively lowers serum glucose levels in diabetic rats. Additionally, it reduces the levels of IL-6, TNF-α, and VCAM-1 in the same group. When used in conjunction with losartan, rosiglitazone raises glucose levels compared to those in diabetic and losartan-treated groups alone. Moreover, rosiglitazone markedly improves endothelial dysfunction, as evidenced by a significantly reduced contractile response to PE and Ang II, along with enhanced ACh-induced relaxation in aortas from diabetic rats.