SRS16-86 is an inhibitor of ferroptosis.[1] It inhibits ferroptosis induced by erastin in HT-1080 and NIH3T3 cells when used at a concentration of 1 μM. SRS16-86 (2 mg/kg) prevents renal tubular damage and increases in serum levels of urea and creatine in a mouse model of renal ischemia-reperfusion injury (IRI). 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.[2] It also increases tissue sparing and improves locomotor recovery in the same model.

Reference:
1. Linkermann, A., Skouta, R., Himmerkus, N., et al. Synchronized renal tubular cell death involves ferroptosis. Proc. Natl. Acad. Sci. U.S.A. 111(47), 16836-16841 (2014).
2. Zhang, Y., Sun, C., Zhao, C., et al. Ferroptosis inhibitor SRS 16-86 attenuates ferroptosis and promotes functional recovery in contusion spinal cord injury. Brain Res. 1706, 48-57 (2019).