Size | Price | Stock | Qty |
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10mg |
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Atorvastatin sodium (Tozalip; Torvast; Cardyl; CI-981; CI981; liptonorm), the sodium salt of Atorvastatin which is a stastin class of LDL cholesterol-lowering/hypolipidemic drug, is a potent and selective inhibitor of HMG-CoA reductase. Atorvastatin isthe best-selling drug in the history of pharmaceuticals with a total of around US$130 billion for Pfizer during its 14 years on the market, making it the world's bestselling drug of all time. It acts by blocking the production of cholesterol. Atorvastatin is used primarily for lowering blood cholesterol and for prevention of events associated with cardiovascular disease.
ln Vitro |
Following myocardial infarction, atorvastatin sodium decreases the expression of GRP78, caspase-12, and CHOP in cardiomyocytes and stimulates the endoplasmic reticulum (ER) in response to angiotensin II (Ang II) stimulation and heart failure. \sup>[4].
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ln Vivo |
Atorvastatin (20–30 mg/kg; once daily; intracavitary gavage; 28 days; ApoE−/− mice) sodium significantly decreases arthritic cell number, endoplasmic reticulum (ER) protein signaling, and pro-inflammatory cytokines like IL-6, IL-8, and IL-1β were significantly inhibited after treatment with Ang II atorvastatin sodium [5].
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References | |
Additional Infomation |
Atorvastatin Sodium is the sodium salt of atorvastatin, a synthetic lipid-lowering agent. Atorvastatin competitively inhibits hepatic hydroxymethyl-glutaryl coenzyme A (HMG-CoA) reductase, the enzyme which catalyzes the conversion of HMG-CoA to mevalonate, a key step in cholesterol synthesis. This agent increases the number of LDL receptors on hepatic cell surfaces, enhancing the uptake and catabolism of LDL and reducing LDL production and the number of LDL particles, and lowers plasma cholesterol and lipoprotein levels. Like other statins, atorvastatin may also display direct antineoplastic activity, possibly by inhibiting farnesylation and geranylgeranylation of proteins such as small GTP-binding proteins, which may result in the arrest of cells in the G1 phase of the cell cycle. This agent may also sensitize tumor cells to cyctostatic drugs, possibly through the mTOR-dependent inhibition of Akt phosphorylation.
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Molecular Formula |
C33H34FN2NAO5
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Molecular Weight |
580.62
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Exact Mass |
580.234
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CAS # |
134523-01-6
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Related CAS # |
134523-03-8 (calcium);344423-98-9 (calcium trihydrate);134523-00-5 (free acid);134523-01-6 (sodium); 874114-41-7 (magnesium);
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PubChem CID |
23665101
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Appearance |
Typically exists as solid at room temperature
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Density |
1.2±0.1 g/cm3
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Boiling Point |
722.2±60.0ºC at 760 mmHg
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Flash Point |
390.6±32.9ºC
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LogP |
5.051
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Hydrogen Bond Donor Count |
3
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Hydrogen Bond Acceptor Count |
6
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Rotatable Bond Count |
12
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Heavy Atom Count |
42
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Complexity |
829
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Defined Atom Stereocenter Count |
2
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SMILES |
[Na+].O=C(C[C@@H](C[C@@H](CCN1C(C(C)C)=C(C(NC2=CC=CC=C2)=O)C(C2=CC=CC=C2)=C1C1=CC=C(F)C=C1)O)O)[O-]
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InChi Key |
VVRPOCPLIUDBSA-CNZCJKERSA-M
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InChi Code |
InChI=1S/C33H35FN2O5.Na/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);/q;+1/p-1/t26-,27-;/m1./s1
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Chemical Name |
sodium;(3R,5R)-7-[2-(4-fluorophenyl)-3-phenyl-4-(phenylcarbamoyl)-5-propan-2-ylpyrrol-1-yl]-3,5-dihydroxyheptanoate
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HS Tariff Code |
2934.99.9001
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Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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Solubility (In Vitro) |
May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples
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Solubility (In Vivo) |
Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.
Injection Formulations
Injection Formulation 1: DMSO : Tween 80: Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution. Injection Formulation 2: DMSO : PEG300 :Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline) Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil) Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals). View More
Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)] Oral Formulations
Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium) Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals). View More
Oral Formulation 3: Dissolved in PEG400  (Please use freshly prepared in vivo formulations for optimal results.) |
Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
1 mM | 1.7223 mL | 8.6115 mL | 17.2230 mL | |
5 mM | 0.3445 mL | 1.7223 mL | 3.4446 mL | |
10 mM | 0.1722 mL | 0.8611 mL | 1.7223 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration: mg/mL;
Method for preparing DMSO stock solution: mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation::Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O,mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
Effect of atorvastatin (ATV) on hypernociception induced by LPS or antigen challenge. (a) The mice were pretreated for 3 consecutive days with ATV (1, 3, 10, 30 and 90 mg kg−1 p.o.) or PBS, once a day. The last dose of ATV was administered 2 h before i.pl injection of LPS (100 ng paw−1, 25 μl) or saline. (b) Mice were pretreated for 1, 2 or 3 consecutive days with ATV (30 mg kg−1 p.o.) or PBS once a day. Two hours after last the dose of ATV, LPS (100 ng paw−1) or saline were i.pl injected. (c) Sensitized mice (Im.) were pretreated for 3 consecutive days with ATV (30 mg kg−1 p.o.) or PBS once a day. The last dose was administered 2 h before antigen challenge. Results from the false immunized mice are shown as the F.I group. In all panels, the mechanical hypernociception was determined at fixed times between 0.5 and 24 h after stimulus injection. The results are expressed as the mean±s.e.m. of five animals per group. The withdrawal threshold base line of the animals pretreated for 3 days with PBS before the i.pl injection of the hypernociceptive stimuli was 9.8±0.10 g (n=10). *Significant difference compared with the paws injected with saline and **with PBS-treated group (P<0.05).[4]. Atorvastatin inhibits myocardial cell apoptosis in a rat model with post-myocardial infarction heart failure by downregulating ER stress response. Int J Med Sci. 2011;8(7):564-72. td> |
Effect of atorvastatin (ATV) on BK, TNF-α, IL-1β-, keratinocyte-derived chemokine (KC)- and PGE2-induced hypernociception. The animals were pretreated for 3 days with ATV (30 mg kg−1 p.o.) once a day. The last dose was administered 2 h before injection of the hypernociceptive stimuli. Mechanical hypernociception was determined 3 h after stimulus injection. *Statistically significant difference compared with the paws injected with saline and **with PBS pretreated group (P<0.05).[4]. Atorvastatin inhibits myocardial cell apoptosis in a rat model with post-myocardial infarction heart failure by downregulating ER stress response. Int J Med Sci. 2011;8(7):564-72. td> |
Effect of NO synthesis inhibition on atorvastatin (ATV)-induced antinociception. The antinociceptive effect of ATV (30 mg kg−1 p.o.) was determined in animals pretreated with L-NAME (90 mg kg−1 i.p.), L-NMMA (90 mg kg−1 i.p.), 1400W (1.5 mg kg−1 i.v.) and in iNOS-deficient (−/−) mice. Mechanical hypernociception was assessed 3 h after injection of LPS (a) (100 ng paw−1) or PGE2 (b) (100 ng paw−1). The results are expressed as the mean±s.e.m. of five animals per group. *Statistically significant difference compared with the paws injected with saline and **with PBS-treated group and #with ATV-pretreated group (P<0.05).[4]. Atorvastatin inhibits myocardial cell apoptosis in a rat model with post-myocardial infarction heart failure by downregulating ER stress response. Int J Med Sci. 2011;8(7):564-72. td> |