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Releases NO and superoxide anion under physiological conditions
BML-CN245-0020 20 mg 66.00 USD
BML-CN245-0100 100 mg 270.00 USD
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Replaces Prod. #: ALX-430-002

SIN-1 is a metabolite of molsidomine which decomposes spontaneously in solution in the presence of oxygen, releasing NO and superoxide anion under physiological conditions. Since NO and superoxide react to form peroxynitrite, SIN-1 may actually produce peroxynitrite under physiological conditions. It is a potent vasodilator and inhibitor of platelet aggregation and produces significant protective effects in myocardial ischemia-reperfusion. The effects of SIN-1 are markedly attenuated by nitroglycerin-induced tolerance. Inhibits cysteine proteases.

Product Specification

Alternative Name:SIN-1, Linsidomine
Formula:C6H10N4O2 . HCl
Purity:≥98% (HPLC)
Identity:Determined by NMR.
Appearance:White to off-white solid.
Solubility:Soluble in water (25mg/ml), 100% ethanol or DMSO (>5mg/ml).
Long Term Storage:-20°C
Handling:Use freshly prepared solutions.
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Product Literature References

Modification of HSP proteins and Ca2+ are responsible for the NO-derived peroxynitrite mediated neurological damage in PC12 cell: J. Wen, et al.; Int. J. Clin. Exp. Pathol. 8, 4492 (2015), Abstract; Full Text
EPR detection of cellular and mitochondrial superoxide using cyclic hydroxylamines: S.I. Dikalov, et al.; Free Rad. Res. 45, 417 (2011), Abstract;
Interactions of peroxynitrite with uric acid in the presence of ascorbate and thiols: implications for uncoupling endothelial nitric oxide synthase: N. Kuzkaya et al.; Biochem. Pharmacol. 70, 343 (2005), Abstract;
New glycosidase activated nitric oxide donors: glycose and 3-morphorlinosydnonimine conjugates: T.B. Cai et al.; J. Org. Chem. 70, 3518 (2005), Abstract;
In vitro cytotoxicity of glyco-S-nitrosothiols. a novel class of nitric oxide donors: H. Babich & H.L. Zuckerbaun; Toxicol. In Vitro 15, 181 (2001), Abstract;
An activity in rat tissues that modifies nitrotyrosine-containing proteins: Y. Kamisaki et al.; PNAS 95, 11584 (1998), Abstract;
A redox-based mechanism for the neuroprotective and neurodestructive effects of nitric oxide and related nitroso-compounds: S.A. Lipton et al.; Nature 364, 626 (1993), Abstract;
Neuronal growth cone collapse and inhibition of protein fatty acylation by nitric oxide: D.T. Hess et al.; Nature 366, 562 (1993), Abstract;
Nitric oxide regulates cardiac Ca2+ current. Involvement of cGMP-inhibited and cGMP-stimulated phosphodiesterases through guanylyl cyclase activation: P.F. Mery et al.; J. Biol. Chem. 268, 26286 (1993), Abstract;
Cardioprotection and attenuation of endothelial dysfunction by organic nitric oxide donors in myocardial ischemia-reperfusion: M.R. Siegfried et al.; J. Pharmacol. Exp. Ther. 260, 668 (1992), Abstract;
Effect of nitric oxide production on the redox modulatory site of the NMDA receptor-channel complex: S.Z. Lei et al.; Neuron 8, 1087 (1992), Abstract;
Production of hydroxyl radicals from the simultaneous generation of superoxide and nitric oxide: N. Hogg et al.; Biochem. J. 281 , 419 (1992), Abstract;
Nitroglycerin-induced tolerance affects multiple sites in the organic nitrate bioconversion cascade: P.J. Henry et al.; J. Pharmacol. Exp. Ther. 248, 762 (1989), Abstract;
Molsidomine: alternative approaches to treat myocardial ischemia: R.-E. Nitz & V.B. Fiedler; Pharmacotherapy 7, 28 (1987), Abstract;
Regulation of cyclic GMP formation by soluble guanylate cyclase: stimulation by NO-containing compounds: E. Bohme et al.; Adv. Cyclic Nucleotide Protein Phosphorylation Res. 17, 259 (1984), Abstract;
Inhibition of platelet aggregation and stimulation of guanylate cyclase by an antianginal agent molsidomine and its metabolites: M. Nishikawa et al.; J. Phar.macol. Exp. Ther. 220, 183 (1982), Abstract;

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