Fluoflavine

Fluoflavine (ML-090) (0.09 μM; during OGD and 2 hours of reoxygenation) significantly reduces OGD-induced superoxide production in primary RGCs, with efficacy comparable to a nonselective NAD(P)H oxidase inhibitor^[1].
Fluoflavine (0.09 μM; during 4 hours of OGD and 24 hours of reoxygenation) potently protects primary from OGD-induced apoptotic and necrotic death, with efficacy comparable to nonselective NAD(P)H oxidase inhibitors^[1].
Fluoflavine (10 μM; 30 min preincubation, 2 h IL-33 treatment) attenuates IL-33-induced barrier disruption in HRMVECs, as demonstrated by reduced FITC-dextran flux^[2].
Fluoflavine (10 μM; 30 min preincubation, 30 min IL-33 treatment) reduces IL-33-induced ZO-1 serine/threonine phosphorylation in HRMVECs^[2].
Fluoflavine (10 μM; 30 min preincubation, 30 min IL-33 treatment) attenuates IL-33-induced PKCδ phosphorylation in HRMVECs^[2].
Fluoflavine (10 μM; 30 min preincubation, 2 h IL-33 treatment) reverses IL-33-induced tight junction disruption in HRMVECs, as shown by restored ZO-1 localization at cell junctions^[2].
Fluoflavine (10 μM; 30 min preincubation, 24 h IL-33 treatment) reduces IL-33-induced proliferation of HRMVECs^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.