FeTPPS

Peroxynitrite is a highly reactive nitrogen species formed from the reaction of nitric oxide (NO) and superoxide.[1] FeTPPS is a ferric porphyrin complex that causes the decomposition of peroxynitrite by catalytic isomerization to produce nitrate both in vitro and in vivo. The conversion of this reactive nitrogen species to nitrate results in cytoprotection (EC50 = 5 µM). [2][3] FeTPPS does not complex with NO and does not alter superoxide directly. It is commonly used to elucidate the roles of peroxynitrite in oxidative stress, cell damage, and intracellular signaling. [4][5][6]

Reference:
[1]. Chen, X., Chen, H., Deng, R., et al. Pros and cons of current approaches for detecting peroxynitrite and their applications. Biomed.J. 37(3), 120-126 (2014).
[2]. Lauzier, B., Sicard, P., Bouchot, O., et al. A peroxynitrite decomposition catalyst: FeTPPS confers cardioprotection during reperfusion after cardioplegic arrest in a working isolated rat heart model. Fundamental Clinical Pharmacology 21, 173-180 (2007).
[3]. Misko, T.P., Highkin, M.K., Veenhuizen, A.W., et al. Characterization of the cytoprotective action of peroxynitrite decomposition catalysts. The Journal of Biological Chemisty 273(25), 15646-15653 (1998).
[4]. Ishrat, T., Kozak, A., Alhusban, A., et al. Role of matrix metalloproteinase activity in the neurovascular protective effects of angiotensin antagonism. Stroke Res.Treat. 2014, 1-9 (2014).
[5]. Li, J., Loukili, N., Rosenblatt-Velin, N., et al. Peroxynitrite is a key mediator of the cardioprotection afforded by ischemic postconditioning in vivo. PLoS One 8(7), 1-8 (2013).
[6]. Kiss, A., Tratsiakovich, Y., Gonon, A.T., et al. The role of arginase and rho kinase in cardioprotection from remote ischemic perconditioning in non-diabetic and diabetic rat in vivo. PLoS One 9(8), 1-8 (2014).