U.S. Department of Health & Human Services Divider Arrow National Institutes of Health Divider Arrow NCATS

Details

Stereochemistry ABSOLUTE
Molecular Formula C22H28FN3O6S
Molecular Weight 481.538
Optical Activity UNSPECIFIED
Defined Stereocenters 2 / 2
E/Z Centers 1
Charge 0

SHOW SMILES / InChI
Structure of ROSUVASTATIN

SMILES

CC(C)C1=NC(=NC(C2=CC=C(F)C=C2)=C1\C=C\[C@@H](O)C[C@@H](O)CC(O)=O)N(C)S(C)(=O)=O

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

HIDE SMILES / InChI

Description

CRESTOR (rosuvastatin calcium) is an inhibitor of HMG-CoA reductase. It has been widely launched for the treatment of patients with dyslipidaemia and has also been approved in the US and EU to slow the progression of atherosclerosis.

CNS Activity

Originator

Approval Year

2003
176
Targets

Targets

Primary TargetPharmacologyConditionPotency
Inhibitor
8297
Conditions

Conditions

ConditionModalityTargetsHighest PhaseProduct
Primary
Approved
8429
CRESTOR

Approved Use

CRESTOR 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 Date

2003
Primary
Approved
8429
CRESTOR

Approved Use

CRESTOR 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 Date

2003
Primary
Approved
8429
CRESTOR

Approved Use

CRESTOR 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 Date

2003
Primary
Approved
8429
CRESTOR

Approved Use

CRESTOR 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 Date

2003
Primary
Approved
8429
CRESTOR

Approved Use

CRESTOR 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 Date

2003
Cmax

Cmax

ValueDoseCo-administeredAnalytePopulation
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
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
AUC

AUC

ValueDoseCo-administeredAnalytePopulation
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
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
T1/2

T1/2

ValueDoseCo-administeredAnalytePopulation
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
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
Funbound

Funbound

ValueDoseCo-administeredAnalytePopulation
12%
DRUG LABEL
https://www.accessdata.fda.gov/drugsatfda_docs/label/2018/208647s000lbl.pdf
ROSUVASTATIN plasma
Homo sapiens
population: UNKNOWN
age: UNKNOWN
sex: UNKNOWN
food status: UNKNOWN
Doses

Doses

DosePopulationAdverse events​
40 mg 1 times / day multiple, oral
Recommended
Dose: 40 mg, 1 times / day
Route: oral
Route: multiple
Dose: 40 mg, 1 times / day
Sources:
https://pubmed.ncbi.nlm.nih.gov/22085316
Page: p.2085
unhealthy, 57.4±8.6
n = 691
Health Status: unhealthy
Condition: Coronary atherosclerosis
Age Group: 57.4±8.6
Sex: M+F
Population Size: 691
Sources:
https://pubmed.ncbi.nlm.nih.gov/22085316
Page: p.2085
Disc. AE: Cardiovascular disorder, Myocardial infarction...
AEs leading to
discontinuation/dose reduction:
Cardiovascular disorder (grade 5, 0.3%)
Myocardial infarction (1.6%)
Stroke (0.4%)
Cardiovascular disorder (7.5%)
Aspartate aminotransferase increased (0.4%)
Alanine aminotransferase increased (0.7%)
Creatine kinase increased (grade 3, 0.3%)
Creatine kinase increased (grade 4, 0.1%)
Proteinuria (3.8%)
Creatinine increased (3.3%)
Sources:
https://pubmed.ncbi.nlm.nih.gov/22085316
Page: p.2085
2 mg/kg 1 times / day multiple, oral
Highest studied dose
Dose: 2 mg/kg, 1 times / day
Route: oral
Route: multiple
Dose: 2 mg/kg, 1 times / day
Co-administed with::
erlotinib, p.o(150 mg; q.d)
Sources:
https://pubmed.ncbi.nlm.nih.gov/27036206
Page: p.4, 8
unhealthy, 58
n = 8
Health Status: unhealthy
Condition: Cancer
Age Group: 58
Sex: M+F
Population Size: 8
Sources:
https://pubmed.ncbi.nlm.nih.gov/27036206
Page: p.4, 8
DLT: Rhabdomyolysis...
Dose limiting toxicities:
Rhabdomyolysis (grade 5, 12.5%)
Sources:
https://pubmed.ncbi.nlm.nih.gov/27036206
Page: p.4, 8
1 mg/kg 1 times / day multiple, oral
MTD
Dose: 1 mg/kg, 1 times / day
Route: oral
Route: multiple
Dose: 1 mg/kg, 1 times / day
Co-administed with::
erlotinib, p.o(150 mg; q.d)
Sources:
https://pubmed.ncbi.nlm.nih.gov/27036206
Page: p.4, 8
unhealthy, 58
n = 10
Health Status: unhealthy
Condition: Cancer
Age Group: 58
Sex: M+F
Population Size: 10
Sources:
https://pubmed.ncbi.nlm.nih.gov/27036206
Page: p.4, 8
Sources:
https://pubmed.ncbi.nlm.nih.gov/27036206
Page: p.4, 8
AEs

AEs

AESignificanceDosePopulation
Aspartate aminotransferase increased 0.4%
Disc. AE
40 mg 1 times / day multiple, oral
Recommended
Dose: 40 mg, 1 times / day
Route: oral
Route: multiple
Dose: 40 mg, 1 times / day
Sources:
https://pubmed.ncbi.nlm.nih.gov/22085316
Page: p.2085
unhealthy, 57.4±8.6
n = 691
Health Status: unhealthy
Condition: Coronary atherosclerosis
Age Group: 57.4±8.6
Sex: M+F
Population Size: 691
Sources:
https://pubmed.ncbi.nlm.nih.gov/22085316
Page: p.2085
Stroke 0.4%
Disc. AE
40 mg 1 times / day multiple, oral
Recommended
Dose: 40 mg, 1 times / day
Route: oral
Route: multiple
Dose: 40 mg, 1 times / day
Sources:
https://pubmed.ncbi.nlm.nih.gov/22085316
Page: p.2085
unhealthy, 57.4±8.6
n = 691
Health Status: unhealthy
Condition: Coronary atherosclerosis
Age Group: 57.4±8.6
Sex: M+F
Population Size: 691
Sources:
https://pubmed.ncbi.nlm.nih.gov/22085316
Page: p.2085
Alanine aminotransferase increased 0.7%
Disc. AE
40 mg 1 times / day multiple, oral
Recommended
Dose: 40 mg, 1 times / day
Route: oral
Route: multiple
Dose: 40 mg, 1 times / day
Sources:
https://pubmed.ncbi.nlm.nih.gov/22085316
Page: p.2085
unhealthy, 57.4±8.6
n = 691
Health Status: unhealthy
Condition: Coronary atherosclerosis
Age Group: 57.4±8.6
Sex: M+F
Population Size: 691
Sources:
https://pubmed.ncbi.nlm.nih.gov/22085316
Page: p.2085
Myocardial infarction 1.6%
Disc. AE
40 mg 1 times / day multiple, oral
Recommended
Dose: 40 mg, 1 times / day
Route: oral
Route: multiple
Dose: 40 mg, 1 times / day
Sources:
https://pubmed.ncbi.nlm.nih.gov/22085316
Page: p.2085
unhealthy, 57.4±8.6
n = 691
Health Status: unhealthy
Condition: Coronary atherosclerosis
Age Group: 57.4±8.6
Sex: M+F
Population Size: 691
Sources:
https://pubmed.ncbi.nlm.nih.gov/22085316
Page: p.2085
Creatinine increased 3.3%
Disc. AE
40 mg 1 times / day multiple, oral
Recommended
Dose: 40 mg, 1 times / day
Route: oral
Route: multiple
Dose: 40 mg, 1 times / day
Sources:
https://pubmed.ncbi.nlm.nih.gov/22085316
Page: p.2085
unhealthy, 57.4±8.6
n = 691
Health Status: unhealthy
Condition: Coronary atherosclerosis
Age Group: 57.4±8.6
Sex: M+F
Population Size: 691
Sources:
https://pubmed.ncbi.nlm.nih.gov/22085316
Page: p.2085
Proteinuria 3.8%
Disc. AE
40 mg 1 times / day multiple, oral
Recommended
Dose: 40 mg, 1 times / day
Route: oral
Route: multiple
Dose: 40 mg, 1 times / day
Sources:
https://pubmed.ncbi.nlm.nih.gov/22085316
Page: p.2085
unhealthy, 57.4±8.6
n = 691
Health Status: unhealthy
Condition: Coronary atherosclerosis
Age Group: 57.4±8.6
Sex: M+F
Population Size: 691
Sources:
https://pubmed.ncbi.nlm.nih.gov/22085316
Page: p.2085
Cardiovascular disorder 7.5%
Disc. AE
40 mg 1 times / day multiple, oral
Recommended
Dose: 40 mg, 1 times / day
Route: oral
Route: multiple
Dose: 40 mg, 1 times / day
Sources:
https://pubmed.ncbi.nlm.nih.gov/22085316
Page: p.2085
unhealthy, 57.4±8.6
n = 691
Health Status: unhealthy
Condition: Coronary atherosclerosis
Age Group: 57.4±8.6
Sex: M+F
Population Size: 691
Sources:
https://pubmed.ncbi.nlm.nih.gov/22085316
Page: p.2085
Creatine kinase increased grade 3, 0.3%
Disc. AE
40 mg 1 times / day multiple, oral
Recommended
Dose: 40 mg, 1 times / day
Route: oral
Route: multiple
Dose: 40 mg, 1 times / day
Sources:
https://pubmed.ncbi.nlm.nih.gov/22085316
Page: p.2085
unhealthy, 57.4±8.6
n = 691
Health Status: unhealthy
Condition: Coronary atherosclerosis
Age Group: 57.4±8.6
Sex: M+F
Population Size: 691
Sources:
https://pubmed.ncbi.nlm.nih.gov/22085316
Page: p.2085
Creatine kinase increased grade 4, 0.1%
Disc. AE
40 mg 1 times / day multiple, oral
Recommended
Dose: 40 mg, 1 times / day
Route: oral
Route: multiple
Dose: 40 mg, 1 times / day
Sources:
https://pubmed.ncbi.nlm.nih.gov/22085316
Page: p.2085
unhealthy, 57.4±8.6
n = 691
Health Status: unhealthy
Condition: Coronary atherosclerosis
Age Group: 57.4±8.6
Sex: M+F
Population Size: 691
Sources:
https://pubmed.ncbi.nlm.nih.gov/22085316
Page: p.2085
Cardiovascular disorder grade 5, 0.3%
Disc. AE
40 mg 1 times / day multiple, oral
Recommended
Dose: 40 mg, 1 times / day
Route: oral
Route: multiple
Dose: 40 mg, 1 times / day
Sources:
https://pubmed.ncbi.nlm.nih.gov/22085316
Page: p.2085
unhealthy, 57.4±8.6
n = 691
Health Status: unhealthy
Condition: Coronary atherosclerosis
Age Group: 57.4±8.6
Sex: M+F
Population Size: 691
Sources:
https://pubmed.ncbi.nlm.nih.gov/22085316
Page: p.2085
Rhabdomyolysis grade 5, 12.5%
DLT, Disc. AE
2 mg/kg 1 times / day multiple, oral
Highest studied dose
Dose: 2 mg/kg, 1 times / day
Route: oral
Route: multiple
Dose: 2 mg/kg, 1 times / day
Co-administed with::
erlotinib, p.o(150 mg; q.d)
Sources:
https://pubmed.ncbi.nlm.nih.gov/27036206
Page: p.4, 8
unhealthy, 58
n = 8
Health Status: unhealthy
Condition: Cancer
Age Group: 58
Sex: M+F
Population Size: 8
Sources:
https://pubmed.ncbi.nlm.nih.gov/27036206
Page: p.4, 8
Overview

Overview

CYP3A4CYP2C9CYP2D6hERG
substrate
1737
substrate
1037
substrate
1217
inhibitor
1612

OverviewOther

Other InhibitorOther SubstrateOther Inducer
CYP 450
18

P-gp
1461

BCRP
699
CYP2C19
991

OATP1B1
406

OATP1B3
350

OATP2B1
104

BCRP
561

NTCP
17

OAT3
339
CYP 450
10
Drug as perpetrator​

Drug as perpetrator​

TargetModalityActivityMetaboliteClinical evidence
CYP 450
20
 no
CYP 450
20
 no
P-gp
1650
 no
BCRP
773
 yes [Ki 15.4 uM]
Drug as victim

Drug as victim

TargetModalityActivityMetaboliteClinical evidence
CYP2C9
1037
 major
no (co-administration study)
Comment: fluconazole (inhibitor) had no statistically significant interaction with drug
Page: 51.0
CYP2D6
1217
 minor
CYP2C19
991
 minor
no (co-administration study)
Comment: fluconazole (inhibitor) had no statistically significant interaction with drug
Page: 51.0
CYP3A4
1737
 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;
Page: 51.0
BCRP
561
 yes
NTCP
17
 yes
OAT3
339
 yes
OATP1B1
406
 yes
OATP1B3
350
 yes
OATP2B1
104
 yes
Tox targets

Tox targets

TargetModalityActivityMetaboliteClinical evidence
hERG
1647
Sourcing

Sourcing

Vendor/AggregatorIDURL
ChEBI
CHEBI:38545
https://www.ebi.ac.uk/chebi/searchId.do?chebiId=CHEBI:38545
MolPort
MolPort-000-883-884
https://www.molport.com/shop/molecule-link/MolPort-000-883-884
ZINC
ZINC000001535101
http://zinc15.docking.org/substances/ZINC000001535101
eMolecules
877496
https://www.emolecules.com/cgi-bin/more?vid=877496
PubMed

PubMed

TitleDatePubMed
A new HMG-CoA reductase inhibitor, rosuvastatin, exerts anti-inflammatory effects on the microvascular endothelium: the role of mevalonic acid.
2001 Jun
Rosuvastatin, a new HMG-CoA reductase inhibitor, upregulates endothelial nitric oxide synthase and protects from ischemic stroke in mice.
2002 Jun 28
Comparison of the efficacy and safety of rosuvastatin versus atorvastatin, simvastatin, and pravastatin across doses (STELLAR* Trial).
2003 Jul 15
The statin wars: why AstraZeneca must retreat.
2003 Oct 25
Rosuvastatin-induced arrest in progression of renal disease.
2004
Rosuvastatin alone or with extended-release niacin: a new therapeutic option for patients with combined hyperlipidemia.
2004 Fall
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
Chronic treatment with rosuvastatin modulates nitric oxide synthase expression and reduces ischemia-reperfusion injury in rat hearts.
2005 Jun 1
Rosuvastatin-associated hepatitis with autoimmune features.
2005 May
Statin therapy alters the relationship between apolipoprotein B and low-density lipoprotein cholesterol and non-high-density lipoprotein cholesterol targets in high-risk patients: the MERCURY II (Measuring Effective Reductions in Cholesterol Using Rosuvastatin) trial.
2008 Aug 19
Vascular and neural dysfunction in Zucker diabetic fatty rats: a difficult condition to reverse.
2008 Jan
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
Functional characterization of mouse organic anion transporting peptide 1a4 in the uptake and efflux of drugs across the blood-brain barrier.
2010 Jan
Rosuvastatin in the prevention of stroke among men and women with elevated levels of C-reactive protein: justification for the Use of Statins in Prevention: an Intervention Trial Evaluating Rosuvastatin (JUPITER).
2010 Jan 5
Biliary efflux transporters involved in the clearance of rosuvastatin in sandwich culture of primary rat hepatocytes.
2010 Mar
Effect of rosuvastatin on cholestasis-induced hepatic injury in rat livers.
2010 Mar-Apr
Rosuvastatin induces apoptosis in CD4(+)CD28 (null) T cells in patients with acute coronary syndromes.
2011 Feb
Rosuvastatin attenuates the elevation in blood pressure induced by overexpression of human C-reactive protein.
2011 Jul
Renal toxicity of lisinopril and rosuvastatin, alone and in combination, in Wistar rats.
2011 Oct
Detection of statin cytotoxicity is increased in cells expressing the OATP1B1 transporter.
2013 Jul
ATP-dependent transport of statins by human and rat MRP2/Mrp2.
2013 Jun 1
Patents

Patents

JP2003511458A
17
JP2004511521A
14
JP2004536047A
24
JP2005504091A
6
JP2005511593A
14
JP2005523255A
21
JP2005531588A
8
JP2006117645A
4
JP2006521344A
15
JP2007182452A
4
JP2007277267A
4
JP2007501217A
6
JP2007503381A
7
JP2007506720A
4
JP2007508039A
114
JP2007508249A
16
JP2007509995A
6
JP2007512228A
19
JP2007513077A
6
JP2007514770A
75
JP2007516294A
6
JP2007520453A
33
JP2007524644A
48
JP2008024712A
4
JP2008523059A
20
JP2008526781A
4
JP2008535928A
8
JP2008539832A
82
JP2008543840A
4
JP2008543841A
4
JP2009024008A
4
JP2009509013A
52
JP2009525790A
101
JP2009531466A
75
JP2009538831A
25
JP2010031047A
4
JP2010090094A
13
JP2010500290A
18
JP2010501643A
4
JP2010510807A
4
JP2010516437A
42
JP2010522245A
4
JP2010533188A
4
JP2011510003A
48
JP2011510038A
4
JP2011510067A
57
JP2011513246A
25
JP2011524416A
138
JP2011529067A
35
JP2011529928A
14
JP4365554B2
22

Sample Use Guides

In Vivo Use Guide
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
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.
Name Type Language
ROSUVASTATIN
HSDB   INN   MI   VANDF   WHO-DD  
INN  
Official Name English
ROSUVASTATIN [HSDB]
Common Name English
ZD4522
Code English
ROSUVASTATIN [MI]
Common Name English
6-HEPTENOIC ACID, 7-(4-(4-FLUOROPHENYL)-6-(1-METHYLETHYL)-2-(METHYL(METHYLSULFONYL)AMINO)-5-PYRIMIDINYL)-3,5-DIHYDROXY-, (3R,5S,6E)-
Common Name English
(3R,5S,6E)-7-(4-(4-FLUOROPHENYL)-6-ISOPROPYL-2-(METHYL(METHYLSULFONYL)AMINO)PYRIMIDIN-5-YL)-3,5-DIHYDROXYHEPT-6-ENOIC ACID
Systematic Name English
ROSUVASTATIN [VANDF]
Common Name English
Rosuvastatin [WHO-DD]
Common Name English
CRESTON
Brand Name English
rosuvastatin [INN]
Common Name English
X-PLENDED
Common Name English
ZD-4522
Code English
Classification Tree Code System Code
WHO-ATC C10BX09
Created by admin on Fri Dec 15 15:44:27 GMT 2023 , Edited by admin on Fri Dec 15 15:44:27 GMT 2023
WHO-ATC C10BX14
Created by admin on Fri Dec 15 15:44:27 GMT 2023 , Edited by admin on Fri Dec 15 15:44:27 GMT 2023
WHO-VATC QC10BX05
Created by admin on Fri Dec 15 15:44:27 GMT 2023 , Edited by admin on Fri Dec 15 15:44:27 GMT 2023
WHO-ATC C10BX07
Created by admin on Fri Dec 15 15:44:27 GMT 2023 , Edited by admin on Fri Dec 15 15:44:27 GMT 2023
WHO-ATC C10AA07
Created by admin on Fri Dec 15 15:44:27 GMT 2023 , Edited by admin on Fri Dec 15 15:44:27 GMT 2023
NDF-RT N0000000121
Created by admin on Fri Dec 15 15:44:27 GMT 2023 , Edited by admin on Fri Dec 15 15:44:27 GMT 2023
FDA ORPHAN DRUG 420513
Created by admin on Fri Dec 15 15:44:27 GMT 2023 , Edited by admin on Fri Dec 15 15:44:27 GMT 2023
WHO-ATC A10BH52
Created by admin on Fri Dec 15 15:44:27 GMT 2023 , Edited by admin on Fri Dec 15 15:44:27 GMT 2023
WHO-ATC C10BA06
Created by admin on Fri Dec 15 15:44:27 GMT 2023 , Edited by admin on Fri Dec 15 15:44:27 GMT 2023
WHO-VATC QC10AA07
Created by admin on Fri Dec 15 15:44:27 GMT 2023 , Edited by admin on Fri Dec 15 15:44:27 GMT 2023
WHO-ATC C10BX10
Created by admin on Fri Dec 15 15:44:27 GMT 2023 , Edited by admin on Fri Dec 15 15:44:27 GMT 2023
NCI_THESAURUS C1655
Created by admin on Fri Dec 15 15:44:27 GMT 2023 , Edited by admin on Fri Dec 15 15:44:27 GMT 2023
WHO-ATC C10BX13
Created by admin on Fri Dec 15 15:44:27 GMT 2023 , Edited by admin on Fri Dec 15 15:44:27 GMT 2023
LIVERTOX NBK548620
Created by admin on Fri Dec 15 15:44:27 GMT 2023 , Edited by admin on Fri Dec 15 15:44:27 GMT 2023
WHO-ATC C10BX05
Created by admin on Fri Dec 15 15:44:27 GMT 2023 , Edited by admin on Fri Dec 15 15:44:27 GMT 2023
NDF-RT N0000175589
Created by admin on Fri Dec 15 15:44:27 GMT 2023 , Edited by admin on Fri Dec 15 15:44:27 GMT 2023
WHO-VATC QC10BA06
Created by admin on Fri Dec 15 15:44:27 GMT 2023 , Edited by admin on Fri Dec 15 15:44:27 GMT 2023
Code System Code Type Description
CHEBI
38545
Created by admin on Fri Dec 15 15:44:27 GMT 2023 , Edited by admin on Fri Dec 15 15:44:27 GMT 2023
PRIMARY
NCI_THESAURUS
C66523
Created by admin on Fri Dec 15 15:44:27 GMT 2023 , Edited by admin on Fri Dec 15 15:44:27 GMT 2023
PRIMARY
SMS_ID
100000088232
Created by admin on Fri Dec 15 15:44:27 GMT 2023 , Edited by admin on Fri Dec 15 15:44:27 GMT 2023
PRIMARY
EPA CompTox
DTXSID8048492
Created by admin on Fri Dec 15 15:44:27 GMT 2023 , Edited by admin on Fri Dec 15 15:44:27 GMT 2023
PRIMARY
WIKIPEDIA
ROSUVASTATIN
Created by admin on Fri Dec 15 15:44:27 GMT 2023 , Edited by admin on Fri Dec 15 15:44:27 GMT 2023
PRIMARY
PUBCHEM
446157
Created by admin on Fri Dec 15 15:44:27 GMT 2023 , Edited by admin on Fri Dec 15 15:44:27 GMT 2023
PRIMARY
MESH
C422923
Created by admin on Fri Dec 15 15:44:27 GMT 2023 , Edited by admin on Fri Dec 15 15:44:27 GMT 2023
PRIMARY
DRUG CENTRAL
2406
Created by admin on Fri Dec 15 15:44:27 GMT 2023 , Edited by admin on Fri Dec 15 15:44:27 GMT 2023
PRIMARY
LACTMED
Rosuvastatin
Created by admin on Fri Dec 15 15:44:27 GMT 2023 , Edited by admin on Fri Dec 15 15:44:27 GMT 2023
PRIMARY
FDA UNII
413KH5ZJ73
Created by admin on Fri Dec 15 15:44:27 GMT 2023 , Edited by admin on Fri Dec 15 15:44:27 GMT 2023
PRIMARY
DAILYMED
413KH5ZJ73
Created by admin on Fri Dec 15 15:44:27 GMT 2023 , Edited by admin on Fri Dec 15 15:44:27 GMT 2023
PRIMARY
RXCUI
301542
Created by admin on Fri Dec 15 15:44:27 GMT 2023 , Edited by admin on Fri Dec 15 15:44:27 GMT 2023
PRIMARY RxNorm
CAS
287714-41-4
Created by admin on Fri Dec 15 15:44:27 GMT 2023 , Edited by admin on Fri Dec 15 15:44:27 GMT 2023
PRIMARY
ChEMBL
CHEMBL1496
Created by admin on Fri Dec 15 15:44:27 GMT 2023 , Edited by admin on Fri Dec 15 15:44:27 GMT 2023
PRIMARY
EVMPD
SUB20634
Created by admin on Fri Dec 15 15:44:27 GMT 2023 , Edited by admin on Fri Dec 15 15:44:27 GMT 2023
PRIMARY
DRUG BANK
DB01098
Created by admin on Fri Dec 15 15:44:27 GMT 2023 , Edited by admin on Fri Dec 15 15:44:27 GMT 2023
PRIMARY
MERCK INDEX
m9672
Created by admin on Fri Dec 15 15:44:27 GMT 2023 , Edited by admin on Fri Dec 15 15:44:27 GMT 2023
PRIMARY Merck Index
IUPHAR
2954
Created by admin on Fri Dec 15 15:44:27 GMT 2023 , Edited by admin on Fri Dec 15 15:44:27 GMT 2023
PRIMARY
INN
8021
Created by admin on Fri Dec 15 15:44:27 GMT 2023 , Edited by admin on Fri Dec 15 15:44:27 GMT 2023
PRIMARY
HSDB
7317
Created by admin on Fri Dec 15 15:44:27 GMT 2023 , Edited by admin on Fri Dec 15 15:44:27 GMT 2023
PRIMARY
ACTIVE MOIETY
Structure of ROSUVASTATIN
METABOLITE INACTIVE (PARENT)
Structure of ROSUVASTATIN LACTONE
METABOLITE LESS ACTIVE (PARENT)
Structure of N-DESMETHYL ROSUVASTATIN
SALT/SOLVATE (PARENT)
Structure of ROSUVASTATIN ZINC
SALT/SOLVATE (PARENT)
Structure of ROSUVASTATIN CALCIUM
NIH
NCATS
PRIVACY ACT
ACCESSIBILITY
DISCLAIMER
HHS VULNERABILITY DISCLOSURE
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