SRS16-86, a ferrostatin analog, is a novel third-generation inhibitor of ferroptosis. It is the first compound in this class that is stable in plasma and liver microsomes and that demonstrates high efficacy when supplied alone or in combination therapy.
Ferroptosis is a newly discovered type of cell death triggered by intracellular phospholipid peroxidation that is morphologically, biologically and genetically distinct from other types of cell death. Ferroptosis is classified as regulated necrosis and is more immunogenic than apoptosis[1]. SRS16-86 is a novel third-generation ferrostatin, is an inhibitor of ferroptosis. SRS16-86 is more stable to metabolism and plasma than Ferrostatin-1 in vivo. SRS16-86 can be used for renal ischemia-reperfusion injury (IRI) and spinal cord injury (SCI) research[2]. In a rat model of spinal cord injury, SRS16-86 (15 mg/kg) increases the levels of glutathione peroxidase 4 (GPX4), system xc- cystine/glutamate transporter (xCT), and glutathione (GSH) and decreases levels of IL-1β, TNF-α, ICAM-1, and the lipid peroxidation marker 4-hydroxy nonenal (4HNE) in injured spinal cord epicenters. It also increases tissue sparing and improves locomotor recovery in the same model[3].
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