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Merck
모든 사진(1)

Key Documents

SML2598

Sigma-Aldrich

Ataciguat

≥98% (HPLC)

동의어(들):

5-Chloro-2-[[(5-chloro-2-thienyl)sulfonyl]amino]-N-[4-(4-morpholinylsulfonyl)phenyl]-benzamide, 5-Chloro-2-[[(5-chlorothien-2-yl)sulfonyl]amino]-N-[4-[(morpholin-4-yl)sulfonyl]phenyl]benzamide, HMR-1766, HMR1766

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About This Item

실험식(Hill 표기법):
C21H19Cl2N3O6S3
CAS Number:
Molecular Weight:
576.49
MDL number:
UNSPSC 코드:
12352202
NACRES:
NA.77

분석

≥98% (HPLC)

형태

powder

색상

white to beige

solubility

DMSO: 2 mg/mL, clear

저장 온도

−20°C

InChI

1S/C21H19Cl2N3O6S3/c22-14-1-6-18(25-34(28,29)20-8-7-19(23)33-20)17(13-14)21(27)24-15-2-4-16(5-3-15)35(30,31)26-9-11-32-12-10-26/h1-8,13,25H,9-12H2,(H,24,27)

InChI key

PQHLRGARXNPFCF-UHFFFAOYSA-N

생화학적/생리학적 작용

Ataciguat (HMR-1766) is a soluble guanylate cyclase (sGC) activator

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point (°F)

Not applicable

Flash Point (°C)

Not applicable


시험 성적서(COA)

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문서 라이브러리 방문

Ariane Migliato Martinelli et al.
Journal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques, 21(1), 38-45 (2018-02-17)
In endothelial cells, investigate if the soluble guanylate cyclase (sGC) activation or stimulation is able to potentiate the relaxation in vessels. Aortic and coronary rings with and without endothelium were placed in a myograph and cumulative concentration-effect curves for DETA-NO
Zongmin Zhou et al.
American journal of physiology. Heart and circulatory physiology, 295(4), H1763-H1771 (2008-09-02)
Many vascular diseases are characterized by increased levels of ROS that destroy the biological activity of nitric oxide and limit cGMP formation. In the present study, we investigated the cGMP-forming ability of HMR-1766 in cells exposed to oxidative stress. Pretreatment
Daniela Fraccarollo et al.
Basic research in cardiology, 109(4), 421-421 (2014-06-09)
Impaired nitric oxide (NO)-soluble guanylate cyclase (sGC)-cGMP signaling is involved in the pathogenesis of ischemic heart diseases, yet the impact of long-term sGC activation on progressive cardiac remodeling and heart failure after myocardial infarction (MI) has not been explored. Moreover

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