Bioactivity | SRS16-86 is a potent inhibitor of ferroptosis[1]. SRS16-86 is more stable than 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][3]. |
Invitro | SRS16-86 (1 µM; 24 hours; in the presence or absence of erastin) inhibits ferroptosis in HT-1080 cells and NIH 3T3 cells[2]. |
In Vivo | SRS16-86 (intraperitoneal injection; 2 mg/kg; 15 min before the onset of surgery) protects mice from functional acute renal failure and structural organ damage after ischemia–reperfusion injury (IRI)[2].SRS16-86 (intraperitoneal injection; 2 mg/kg; 4 weeks) combination therapy with [Nec-1+SfA] is superior in the prevention of renal IRI compared with the double-combination therapy with [Nec-1+SfA]. Addition of 16-86 reduces plasma levels of serum urea and serum creatinine in IRI mice model[2].SRS16-86 (intraperitoneal injection; 15 mg/kg; once a day; 7 days) enhances functional recovery after SCI, it decreases the levels of proinflammatory cytokines and the inflammatory adhesion factor in injured spinal cord in rats[3]. Animal Model: |
Name | SRS16-86 |
CAS | 1793052-96-6 |
Formula | C26H32N4O2 |
Molar Mass | 432.56 |
Appearance | Solid |
Transport | Room temperature in continental US; may vary elsewhere. |
Storage | 4°C, protect from light *In solvent : -80°C, 6 months; -20°C, 1 month (protect from light) |
Reference | [1]. Sam Hofmans, et al. Novel Ferroptosis Inhibitors with Improved Potency and ADME Properties. J Med Chem. 2016 Mar 10;59(5):2041-53. [2]. Andreas Linkermann, et al. Synchronized renal tubular cell death involves ferroptosis.Proc Natl Acad Sci U S A. 2014 Nov 25;111(47):16836-41. [3]. Yan Zhang, et al. Ferroptosis inhibitor SRS 16-86 attenuates ferroptosis and promotes functional recovery in contusion spinal cord injury. Brain Res. 2019 Mar 1;1706:48-57. |