Molsidomine

Warning

H302 (100%): Harmful if swallowed [Warning Acute toxicity, oral]

P264, P270, P301+P317, P330, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 47 reports by companies from 2 notifications to the ECHA C&L Inventory.

Drug-Induced Liver Injury Severity and Toxicity (DILIst)

Molsidomine

DILI Positive

DOI:10.1016/j.drudis.2019.09.022

C - Cardiovascular system

QC - Cardiovascular system

Molsidomine, a cardiovascular drug, acts in a similar fashion to organic nitrates. The SIN-1A metabolite of molsidomine has a pharmacologically active group of nitric oxide, which increases levels of cyclic GMP, and decreases intracellular calcium ions in smooth muscle cells. This leads to relaxation of smooth muscle in the blood vessels, and inhibits platelet aggregation.

Molsidomine hepatically metabolized to _linsidomine_. Linsidomine releases nitric oxide (NO) from endothelial cells when it decays, and acts as the active vasodilating metabolite responsible for molsidomine's pharmacological effects. Oral absorption of Molsidomine is found to be 95.5% ±4.5. Presystemic metabolism is noted to be 56% and metabolism is reported extensive by Liver. Renal Excretion accounts for 95 % and plasma half-life is 5 hr. Back to top

Drugs used to cause dilation of the blood vessels.

A diverse group of agents, with unique chemical structures and biochemical requirements, which generate NITRIC OXIDE. These compounds have been used in the treatment of cardiovascular diseases and the management of acute myocardial infarction, acute and chronic congestive heart failure, and surgical control of blood pressure. (Adv Pharmacol 1995;34:361-81)

Peak plasma drug concentration (tmax) occurs from 1 to 2 hours after administration.

98 L

renal excretion is the main route of elimination of the metabolites in humans (90% to 95%) About 2% of the ingested drug is excreted unchanged in the urine.