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

Details

Stereochemistry ABSOLUTE
Molecular Formula C22H28FN3O6S
Molecular Weight 481.5396
Optical Activity UNSPECIFIED
Defined Stereocenters 2 / 2
E/Z Centers 1
Charge 0

SHOW SMILES / InChI
Structure of ROSUVASTATIN

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

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
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
experiment_type: multiple
dose_type: Recommended
co-adm with
    data_source:
    https://pubmed.ncbi.nlm.nih.gov/22085316
    unhealthy, 57.4±8.6
    population: unhealthy
    age: 57.4±8.6
    sex: M+F
    food_status:
    n:
    data_source:
    https://pubmed.ncbi.nlm.nih.gov/22085316
    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%)

    data_source:
    https://pubmed.ncbi.nlm.nih.gov/22085316
    2 mg/kg 1 times / day multiple, oral
    Highest studied dose
    dose: 2 mg/kg 1 times / day
    route: oral
    experiment_type: multiple
    dose_type: Highest studied dose
    co-adm with
      data_source:
      https://pubmed.ncbi.nlm.nih.gov/27036206
      unhealthy, 58
      population: unhealthy
      age: 58
      sex: M+F
      food_status:
      n:
      data_source:
      https://pubmed.ncbi.nlm.nih.gov/27036206
      DLT: Rhabdomyolysis...
      Dose limiting toxicities:
      Rhabdomyolysis (grade 5, 12.5%)

      data_source:
      https://pubmed.ncbi.nlm.nih.gov/27036206
      1 mg/kg 1 times / day multiple, oral
      MTD
      dose: 1 mg/kg 1 times / day
      route: oral
      experiment_type: multiple
      dose_type: MTD
      co-adm with
        data_source:
        https://pubmed.ncbi.nlm.nih.gov/27036206
        unhealthy, 58
        population: unhealthy
        age: 58
        sex: M+F
        food_status:
        n:
        data_source:
        https://pubmed.ncbi.nlm.nih.gov/27036206
        AEs

        AEs

        AESignificanceDosePopulation
        Rhabdomyolysis grade 5,12.5%
        DLT
        2 mg/kg 1 times / day multiple, oral
        Highest studied dose
        dose: 2 mg/kg 1 times / day
        route: oral
        experiment_type: multiple
        dose_type: Highest studied dose
        co-adm with
          data_source:
          https://pubmed.ncbi.nlm.nih.gov/27036206
          unhealthy, 58
          population:
          age:
          sex:
          food_status:
          n:
          data_source:
          https://pubmed.ncbi.nlm.nih.gov/27036206
          Aspartate aminotransferase increased 0.4%
          Disc. AE
          40 mg 1 times / day multiple, oral
          Recommended
          dose: 40 mg 1 times / day
          route: oral
          experiment_type: multiple
          dose_type: Recommended
          co-adm with
            data_source:
            https://pubmed.ncbi.nlm.nih.gov/22085316
            unhealthy, 57.4±8.6
            population:
            age:
            sex:
            food_status:
            n:
            data_source:
            https://pubmed.ncbi.nlm.nih.gov/22085316
            Stroke 0.4%
            Disc. AE
            40 mg 1 times / day multiple, oral
            Recommended
            dose: 40 mg 1 times / day
            route: oral
            experiment_type: multiple
            dose_type: Recommended
            co-adm with
              data_source:
              https://pubmed.ncbi.nlm.nih.gov/22085316
              unhealthy, 57.4±8.6
              population:
              age:
              sex:
              food_status:
              n:
              data_source:
              https://pubmed.ncbi.nlm.nih.gov/22085316
              Alanine aminotransferase increased 0.7%
              Disc. AE
              40 mg 1 times / day multiple, oral
              Recommended
              dose: 40 mg 1 times / day
              route: oral
              experiment_type: multiple
              dose_type: Recommended
              co-adm with
                data_source:
                https://pubmed.ncbi.nlm.nih.gov/22085316
                unhealthy, 57.4±8.6
                population:
                age:
                sex:
                food_status:
                n:
                data_source:
                https://pubmed.ncbi.nlm.nih.gov/22085316
                Myocardial infarction 1.6%
                Disc. AE
                40 mg 1 times / day multiple, oral
                Recommended
                dose: 40 mg 1 times / day
                route: oral
                experiment_type: multiple
                dose_type: Recommended
                co-adm with
                  data_source:
                  https://pubmed.ncbi.nlm.nih.gov/22085316
                  unhealthy, 57.4±8.6
                  population:
                  age:
                  sex:
                  food_status:
                  n:
                  data_source:
                  https://pubmed.ncbi.nlm.nih.gov/22085316
                  Creatinine increased 3.3%
                  Disc. AE
                  40 mg 1 times / day multiple, oral
                  Recommended
                  dose: 40 mg 1 times / day
                  route: oral
                  experiment_type: multiple
                  dose_type: Recommended
                  co-adm with
                    data_source:
                    https://pubmed.ncbi.nlm.nih.gov/22085316
                    unhealthy, 57.4±8.6
                    population:
                    age:
                    sex:
                    food_status:
                    n:
                    data_source:
                    https://pubmed.ncbi.nlm.nih.gov/22085316
                    Proteinuria 3.8%
                    Disc. AE
                    40 mg 1 times / day multiple, oral
                    Recommended
                    dose: 40 mg 1 times / day
                    route: oral
                    experiment_type: multiple
                    dose_type: Recommended
                    co-adm with
                      data_source:
                      https://pubmed.ncbi.nlm.nih.gov/22085316
                      unhealthy, 57.4±8.6
                      population:
                      age:
                      sex:
                      food_status:
                      n:
                      data_source:
                      https://pubmed.ncbi.nlm.nih.gov/22085316
                      Cardiovascular disorder 7.5%
                      Disc. AE
                      40 mg 1 times / day multiple, oral
                      Recommended
                      dose: 40 mg 1 times / day
                      route: oral
                      experiment_type: multiple
                      dose_type: Recommended
                      co-adm with
                        data_source:
                        https://pubmed.ncbi.nlm.nih.gov/22085316
                        unhealthy, 57.4±8.6
                        population:
                        age:
                        sex:
                        food_status:
                        n:
                        data_source:
                        https://pubmed.ncbi.nlm.nih.gov/22085316
                        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
                        experiment_type: multiple
                        dose_type: Recommended
                        co-adm with
                          data_source:
                          https://pubmed.ncbi.nlm.nih.gov/22085316
                          unhealthy, 57.4±8.6
                          population:
                          age:
                          sex:
                          food_status:
                          n:
                          data_source:
                          https://pubmed.ncbi.nlm.nih.gov/22085316
                          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
                          experiment_type: multiple
                          dose_type: Recommended
                          co-adm with
                            data_source:
                            https://pubmed.ncbi.nlm.nih.gov/22085316
                            unhealthy, 57.4±8.6
                            population:
                            age:
                            sex:
                            food_status:
                            n:
                            data_source:
                            https://pubmed.ncbi.nlm.nih.gov/22085316
                            Cardiovascular disorder grade 5,0.3%
                            Disc. AE
                            40 mg 1 times / day multiple, oral
                            Recommended
                            dose: 40 mg 1 times / day
                            route: oral
                            experiment_type: multiple
                            dose_type: Recommended
                            co-adm with
                              data_source:
                              https://pubmed.ncbi.nlm.nih.gov/22085316
                              unhealthy, 57.4±8.6
                              population:
                              age:
                              sex:
                              food_status:
                              n:
                              data_source:
                              https://pubmed.ncbi.nlm.nih.gov/22085316
                              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
                              A new HMG-CoA reductase inhibitor, rosuvastatin, exerts anti-inflammatory effects on the microvascular endothelium: the role of mevalonic acid.
                              2001 Jun
                              The statin wars.
                              2003 Nov 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
                              Rosuvastatin treatment reverses impaired coronary artery vasodilation in fructose-fed, insulin-resistant rats.
                              2004 Jul
                              Effects of switching statins on lipid and apolipoprotein ratios in the MERCURY I study.
                              2005 Apr 20
                              Bile salt export pump (BSEP/ABCB11) can transport a nonbile acid substrate, pravastatin.
                              2005 Aug
                              Aggravation of focal cerebral ischemia by tissue plasminogen activator is reversed by 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor but does not depend on endothelial NO synthase.
                              2005 Feb
                              Comparison of rosuvastatin with atorvastatin, simvastatin and pravastatin in achieving cholesterol goals and improving plasma lipids in hypercholesterolaemic patients with or without the metabolic syndrome in the MERCURY I trial.
                              2005 Jul
                              Chronic treatment with rosuvastatin modulates nitric oxide synthase expression and reduces ischemia-reperfusion injury in rat hearts.
                              2005 Jun 1
                              Rosuvastatin, but not simvastatin, provides end-organ protection in stroke-prone rats by antiinflammatory effects.
                              2005 Mar
                              Rosuvastatin-associated hepatitis with autoimmune features.
                              2005 May
                              Binding thermodynamics of statins to HMG-CoA reductase.
                              2005 Sep 6
                              Effect of very high-intensity statin therapy on regression of coronary atherosclerosis: the ASTEROID trial.
                              2006 Apr 5
                              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
                              Rosuvastatin treatment protects against nitrate-induced oxidative stress in eNOS knockout mice: implication of the NAD(P)H oxidase pathway.
                              2006 Jun
                              Statin-associated myasthenia gravis: report of 4 cases and review of the literature.
                              2006 Mar
                              Drug and bile acid transporters in rosuvastatin hepatic uptake: function, expression, and pharmacogenetics.
                              2006 May
                              An overview of statin-associated proteinuria.
                              2006 May
                              Design and synthesis of hepatoselective, pyrrole-based HMG-CoA reductase inhibitors.
                              2007 Aug 15
                              Statin treatment and 3' polyadenylation of eNOS mRNA.
                              2007 Dec
                              Myopathy caused by a combination rosuvastatin and fenofibrate.
                              2007 Feb
                              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
                              Rosuvastatin-associated adverse effects and drug-drug interactions in the clinical setting of dyslipidemia.
                              2010
                              WT-1 mRNA expression is modulated by nitric oxide availability and Hsp70 interaction after neonatal unilateral ureteral obstruction.
                              2010 Dec
                              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
                              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.
                              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 [WHO-DD]
                              Common Name English
                              ROSUVASTATIN [VANDF]
                              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 Sat Jun 26 15:30:50 UTC 2021 , Edited by admin on Sat Jun 26 15:30:50 UTC 2021
                              WHO-ATC C10BX14
                              Created by admin on Sat Jun 26 15:30:50 UTC 2021 , Edited by admin on Sat Jun 26 15:30:50 UTC 2021
                              WHO-VATC QC10BX05
                              Created by admin on Sat Jun 26 15:30:50 UTC 2021 , Edited by admin on Sat Jun 26 15:30:50 UTC 2021
                              WHO-ATC C10BX07
                              Created by admin on Sat Jun 26 15:30:50 UTC 2021 , Edited by admin on Sat Jun 26 15:30:50 UTC 2021
                              WHO-ATC C10AA07
                              Created by admin on Sat Jun 26 15:30:50 UTC 2021 , Edited by admin on Sat Jun 26 15:30:50 UTC 2021
                              NDF-RT N0000000121
                              Created by admin on Sat Jun 26 15:30:50 UTC 2021 , Edited by admin on Sat Jun 26 15:30:50 UTC 2021
                              FDA ORPHAN DRUG 420513
                              Created by admin on Sat Jun 26 15:30:50 UTC 2021 , Edited by admin on Sat Jun 26 15:30:50 UTC 2021
                              WHO-ATC A10BH52
                              Created by admin on Sat Jun 26 15:30:50 UTC 2021 , Edited by admin on Sat Jun 26 15:30:50 UTC 2021
                              WHO-ATC C10BA06
                              Created by admin on Sat Jun 26 15:30:50 UTC 2021 , Edited by admin on Sat Jun 26 15:30:50 UTC 2021
                              WHO-VATC QC10AA07
                              Created by admin on Sat Jun 26 15:30:50 UTC 2021 , Edited by admin on Sat Jun 26 15:30:50 UTC 2021
                              WHO-ATC C10BX10
                              Created by admin on Sat Jun 26 15:30:50 UTC 2021 , Edited by admin on Sat Jun 26 15:30:50 UTC 2021
                              NCI_THESAURUS C1655
                              Created by admin on Sat Jun 26 15:30:50 UTC 2021 , Edited by admin on Sat Jun 26 15:30:50 UTC 2021
                              WHO-ATC C10BX13
                              Created by admin on Sat Jun 26 15:30:50 UTC 2021 , Edited by admin on Sat Jun 26 15:30:50 UTC 2021
                              LIVERTOX 864
                              Created by admin on Sat Jun 26 15:30:50 UTC 2021 , Edited by admin on Sat Jun 26 15:30:50 UTC 2021
                              WHO-ATC C10BX05
                              Created by admin on Sat Jun 26 15:30:50 UTC 2021 , Edited by admin on Sat Jun 26 15:30:50 UTC 2021
                              NDF-RT N0000175589
                              Created by admin on Sat Jun 26 15:30:50 UTC 2021 , Edited by admin on Sat Jun 26 15:30:50 UTC 2021
                              WHO-VATC QC10BA06
                              Created by admin on Sat Jun 26 15:30:50 UTC 2021 , Edited by admin on Sat Jun 26 15:30:50 UTC 2021
                              Code System Code Type Description
                              NCI_THESAURUS
                              C66523
                              Created by admin on Sat Jun 26 15:30:50 UTC 2021 , Edited by admin on Sat Jun 26 15:30:50 UTC 2021
                              PRIMARY
                              EPA CompTox
                              287714-41-4
                              Created by admin on Sat Jun 26 15:30:50 UTC 2021 , Edited by admin on Sat Jun 26 15:30:50 UTC 2021
                              PRIMARY
                              WIKIPEDIA
                              ROSUVASTATIN
                              Created by admin on Sat Jun 26 15:30:50 UTC 2021 , Edited by admin on Sat Jun 26 15:30:50 UTC 2021
                              PRIMARY
                              PUBCHEM
                              446157
                              Created by admin on Sat Jun 26 15:30:50 UTC 2021 , Edited by admin on Sat Jun 26 15:30:50 UTC 2021
                              PRIMARY
                              MESH
                              C422923
                              Created by admin on Sat Jun 26 15:30:50 UTC 2021 , Edited by admin on Sat Jun 26 15:30:50 UTC 2021
                              PRIMARY
                              DRUG CENTRAL
                              2406
                              Created by admin on Sat Jun 26 15:30:50 UTC 2021 , Edited by admin on Sat Jun 26 15:30:50 UTC 2021
                              PRIMARY
                              LACTMED
                              Rosuvastatin
                              Created by admin on Sat Jun 26 15:30:50 UTC 2021 , Edited by admin on Sat Jun 26 15:30:50 UTC 2021
                              PRIMARY
                              FDA UNII
                              413KH5ZJ73
                              Created by admin on Sat Jun 26 15:30:50 UTC 2021 , Edited by admin on Sat Jun 26 15:30:50 UTC 2021
                              PRIMARY
                              RXCUI
                              301542
                              Created by admin on Sat Jun 26 15:30:50 UTC 2021 , Edited by admin on Sat Jun 26 15:30:50 UTC 2021
                              PRIMARY RxNorm
                              CAS
                              287714-41-4
                              Created by admin on Sat Jun 26 15:30:50 UTC 2021 , Edited by admin on Sat Jun 26 15:30:50 UTC 2021
                              PRIMARY
                              ChEMBL
                              CHEMBL1496
                              Created by admin on Sat Jun 26 15:30:50 UTC 2021 , Edited by admin on Sat Jun 26 15:30:50 UTC 2021
                              PRIMARY
                              EVMPD
                              SUB20634
                              Created by admin on Sat Jun 26 15:30:50 UTC 2021 , Edited by admin on Sat Jun 26 15:30:50 UTC 2021
                              PRIMARY
                              DRUG BANK
                              DB01098
                              Created by admin on Sat Jun 26 15:30:50 UTC 2021 , Edited by admin on Sat Jun 26 15:30:50 UTC 2021
                              PRIMARY
                              MERCK INDEX
                              M9672
                              Created by admin on Sat Jun 26 15:30:50 UTC 2021 , Edited by admin on Sat Jun 26 15:30:50 UTC 2021
                              PRIMARY Merck Index
                              IUPHAR
                              2954
                              Created by admin on Sat Jun 26 15:30:50 UTC 2021 , Edited by admin on Sat Jun 26 15:30:50 UTC 2021
                              PRIMARY
                              INN
                              8021
                              Created by admin on Sat Jun 26 15:30:50 UTC 2021 , Edited by admin on Sat Jun 26 15:30:50 UTC 2021
                              PRIMARY
                              HSDB
                              7317
                              Created by admin on Sat Jun 26 15:30:50 UTC 2021 , Edited by admin on Sat Jun 26 15:30:50 UTC 2021
                              PRIMARY