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Details

Stereochemistry ABSOLUTE
Molecular Formula 2C22H27FN3O6S.Ca
Molecular Weight 1001.1413
Optical Activity UNSPECIFIED
Defined Stereocenters 4 / 4
E/Z Centers 2
Charge 0

SHOW SMILES / InChI
Structure of ROSUVASTATIN CALCIUM

SMILES

CC(C)c1c(/C(/[H])=C(\[H])/[C@]([H])(C[C@]([H])(CC(=O)[O-])O)O)c(-c2ccc(cc2)F)nc(n1)N(C)S(=O)(=O)C.CC(C)c1c(/C(/[H])=C(\[H])/[C@]([H])(C[C@]([H])(CC(=O)[O-])O)O)c(-c2ccc(cc2)F)nc(n1)N(C)S(=O)(=O)C.[Ca+2]

InChI

InChIKey=LALFOYNTGMUKGG-BGRFNVSISA-L
InChI=1S/2C22H28FN3O6S.Ca/c2*1-13(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;/h2*5-10,13,16-17,27-28H,11-12H2,1-4H3,(H,29,30);/q;;+2/p-2/b2*10-9+;/t2*16-,17-;/m11./s1

HIDE SMILES / InChI

Molecular Formula C22H27FN3O6S
Molecular Weight 480.5316
Charge -1
Count
Stereochemistry ABSOLUTE
Additional Stereochemistry No
Defined Stereocenters 2 / 2
E/Z Centers 1
Optical Activity UNSPECIFIED

Molecular Formula Ca
Molecular Weight 40.078
Charge 2
Count
Stereochemistry ACHIRAL
Additional Stereochemistry No
Defined Stereocenters 0 / 0
E/Z Centers 0
Optical Activity NONE

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

TargetsConditions

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

1060646400000
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

1060646400000
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

1060646400000
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

1060646400000
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

1060646400000
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:
unhealthy, 57.4±8.6
Health Status: unhealthy
Age Group: 57.4±8.6
Sex: M+F
Sources:
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:
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
Sources:
unhealthy, 58
Health Status: unhealthy
Age Group: 58
Sex: M+F
Sources:
DLT: Rhabdomyolysis...
Dose limiting toxicities:
Rhabdomyolysis (grade 5, 12.5%)
Sources:
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
Sources:
unhealthy, 58
Health Status: unhealthy
Age Group: 58
Sex: M+F
Sources:
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:
unhealthy, 57.4±8.6
Health Status: unhealthy
Age Group: 57.4±8.6
Sex: M+F
Sources:
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:
unhealthy, 57.4±8.6
Health Status: unhealthy
Age Group: 57.4±8.6
Sex: M+F
Sources:
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:
unhealthy, 57.4±8.6
Health Status: unhealthy
Age Group: 57.4±8.6
Sex: M+F
Sources:
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:
unhealthy, 57.4±8.6
Health Status: unhealthy
Age Group: 57.4±8.6
Sex: M+F
Sources:
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:
unhealthy, 57.4±8.6
Health Status: unhealthy
Age Group: 57.4±8.6
Sex: M+F
Sources:
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:
unhealthy, 57.4±8.6
Health Status: unhealthy
Age Group: 57.4±8.6
Sex: M+F
Sources:
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:
unhealthy, 57.4±8.6
Health Status: unhealthy
Age Group: 57.4±8.6
Sex: M+F
Sources:
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:
unhealthy, 57.4±8.6
Health Status: unhealthy
Age Group: 57.4±8.6
Sex: M+F
Sources:
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:
unhealthy, 57.4±8.6
Health Status: unhealthy
Age Group: 57.4±8.6
Sex: M+F
Sources:
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:
unhealthy, 57.4±8.6
Health Status: unhealthy
Age Group: 57.4±8.6
Sex: M+F
Sources:
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
Sources:
unhealthy, 58
Health Status: unhealthy
Age Group: 58
Sex: M+F
Sources:
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
minor
minor
no (co-administration study)
Comment: fluconazole (inhibitor) had no statistically significant interaction with drug
Page: 51
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
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
Structural mechanism for statin inhibition of HMG-CoA reductase.
2001 May 11
Rosuvastatin, a new HMG-CoA reductase inhibitor, upregulates endothelial nitric oxide synthase and protects from ischemic stroke in mice.
2002 Jun 28
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-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
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
Binding thermodynamics of statins to HMG-CoA reductase.
2005 Sep 6
Rosuvastatin 5 and 10 mg/d: a pilot study of the effects in hypercholesterolemic adults unable to tolerate other statins and reach LDL cholesterol goals with nonstatin lipid-lowering therapies.
2006 Jun
Statin-associated myasthenia gravis: report of 4 cases and review of the literature.
2006 Mar
Statin treatment and 3' polyadenylation of eNOS mRNA.
2007 Dec
McArdle disease with rhabdomyolysis induced by rosuvastatin: case report.
2007 Sep
Rosuvastatin protects against oxidative stress and DNA damage in vitro via upregulation of glutathione synthesis.
2008 Aug
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
In-vivo effects of simvastatin and rosuvastatin on global gene expression in peripheral blood leucocytes in a human inflammation model.
2008 Feb
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
Rosuvastatin prevents endothelial cell death and reduces atherosclerotic lesion formation in ApoE-deficient mice.
2009 Jan
WT-1 mRNA expression is modulated by nitric oxide availability and Hsp70 interaction after neonatal unilateral ureteral obstruction.
2010 Dec
Case report. Hyperlipoproteinaemia(a): which is the optimal therapy? A case report.
2010 Oct
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
Rosuvastatin induces apoptosis in cultured human papillary thyroid cancer cells.
2011 Jul
Rosuvastatin prevents myocardial necrosis in an experimental model of acute myocardial infarction.
2011 May
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
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
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 Jun 25 21:07:42 UTC 2021
Edited
by admin
on Fri Jun 25 21:07:42 UTC 2021
Record UNII
83MVU38M7Q
Record Status Validated (UNII)
Record Version
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Name Type Language
ROSUVASTATIN CALCIUM
JAN   MART.   ORANGE BOOK   USAN   WHO-DD  
USAN  
Official Name English
ROSUVASTATIN CALCIUM [JAN]
Common Name English
ROSUVASTATIN CALCIUM [MART.]
Common Name English
ROSUVASTATIN CALCIUM [ORANGE BOOK]
Common Name English
ROSUVASTATIN CALCIUM SALT
MI  
Common Name English
BIS((E)-7-(4-(4-FLUOROPHENYL)-6-ISOPROPYL-2-(METHYL(METHYLSULFONYL)AMINO)-PYRIMIDE-5-YL)-(3R,5S)3,5-DIHYDROXYLHEPT-6-ENOIC ACID) CALCIUM
Systematic Name English
ZD4522 CALCIUM
Code English
ROSUVASTATIN CALCIUM SALT [MI]
Common Name English
ROSUVASTATIN CALCIUM [USP-RS]
Common Name English
ROSUVASTATIN CALCIUM [USAN]
Common Name English
ROSUVASTATIN CALCIUM COMPONENT OF ROSZET
Brand Name English
NSC-747274
Code English
6-HEPTENOIC ACID, 7-(4-(4-FLUOROPHENYL)-6-(1-METHYLETHYL)-2-(METHYLSULFONYL)AMINO)-5-PYRIMIDINYL)-3,5-DIHYDROXY-, CALCIUM SALT (2:1), (3R,5S,6E)-
Systematic Name English
NSC-758930
Code English
ZD-4522 CALCIUM
Code English
EZALLOR
Brand Name English
ROSUVASTATIN CALCIUM [EP MONOGRAPH]
Common Name English
ROSUVASTATIN CALCIUM [WHO-DD]
Common Name English
ROSUVASTATIN (AS CALCIUM)
Common Name English
CRESTOR
Brand Name English
(S-((R*,S*-(E)))- 7-(4-(4-FLUOROPHENYL)-6-(1-METHYLETHYL)-2-(METHYL(METHYLSULFONYL) AMINO)-5-PYRIMIDINYL)-3,5-DIHYDROXY-6-HEPTENOIC ACID, CALCIUM SALT (2:1)
Systematic Name English
ROZAVEL
Common Name English
SUVIKAN
Common Name English
ROSTAR
Common Name English
ROSUVASTATIN CALCIUM [USP MONOGRAPH]
Common Name English
ROSZET COMPONENT ROSUVASTATIN CALCIUM
Brand Name English
FORTIUS
Common Name English
ROSUVASTATIN HEMICALCIUM
Common Name English
(S-(R*,S*-(E)))-7-(4-(4-FLUOROPHENYL)-6-(1-METHYLETHYL)-2-(METHYL(METHYLSULFONYL)AMINO)-5-PYRIMIDINYL)-3,5-DIHYDROXY-6-HEPTENOIC ACID, CALCIUM SALT
Systematic Name English
S-4522
Code English
Classification Tree Code System Code
NCI_THESAURUS C1655
Created by admin on Fri Jun 25 21:07:42 UTC 2021 , Edited by admin on Fri Jun 25 21:07:42 UTC 2021
Code System Code Type Description
PUBCHEM
5282455
Created by admin on Fri Jun 25 21:07:42 UTC 2021 , Edited by admin on Fri Jun 25 21:07:42 UTC 2021
PRIMARY
DRUG BANK
DBSALT000154
Created by admin on Fri Jun 25 21:07:42 UTC 2021 , Edited by admin on Fri Jun 25 21:07:42 UTC 2021
PRIMARY
CAS
147098-20-2
Created by admin on Fri Jun 25 21:07:42 UTC 2021 , Edited by admin on Fri Jun 25 21:07:42 UTC 2021
PRIMARY
FDA UNII
83MVU38M7Q
Created by admin on Fri Jun 25 21:07:42 UTC 2021 , Edited by admin on Fri Jun 25 21:07:42 UTC 2021
PRIMARY
RXCUI
323828
Created by admin on Fri Jun 25 21:07:42 UTC 2021 , Edited by admin on Fri Jun 25 21:07:42 UTC 2021
PRIMARY RxNorm
NCI_THESAURUS
C61933
Created by admin on Fri Jun 25 21:07:42 UTC 2021 , Edited by admin on Fri Jun 25 21:07:42 UTC 2021
PRIMARY
USP_CATALOG
1606015
Created by admin on Fri Jun 25 21:07:42 UTC 2021 , Edited by admin on Fri Jun 25 21:07:42 UTC 2021
PRIMARY USP-RS
EPA CompTox
147098-20-2
Created by admin on Fri Jun 25 21:07:42 UTC 2021 , Edited by admin on Fri Jun 25 21:07:42 UTC 2021
PRIMARY
EVMPD
SUB20721
Created by admin on Fri Jun 25 21:07:42 UTC 2021 , Edited by admin on Fri Jun 25 21:07:42 UTC 2021
PRIMARY
ChEMBL
CHEMBL1496
Created by admin on Fri Jun 25 21:07:42 UTC 2021 , Edited by admin on Fri Jun 25 21:07:42 UTC 2021
PRIMARY
MERCK INDEX
M9672
Created by admin on Fri Jun 25 21:07:42 UTC 2021 , Edited by admin on Fri Jun 25 21:07:42 UTC 2021
PRIMARY Merck Index
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TITRATION
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IMPURITY -> PARENT
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CHROMATOGRAPHIC PURITY (HPLC/UV)
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ACTIVE MOIETY