Ataciguat
mRNA synthesis
In vitro transcription of capped mRNA with modified nucleotides and Poly(A) tail
Tyramide Signal Amplification (TSA)
TSA (Tyramide Signal Amplification), used for signal amplification of ISH, IHC and IC etc.
Phos Binding Reagent Acrylamide
Separation of phosphorylated and non-phosphorylated proteins without phospho-specific antibody
Cell Counting Kit-8 (CCK-8)
A convenient and sensitive way for cell proliferation assay and cytotoxicity assay
SYBR Safe DNA Gel Stain
Safe and sensitive stain for visualization of DNA or RNA in agarose or acrylamide gels.
Inhibitor Cocktails
Protect the integrity of proteins from multiple proteases and phosphatases for different applications.
Ataciguat, formerly named as HMR 1766, is a novel activator of soluble guanylyl cyclase (sGC) [1].
The sGC is activated in the presence of NO, converts GTP to cyclic GMP (cGMP). The sGC shows a direct role in controlling various physiological processes, including the cardiovascular and neural systems [2].
In aortic rings from CHF rats, ataciguat normalized the impaired endothelium-dependent, NO-mediated vasorelaxation as well as vascular sensitivity to exogenous NO. In platelets from CHF rats, ataciguat normalized the attenuated the in vivo VASP phosphorylation. Treatment with ataciguat reduced the platelet activation in CHF [1]. Ataciguat normalized platelet activation by reducing P-selectin expression and increasing platelet vasodilator stimulated phosphoprotein (VASP) phosphorylation. In isolated aortic rings from control and placebo treated STZ rats, activation of sGC by ataciguat normalized vascular function and restored endothelium dependent relaxation [3]. In a mouse model of coronary thrombosis, treatment with ataciguat significantly reduced atherosclerotic plaque formation and markedly improved endothelium-dependent vasodilatation. Ataciguat treatment showed no effect on endothelium-independent vasorelaxation or vasoconstriction. Ataciguat increased expression of vascular P-VASP, showed no effect on eNOS and sGC expression, and reduced vascular VCAM-1 expression [3].
References:
[1] Schfer A, Fraccarollo D, Werner L, et al. Guanylyl cyclase activator ataciguat improves vascular function and reduces platelet activation in heart failure[J]. Pharmacological research, 2010, 62(5): 432-438.
[2] Poulos T L. Soluble guanylate cyclase[J]. Current opinion in structural biology, 2006, 16(6): 736-743.
[3] van Eickels M, Wassmann S, Schfer A, et al. Role of the sGC activator ataciguat sodium (HMR1766) in cardiovascular disease[J]. BMC Pharmacology, 2007, 7: 1-2.
Physical Appearance | A crystalline solid |
Storage | Store at -20°C |
M.Wt | 576.5 |
Cas No. | 254877-67-3 |
Formula | C21H19Cl2N3O6S3 |
Synonyms | HMR 1766 |
Solubility | ≤1mg/ml in dimethyl formamide |
Chemical Name | 5-chloro-2-[[(5-chloro-2-thienyl)sulfonyl]amino]-N-[4-(4-morpholinylsulfonyl)phenyl]-benzamide |
SDF | Download SDF |
Canonical SMILES | O=S(N1CCOCC1)(C2=CC=C(NC(C3=CC(Cl)=CC=C3NS(C4=CC=C(Cl)S4)(=O)=O)=O)C=C2)=O |
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