PKM2-IN-3 is a potent PKM2 kinase inhibitor, displaying an IC 50 value of 4.1 μM. The compound effectively suppresses PKM2-mediated glycolysis and NLRP3 activation, thereby exerting an anti-neuroinflammatory effect.

PKM2:4.1 μM (IC50)

PKM2-IN-3 (compound 10i) inhibits the TNF-α release of LPS-stimulated RAW264.7 macrophages, with an IC 50 value of 5.2 μM. PKM2-IN-3 exhibits the lowest toxicity with a CC 50 value of 43.6 μM[1]. PKM2-IN-3 (0.1-100 μM; 20 min) inhibits PKM2 kinase activity in a cell-free molecular level with an IC 50 value of 4.1 μM[1].

PKM2-IN-3 (1, 10 mg/kg; i.p.; daily for 3 days ) significantly reverses the LPS-induced mice behavior changes in open field test[1]. PKM2-IN-3 (1, 10 mg/kg; i.v.; injected at 4 hours and 24 hours after ischemia onset) reduces the infarct volume and improves neurological deficits of tMCAO rats[1]. Animal Model: LPS-induced mice (male 6-8 weeks old; 20.0-22.0 g)[1]Dosage: 1, 10 mg/kg Administration: i.p.; daily for 3 days Result: Reversed the LPS-induced mice behavior changes in open field test. Animal Model: tMCAO Sprague-Dawley rats (Male 8-10 weeks old; 250.0-280.0 g)[1]Dosage: 1, 10 mg/kg Administration: i.v.; injected at 4 hours and 24 hours after ischemia onset Result: Reduced the infarct volume and improved neurological deficits of tMCAO rats.