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]. In Vitro:Linsidomine hydrochloride (0-5 mM; 0-24 h) reduces the activity of hypertrophic chondrocytes, induces hypertrophic chondrocyte necrosis and apoptosis of non-hypertrophic ATDC5 and C28/I2 cells^[1].
Linsidomine hydrochloride (30-1000 μM; 190 min) prevents Zn²⁺ induced neuronal death, but is eliminated by uric acid (HY-B2130)^[2].
Linsidomine hydrochloride (100-300 μM; 0-190 min) increases the production of reactive oxygen species and active nitrogen, inhibits the Zn²⁺ induced glutathione reductase inactivation and the increase of oxidized glutathione/total glutathione ratio in PC12 cells^[2].
Linsidomine hydrochloride (1 mM; 2-3 h) induces nuclear accumulation of Nrf2 in EAhy926 and HUVECs cells^[3].
Linsidomine hydrochloride (0-500 μM; 30 min) inhibits platelet-derived growth factor BB-induced cell migration and proliferation by annexin A2 in rat aortic smooth muscle cells^[4].
Linsidomine hydrochloride (1-5 mM, 24 h) induces the accumulation of LC3-II, and the formation of autophagosome, inducing autophagy in serum starved EAhy926 cell^[4]. In Vivo:Linsidomine hydrochloride (0.01-0.1 mg/kg; ip; 14 days) attenuates neointima formation in balloon-injured rat carotid arteries^[4].