Atorvastatin - CAS 134523-00-5
Catalog number: 134523-00-5
Category: Inhibitor
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Molecular Formula:
C33H35FN2O5
Molecular Weight:
558.64
COA:
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Targets:
HMG-CoA Reductase (HMGCR)
Description:
Atorvastatin, a HMG-CoA reductase inhibitor, could be used to reduce cholesterol and prevent cardiovascular related disease.
Purity:
95%
Appearance:
Crystalline powder
Synonyms:
Atorvastatin;(3R,5R)-7-[2-(4-Fluorophenyl)-5-isopropyl-3-phenyl-4-(pheynylcarbamoyl)pyrrol-1-yl]-3,5-dihydro heptanoic acid
Solubility:
DMSO 100 mg/mL; Water <1 mg/mL
Storage:
-20ºC Freeze
MSDS:
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Application:
Atorvastatin is a HMG-CoA reductase inhibitor that could be used to reduce cholesterol and prevent cardiovascular related disease.
Shelf Life:
As supplied, 2 years from the QC date provided on the Certificate of Analysis, when stored properly
Quantity:
Milligrams-Grams
Boiling Point:
722.198ºC at 760 mmHg
Melting Point:
176-178ºC
Density:
1.236 g/cm3
InChIKey:
XUKUURHRXDUEBC-KAYWLYCHSA-N
InChI:
InChI=1S/C33H35FN2O5/c1-21(2)31-30(33(41)35-25-11-7-4-8-12-25)29(22-9-5-3-6-10-22)32(23-13-15-24(34)16-14-23)36(31)18-17-26(37)19-27(38)20-28(39)40/h3-16,21,26-27,37-38H,17-20H2,1-2H3,(H,35,41)(H,39,40)/t26-,27-/m1/s1
Canonical SMILES:
CC(C)C1=C(C(=C(N1CCC(CC(CC(=O)O)O)O)C2=CC=C(C=C2)F)C3=CC=CC=C3)C(=O)NC4=CC=CC=C4
1.Liquid chromatography-tandem mass spectrometry assay for the simultaneous quantification of simvastatin, lovastatin, atorvastatin, and their major metabolites in human plasma.
Wang J;Luzum JA;Phelps MA;Kitzmiller JP J Chromatogr B Analyt Technol Biomed Life Sci. 2015 Mar 1;983-984:18-25. doi: 10.1016/j.jchromb.2014.12.029. Epub 2015 Jan 13.
Millions of individuals are treated with a variety of statins that are metabolized to a variety of active metabolites. A single assay capable of simultaneously quantifying commonly used statins and their major metabolites has not been previously reported. Herein we describe the development and validation of a novel and robust liquid chromatography-tandem mass spectrometry assay for simultaneously quantifying simvastatin, lovastatin, atorvastatin, and their metabolites, simvastatin acid, lovastatin acid, para-hydroxy atorvastatin, and ortho-hydroxy atorvastatin in human plasma. Plasma samples were processed with a simple protein precipitation technique using acetonitrile, followed by chromatographic separation using an Agilent Zorbax Extend C18 column. A 12.0min linear gradient elution was used at a flow rate of 400μL/min with a mobile phase of water and methanol, both modified with 2mM ammonium formate and 0.2% formic acid. The analytes and internal standard, hesperetin, were detected using the selected reaction monitoring mode on a TSQ Quantum Discovery mass spectrometer with positive electrospray ionization. The assay exhibited a linear range of 1-1000nM for simvastatin acid and lovastatin acid, and a linear range of 0.
2.The role of atorvastatin in suppressing tumor growth of uterine fibroids.
Shen Z;Li S;Sheng B;Shen Q;Sun LZ;Zhu H;Zhu X J Transl Med. 2018 Mar 9;16(1):53. doi: 10.1186/s12967-018-1430-x.
BACKGROUND: ;Medical therapeutic options remain quite limited for uterine fibroids treatment. Statins, competitive inhibitors of 3-hydroxy-3-methylglutaryl-coenzyme A reductase, have anti-tumoral effects on multiple cancer types, however, little is known about their effects on uterine fibroids.;METHODS: ;Initially, we conducted a retrospective study of 120 patients with uterine fibroids and hyperlipidemia from the Second Affiliated Hospital of Wenzhou Medical University. Then, we evaluated the effect of atorvastatin on proliferation and apoptosis both in immortalized uterine fibroids cells and primary uterine fibroids cells. Furthermore, the molecular mechanism by which atorvastatin suppressed uterine fibroids cell growth was explored.;RESULTS: ;Our results showed that atorvastatin use for 1 or 2 years significantly suppressed growth of uterine fibroids. Atorvastatin inhibited the proliferation of immortalized and primary uterine fibroids cells in a dose and time-dependent manner and stimulated apoptosis of uterine fibroids cells by inducing caspase-3 activation, up-regulating Bim and down-regulating Bcl-2. Additionally, atorvastatin treatment suppressed phosphorylation of ERK1/2 and JNK.
3.Effect of Steady-State Faldaprevir on Pharmacokinetics of Atorvastatin or Rosuvastatin in Healthy Volunteers: A Prospective Open-Label, Fixed-Sequence Crossover Study.
Huang F;Marzin K;Koenen R;Kammerer KP;Strelkowa N;Elgadi M;Quinson AM;Haertter S J Clin Pharmacol. 2017 Oct;57(10):1305-1314. doi: 10.1002/jcph.931. Epub 2017 May 17.
Faldaprevir (FDV) is a potent, orally administered inhibitor of hepatitis C virus protease. It inhibits multiple cytochrome P-450 enzymes and multiple membrane transporters. The objective of this study was to evaluate the effect of steady-state faldaprevir on the pharmacokinetics (PK) of a single dose of atorvastatin or rosuvastatin. In this single-center, open-label, fixed-sequence crossover study, 33 healthy adult male and female volunteers were given either atorvastatin 10 mg (n = 16) or rosuvastatin 10 mg (n = 17) on day 1. Subjects subsequently received 240 mg twice daily of faldaprevir (loading dose) on day 5, followed by 240 mg faldaprevir once daily from day 6 to day 10, with an additional single dose of atorvastatin (10 mg) or rosuvastatin (10 mg) given on day 10. PK samples for the statins were collected on days 1-3 and days 10-12. Concomitant administration with faldaprevir led to approximately 9-fold and 34-fold increases in AUC;0-∞; and C;max; , respectively, of atorvastatin and approximately 15-fold and 33-fold increases in AUC;0-∞; and C;max; , respectively, of rosuvastatin, compared with the statins given alone. Exposure to the major metabolites (ortho-hydroxyatorvastatin and N-desmethylrosuvastatin) was increased to a similar magnitude as that of the parent compounds.
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CAS 134523-00-5 Atorvastatin

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