- Atorvastatin
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- $3.00 / 1kg
-
2024-04-12
- CAS:110862-48-1
- Min. Order: 1kg
- Purity: 99.9%
- Supply Ability: 10 tons
- Atorvastatin
-
- $35.00/ kg
-
2024-03-12
- CAS:110862-48-1
- Min. Order: 1kg
- Purity: 99.8%
- Supply Ability: 200tons/year
- Atorvastatin
-
- $0.00 / 25KG
-
2023-01-31
- CAS:110862-48-1
- Min. Order: 1KG
- Purity: 99%
- Supply Ability: 50000KG/month
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| | Atorvastatin Basic information |
| Product Name: | Atorvastatin | | Synonyms: | 1H-Pyrrole-1-heptanoic acid, 2-(4-fluorophenyl)-β,δ-dihydroxy-5-(1-methylethyl)-3-phenyl-4-[(phenylamino)carbonyl]-, (βR,δR)-rel-;1H-PYRROLE-1-HEPTANOIC ACID;(3S,5S)-7-[2-(4-Fluorophenyl)-3-phenyl-4-(phenylcarbamoyl)-5-propan-2-ylpyrrol-1-yl]-3,5-dihydroxyheptanoic acid;Atorvastatin;Atorvastatin(Relative);Atorvastatin, ?>98.0%;calcium 7-[4-[anilino(oxo)methyl]-2-(4-fluorophenyl)-3-phenyl-5-propan-2-yl-1-pyrrolyl]-3,5-dihydroxyheptanoate;Atorvastatin isomer | | CAS: | 110862-48-1 | | MF: | C33H35FN2O5 | | MW: | 558.64 | | EINECS: | 214-486-9 | | Product Categories: | Cardiovascular Agents | | Mol File: | 110862-48-1.mol |  |
| | Atorvastatin Chemical Properties |
| Boiling point | 722.2±60.0 °C(Predicted) | | density | 1.23±0.1 g/cm3(Predicted) | | pka | 4.29±0.10(Predicted) |
| | Atorvastatin Usage And Synthesis |
| Definition | ChEBI: Atorvastatin is a dihydroxy monocarboxylic acid that is a member of the drug class known as statins, used primarily for lowering blood cholesterol and for preventing cardiovascular diseases. It has a role as an environmental contaminant and a xenobiotic. It is an aromatic amide, a member of monofluorobenzenes, a statin (synthetic), a dihydroxy monocarboxylic acid and a member of pyrroles. It is functionally related to a heptanoic acid. It is a conjugate acid of an atorvastatin(1-). | | Clinical Use | Hyperlipidaemia and hypercholesterolaemia | | Drug interactions | Potentially hazardous interactions with other drugs
Anti-arrhythmics: concentration possibly increased
by dronedarone.
Antibacterials: azithromycin, erythromycin,
clarithromycin or fusidic acid possibly increased
risk of myopathy - avoid atorvastatin for at least
7 days after fusidic acid stopped; concentration
increased by clarithromycin - do not exceed 20 mg
of atorvastatin1
; avoid with telithromycin; increased
risk of myopathy with daptomycin; concentration
possibly reduced by rifampicin.
Anticoagulants: may transiently reduce anticoagulant
effect of warfarin.
Antifungals: increased risk of myopathy with
itraconazole - do not exceed 40 mg of atorvastatin1
;
increased risk of myopathy with fluconazole,
ketoconazole, posaconazole, voriconazole and
possibly other imidazoles and triazoles - avoid.
Antivirals: increased risk of myopathy with
atazanavir, boceprevir (reduce atorvastatin dose),
and possibly darunavir, fosamprenavir, indinavir,
lopinavir, ritonavir, saquinavir or tipranavir (max
dose of atorvastatin 10 mg); concentration reduced
by efavirenz and possibly etravirine; avoid with
dasabuvir, ombitasvir, paritaprevir and telaprevir;
possible increased risk of myopathy with ledipasvir
- reduce atorvastatin dose; concentration increased
by simeprevir - consider reducing atorvastatin
dose.
Calcium channel blockers: concentration increased
by diltiazem - increased risk of myopathy;
concentration of verapamil increased also possible
increased risk of myopathy - consider reducing
atorvastatin dose.
Ciclosporin: increased risk of myopathy - do not
exceed 10 mg of atorvastatin.1 Cobicistat: reduce atorvastatin dose.
Colchicine: possible increased risk of myopathy.
Grapefruit juice: concentration possibly increased.
Lipid lowering agents: increased risk of myopathy
with fibrates, gemfibrozil (avoid) and nicotinic acid. | | Metabolism | Atorvastatin undergoes extensive presystemic clearance
in gastrointestinal mucosa and/or hepatic first-pass
metabolism. Atorvastatin is metabolised by cytochrome
P450 3A4 to ortho- and parahydroxylated derivatives
and various beta-oxidation products. These products are
further metabolised via glucuronidation. Approximately
70% of circulating inhibitory activity for HMG-CoA
reductase is attributed to active metabolites.
Atorvastatin is eliminated primarily in bile as active
metabolites following hepatic and/or extrahepatic
metabolism, but does not appear to undergo significant
enterohepatic recirculation. |
| | Atorvastatin Preparation Products And Raw materials |
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