(S)-(+)-Niguldipine hydrochloride - CAS 113145-69-0
Category: Inhibitor
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Molecular Formula:
Molecular Weight:
Adrenergic Receptor
(S)-(+)-Niguldipine hydrochloride, the more active enantiomer of Niguldipine hydrochloride, acts as a potent, selective α1A-adrenoceptor antagonist (Ki = 0.16 nM), and also is a L-type Ca2+ channel blocker.
Related CAS:
(S)-1,4-Dihydro-2,6-dimethyl-4-(3-nitrophenyl)-3,5-pyridinedicarboxylic Acid 3-(4,4-Diphenyl-1-piperidinyl)propyl Methyl Ester Monohydrochloride; (+)-Niguldipine Hydrochloride; (S)-Niguldipine Hydrochloride; B 8509-034; BY 934; Niguldipine Hydrochloride
Store in a cool and dry place (or refer to the Certificate of Analysis).
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1.Trophic effects induced by alpha1D-adrenoceptors on endothelial cells are potentiated by hypoxia.
Vinci MC;Bellik L;Filippi S;Ledda F;Parenti A Am J Physiol Heart Circ Physiol. 2007 Oct;293(4):H2140-7. Epub 2007 Jul 27.
Catecholamines have been shown to be involved in vascular remodeling through the stimulation of alpha(1)-adrenoceptors (alpha(1)-ARs). Recently, it has been demonstrated that catecholamines can stimulate angiogenesis in pathological conditions, even if the mechanisms and the AR subtypes involved still remain unclear. We investigated the influence of hypoxia (3% O(2)) on the ability of picomolar concentrations of phenylephrine (PHE), which are unable to induce any vascular contraction, to induce a trophic effect in human endothelial cells through stimulation of the alpha(1D)-subtype ARs. PHE, at picomolar concentrations, significantly promoted pseudocapillary formation from fragments of human mature vessels in vitro. Exposure to hypoxia significantly potentiated this effect, which was inhibited by the selective alpha(1D)-AR antagonist BMY-7378 and by the nitric oxide synthase inhibitor L-NAME, suggesting that alpha(1D)-ARs were involved in this effect through activation of the nitric oxide pathway. Proliferation and migration of HUVEC were also affected by picomolar PHE concentrations. Again, these effects were significantly potentiated in cells exposed to hypoxia and were inhibited by BMY-7378 and by N(G)-nitro-L-arginine methyl ester.
2.A high-performance liquid chromatographic method for determination of the niguldipine analogue DHP-014.
Zhou XF;Wang Q;Coburn RA;Morris ME Biomed Chromatogr. 2006 Jan;20(1):48-53.
A simple and reliable reversed-phase high-performance liquid chromatography method was developed and validated for the determination of DHP-014, a niguldipine analogue with potent P-glycoprotein inhibitory and negligible calcium channel blocking properties, in rat plasma. DHP-014 and niguldipine hydrochloride (the internal standard) were extracted from rat plasma by liquid extraction using hexane. DHP-014 was then separated by HPLC on a C18 column and quantified by ultraviolet detection at 238 nm. The mobile phase consisted of acetonitrile-aqueous 5 mM phosphate buffer (65:35, v/v) containing 0.4% (v/v) triethylamine adjusted to pH 7.0. The mean extraction efficiency of DHP-014 was 109.0 +/- 12.9, 97.7 +/- 8.0 and 102.9 +/- 7.5% for DHP-014 concentrations of 10, 50 and 100 nM, respectively (n = 5). The method was linear over the concentration range 2.5-200 nM with a regression coefficient of 0.998. The limit of detection of DHP-014 in rat plasma was 1.0 nM. The intra- and inter-day coefficients of variation for DHP-014 in rat plasma were 4.7-7.9 and 6.9-9.9%, respectively. The intra- and inter-day accuracy was 98.2-99.5 and 97.9-103%, respectively. The bioanalytical technique was used to determine DHP-014 in plasma samples in a pharmacokinetic study of DHP-014 administered to female Sprague-Dawley rats.
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CAS 113145-69-0 (S)-(+)-Niguldipine hydrochloride

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