Details
Stereochemistry | ABSOLUTE |
Molecular Formula | C22H28FN3O6S |
Molecular Weight | 481.538 |
Optical Activity | ( + ) |
Defined Stereocenters | 2 / 2 |
E/Z Centers | 1 |
Charge | 0 |
SHOW SMILES / InChI
SMILES
CC(C)C1=C(\C=C\[C@@H](O)C[C@@H](O)CC(O)=O)C(=NC(=N1)N(C)S(C)(=O)=O)C2=CC=C(F)C=C2
InChI
InChIKey=BPRHUIZQVSMCRT-VEUZHWNKSA-N
InChI=1S/C22H28FN3O6S/c1-13(2)20-18(10-9-16(27)11-17(28)12-19(29)30)21(14-5-7-15(23)8-6-14)25-22(24-20)26(3)33(4,31)32/h5-10,13,16-17,27-28H,11-12H2,1-4H3,(H,29,30)/b10-9+/t16-,17-/m1/s1
Originator
Approval Year
Targets
Primary Target | Pharmacology | Condition | Potency |
---|---|---|---|
Target ID: CHEMBL402 |
Conditions
Condition | Modality | Targets | Highest Phase | Product |
---|---|---|---|---|
Primary | CRESTOR Approved UseCRESTOR is an HMG Co-A reductase inhibitor indicated for: ••patients with primary hyperlipidemia and mixed dyslipidemia as an adjunct to diet to reduce elevated total-C, LDL-C, ApoB, nonHDL-C, and TG levels and to increase HDL-C (1.1) ••patients with hypertriglyceridemia as an adjunct to diet (1.2) ••patients with primary dysbetalipoproteinemia (Type III hyperlipoproteinemia) as an adjunct to diet (1.3) ••patients with homozygous familial hypercholesterolemia (HoFH) to reduce LDL-C, total-C, and ApoB (1.4) ••slowing the progression of atherosclerosis as part of a treatment strategy to lower total-C and LDL-C as an adjunct to diet (1.5) ••pediatric patients 10 to 17 years of age with heterozygous familial hypercholesterolemia (HeFH) to reduce elevated total-C, LDL-C and ApoB after failing an adequate trial of diet therapy (1.1) ••risk reduction of MI, stroke, and arterial revascularization procedures in patients without clinically evident CHD, but with multiple risk factors (1.6) Limitations of use (1.7): ••CRESTOR has not been studied in Fredrickson Type I and V dyslipidemias. 1.1 Hyperlipidemia and Mixed Dyslipidemia CRESTOR is indicated as adjunctive therapy to diet to reduce elevated Total-C, LDL-C, ApoB, nonHDL-C, and triglycerides and to increase HDL-C in adult patients with primary hyperlipidemia or mixed dyslipidemia. Lipid-altering agents should be used in addition to a diet restricted in saturated fat and cholesterol when response to diet and nonpharmacological interventions alone has been inadequate. Pediatric Patients 10 to 17 years of age with Heterozygous Familial Hypercholesterolemia (HeFH) Adjunct to diet to reduce Total-C, LDL-C and ApoB levels in adolescent boys and girls, who are at least one year post-menarche, 10-17 years of age with heterozygous familial hypercholesterolemia if after an adequate trial of diet therapy the following findings are present: LDL-C > 190 mg/dL or > 160 mg/dL and there is a positive family history of premature cardiovascular disease (CVD) or two or more other CVD risk factors. 1.2 Hypertriglyceridemia CRESTOR is indicated as adjunctive therapy to diet for the treatment of adult patients with hypertriglyceridemia. 1.3 Primary Dysbetalipoproteinemia (Type III Hyperlipoproteinemia) CRESTOR is indicated as an adjunct to diet for the treatment of patients with primary dysbetalipoproteinemia (Type III Hyperlipoproteinemia). 1.4 Homozygous Familial Hypercholesterolemia CRESTOR is indicated as adjunctive therapy to other lipid-lowering treatments (e.g., LDL apheresis) or alone if such treatments are unavailable to reduce LDL-C, Total-C, and ApoB in adult patients with homozygous familial hypercholesterolemia. 1.5 Slowing of the Progression of Atherosclerosis CRESTOR is indicated as adjunctive therapy to diet to slow the progression of atherosclerosis in adult patients as part of a treatment strategy to lower Total-C and LDL-C to target levels. 1.6 Primary Prevention of Cardiovascular Disease In individuals without clinically evident coronary heart disease but with an increased risk of cardiovascular disease based on age ≥ 50 years old in men and ≥ 60 years old in women, hsCRP ≥ 2 mg/L, and the presence of at least one additional cardiovascular disease risk factor such as hypertension, low HDL-C, smoking, or a family history of premature coronary heart disease, CRESTOR is indicated to: ••reduce the risk of stroke ••reduce the risk of myocardial infarction ••reduce the risk of arterial revascularization procedures 1.7 Limitations of Use CRESTOR has not been studied in Fredrickson Type I and V dyslipidemias. Launch Date2003 |
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Primary | CRESTOR Approved UseCRESTOR is an HMG Co-A reductase inhibitor indicated for: ••patients with primary hyperlipidemia and mixed dyslipidemia as an adjunct to diet to reduce elevated total-C, LDL-C, ApoB, nonHDL-C, and TG levels and to increase HDL-C (1.1) ••patients with hypertriglyceridemia as an adjunct to diet (1.2) ••patients with primary dysbetalipoproteinemia (Type III hyperlipoproteinemia) as an adjunct to diet (1.3) ••patients with homozygous familial hypercholesterolemia (HoFH) to reduce LDL-C, total-C, and ApoB (1.4) ••slowing the progression of atherosclerosis as part of a treatment strategy to lower total-C and LDL-C as an adjunct to diet (1.5) ••pediatric patients 10 to 17 years of age with heterozygous familial hypercholesterolemia (HeFH) to reduce elevated total-C, LDL-C and ApoB after failing an adequate trial of diet therapy (1.1) ••risk reduction of MI, stroke, and arterial revascularization procedures in patients without clinically evident CHD, but with multiple risk factors (1.6) Limitations of use (1.7): ••CRESTOR has not been studied in Fredrickson Type I and V dyslipidemias. 1.1 Hyperlipidemia and Mixed Dyslipidemia CRESTOR is indicated as adjunctive therapy to diet to reduce elevated Total-C, LDL-C, ApoB, nonHDL-C, and triglycerides and to increase HDL-C in adult patients with primary hyperlipidemia or mixed dyslipidemia. Lipid-altering agents should be used in addition to a diet restricted in saturated fat and cholesterol when response to diet and nonpharmacological interventions alone has been inadequate. Pediatric Patients 10 to 17 years of age with Heterozygous Familial Hypercholesterolemia (HeFH) Adjunct to diet to reduce Total-C, LDL-C and ApoB levels in adolescent boys and girls, who are at least one year post-menarche, 10-17 years of age with heterozygous familial hypercholesterolemia if after an adequate trial of diet therapy the following findings are present: LDL-C > 190 mg/dL or > 160 mg/dL and there is a positive family history of premature cardiovascular disease (CVD) or two or more other CVD risk factors. 1.2 Hypertriglyceridemia CRESTOR is indicated as adjunctive therapy to diet for the treatment of adult patients with hypertriglyceridemia. 1.3 Primary Dysbetalipoproteinemia (Type III Hyperlipoproteinemia) CRESTOR is indicated as an adjunct to diet for the treatment of patients with primary dysbetalipoproteinemia (Type III Hyperlipoproteinemia). 1.4 Homozygous Familial Hypercholesterolemia CRESTOR is indicated as adjunctive therapy to other lipid-lowering treatments (e.g., LDL apheresis) or alone if such treatments are unavailable to reduce LDL-C, Total-C, and ApoB in adult patients with homozygous familial hypercholesterolemia. 1.5 Slowing of the Progression of Atherosclerosis CRESTOR is indicated as adjunctive therapy to diet to slow the progression of atherosclerosis in adult patients as part of a treatment strategy to lower Total-C and LDL-C to target levels. 1.6 Primary Prevention of Cardiovascular Disease In individuals without clinically evident coronary heart disease but with an increased risk of cardiovascular disease based on age ≥ 50 years old in men and ≥ 60 years old in women, hsCRP ≥ 2 mg/L, and the presence of at least one additional cardiovascular disease risk factor such as hypertension, low HDL-C, smoking, or a family history of premature coronary heart disease, CRESTOR is indicated to: ••reduce the risk of stroke ••reduce the risk of myocardial infarction ••reduce the risk of arterial revascularization procedures 1.7 Limitations of Use CRESTOR has not been studied in Fredrickson Type I and V dyslipidemias. Launch Date2003 |
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Primary | CRESTOR Approved UseCRESTOR is an HMG Co-A reductase inhibitor indicated for: ••patients with primary hyperlipidemia and mixed dyslipidemia as an adjunct to diet to reduce elevated total-C, LDL-C, ApoB, nonHDL-C, and TG levels and to increase HDL-C (1.1) ••patients with hypertriglyceridemia as an adjunct to diet (1.2) ••patients with primary dysbetalipoproteinemia (Type III hyperlipoproteinemia) as an adjunct to diet (1.3) ••patients with homozygous familial hypercholesterolemia (HoFH) to reduce LDL-C, total-C, and ApoB (1.4) ••slowing the progression of atherosclerosis as part of a treatment strategy to lower total-C and LDL-C as an adjunct to diet (1.5) ••pediatric patients 10 to 17 years of age with heterozygous familial hypercholesterolemia (HeFH) to reduce elevated total-C, LDL-C and ApoB after failing an adequate trial of diet therapy (1.1) ••risk reduction of MI, stroke, and arterial revascularization procedures in patients without clinically evident CHD, but with multiple risk factors (1.6) Limitations of use (1.7): ••CRESTOR has not been studied in Fredrickson Type I and V dyslipidemias. 1.1 Hyperlipidemia and Mixed Dyslipidemia CRESTOR is indicated as adjunctive therapy to diet to reduce elevated Total-C, LDL-C, ApoB, nonHDL-C, and triglycerides and to increase HDL-C in adult patients with primary hyperlipidemia or mixed dyslipidemia. Lipid-altering agents should be used in addition to a diet restricted in saturated fat and cholesterol when response to diet and nonpharmacological interventions alone has been inadequate. Pediatric Patients 10 to 17 years of age with Heterozygous Familial Hypercholesterolemia (HeFH) Adjunct to diet to reduce Total-C, LDL-C and ApoB levels in adolescent boys and girls, who are at least one year post-menarche, 10-17 years of age with heterozygous familial hypercholesterolemia if after an adequate trial of diet therapy the following findings are present: LDL-C > 190 mg/dL or > 160 mg/dL and there is a positive family history of premature cardiovascular disease (CVD) or two or more other CVD risk factors. 1.2 Hypertriglyceridemia CRESTOR is indicated as adjunctive therapy to diet for the treatment of adult patients with hypertriglyceridemia. 1.3 Primary Dysbetalipoproteinemia (Type III Hyperlipoproteinemia) CRESTOR is indicated as an adjunct to diet for the treatment of patients with primary dysbetalipoproteinemia (Type III Hyperlipoproteinemia). 1.4 Homozygous Familial Hypercholesterolemia CRESTOR is indicated as adjunctive therapy to other lipid-lowering treatments (e.g., LDL apheresis) or alone if such treatments are unavailable to reduce LDL-C, Total-C, and ApoB in adult patients with homozygous familial hypercholesterolemia. 1.5 Slowing of the Progression of Atherosclerosis CRESTOR is indicated as adjunctive therapy to diet to slow the progression of atherosclerosis in adult patients as part of a treatment strategy to lower Total-C and LDL-C to target levels. 1.6 Primary Prevention of Cardiovascular Disease In individuals without clinically evident coronary heart disease but with an increased risk of cardiovascular disease based on age ≥ 50 years old in men and ≥ 60 years old in women, hsCRP ≥ 2 mg/L, and the presence of at least one additional cardiovascular disease risk factor such as hypertension, low HDL-C, smoking, or a family history of premature coronary heart disease, CRESTOR is indicated to: ••reduce the risk of stroke ••reduce the risk of myocardial infarction ••reduce the risk of arterial revascularization procedures 1.7 Limitations of Use CRESTOR has not been studied in Fredrickson Type I and V dyslipidemias. Launch Date2003 |
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Primary | CRESTOR Approved UseCRESTOR is an HMG Co-A reductase inhibitor indicated for: ••patients with primary hyperlipidemia and mixed dyslipidemia as an adjunct to diet to reduce elevated total-C, LDL-C, ApoB, nonHDL-C, and TG levels and to increase HDL-C (1.1) ••patients with hypertriglyceridemia as an adjunct to diet (1.2) ••patients with primary dysbetalipoproteinemia (Type III hyperlipoproteinemia) as an adjunct to diet (1.3) ••patients with homozygous familial hypercholesterolemia (HoFH) to reduce LDL-C, total-C, and ApoB (1.4) ••slowing the progression of atherosclerosis as part of a treatment strategy to lower total-C and LDL-C as an adjunct to diet (1.5) ••pediatric patients 10 to 17 years of age with heterozygous familial hypercholesterolemia (HeFH) to reduce elevated total-C, LDL-C and ApoB after failing an adequate trial of diet therapy (1.1) ••risk reduction of MI, stroke, and arterial revascularization procedures in patients without clinically evident CHD, but with multiple risk factors (1.6) Limitations of use (1.7): ••CRESTOR has not been studied in Fredrickson Type I and V dyslipidemias. 1.1 Hyperlipidemia and Mixed Dyslipidemia CRESTOR is indicated as adjunctive therapy to diet to reduce elevated Total-C, LDL-C, ApoB, nonHDL-C, and triglycerides and to increase HDL-C in adult patients with primary hyperlipidemia or mixed dyslipidemia. Lipid-altering agents should be used in addition to a diet restricted in saturated fat and cholesterol when response to diet and nonpharmacological interventions alone has been inadequate. Pediatric Patients 10 to 17 years of age with Heterozygous Familial Hypercholesterolemia (HeFH) Adjunct to diet to reduce Total-C, LDL-C and ApoB levels in adolescent boys and girls, who are at least one year post-menarche, 10-17 years of age with heterozygous familial hypercholesterolemia if after an adequate trial of diet therapy the following findings are present: LDL-C > 190 mg/dL or > 160 mg/dL and there is a positive family history of premature cardiovascular disease (CVD) or two or more other CVD risk factors. 1.2 Hypertriglyceridemia CRESTOR is indicated as adjunctive therapy to diet for the treatment of adult patients with hypertriglyceridemia. 1.3 Primary Dysbetalipoproteinemia (Type III Hyperlipoproteinemia) CRESTOR is indicated as an adjunct to diet for the treatment of patients with primary dysbetalipoproteinemia (Type III Hyperlipoproteinemia). 1.4 Homozygous Familial Hypercholesterolemia CRESTOR is indicated as adjunctive therapy to other lipid-lowering treatments (e.g., LDL apheresis) or alone if such treatments are unavailable to reduce LDL-C, Total-C, and ApoB in adult patients with homozygous familial hypercholesterolemia. 1.5 Slowing of the Progression of Atherosclerosis CRESTOR is indicated as adjunctive therapy to diet to slow the progression of atherosclerosis in adult patients as part of a treatment strategy to lower Total-C and LDL-C to target levels. 1.6 Primary Prevention of Cardiovascular Disease In individuals without clinically evident coronary heart disease but with an increased risk of cardiovascular disease based on age ≥ 50 years old in men and ≥ 60 years old in women, hsCRP ≥ 2 mg/L, and the presence of at least one additional cardiovascular disease risk factor such as hypertension, low HDL-C, smoking, or a family history of premature coronary heart disease, CRESTOR is indicated to: ••reduce the risk of stroke ••reduce the risk of myocardial infarction ••reduce the risk of arterial revascularization procedures 1.7 Limitations of Use CRESTOR has not been studied in Fredrickson Type I and V dyslipidemias. Launch Date2003 |
|||
Primary | CRESTOR Approved UseCRESTOR is an HMG Co-A reductase inhibitor indicated for: ••patients with primary hyperlipidemia and mixed dyslipidemia as an adjunct to diet to reduce elevated total-C, LDL-C, ApoB, nonHDL-C, and TG levels and to increase HDL-C (1.1) ••patients with hypertriglyceridemia as an adjunct to diet (1.2) ••patients with primary dysbetalipoproteinemia (Type III hyperlipoproteinemia) as an adjunct to diet (1.3) ••patients with homozygous familial hypercholesterolemia (HoFH) to reduce LDL-C, total-C, and ApoB (1.4) ••slowing the progression of atherosclerosis as part of a treatment strategy to lower total-C and LDL-C as an adjunct to diet (1.5) ••pediatric patients 10 to 17 years of age with heterozygous familial hypercholesterolemia (HeFH) to reduce elevated total-C, LDL-C and ApoB after failing an adequate trial of diet therapy (1.1) ••risk reduction of MI, stroke, and arterial revascularization procedures in patients without clinically evident CHD, but with multiple risk factors (1.6) Limitations of use (1.7): ••CRESTOR has not been studied in Fredrickson Type I and V dyslipidemias. 1.1 Hyperlipidemia and Mixed Dyslipidemia CRESTOR is indicated as adjunctive therapy to diet to reduce elevated Total-C, LDL-C, ApoB, nonHDL-C, and triglycerides and to increase HDL-C in adult patients with primary hyperlipidemia or mixed dyslipidemia. Lipid-altering agents should be used in addition to a diet restricted in saturated fat and cholesterol when response to diet and nonpharmacological interventions alone has been inadequate. Pediatric Patients 10 to 17 years of age with Heterozygous Familial Hypercholesterolemia (HeFH) Adjunct to diet to reduce Total-C, LDL-C and ApoB levels in adolescent boys and girls, who are at least one year post-menarche, 10-17 years of age with heterozygous familial hypercholesterolemia if after an adequate trial of diet therapy the following findings are present: LDL-C > 190 mg/dL or > 160 mg/dL and there is a positive family history of premature cardiovascular disease (CVD) or two or more other CVD risk factors. 1.2 Hypertriglyceridemia CRESTOR is indicated as adjunctive therapy to diet for the treatment of adult patients with hypertriglyceridemia. 1.3 Primary Dysbetalipoproteinemia (Type III Hyperlipoproteinemia) CRESTOR is indicated as an adjunct to diet for the treatment of patients with primary dysbetalipoproteinemia (Type III Hyperlipoproteinemia). 1.4 Homozygous Familial Hypercholesterolemia CRESTOR is indicated as adjunctive therapy to other lipid-lowering treatments (e.g., LDL apheresis) or alone if such treatments are unavailable to reduce LDL-C, Total-C, and ApoB in adult patients with homozygous familial hypercholesterolemia. 1.5 Slowing of the Progression of Atherosclerosis CRESTOR is indicated as adjunctive therapy to diet to slow the progression of atherosclerosis in adult patients as part of a treatment strategy to lower Total-C and LDL-C to target levels. 1.6 Primary Prevention of Cardiovascular Disease In individuals without clinically evident coronary heart disease but with an increased risk of cardiovascular disease based on age ≥ 50 years old in men and ≥ 60 years old in women, hsCRP ≥ 2 mg/L, and the presence of at least one additional cardiovascular disease risk factor such as hypertension, low HDL-C, smoking, or a family history of premature coronary heart disease, CRESTOR is indicated to: ••reduce the risk of stroke ••reduce the risk of myocardial infarction ••reduce the risk of arterial revascularization procedures 1.7 Limitations of Use CRESTOR has not been studied in Fredrickson Type I and V dyslipidemias. Launch Date2003 |
Cmax
Value | Dose | Co-administered | Analyte | Population |
---|---|---|---|---|
10.22 ng/mL EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/18042475 |
5 mg single, oral dose: 5 mg route of administration: Oral experiment type: SINGLE co-administered: |
ROSUVASTATIN plasma | Homo sapiens population: HEALTHY age: ADULT sex: FEMALE / MALE food status: FASTED |
|
25.86 ng/mL EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/18042475 |
10 mg single, oral dose: 10 mg route of administration: Oral experiment type: SINGLE co-administered: |
ROSUVASTATIN plasma | Homo sapiens population: HEALTHY age: ADULT sex: FEMALE / MALE food status: FASTED |
|
44.99 ng/mL EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/18042475 |
20 mg single, oral dose: 20 mg route of administration: Oral experiment type: SINGLE co-administered: |
ROSUVASTATIN plasma | Homo sapiens population: HEALTHY age: ADULT sex: FEMALE / MALE food status: FASTED |
AUC
Value | Dose | Co-administered | Analyte | Population |
---|---|---|---|---|
75.93 ng × h/mL EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/18042475 |
5 mg single, oral dose: 5 mg route of administration: Oral experiment type: SINGLE co-administered: |
ROSUVASTATIN plasma | Homo sapiens population: HEALTHY age: ADULT sex: FEMALE / MALE food status: FASTED |
|
216.77 ng × h/mL EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/18042475 |
10 mg single, oral dose: 10 mg route of administration: Oral experiment type: SINGLE co-administered: |
ROSUVASTATIN plasma | Homo sapiens population: HEALTHY age: ADULT sex: FEMALE / MALE food status: FASTED |
|
311.35 ng × h/mL EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/18042475 |
20 mg single, oral dose: 20 mg route of administration: Oral experiment type: SINGLE co-administered: |
ROSUVASTATIN plasma | Homo sapiens population: HEALTHY age: ADULT sex: FEMALE / MALE food status: FASTED |
T1/2
Value | Dose | Co-administered | Analyte | Population |
---|---|---|---|---|
13.01 h EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/18042475 |
5 mg single, oral dose: 5 mg route of administration: Oral experiment type: SINGLE co-administered: |
ROSUVASTATIN plasma | Homo sapiens population: HEALTHY age: ADULT sex: FEMALE / MALE food status: FASTED |
|
13.33 h EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/18042475 |
10 mg single, oral dose: 10 mg route of administration: Oral experiment type: SINGLE co-administered: |
ROSUVASTATIN plasma | Homo sapiens population: HEALTHY age: ADULT sex: FEMALE / MALE food status: FASTED |
|
15.4 h EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/18042475 |
20 mg single, oral dose: 20 mg route of administration: Oral experiment type: SINGLE co-administered: |
ROSUVASTATIN plasma | Homo sapiens population: HEALTHY age: ADULT sex: FEMALE / MALE food status: FASTED |
Funbound
Value | Dose | Co-administered | Analyte | Population |
---|---|---|---|---|
12% |
ROSUVASTATIN plasma | Homo sapiens population: UNKNOWN age: UNKNOWN sex: UNKNOWN food status: UNKNOWN |
Overview
CYP3A4 | CYP2C9 | CYP2D6 | hERG |
---|---|---|---|
OverviewOther
Other Inhibitor | Other Substrate | Other Inducer |
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Drug as perpetrator
Target | Modality | Activity | Metabolite | Clinical evidence |
---|---|---|---|---|
Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2003/21-366_Crestor_Pharmr_P2.pdf#page=16 Page: 16.0 |
no | |||
Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2003/21-366_Crestor_Pharmr_P2.pdf#page=16 Page: 16.0 |
no | |||
Page: 11.0 |
no | |||
yes [Ki 15.4 uM] |
Drug as victim
Target | Modality | Activity | Metabolite | Clinical evidence |
---|---|---|---|---|
Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2003/21-366_Crestor_BioPharmr.pdf#page=51 Page: 51.0 |
major | no (co-administration study) Comment: fluconazole (inhibitor) had no statistically significant interaction with drug Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2003/21-366_Crestor_BioPharmr.pdf#page=51 Page: 51.0 |
||
Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2003/21-366_Crestor_BioPharmr.pdf#page=51 Page: 51.0 |
minor | |||
Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2003/21-366_Crestor_BioPharmr.pdf#page=51 Page: 51.0 |
minor | no (co-administration study) Comment: fluconazole (inhibitor) had no statistically significant interaction with drug Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2003/21-366_Crestor_BioPharmr.pdf#page=51 Page: 51.0 |
||
Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2003/21-366_Crestor_BioPharmr.pdf#page=51 Page: 51.0 |
minor | yes (co-administration study) Comment: Itraconazole increased exposure of rosuvastatin based on AUC by 39% and 28%; no significant effect of ketoconazole on rosuvastatin; Rosuvastatin exposure decreased in presence of erythromycin for 20% and 31% of AUC and Cmax, respectively; Cyclosporine increased rosuvastatin Cmax and AUC by ~10- and 7-fold, respectively; Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2003/21-366_Crestor_BioPharmr.pdf#page=51 Page: 51.0 |
||
yes | ||||
yes | ||||
yes | ||||
yes | ||||
yes | ||||
yes |
Tox targets
Target | Modality | Activity | Metabolite | Clinical evidence |
---|---|---|---|---|
PubMed
Title | Date | PubMed |
---|---|---|
A new HMG-CoA reductase inhibitor, rosuvastatin, exerts anti-inflammatory effects on the microvascular endothelium: the role of mevalonic acid. | 2001 Jun |
|
Preclinical and clinical pharmacology of Rosuvastatin, a new 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor. | 2001 Mar 8 |
|
Rosuvastatin, a new HMG-CoA reductase inhibitor, upregulates endothelial nitric oxide synthase and protects from ischemic stroke in mice. | 2002 Jun 28 |
|
Direct vascular and cardioprotective effects of rosuvastatin, a new HMG-CoA reductase inhibitor. | 2002 Sep 18 |
|
Beneficial effects of rosuvastatin alone and in combination with extended-release niacin in patients with a combined hyperlipidemia and low high-density lipoprotein cholesterol levels. | 2003 Jun 1 |
|
Rosuvastatin-induced arrest in progression of renal disease. | 2004 |
|
Effects of switching statins on lipid and apolipoprotein ratios in the MERCURY I study. | 2005 Apr 20 |
|
Bile salt export pump (BSEP/ABCB11) can transport a nonbile acid substrate, pravastatin. | 2005 Aug |
|
Aggravation of focal cerebral ischemia by tissue plasminogen activator is reversed by 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor but does not depend on endothelial NO synthase. | 2005 Feb |
|
Comparison of rosuvastatin with atorvastatin, simvastatin and pravastatin in achieving cholesterol goals and improving plasma lipids in hypercholesterolaemic patients with or without the metabolic syndrome in the MERCURY I trial. | 2005 Jul |
|
Chronic treatment with rosuvastatin modulates nitric oxide synthase expression and reduces ischemia-reperfusion injury in rat hearts. | 2005 Jun 1 |
|
Rosuvastatin, but not simvastatin, provides end-organ protection in stroke-prone rats by antiinflammatory effects. | 2005 Mar |
|
Binding thermodynamics of statins to HMG-CoA reductase. | 2005 Sep 6 |
|
Myopathy caused by a combination rosuvastatin and fenofibrate. | 2007 Feb |
|
Rationale and design of the carotid plaque in human for all evaluations with aggressive rosuvastatin therapy (CHALLENGER trial): evaluation by magnetic resonance imaging. | 2009 Jan |
|
Rosuvastatin attenuates the elevation in blood pressure induced by overexpression of human C-reactive protein. | 2011 Jul |
|
Statins alter the hepatobiliary transport of unconjugated and conjugated bilirubin in sandwich-cultured rat hepatocytes. | 2014 Sep |
Patents
Sample Use Guides
The dose range for CRESTOR (rosuvastatin calcium) is 5 to 40 mg orally once daily. The usual starting dose is 10-20 mg.
Route of Administration:
Oral
In Vitro Use Guide
Sources: https://www.ncbi.nlm.nih.gov/pubmed/27813604
HUVECs treated with 30 mM glucose were used to simulate high-glucose conditions, and rosuvastatin concentrations ranging from 0.1 to 10 nM were used.
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Classification Tree | Code System | Code | ||
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WHO-ATC |
C10BX09
Created by
admin on Mon Mar 31 18:07:13 GMT 2025 , Edited by admin on Mon Mar 31 18:07:13 GMT 2025
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WHO-ATC |
C10BX14
Created by
admin on Mon Mar 31 18:07:13 GMT 2025 , Edited by admin on Mon Mar 31 18:07:13 GMT 2025
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WHO-VATC |
QC10BX05
Created by
admin on Mon Mar 31 18:07:13 GMT 2025 , Edited by admin on Mon Mar 31 18:07:13 GMT 2025
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WHO-ATC |
C10BX07
Created by
admin on Mon Mar 31 18:07:13 GMT 2025 , Edited by admin on Mon Mar 31 18:07:13 GMT 2025
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WHO-ATC |
C10AA07
Created by
admin on Mon Mar 31 18:07:13 GMT 2025 , Edited by admin on Mon Mar 31 18:07:13 GMT 2025
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NDF-RT |
N0000000121
Created by
admin on Mon Mar 31 18:07:13 GMT 2025 , Edited by admin on Mon Mar 31 18:07:13 GMT 2025
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FDA ORPHAN DRUG |
420513
Created by
admin on Mon Mar 31 18:07:13 GMT 2025 , Edited by admin on Mon Mar 31 18:07:13 GMT 2025
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WHO-ATC |
A10BH52
Created by
admin on Mon Mar 31 18:07:13 GMT 2025 , Edited by admin on Mon Mar 31 18:07:13 GMT 2025
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WHO-ATC |
C10BA06
Created by
admin on Mon Mar 31 18:07:13 GMT 2025 , Edited by admin on Mon Mar 31 18:07:13 GMT 2025
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WHO-VATC |
QC10AA07
Created by
admin on Mon Mar 31 18:07:13 GMT 2025 , Edited by admin on Mon Mar 31 18:07:13 GMT 2025
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WHO-ATC |
C10BX10
Created by
admin on Mon Mar 31 18:07:13 GMT 2025 , Edited by admin on Mon Mar 31 18:07:13 GMT 2025
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NCI_THESAURUS |
C1655
Created by
admin on Mon Mar 31 18:07:13 GMT 2025 , Edited by admin on Mon Mar 31 18:07:13 GMT 2025
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WHO-ATC |
C10BX13
Created by
admin on Mon Mar 31 18:07:13 GMT 2025 , Edited by admin on Mon Mar 31 18:07:13 GMT 2025
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LIVERTOX |
NBK548620
Created by
admin on Mon Mar 31 18:07:13 GMT 2025 , Edited by admin on Mon Mar 31 18:07:13 GMT 2025
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WHO-ATC |
C10BX05
Created by
admin on Mon Mar 31 18:07:13 GMT 2025 , Edited by admin on Mon Mar 31 18:07:13 GMT 2025
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NDF-RT |
N0000175589
Created by
admin on Mon Mar 31 18:07:13 GMT 2025 , Edited by admin on Mon Mar 31 18:07:13 GMT 2025
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WHO-VATC |
QC10BA06
Created by
admin on Mon Mar 31 18:07:13 GMT 2025 , Edited by admin on Mon Mar 31 18:07:13 GMT 2025
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Code System | Code | Type | Description | ||
---|---|---|---|---|---|
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38545
Created by
admin on Mon Mar 31 18:07:13 GMT 2025 , Edited by admin on Mon Mar 31 18:07:13 GMT 2025
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PRIMARY | |||
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C66523
Created by
admin on Mon Mar 31 18:07:13 GMT 2025 , Edited by admin on Mon Mar 31 18:07:13 GMT 2025
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PRIMARY | |||
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100000088232
Created by
admin on Mon Mar 31 18:07:13 GMT 2025 , Edited by admin on Mon Mar 31 18:07:13 GMT 2025
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PRIMARY | |||
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DTXSID8048492
Created by
admin on Mon Mar 31 18:07:13 GMT 2025 , Edited by admin on Mon Mar 31 18:07:13 GMT 2025
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PRIMARY | |||
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ROSUVASTATIN
Created by
admin on Mon Mar 31 18:07:13 GMT 2025 , Edited by admin on Mon Mar 31 18:07:13 GMT 2025
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PRIMARY | |||
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446157
Created by
admin on Mon Mar 31 18:07:13 GMT 2025 , Edited by admin on Mon Mar 31 18:07:13 GMT 2025
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PRIMARY | |||
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C422923
Created by
admin on Mon Mar 31 18:07:13 GMT 2025 , Edited by admin on Mon Mar 31 18:07:13 GMT 2025
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PRIMARY | |||
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2406
Created by
admin on Mon Mar 31 18:07:13 GMT 2025 , Edited by admin on Mon Mar 31 18:07:13 GMT 2025
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PRIMARY | |||
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Rosuvastatin
Created by
admin on Mon Mar 31 18:07:13 GMT 2025 , Edited by admin on Mon Mar 31 18:07:13 GMT 2025
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PRIMARY | |||
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413KH5ZJ73
Created by
admin on Mon Mar 31 18:07:13 GMT 2025 , Edited by admin on Mon Mar 31 18:07:13 GMT 2025
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PRIMARY | |||
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413KH5ZJ73
Created by
admin on Mon Mar 31 18:07:13 GMT 2025 , Edited by admin on Mon Mar 31 18:07:13 GMT 2025
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PRIMARY | |||
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301542
Created by
admin on Mon Mar 31 18:07:13 GMT 2025 , Edited by admin on Mon Mar 31 18:07:13 GMT 2025
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PRIMARY | RxNorm | ||
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287714-41-4
Created by
admin on Mon Mar 31 18:07:13 GMT 2025 , Edited by admin on Mon Mar 31 18:07:13 GMT 2025
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PRIMARY | |||
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CHEMBL1496
Created by
admin on Mon Mar 31 18:07:13 GMT 2025 , Edited by admin on Mon Mar 31 18:07:13 GMT 2025
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PRIMARY | |||
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SUB20634
Created by
admin on Mon Mar 31 18:07:13 GMT 2025 , Edited by admin on Mon Mar 31 18:07:13 GMT 2025
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PRIMARY | |||
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DB01098
Created by
admin on Mon Mar 31 18:07:13 GMT 2025 , Edited by admin on Mon Mar 31 18:07:13 GMT 2025
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PRIMARY | |||
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m9672
Created by
admin on Mon Mar 31 18:07:13 GMT 2025 , Edited by admin on Mon Mar 31 18:07:13 GMT 2025
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PRIMARY | Merck Index | ||
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2954
Created by
admin on Mon Mar 31 18:07:13 GMT 2025 , Edited by admin on Mon Mar 31 18:07:13 GMT 2025
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PRIMARY | |||
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8021
Created by
admin on Mon Mar 31 18:07:13 GMT 2025 , Edited by admin on Mon Mar 31 18:07:13 GMT 2025
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PRIMARY | |||
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7317
Created by
admin on Mon Mar 31 18:07:13 GMT 2025 , Edited by admin on Mon Mar 31 18:07:13 GMT 2025
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PRIMARY |
ACTIVE MOIETY
METABOLITE INACTIVE (PARENT)
METABOLITE LESS ACTIVE (PARENT)
SALT/SOLVATE (PARENT)
SALT/SOLVATE (PARENT)
SALT/SOLVATE (PARENT)