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Merck
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SML2598

Sigma-Aldrich

Ataciguat

≥98% (HPLC)

别名:

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

经验公式（希尔记法）:
C21H19Cl2N3O6S3
CAS号:
254877-67-3
分子量:
576.49
MDL號碼:
MFCD09837865
分類程式碼代碼:
12352202
NACRES:
NA.77

化驗

≥98% (HPLC)

形狀

powder

顏色

white to beige

溶解度

DMSO: 2 mg/mL, clear

儲存溫度

−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 密鑰

PQHLRGARXNPFCF-UHFFFAOYSA-N

生化／生理作用

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

儲存類別代碼

11 - Combustible Solids

水污染物質分類（WGK）

WGK 3

閃點（°F）

Not applicable

閃點（°C）

Not applicable

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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
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
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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