Linsidomine (hydrochloride)

Linsidomine hydrochloride (SIN-1 chloride) is a spontaneous ROS/RNS generator and peroxynitrite donor. Linsidomine hydrochloride is a vasodilator and platelet aggregation inhibitor. Linsidomine hydrochloride induces oxidative stress-induced chondrocyte apoptosis and necrosis. Linsidomine hydrochloride inhibits the migration, proliferation and neointima formation of vascular smooth muscle cells by inhibiting the expression of annexin A2. In addition, low doses of Linsidomine hydrochloride shows protective effects on Zn2+ treated nerve cells[1][2][3][4].

Product Specifications

CAS Number

[16142-27-1]

Product Name Alternative

SIN-1 (chloride)

UNSPSC

12352005

Hazard Statement

H302

Target

Annexin A; Apoptosis; Autophagy; NF-κB; Reactive Oxygen Species (ROS)

Type

Reference compound

Related Pathways

Apoptosis; Autophagy; Cytoskeleton; Immunology/Inflammation; Metabolic Enzyme/Protease; NF-κB

Applications

Neuroscience-Neuromodulation

Field of Research

Cancer; Inflammation/Immunology; Neurological Disease; Cardiovascular Disease

Assay Protocol

https://www.medchemexpress.com/linsidomine-hydrochloride.html

Purity

99.97

Solubility

DMSO : 50 mg/mL (ultrasonic; warming; heat to 60°C) |H2O : 50 mg/mL (ultrasonic)

Smiles

NC1=C[N+](N2CCOCC2)=NO1.[Cl-]

Molecular Formula

C6H11ClN4O2

Molecular Weight

206.63

Precautions

H302

References & Citations

[1]He Y, et al. 3-morpholinosydnonimine (SIN-1) -induced oxidative stress leads to necrosis in hypertrophic chondrocytes in vitro. Biomed Pharmacother. 2018 Oct;106:1696-1704. |[2]An JM, et al. Neuroprotective effect of 3-morpholinosydnonimine against Zn²⁺-induced PC12 cell death. Eur J Pharmacol. 2015 Feb 5;748:37-44.|[3]Mattart L, et al. The peroxynitrite donor 3-morpholinosydnonimine activates Nrf2 and the UPR leading to a cytoprotective response in endothelial cells. Cell Signal. 2012 Jan;24 (1) :199-213.|[4]Won KJ, et al. 3-morpholinosydnonimine participates in the attenuation of neointima formation via inhibition of annexin A2-mediated vascular smooth muscle cell migration. Proteomics. 2011 Jan;11 (2) :193-201.