| Stereochemistry | ABSOLUTE |
| Molecular Formula | C24H36O5 |
| Molecular Weight | 404.5396 |
| 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](C)C=C1C=C[C@H](C)[C@@H]2CC[C@@H]3C[C@@H](O)CC(=O)O3)OC(=O)[C@@H](C)CC
InChI
InChIKey=PCZOHLXUXFIOCF-BXMDZJJMSA-N
InChI=1S/C24H36O5/c1-5-15(3)24(27)29-21-11-14(2)10-17-7-6-16(4)20(23(17)21)9-8-19-12-18(25)13-22(26)28-19/h6-7,10,14-16,18-21,23,25H,5,8-9,11-13H2,1-4H3/t14-,15-,16-,18+,19+,20-,21-,23-/m0/s1
| Molecular Formula | C24H36O5 |
| Molecular Weight | 404.5396 |
| 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 |
Lovastatin acid is an active metabolite of hypolipidemic drug Lovastatin. Lovastatin acid inhibits HMG-CoA reductase. This enzyme catalyzes the conversion of HMG-CoA to mevalonate, which is an early and rate limiting step in the biosynthesis of cholesterol. Lovastatin has been shown to reduce both normal and elevated low-density lipoprotein cholesterol (LDL-C). Lovastatin in approved for prevention of cardiovascular events and hypercholesterolemia. Off-label use of lovastatin includes treatmetn of diabetic dyslipidemia, familial dysbetalipoproteinemia, familial combined hyperlipidemia, or nephrotic hyperlipidemia. Lovastatin was tested in clinical trials agains radioation injury during therapy of prostate cancer.
CNS Activity
Originator
Approval Year
Doses
AEs
Sourcing
PubMed
Patents
Sample Use Guides
Hyperlipidemia and Mixed Dyslipidemia: (Fredrickson Types IIa and IIb). The recommended dosing range is 20-60 mg/day, in single doses taken in the evening at bedtime.
Route of Administration:
Oral
Flow cytometry revealed significant increases in three of four lung cancer cell lines in apoptosis and necrosis after lovastatin treatment at 10 uM for 72 h. Lovastatin adversely affected lung cancer cell survival with increases in cell-cycle check-point inhibitors p21WAF and/or p27KIP and a decrease in cyclin D1. All four lung cancer cell lines had a decrease in glutathione after lovastatin treatment consistent with reduced protection against reactive oxidant species. Three of four lung cancer cell lines had increased cytochrome c release with reduced pro-caspase-3 and increases in activated caspase-3. Lovastatin induces apoptosis and necrosis in lung cancer cell lines by causing alterations in the cell cycle, reducing glutathione, and activating p53, Bax protein, and caspases while increasing cytochrome c in apoptosis pathways.
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| Name | Property Type | Amount | Referenced Substance | Defining | Parameters | References |
|---|---|---|---|---|---|---|
| Tmax | PHARMACOKINETIC |
2 hours (average) |
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| Biological Half-life | PHARMACOKINETIC |
[1.1 to 1.7] hours (average) |
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| MAXIMUM TOLERATED DOSE | TOXICITY |
80 mg/day (average) ORAL IMMEDIATE-RELEASE DOSE |
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| ORAL BIOAVAILABILITY | PHARMACOKINETIC |
LESS THAN 5% (HYPERCHOLESTEROLEMIA) |
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