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3-amino-crotonic acid 6-(5-phenyl-3-pyrazolyloxy)hexyl ester is a chemical with a specific purpose. Lookchem provides you with multiple data and supplier information of this chemical.

86385-48-0

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86385-48-0 Usage

Check Digit Verification of cas no

The CAS Registry Mumber 86385-48-0 includes 8 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 5 digits, 8,6,3,8 and 5 respectively; the second part has 2 digits, 4 and 8 respectively.
Calculate Digit Verification of CAS Registry Number 86385-48:
(7*8)+(6*6)+(5*3)+(4*8)+(3*5)+(2*4)+(1*8)=170
170 % 10 = 0
So 86385-48-0 is a valid CAS Registry Number.

86385-48-0Downstream Products

86385-48-0Relevant academic research and scientific papers

Effects of a calcium-channel blocker (CV159) on hepatic ischemia/reperfusion injury in rats: Evaluation with selective NO/pO2 electrodes and an electron paramagnetic resonance spin-trapping method

Hataji, Keizo,Watanabe, Taiji,Oowada, Shigeru,Nagaya, Masaki,Kamibayashi, Masato,Murakami, Eiichi,Kawakami, Hiroyoshi,Ishiuchi, Atsuko,Kumai, Toshio,Nakano, Hiroshi,Kobayashi, Shinichi,Otsubo, Takehito

, p. 77 - 83 (2010)

Nitric oxide (NO) and the partial pressure of oxygen (pO2) in the liver were simultaneously quantified in rats with partial hepatic ischemia/reperfusion injury (PHIRI). Real-time NO/pO2 monitoring and immunohistochemical analysis for superoxide dismutase and inducible nitric oxide synthase (iNOS) and endothelial NOS (eNOS) were performed to evaluate the protective effects of a dihydropyridine-type calcium-channel blocker-CV159-on PHIRI. Serum high-mobility-group box-1 (HMGB-1) was measured to assess cellular necrosis. Moreover, we used in vitro/ex vivo electron paramagnetic resonance spin trapping to assess the hydroxyl radical ( ?OH)-scavenging activity (OHSA) of CV159 and the liver tissue. The NO levels were significantly higher in CV159-treated rats than in control rats throughout the ischemic phase. Immediately after reperfusion, the levels temporarily increased in waves and then gradually decreased in the treated rats but remained constant in the control rats. pO 2 was continually higher in the treated rats. In these rats, hepatic eNOS expression increased, whereas iNOS expression decreased. The treated rats exhibited significantly higher cytosolic and mitochondrial concentrations NOx (NO2+NO3). The serum HMGB-1 levels significantly decreased in the treated rats. Moreover, CV159 directly scavenged ·OH and both mitochondrial and cytosolic OHSA were preserved in the treated rats. Thus, CV159-mediated inhibition of intracellular Ca2+ overloading may effectively minimize organ damage and also have ·OH-scavenging activity and the cytoprotective effects of eNOS-derived NO.

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