Fluoflavine  (Synonyms: ML-090)

Fluoflavine (ML-090) is a selective NOX1 inhibitor and reactive oxygen species inhibitor. Fluoflavine reduces reactive oxygen species production, NOX1-mediated downstream signaling events, and oxygen-glucose deprivation-induced retinal ganglion cell death. Fluoflavine inhibits NADPH oxidase activity and pathological retinal neovascularization induced by oxygen-induced retinopathy in the retinas of ischemic mice. Fluoflavine can be used in studies related to retinal ischemia-reperfusion injury and proliferative retinopathy^[1][2].

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.

234.26

C₁₄H₁₀N₄

531-46-4

Solid

Light yellow to yellow

C1(N2)=NC3=C(C=CC=C3)NC1=NC4=C2C=CC=C4

Room temperature in continental US; may vary elsewhere.

• [1]. Dvoriantchikova G, et al. Neuronal NAD(P)H oxidases contribute to ROS production and mediate RGC death after ischemia. Invest Ophthalmol Vis Sci. 2012;53(6):2823-2830. Published 2012 May 14.  [Content Brief]

  [2]. Kaur G, et al. NADPH oxidase 1-PKCδ-dependent ZO-1 phosphorylation mediates IL-33-induced inner blood-retinal barrier disruption in proliferative retinopathies. Am J Physiol Cell Physiol. 2025;329(5):C1577-C1592.  [Content Brief]