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Merck

M2901

Sigma-Aldrich

Molsidomin

Synonym(e):

N-(Ethoxycarbonyl)-3-morpholinosydnonimin

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About This Item

Empirische Formel (Hill-System):
C9H14N4O4
CAS-Nummer:
Molekulargewicht:
242.23
EG-Nummer:
MDL-Nummer:
UNSPSC-Code:
12352200
PubChem Substanz-ID:
NACRES:
NA.77

Lagertemp.

2-8°C

SMILES String

CCOC(=O)N=C1O[N-][N+](=C1)N2CCOCC2

InChI

1S/C9H14N4O4/c1-2-16-9(14)10-8-7-13(11-17-8)12-3-5-15-6-4-12/h7H,2-6H2,1H3/b10-8-

InChIKey

XLFWDASMENKTKL-NTMALXAHSA-N

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Anwendung

Molsidomine has been used as nitric oxide (NO)-releasing vasodilator to study the effect of NO on angiostatin production in aging rat kidneys.[1]

Biochem./physiol. Wirkung

Molsidomine is an effective vasodilator[2] and a long-lasting nitric oxide (NO) donor.[1] It is a pro-drug that is enzymatically decarboxylated to form 3-morpholinosydnone imine (SIN-1) in the liver. Molsidomine is used as an anti-anginal agent and possesses antioxidant properties. It may be used to treat cisplatin-induced oxidative stress in the liver tissue.[2] Molsidomine has also been used during angina pectoris, heart failure, and after myocardial infarction.[3]
Orally active, long acting vasodilator; antianginal; converted by the liver to the active metabolite, SIN-1

Piktogramme

Exclamation mark

Signalwort

Warning

H-Sätze

Gefahreneinstufungen

Acute Tox. 4 Oral

Lagerklassenschlüssel

11 - Combustible Solids

WGK

WGK 3

Persönliche Schutzausrüstung

dust mask type N95 (US), Eyeshields, Gloves


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Molsidomine
Meyler's Side Effects of Drugs: The International Encyclopedia of Adverse Drug Reactions and Interactions (2016)
R E Nitz et al.
Pharmacotherapy, 7(1), 28-37 (1987-01-01)
The long-acting antianginal drug molsidomine has been shown experimentally to reduce myocardial infarct size when administered prior to or after cardiac insult. This is due to several drug actions. Dilation of postcapillary capacitance vessels diminishes venous return, preload, heart dimensions
Istvan Kovanecz et al.
The journal of sexual medicine, 9(11), 2814-2826 (2012-09-15)
Long-term daily administration of phosphodiesterase type 5 (PDE5) inhibitors in the rat prevents or reverses corporal veno-occlusive dysfunction (CVOD) and smooth muscle cell (CSMC) loss and fibrosis, in both aging and bilateral cavernosal nerve resection (BCNR) models for erectile dysfunction.
Roberta Buono et al.
Stem cells (Dayton, Ohio), 30(2), 197-209 (2011-11-16)
Satellite cells are myogenic precursors that proliferate, activate, and differentiate on muscle injury to sustain the regenerative capacity of adult skeletal muscle; in this process, they self-renew through the return to quiescence of the cycling progeny. This mechanism, while efficient
Jerzy Sacha et al.
Annals of noninvasive electrocardiology : the official journal of the International Society for Holter and Noninvasive Electrocardiology, Inc, 17(3), 286-290 (2012-07-24)
Myocardial ischemia during coronary spasm may generate malignant ventricular arrhythmias. The J-wave pattern was suggested to be a marker of a disorder associated with life-threatening arrhythmias. We report the case of a patient with vasospastic angina and J-wave pattern in

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