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

Molecular Formula C22H28FN3O6S
Molecular Weight 481.538
Charge 0
Count
Stereochemistry ABSOLUTE
Additional Stereochemistry No
Defined Stereocenters 2 / 2
E/Z Centers 1
Optical Activity UNSPECIFIED

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.

Approval Year

Targets

Targets

Primary TargetPharmacologyConditionPotency
Conditions

Conditions

ConditionModalityTargetsHighest PhaseProduct
Primary
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
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
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
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
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
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
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
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
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
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
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
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
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
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%
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: 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: 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: 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: Page: p.4, 8
unhealthy, 58
n = 8
Health Status: unhealthy
Condition: Cancer
Age Group: 58
Sex: M+F
Population Size: 8
Sources: Page: p.4, 8
DLT: Rhabdomyolysis...
Dose limiting toxicities:
Rhabdomyolysis (grade 5, 12.5%)
Sources: 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: Page: p.4, 8
unhealthy, 58
n = 10
Health Status: unhealthy
Condition: Cancer
Age Group: 58
Sex: M+F
Population Size: 10
Sources: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: 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: Page: p.4, 8
unhealthy, 58
n = 8
Health Status: unhealthy
Condition: Cancer
Age Group: 58
Sex: M+F
Population Size: 8
Sources: Page: p.4, 8
Overview

Overview

OverviewOther

Drug as perpetrator​Drug as victim

Drug as victim

TargetModalityActivityMetaboliteClinical evidence
major
no (co-administration study)
Comment: fluconazole (inhibitor) had no statistically significant interaction with drug
Page: 51.0
minor
minor
no (co-administration study)
Comment: fluconazole (inhibitor) had no statistically significant interaction with drug
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;
Page: 51.0
yes
yes
yes
yes
yes
yes
Tox targets

Tox targets

TargetModalityActivityMetaboliteClinical evidence
PubMed

PubMed

TitleDatePubMed
Preclinical and clinical pharmacology of Rosuvastatin, a new 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor.
2001 Mar 8
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
The statin wars: why AstraZeneca must retreat.
2003 Oct 25
Rosuvastatin alone or with extended-release niacin: a new therapeutic option for patients with combined hyperlipidemia.
2004 Fall
Rosuvastatin-associated hepatitis with autoimmune features.
2005 May
An overview of statin-associated proteinuria.
2006 May
McArdle disease with rhabdomyolysis induced by rosuvastatin: case report.
2007 Sep
Effect of rosuvastatin on cholestasis-induced hepatic injury in rat livers.
2010 Mar-Apr
Rosuvastatin attenuates the elevation in blood pressure induced by overexpression of human C-reactive protein.
2011 Jul
Rosuvastatin induces apoptosis in cultured human papillary thyroid cancer cells.
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

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
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.
Substance Class Chemical
Created
by admin
on Fri Dec 15 15:44:27 GMT 2023
Edited
by admin
on Fri Dec 15 15:44:27 GMT 2023
Record UNII
413KH5ZJ73
Record Status Validated (UNII)
Record Version
  • Download
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
Related Record Type Details
SALT/SOLVATE -> PARENT
EXCRETED UNCHANGED
FECAL
TARGET -> INHIBITOR
SALT/SOLVATE -> PARENT
TRANSPORTER -> SUBSTRATE
Km
TRANSPORTER -> SUBSTRATE
TRANSPORTER -> INHIBITOR
TRANSPORTER -> SUBSTRATE
METABOLIC ENZYME -> SUBSTRATE
MAJOR
BINDER->LIGAND
Related Record Type Details
METABOLITE LESS ACTIVE -> PARENT
N-desmethyl rosuvastatin has approximately one-sixth to one-half the HMG-CoA reductase inhibitory activity of the parent compound.
METABOLITE LESS ACTIVE -> PARENT
METABOLITE INACTIVE -> PARENT
Related Record Type Details
ACTIVE MOIETY
Name Property Type Amount Referenced Substance Defining Parameters References
Biological Half-life PHARMACOKINETIC
ORAL BIOAVAILABILITY PHARMACOKINETIC
Volume of Distribution PHARMACOKINETIC
MAXIMUM TOLERATED DOSE TOXICITY
Tmax PHARMACOKINETIC