Stereochemistry | ABSOLUTE |
Molecular Formula | C23H36O7 |
Molecular Weight | 424.5277 |
Optical Activity | UNSPECIFIED |
Defined Stereocenters | 8 / 8 |
E/Z Centers | 0 |
Charge | 0 |
SHOW SMILES / InChI
SMILES
[H][C@]12[C@H](C[C@H](O)C=C1C=C[C@H](C)[C@@H]2CC[C@@H](O)C[C@@H](O)CC(O)=O)OC(=O)[C@@H](C)CC
InChI
InChIKey=TUZYXOIXSAXUGO-PZAWKZKUSA-N
InChI=1S/C23H36O7/c1-4-13(2)23(29)30-20-11-17(25)9-15-6-5-14(3)19(22(15)20)8-7-16(24)10-18(26)12-21(27)28/h5-6,9,13-14,16-20,22,24-26H,4,7-8,10-12H2,1-3H3,(H,27,28)/t13-,14-,16+,17+,18+,19-,20-,22-/m0/s1
Molecular Formula | C23H36O7 |
Molecular Weight | 424.5277 |
Charge | 0 |
Count |
MOL RATIO
1 MOL RATIO (average) |
Stereochemistry | ABSOLUTE |
Additional Stereochemistry | No |
Defined Stereocenters | 8 / 8 |
E/Z Centers | 0 |
Optical Activity | UNSPECIFIED |
Pravastatin (marketed as Pravachol or Selektine) is a member of the drug class of statins, used in combination with diet, exercise, and weight loss for lowering cholesterol and preventing cardiovascular disease. Pravastatin acts as a lipoprotein-lowering drug through two pathways. In the major pathway, pravastatin inhibits the function of hydroxymethylglutaryl-CoA (HMG-CoA) reductase. As a reversible competitive inhibitor, pravastatin sterically hinders the action of HMG-CoA reductase by occupying the active site of the enzyme. Taking place primarily in the liver, this enzyme is responsible for the conversion of HMG-CoA to mevalonate in the rate-limiting step of the biosynthetic pathway for cholesterol. Pravastatin also inhibits the synthesis of very-low-density lipoproteins, which are the precursor to low-density lipoproteins (LDL). These reductions increase the number of cellular LDL receptors, thus LDL uptake increases, removing it from the bloodstream. Pravastatin is primarily used for the treatment of dyslipidemia and the prevention of cardiovascular disease. It is recommended to be used only after other measures, such as diet, exercise, and weight reduction, have not improved cholesterol levels. The evidence for the use of pravastatin is generally weaker than for other statins. The antihypertensive and lipid-lowering treatment to prevent heart attack trial (ALLHAT), failed to demonstrate a difference in all-cause mortality or nonfatal myocardial infarction/fatal coronary heart disease rates between patients receiving pravastatin 40 mg daily (a common starting dose) and those receiving usual care. Pravastatin is generally well tolerated; adverse reactions have usually been mild and transient. In 4-month-long placebo-controlled trials, 1.7% of Pravastatin-treated patients and 1.2% of placebo-treated patients were discontinued from treatment because of adverse experiences attributed to study drug therapy; this difference was not statistically significant.
CNS Activity
Originator
Approval Year
AUC
Overview
CYP3A4 | CYP2C9 | CYP2D6 | hERG |
---|---|---|---|
Drug as perpetrator
Drug as victim
Sourcing
Sample Use Guides
May be beneficial for prophylaxis of cardiovascular events in at-risk patients, even if patients have normal levels of cholesterol.
10-40 mg PO qDay; not to exceed 80 mg/day
Initiate with 10 mg qHS if taking immunosuppressants like cyclosporine concurrently; not to exceed 20 mg/day
Limit maximum to 40 mg/day if taking concurrently with clarithromycin
Dose adjustments should be made at intervals of 4 weeks or more; individualize dosing according to baseline LDL cholesterol levels
Route of Administration:
Oral
Pravastatin activity was evaluated using cellular steroidgenesis assay in Hep G2cells (human hepatoma cell line) cultured with 5% lipoprotein deficient serum containing medium for 48 h. The activities were determined by decreased incorporation of sodium [2-14C] acetate into non-saponifiable lipids.