Details
| 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
CC[C@H](C)C(=O)O[C@H]1C[C@@H](C)C=C2C=C[C@H](C)[C@H](CC[C@@H]3C[C@@H](O)CC(=O)O3)[C@@H]12
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 |
|
| Stereochemistry | ABSOLUTE |
| Additional Stereochemistry | No |
| Defined Stereocenters | 8 / 8 |
| E/Z Centers | 0 |
| Optical Activity | UNSPECIFIED |
DescriptionSources: http://www.accessdata.fda.gov/drugsatfda_docs/label/2014/021316s031lbl.pdfhttp://www.accessdata.fda.gov/drugsatfda_docs/label/2012/019643s085lbl.pdfCurator's Comment: description was created based on several sources, including https://clinicaltrials.gov/show/NCT00580970 | http://medical-dictionary.thefreedictionary.com/lovastatin
Sources: http://www.accessdata.fda.gov/drugsatfda_docs/label/2014/021316s031lbl.pdfhttp://www.accessdata.fda.gov/drugsatfda_docs/label/2012/019643s085lbl.pdf
Curator's Comment: description was created based on several sources, including https://clinicaltrials.gov/show/NCT00580970 | http://medical-dictionary.thefreedictionary.com/lovastatin
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
Sources: https://www.ncbi.nlm.nih.gov/pubmed/20467214https://www.ncbi.nlm.nih.gov/pubmed/6933445
Curator's Comment: # Merck
Approval Year
Targets
| Primary Target | Pharmacology | Condition | Potency |
|---|---|---|---|
| 0.64 nM [Ki] | |||
Target ID: CHEMBL402 Sources: https://www.ncbi.nlm.nih.gov/pubmed/3055919 |
0.64 nM [IC50] | ||
Target ID: CHEMBL402 Sources: https://www.ncbi.nlm.nih.gov/pubmed/12405293 |
Conditions
| Condition | Modality | Targets | Highest Phase | Product |
|---|---|---|---|---|
| Preventing | ALTOPREV Approved Use1.1 Prevention of Coronary Heart Disease In patients without symptomatic coronary heart disease (CHD), but at high risk, Altoprev® is indicated to reduce the risk of: Myocardial infarction; Unstable angina; Coronary revascularization procedures; Coronary Heart Disease. Altoprev is indicated to slow the progression of coronary atherosclerosis in patients with coronary heart disease as part of a treatment strategy to lower Total-C and LDL-C to target levels. Hyperlipidemia Altoprev is indicated as an adjunct to diet for the reduction of elevated Total-C, LDL-C, Apo B, and TG, and to increase HDL-C in patients with primary hypercholesterolemia (heterozygous familial and non-familial) and mixed dyslipidemia (Fredrickson types IIa and IIb). Launch Date2002 |
|||
| Palliative | ALTOPREV Approved Use1.1 Prevention of Coronary Heart Disease In patients without symptomatic coronary heart disease (CHD), but at high risk, Altoprev® is indicated to reduce the risk of: Myocardial infarction; Unstable angina; Coronary revascularization procedures; Coronary Heart Disease. Altoprev is indicated to slow the progression of coronary atherosclerosis in patients with coronary heart disease as part of a treatment strategy to lower Total-C and LDL-C to target levels. Hyperlipidemia Altoprev is indicated as an adjunct to diet for the reduction of elevated Total-C, LDL-C, Apo B, and TG, and to increase HDL-C in patients with primary hypercholesterolemia (heterozygous familial and non-familial) and mixed dyslipidemia (Fredrickson types IIa and IIb). Launch Date2002 |
|||
| Preventing | MEVACOR Approved UseAfter oral ingestion, lovastatin, which is an inactive lactone, is hydrolyzed to the lovastatin acid. This is a principal metabolite and an inhibitor of 3-hydroxy-3-methylglutarylcoenzyme A (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). Launch Date1987 |
|||
| Primary | MEVACOR Approved UseTherapy with lipid-altering agents should be a component of multiple risk factor intervention in those individuals at significantly increased risk for atherosclerotic vascular disease due to hypercholesterolemia. MEVACOR is indicated as an adjunct to diet for the reduction of elevated total-C and LDL-C levels in patients with primary hypercholesterolemia (Types IIa and IIb***), when the response to diet restricted in saturated fat and cholesterol and to other nonpharmacological measures alone has been inadequate. Launch Date1987 |
|||
| Secondary | Unknown Approved UseUnknown |
Cmax
| Value | Dose | Co-administered | Analyte | Population |
|---|---|---|---|---|
17.6 ng/mL EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/9585793 |
80 mg single, oral dose: 80 mg route of administration: Oral experiment type: SINGLE co-administered: |
LOVASTATIN ACID plasma | Homo sapiens population: HEALTHY age: ADULT sex: FEMALE / MALE food status: FASTED |
|
11.9 ng/mL |
40 mg 1 times / day steady-state, oral dose: 40 mg route of administration: Oral experiment type: STEADY-STATE co-administered: |
LOVASTATIN ACID plasma | Homo sapiens population: UNHEALTHY age: ADULT sex: UNKNOWN food status: UNKNOWN |
AUC
| Value | Dose | Co-administered | Analyte | Population |
|---|---|---|---|---|
76.9 ng × h/mL EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/9585793 |
80 mg single, oral dose: 80 mg route of administration: Oral experiment type: SINGLE co-administered: |
LOVASTATIN ACID plasma | Homo sapiens population: HEALTHY age: ADULT sex: FEMALE / MALE food status: FASTED |
|
83 ng × h/mL |
40 mg 1 times / day steady-state, oral dose: 40 mg route of administration: Oral experiment type: STEADY-STATE co-administered: |
LOVASTATIN ACID plasma | Homo sapiens population: UNHEALTHY age: ADULT sex: UNKNOWN food status: UNKNOWN |
T1/2
| Value | Dose | Co-administered | Analyte | Population |
|---|---|---|---|---|
2.5 h EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/9585793 |
80 mg single, oral dose: 80 mg route of administration: Oral experiment type: SINGLE co-administered: |
LOVASTATIN ACID plasma | Homo sapiens population: HEALTHY age: ADULT sex: FEMALE / MALE food status: FASTED |
Funbound
| Value | Dose | Co-administered | Analyte | Population |
|---|---|---|---|---|
5% |
40 mg 1 times / day steady-state, oral dose: 40 mg route of administration: Oral experiment type: STEADY-STATE co-administered: |
LOVASTATIN ACID plasma | Homo sapiens population: UNHEALTHY age: ADULT sex: UNKNOWN food status: UNKNOWN |
Doses
| Dose | Population | Adverse events |
|---|---|---|
80 mg 1 times / day multiple, oral Recommended Dose: 80 mg, 1 times / day Route: oral Route: multiple Dose: 80 mg, 1 times / day Sources: |
unhealthy, 50 |
Disc. AE: Aspartate aminotransferase increased, Alanine aminotransferase increased... AEs leading to discontinuation/dose reduction: Aspartate aminotransferase increased (grade 2-4, 1.3%) Sources: Alanine aminotransferase increased (grade 2-4, 1.3%) Gastrointestinal disturbance (0.4%) Rash (0.27%) Myalgia (0.13%) Myopathy (0.27%) Arthralgia (0.13%) Insomnia (0.13%) Weight gain (0.13%) |
10 mg/kg 4 times / day multiple, oral Highest studied dose Dose: 10 mg/kg, 4 times / day Route: oral Route: multiple Dose: 10 mg/kg, 4 times / day Sources: |
unhealthy, 56 |
DLT: Creatine phosphokinase increased, Aspartate aminotransferase increased... Dose limiting toxicities: Creatine phosphokinase increased (grade 4, 33.3%) Sources: Aspartate aminotransferase increased (grade 2-3, 33.3%) Alanine aminotransferase increased (grade 2-3, 33.3%) |
7.5 mg/kg 4 times / day multiple, oral MTD Dose: 7.5 mg/kg, 4 times / day Route: oral Route: multiple Dose: 7.5 mg/kg, 4 times / day Sources: |
unhealthy, 56 |
DLT: Creatine phosphokinase increased, Aspartate aminotransferase increased... Dose limiting toxicities: Creatine phosphokinase increased (grade 4, 28.6%) Sources: Aspartate aminotransferase increased (grade 3, 14.3%) Alanine aminotransferase increased (grade 3, 14.3%) |
AEs
| AE | Significance | Dose | Population |
|---|---|---|---|
| Arthralgia | 0.13% Disc. AE |
80 mg 1 times / day multiple, oral Recommended Dose: 80 mg, 1 times / day Route: oral Route: multiple Dose: 80 mg, 1 times / day Sources: |
unhealthy, 50 |
| Insomnia | 0.13% Disc. AE |
80 mg 1 times / day multiple, oral Recommended Dose: 80 mg, 1 times / day Route: oral Route: multiple Dose: 80 mg, 1 times / day Sources: |
unhealthy, 50 |
| Myalgia | 0.13% Disc. AE |
80 mg 1 times / day multiple, oral Recommended Dose: 80 mg, 1 times / day Route: oral Route: multiple Dose: 80 mg, 1 times / day Sources: |
unhealthy, 50 |
| Weight gain | 0.13% Disc. AE |
80 mg 1 times / day multiple, oral Recommended Dose: 80 mg, 1 times / day Route: oral Route: multiple Dose: 80 mg, 1 times / day Sources: |
unhealthy, 50 |
| Myopathy | 0.27% Disc. AE |
80 mg 1 times / day multiple, oral Recommended Dose: 80 mg, 1 times / day Route: oral Route: multiple Dose: 80 mg, 1 times / day Sources: |
unhealthy, 50 |
| Rash | 0.27% Disc. AE |
80 mg 1 times / day multiple, oral Recommended Dose: 80 mg, 1 times / day Route: oral Route: multiple Dose: 80 mg, 1 times / day Sources: |
unhealthy, 50 |
| Gastrointestinal disturbance | 0.4% Disc. AE |
80 mg 1 times / day multiple, oral Recommended Dose: 80 mg, 1 times / day Route: oral Route: multiple Dose: 80 mg, 1 times / day Sources: |
unhealthy, 50 |
| Alanine aminotransferase increased | grade 2-4, 1.3% Disc. AE |
80 mg 1 times / day multiple, oral Recommended Dose: 80 mg, 1 times / day Route: oral Route: multiple Dose: 80 mg, 1 times / day Sources: |
unhealthy, 50 |
| Aspartate aminotransferase increased | grade 2-4, 1.3% Disc. AE |
80 mg 1 times / day multiple, oral Recommended Dose: 80 mg, 1 times / day Route: oral Route: multiple Dose: 80 mg, 1 times / day Sources: |
unhealthy, 50 |
| Alanine aminotransferase increased | grade 2-3, 33.3% DLT |
10 mg/kg 4 times / day multiple, oral Highest studied dose Dose: 10 mg/kg, 4 times / day Route: oral Route: multiple Dose: 10 mg/kg, 4 times / day Sources: |
unhealthy, 56 |
| Aspartate aminotransferase increased | grade 2-3, 33.3% DLT |
10 mg/kg 4 times / day multiple, oral Highest studied dose Dose: 10 mg/kg, 4 times / day Route: oral Route: multiple Dose: 10 mg/kg, 4 times / day Sources: |
unhealthy, 56 |
| Creatine phosphokinase increased | grade 4, 33.3% DLT |
10 mg/kg 4 times / day multiple, oral Highest studied dose Dose: 10 mg/kg, 4 times / day Route: oral Route: multiple Dose: 10 mg/kg, 4 times / day Sources: |
unhealthy, 56 |
| Alanine aminotransferase increased | grade 3, 14.3% DLT |
7.5 mg/kg 4 times / day multiple, oral MTD Dose: 7.5 mg/kg, 4 times / day Route: oral Route: multiple Dose: 7.5 mg/kg, 4 times / day Sources: |
unhealthy, 56 |
| Aspartate aminotransferase increased | grade 3, 14.3% DLT |
7.5 mg/kg 4 times / day multiple, oral MTD Dose: 7.5 mg/kg, 4 times / day Route: oral Route: multiple Dose: 7.5 mg/kg, 4 times / day Sources: |
unhealthy, 56 |
| Creatine phosphokinase increased | grade 4, 28.6% DLT |
7.5 mg/kg 4 times / day multiple, oral MTD Dose: 7.5 mg/kg, 4 times / day Route: oral Route: multiple Dose: 7.5 mg/kg, 4 times / day Sources: |
unhealthy, 56 |
Overview
| CYP3A4 | CYP2C9 | CYP2D6 | hERG |
|---|---|---|---|
OverviewOther
| Other Inhibitor | Other Substrate | Other Inducer |
|---|---|---|
Drug as perpetrator
| Target | Modality | Activity | Metabolite | Clinical evidence |
|---|---|---|---|---|
| moderate [Ki >50 uM] | ||||
| moderate [Ki >50 uM] | ||||
| moderate [Ki >50 uM] | ||||
| no [IC50 >100 uM] | ||||
| no [IC50 >100 uM] | ||||
| yes [IC50 4 uM] | ||||
Sources: https://pubmed.ncbi.nlm.nih.gov/19429419/ |
yes | |||
Sources: https://pubmed.ncbi.nlm.nih.gov/19429419/ |
yes |
Drug as victim
| Target | Modality | Activity | Metabolite | Clinical evidence |
|---|---|---|---|---|
| no | ||||
| no | ||||
| no | ||||
| no | ||||
| no | ||||
| weak | ||||
| yes [Km 26 uM] | ||||
| yes [Km 88 uM] | yes (co-administration study) Comment: Gemfibrozil increased Lovastatin acid AUC24 and Cmax both by 180%. |
|||
| yes | ||||
| yes | yes (pharmacogenomic study) Comment: AUC24 and Cmax were increased by 184% and 230% in OATP1B1*5/*15 or *15/*15 subjects. Sources: https://pubmed.ncbi.nlm.nih.gov/26020121/ |
PubMed
| Title | Date | PubMed |
|---|---|---|
| The widening role of statins: RAS signal transduction and drug-induced cytotoxicity in human leukemia: a commentary to 'interaction of cytosine arabinoside and lovastatin in human leukemia cells'. | 2001-08 |
|
| Interaction of cytosine arabinoside and lovastatin in human leukemia cells. | 2001-08 |
|
| Lovastatin controls signal transduction in vascular smooth muscle cells by modulating phosphorylation levels of mevalonate-independent pathways. | 2001-06-14 |
|
| Use of statins and the subsequent development of deep vein thrombosis. | 2001-06-11 |
|
| Compactin enhances osteogenesis in murine embryonic stem cells. | 2001-06-08 |
|
| Low-dose combination therapy with colesevelam hydrochloride and lovastatin effectively decreases low-density lipoprotein cholesterol in patients with primary hypercholesterolemia. | 2001-06 |
|
| Effect of lovastatin, an HMG CoA reductase inhibitor, on acute renal allograft rejection. | 2001-06 |
|
| Statins selectively inhibit leukocyte function antigen-1 by binding to a novel regulatory integrin site. | 2001-06 |
|
| Liver regeneration after hepatectomy. | 2001-05-31 |
|
| Regulation of sterol regulatory element-binding proteins in hamster intestine by changes in cholesterol flux. | 2001-05-18 |
|
| RhoA is activated during respiratory syncytial virus infection. | 2001-05-10 |
|
| Air Force/Texas Coronary Atherosclerosis Prevention Study (AFCAPS/TEXCAPS): additional perspectives on tolerability of long-term treatment with lovastatin. | 2001-05-01 |
|
| The National Service Framework on coronary heart disease: is it sufficiently evidence-based? | 2001-05 |
|
| Statin induced myopathy does not show up in MIBI scintigraphy. | 2001-05 |
|
| Revised indications for statin therapies. | 2001-05 |
|
| What do the statin trials tell us? | 2001-05 |
|
| Statins--similarities and differences. | 2001-05 |
|
| Should all patients with cardiovascular disease receive statin therapy? | 2001-05 |
|
| Long-term administration of the HMG-CoA reductase inhibitor lovastatin in two patients with cholesteryl ester storage disease. | 2001-05 |
|
| Plasma concentrations of active lovastatin acid are markedly increased by gemfibrozil but not by bezafibrate. | 2001-05 |
|
| The combined effects of novel tocotrienols and lovastatin on lipid metabolism in chickens. | 2001-05 |
|
| Can modulation of endothelial nitric oxide synthase explain the vasculoprotective actions of statins? | 2001-05 |
|
| Cholesterol ester accumulation: an immediate consequence of acute in vivo ischemic renal injury. | 2001-05 |
|
| Deterioration of the protein kinase C-K(ATP) channel pathway in regulation of coronary flow in hypercholesterolaemic rabbits. | 2001-04-27 |
|
| Analysis of 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors using liquid chromatography-electrospray mass spectrometry. | 2001-04-25 |
|
| Differential effects of lovastatin treatment on brain cholesterol levels in normal and apoE-deficient mice. | 2001-04-17 |
|
| Statins are magic when you gotta have heart. | 2001-04-16 |
|
| Assessing the results: phase 1 hyperlipidemia outcomes in 27 health plans. | 2001-04-16 |
|
| New OTC drugs and devices 2000: a selective review. | 2001-04-12 |
|
| Rho GTPases are involved in the regulation of NF-kappaB by genotoxic stress. | 2001-04-01 |
|
| An analysis of nine proprietary Chinese red yeast rice dietary supplements: implications of variability in chemical profile and contents. | 2001-04 |
|
| The effects of the statins lovastatin and cerivastatin on signalling by the prostanoid IP-receptor. | 2001-04 |
|
| Mevastatin, an HMG-CoA reductase inhibitor, reduces stroke damage and upregulates endothelial nitric oxide synthase in mice. | 2001-04 |
|
| A new simvastatin (mevinolin)-resistance marker from Haloarcula hispanica and a new Haloferax volcanii strain cured of plasmid pHV2. | 2001-04 |
|
| Antiviral activity of lovastatin against respiratory syncytial virus in vivo and in vitro. | 2001-04 |
|
| Comparative study of HMG-CoA reductase inhibitors on fibrinogen. | 2001-04 |
|
| Cell cycle-related changes in regulatory volume decrease and volume-sensitive chloride conductance in mouse fibroblasts. | 2001-04 |
|
| High apolipoprotein B with low high-density lipoprotein cholesterol and normal plasma triglycerides and cholesterol. | 2001-03-15 |
|
| Inhibition of human tumor cell growth in vivo by an orally bioavailable inhibitor of human farnesyltransferase, BIM-46228. | 2001-03-01 |
|
| Recent advances in the biosynthetic studies of lovastatin. | 2001-03 |
|
| [Statins do not prevent restenosis after coronary angioplasty: where to go from here?]. | 2001-03 |
|
| [AFCAPS/TexCAPS [The Air Force/Texas Coronary Atherosclerosis Prevention Study]]. | 2001-03 |
|
| Lovastatin blocks basic fibroblast growth factor-induced mitogen-activated protein kinase signaling in coronary smooth muscle cells via phosphatase inhibition. | 2001-03 |
|
| [Effect of cholesterol deficiency on the membrane fluidity of Jurkat T lymphocytes]. | 2001-03 |
|
| Is a statin a statin? | 2001-03 |
|
| Lovastatin and phenylacetate induce apoptosis, but not differentiation, in human malignant glioma cells. | 2001-03 |
|
| HMG-CoA reductase inhibitors and P-glycoprotein modulation. | 2001-03 |
|
| Phase II study of high-dose lovastatin in patients with advanced gastric adenocarcinoma. | 2001 |
|
| Cost effectiveness of HMG-CoA reductase inhibition in Canada. | 2001 |
|
| The cyclin dependent kinase inhibitor p27 and its prognostic role in breast cancer. | 2001 |
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
In Vitro Use Guide
Sources: https://www.ncbi.nlm.nih.gov/pubmed/18034278
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.
| Substance Class |
Chemical
Created
by
admin
on
Edited
Mon Mar 31 17:45:51 GMT 2025
by
admin
on
Mon Mar 31 17:45:51 GMT 2025
|
| Record UNII |
9LHU78OQFD
|
| Record Status |
Validated (UNII)
|
| Record Version |
|
-
Download
| Name | Type | Language | ||
|---|---|---|---|---|
|
Official Name | English | ||
|
Preferred Name | English | ||
|
Common Name | English | ||
|
Common Name | English | ||
|
Common Name | English | ||
|
Brand Name | English | ||
|
Brand Name | English | ||
|
Common Name | English | ||
|
Common Name | English | ||
|
Brand Name | English | ||
|
Common Name | English | ||
|
Common Name | English | ||
|
Code | English | ||
|
Common Name | English | ||
|
Common Name | English | ||
|
Common Name | English | ||
|
Code | English | ||
|
Common Name | English | ||
|
Common Name | English | ||
|
Common Name | English | ||
|
Common Name | English | ||
|
Common Name | English | ||
|
Common Name | English | ||
|
Common Name | English | ||
|
Common Name | English | ||
|
Brand Name | English | ||
|
Common Name | English | ||
|
Code | English | ||
|
Brand Name | English | ||
|
Common Name | English |
| Classification Tree | Code System | Code | ||
|---|---|---|---|---|
|
WHO-ATC |
C10AA02
Created by
admin on Mon Mar 31 17:45:51 GMT 2025 , Edited by admin on Mon Mar 31 17:45:51 GMT 2025
|
||
|
LIVERTOX |
NBK548670
Created by
admin on Mon Mar 31 17:45:51 GMT 2025 , Edited by admin on Mon Mar 31 17:45:51 GMT 2025
|
||
|
WHO-ATC |
C10BA01
Created by
admin on Mon Mar 31 17:45:51 GMT 2025 , Edited by admin on Mon Mar 31 17:45:51 GMT 2025
|
||
|
NCI_THESAURUS |
C54679
Created by
admin on Mon Mar 31 17:45:51 GMT 2025 , Edited by admin on Mon Mar 31 17:45:51 GMT 2025
|
||
|
WHO-VATC |
QC10BA01
Created by
admin on Mon Mar 31 17:45:51 GMT 2025 , Edited by admin on Mon Mar 31 17:45:51 GMT 2025
|
||
|
WHO-VATC |
QC10AA02
Created by
admin on Mon Mar 31 17:45:51 GMT 2025 , Edited by admin on Mon Mar 31 17:45:51 GMT 2025
|
||
|
NDF-RT |
N0000000121
Created by
admin on Mon Mar 31 17:45:51 GMT 2025 , Edited by admin on Mon Mar 31 17:45:51 GMT 2025
|
||
|
NCI_THESAURUS |
C1655
Created by
admin on Mon Mar 31 17:45:51 GMT 2025 , Edited by admin on Mon Mar 31 17:45:51 GMT 2025
|
||
|
NDF-RT |
N0000175589
Created by
admin on Mon Mar 31 17:45:51 GMT 2025 , Edited by admin on Mon Mar 31 17:45:51 GMT 2025
|
| Code System | Code | Type | Description | ||
|---|---|---|---|---|---|
|
Y-5
Created by
admin on Mon Mar 31 17:45:51 GMT 2025 , Edited by admin on Mon Mar 31 17:45:51 GMT 2025
|
PRIMARY | |||
|
6534
Created by
admin on Mon Mar 31 17:45:51 GMT 2025 , Edited by admin on Mon Mar 31 17:45:51 GMT 2025
|
PRIMARY | |||
|
9LHU78OQFD
Created by
admin on Mon Mar 31 17:45:51 GMT 2025 , Edited by admin on Mon Mar 31 17:45:51 GMT 2025
|
PRIMARY | |||
|
6074
Created by
admin on Mon Mar 31 17:45:51 GMT 2025 , Edited by admin on Mon Mar 31 17:45:51 GMT 2025
|
PRIMARY | |||
|
m6914
Created by
admin on Mon Mar 31 17:45:51 GMT 2025 , Edited by admin on Mon Mar 31 17:45:51 GMT 2025
|
PRIMARY | Merck Index | ||
|
CHEMBL503
Created by
admin on Mon Mar 31 17:45:51 GMT 2025 , Edited by admin on Mon Mar 31 17:45:51 GMT 2025
|
PRIMARY | |||
|
1370600
Created by
admin on Mon Mar 31 17:45:51 GMT 2025 , Edited by admin on Mon Mar 31 17:45:51 GMT 2025
|
PRIMARY | |||
|
100000092165
Created by
admin on Mon Mar 31 17:45:51 GMT 2025 , Edited by admin on Mon Mar 31 17:45:51 GMT 2025
|
PRIMARY | |||
|
DTXSID5020784
Created by
admin on Mon Mar 31 17:45:51 GMT 2025 , Edited by admin on Mon Mar 31 17:45:51 GMT 2025
|
PRIMARY | |||
|
Lovastatin
Created by
admin on Mon Mar 31 17:45:51 GMT 2025 , Edited by admin on Mon Mar 31 17:45:51 GMT 2025
|
PRIMARY | |||
|
D008148
Created by
admin on Mon Mar 31 17:45:51 GMT 2025 , Edited by admin on Mon Mar 31 17:45:51 GMT 2025
|
PRIMARY | |||
|
DB00227
Created by
admin on Mon Mar 31 17:45:51 GMT 2025 , Edited by admin on Mon Mar 31 17:45:51 GMT 2025
|
PRIMARY | |||
|
6472
Created by
admin on Mon Mar 31 17:45:51 GMT 2025 , Edited by admin on Mon Mar 31 17:45:51 GMT 2025
|
PRIMARY | RxNorm | ||
|
C620
Created by
admin on Mon Mar 31 17:45:51 GMT 2025 , Edited by admin on Mon Mar 31 17:45:51 GMT 2025
|
PRIMARY | |||
|
53232
Created by
admin on Mon Mar 31 17:45:51 GMT 2025 , Edited by admin on Mon Mar 31 17:45:51 GMT 2025
|
PRIMARY | |||
|
40303
Created by
admin on Mon Mar 31 17:45:51 GMT 2025 , Edited by admin on Mon Mar 31 17:45:51 GMT 2025
|
PRIMARY | |||
|
9LHU78OQFD
Created by
admin on Mon Mar 31 17:45:51 GMT 2025 , Edited by admin on Mon Mar 31 17:45:51 GMT 2025
|
PRIMARY | |||
|
758662
Created by
admin on Mon Mar 31 17:45:51 GMT 2025 , Edited by admin on Mon Mar 31 17:45:51 GMT 2025
|
PRIMARY | |||
|
SUB08604MIG
Created by
admin on Mon Mar 31 17:45:51 GMT 2025 , Edited by admin on Mon Mar 31 17:45:51 GMT 2025
|
PRIMARY | |||
|
1612
Created by
admin on Mon Mar 31 17:45:51 GMT 2025 , Edited by admin on Mon Mar 31 17:45:51 GMT 2025
|
PRIMARY | |||
|
75330-75-5
Created by
admin on Mon Mar 31 17:45:51 GMT 2025 , Edited by admin on Mon Mar 31 17:45:51 GMT 2025
|
PRIMARY | |||
|
2739
Created by
admin on Mon Mar 31 17:45:51 GMT 2025 , Edited by admin on Mon Mar 31 17:45:51 GMT 2025
|
PRIMARY | |||
|
LOVASTATIN
Created by
admin on Mon Mar 31 17:45:51 GMT 2025 , Edited by admin on Mon Mar 31 17:45:51 GMT 2025
|
PRIMARY |
| Related Record | Type | Details | ||
|---|---|---|---|---|
|
TRANSPORTER -> INHIBITOR | |||
|
METABOLIC ENZYME -> SUBSTRATE | |||
|
|
PARENT -> ACTIVE CONSTITUENT ALWAYS PRESENT |
PRESENT FOR CHOLESTEROL CONTROL MAY BE ABSENT IN SOME PRODUCTS
|
||
|
|
OFF TARGET->ACTIVATOR |
Kd
|
||
|
METABOLIC ENZYME -> SUBSTRATE | |||
|
TARGET -> INHIBITOR |
IC50
|
||
|
BINDER->LIGAND |
BINDING
|
| Related Record | Type | Details | ||
|---|---|---|---|---|
|
METABOLITE -> PARENT |
CYP3A
PLASMA
|
||
|
METABOLITE ACTIVE -> PRODRUG |
|
||
|
METABOLITE -> PARENT |
In Vitro metabolite; CYP3A
IN-VITRO
|
| Related Record | Type | Details | ||
|---|---|---|---|---|
|
IMPURITY -> PARENT |
correction factor: for the calculation of content, multiply the peak area of impurity E by 1.6
CHROMATOGRAPHIC PURITY (HPLC/UV)
EP
|
||
|
IMPURITY -> PARENT |
CHROMATOGRAPHIC PURITY (HPLC/UV)
EP
|
||
|
IMPURITY -> PARENT |
CHROMATOGRAPHIC PURITY (HPLC/UV)
EP
|
||
|
IMPURITY -> PARENT |
CHROMATOGRAPHIC PURITY (HPLC/UV)
EP
|
||
|
IMPURITY -> PARENT |
CHROMATOGRAPHIC PURITY (HPLC/UV)
EP
|
||
|
PARENT -> IMPURITY | |||
|
IMPURITY -> PARENT |
CHROMATOGRAPHIC PURITY (HPLC/UV)
EP
|
| Related Record | Type | Details | ||
|---|---|---|---|---|
|
ACTIVE MOIETY |
|
| Name | Property Type | Amount | Referenced Substance | Defining | Parameters | References |
|---|---|---|---|---|---|---|
| Tmax | PHARMACOKINETIC |
|
|
|||
| Biological Half-life | PHARMACOKINETIC |
|
|
|||
| MAXIMUM TOLERATED DOSE | TOXICITY |
|
|
|||
| ORAL BIOAVAILABILITY | PHARMACOKINETIC |
|
|
|||