In Vitro: Aleglitazar exhibits species selectivity with respect to PPARα, with an EC50s of 50 nM, 2.26 µM and 2.34 µM for human PPARα, rat PPARα and mouse PPARα, respectively. Aleglitazar (0.01-40 µM; 12-48 hours) does not significantly increase lactate dehydrogenase (LDH) release at concentrations of 0.1 µM to 20 µM, but significant increases LDH release at concentrations of 30 µM and 40 µM. Aleglitazar (0.01-20 µM; 48 hours) decreases hyperglycaemic conditions (HG, glucose 25 mM)-induced apoptosis, caspase-3 activity and cytochrome-C release. Aleglitazar improves cell viability in cells exposed to hyperglycaemia.
In Vivo: Aleglitazar (0.3-3.0 mg/kg; i.p.; daily; for 7 days) exerts beneficial effects on structural and functional outcomes of mild brain ischemia. Aleglitazar reduces key aspects of microglia activation including NO production, release of proinflammatory cytokines, migration, and phagocytosis. Aleglitazar attenuates inflammatory responses in post-ischemic brain.