NO-Pravastatin
NO-Pravastatin is a derivative of Pravastatin (HY-B0165) covalently linked with an NO donor moiety, endowing it with dual functions of HMG-CoA reductase (HMGCR) inhibition and exogenous nitric oxide (NO) release. NO-Pravastatin activates PPARα/γ and ABCA1, and inhibits LPS (HY-D1056)-induced TNFα production. NO-Pravastatin can be used in research related to gallstones and cardiovascular diseases.
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- CAS. Nr.: 733034-46-3
- Formel: C27H43NO10
- Molecular Weight:541.63
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biologische Aktivität
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Chemical Information
- Reinheit & Dokumentation
- Verweise
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Help & FAQs
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Biologische Aktivität
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PPARα |
PPARγ |
NO-pravastatin (15 μM; 18-24 h) significantly upregulates the expression of ABCA1 and LXRα in cultured canine gallbladder epithelial cells, and inhibits LPS-induced TNFα production in the same cell type[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:cultured canine gallbladder epithelial cells (GBEC)
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Concentration:15 μM
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Incubation Time:24 h
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Result:Significantly increased PPARα protein expression relative to the no-treatment control, at a level similar to the PPARα agonist WY-14643.
Significantly increased PPARγ protein expression relative to the no-treatment control, with a stronger activation effect than simvastatin.
Significantly increased ABCA1 protein expression relative to the no-treatment control, though this induction was less potent than that of PPARα or PPARγ ligands.
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Cell Line:cultured canine gallbladder epithelial cells (GBEC)
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Concentration:15 μM (ABCA1 and LXRα mRNA analysis); 15 μM (TNFα mRNA analysis)
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Incubation Time:24 h (ABCA1 and LXRα mRNA analysis); 18 h pre-treatment prior to 1 h LPS loading (TNFα mRNA analysis)
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Result:Significantly increased ABCA1 mRNA expression relative to the no-treatment control, though this induction was less potent than that of PPARα or PPARγ ligands.
Significantly increased LXRα mRNA expression relative to the no-treatment control.
Almost completely repressed LPS-induced TNFα mRNA production relative to the LPS-only treatment group; simultaneous treatment with NO-pravastatin and LPS did not show this suppressive effect.
Chemical Information
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CAS. Nr. 733034-46-3
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Molecular Weight 541.63
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Formel C27H43NO10
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SMILES
CC[C@H](C)C(O[C@@H]1[C@@]2([H])C(C=C[C@@H]([C@@H]2CC[C@@H](O)C[C@@H](O)CC(OCCCCO[N+]([O-])=O)=O)C)=C[C@H](C1)O)=O
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Reinheit & Dokumentation
Verweise
[1]. Lee J, et al. HMG-CoA reductase inhibitors (statins) activate expression of PPARalpha/PPARgamma and ABCA1 in cultured gallbladder epithelial cells. Digestive diseases and sciences. 2010 Feb;55(2):292-9. [Content Brief]
[2]. Seymour K, et al. Statins and nitric oxide donors affect thrombospondin 1-induced chemotaxis. Vascular and endovascular surgery. 2014;48(7-8):470-5. [Content Brief]
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
NO-Pravastatin Related Classifications
HY-184354 Related Classifications
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