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
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
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 |
Originator
Approval Year
Targets
Primary Target | Pharmacology | Condition | Potency |
---|---|---|---|
Target ID: CHEMBL402 |
Conditions
Condition | Modality | Targets | Highest Phase | Product |
---|---|---|---|---|
Primary | CRESTOR Approved UseCRESTOR is an HMG Co-A reductase inhibitor indicated for: ••patients with primary hyperlipidemia and mixed dyslipidemia as an adjunct to diet to reduce elevated total-C, LDL-C, ApoB, nonHDL-C, and TG levels and to increase HDL-C (1.1) ••patients with hypertriglyceridemia as an adjunct to diet (1.2) ••patients with primary dysbetalipoproteinemia (Type III hyperlipoproteinemia) as an adjunct to diet (1.3) ••patients with homozygous familial hypercholesterolemia (HoFH) to reduce LDL-C, total-C, and ApoB (1.4) ••slowing the progression of atherosclerosis as part of a treatment strategy to lower total-C and LDL-C as an adjunct to diet (1.5) ••pediatric patients 10 to 17 years of age with heterozygous familial hypercholesterolemia (HeFH) to reduce elevated total-C, LDL-C and ApoB after failing an adequate trial of diet therapy (1.1) ••risk reduction of MI, stroke, and arterial revascularization procedures in patients without clinically evident CHD, but with multiple risk factors (1.6) Limitations of use (1.7): ••CRESTOR has not been studied in Fredrickson Type I and V dyslipidemias. 1.1 Hyperlipidemia and Mixed Dyslipidemia CRESTOR is indicated as adjunctive therapy to diet to reduce elevated Total-C, LDL-C, ApoB, nonHDL-C, and triglycerides and to increase HDL-C in adult patients with primary hyperlipidemia or mixed dyslipidemia. Lipid-altering agents should be used in addition to a diet restricted in saturated fat and cholesterol when response to diet and nonpharmacological interventions alone has been inadequate. Pediatric Patients 10 to 17 years of age with Heterozygous Familial Hypercholesterolemia (HeFH) Adjunct to diet to reduce Total-C, LDL-C and ApoB levels in adolescent boys and girls, who are at least one year post-menarche, 10-17 years of age with heterozygous familial hypercholesterolemia if after an adequate trial of diet therapy the following findings are present: LDL-C > 190 mg/dL or > 160 mg/dL and there is a positive family history of premature cardiovascular disease (CVD) or two or more other CVD risk factors. 1.2 Hypertriglyceridemia CRESTOR is indicated as adjunctive therapy to diet for the treatment of adult patients with hypertriglyceridemia. 1.3 Primary Dysbetalipoproteinemia (Type III Hyperlipoproteinemia) CRESTOR is indicated as an adjunct to diet for the treatment of patients with primary dysbetalipoproteinemia (Type III Hyperlipoproteinemia). 1.4 Homozygous Familial Hypercholesterolemia CRESTOR is indicated as adjunctive therapy to other lipid-lowering treatments (e.g., LDL apheresis) or alone if such treatments are unavailable to reduce LDL-C, Total-C, and ApoB in adult patients with homozygous familial hypercholesterolemia. 1.5 Slowing of the Progression of Atherosclerosis CRESTOR is indicated as adjunctive therapy to diet to slow the progression of atherosclerosis in adult patients as part of a treatment strategy to lower Total-C and LDL-C to target levels. 1.6 Primary Prevention of Cardiovascular Disease In individuals without clinically evident coronary heart disease but with an increased risk of cardiovascular disease based on age ≥ 50 years old in men and ≥ 60 years old in women, hsCRP ≥ 2 mg/L, and the presence of at least one additional cardiovascular disease risk factor such as hypertension, low HDL-C, smoking, or a family history of premature coronary heart disease, CRESTOR is indicated to: ••reduce the risk of stroke ••reduce the risk of myocardial infarction ••reduce the risk of arterial revascularization procedures 1.7 Limitations of Use CRESTOR has not been studied in Fredrickson Type I and V dyslipidemias. Launch Date2003 |
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Primary | CRESTOR Approved UseCRESTOR is an HMG Co-A reductase inhibitor indicated for: ••patients with primary hyperlipidemia and mixed dyslipidemia as an adjunct to diet to reduce elevated total-C, LDL-C, ApoB, nonHDL-C, and TG levels and to increase HDL-C (1.1) ••patients with hypertriglyceridemia as an adjunct to diet (1.2) ••patients with primary dysbetalipoproteinemia (Type III hyperlipoproteinemia) as an adjunct to diet (1.3) ••patients with homozygous familial hypercholesterolemia (HoFH) to reduce LDL-C, total-C, and ApoB (1.4) ••slowing the progression of atherosclerosis as part of a treatment strategy to lower total-C and LDL-C as an adjunct to diet (1.5) ••pediatric patients 10 to 17 years of age with heterozygous familial hypercholesterolemia (HeFH) to reduce elevated total-C, LDL-C and ApoB after failing an adequate trial of diet therapy (1.1) ••risk reduction of MI, stroke, and arterial revascularization procedures in patients without clinically evident CHD, but with multiple risk factors (1.6) Limitations of use (1.7): ••CRESTOR has not been studied in Fredrickson Type I and V dyslipidemias. 1.1 Hyperlipidemia and Mixed Dyslipidemia CRESTOR is indicated as adjunctive therapy to diet to reduce elevated Total-C, LDL-C, ApoB, nonHDL-C, and triglycerides and to increase HDL-C in adult patients with primary hyperlipidemia or mixed dyslipidemia. Lipid-altering agents should be used in addition to a diet restricted in saturated fat and cholesterol when response to diet and nonpharmacological interventions alone has been inadequate. Pediatric Patients 10 to 17 years of age with Heterozygous Familial Hypercholesterolemia (HeFH) Adjunct to diet to reduce Total-C, LDL-C and ApoB levels in adolescent boys and girls, who are at least one year post-menarche, 10-17 years of age with heterozygous familial hypercholesterolemia if after an adequate trial of diet therapy the following findings are present: LDL-C > 190 mg/dL or > 160 mg/dL and there is a positive family history of premature cardiovascular disease (CVD) or two or more other CVD risk factors. 1.2 Hypertriglyceridemia CRESTOR is indicated as adjunctive therapy to diet for the treatment of adult patients with hypertriglyceridemia. 1.3 Primary Dysbetalipoproteinemia (Type III Hyperlipoproteinemia) CRESTOR is indicated as an adjunct to diet for the treatment of patients with primary dysbetalipoproteinemia (Type III Hyperlipoproteinemia). 1.4 Homozygous Familial Hypercholesterolemia CRESTOR is indicated as adjunctive therapy to other lipid-lowering treatments (e.g., LDL apheresis) or alone if such treatments are unavailable to reduce LDL-C, Total-C, and ApoB in adult patients with homozygous familial hypercholesterolemia. 1.5 Slowing of the Progression of Atherosclerosis CRESTOR is indicated as adjunctive therapy to diet to slow the progression of atherosclerosis in adult patients as part of a treatment strategy to lower Total-C and LDL-C to target levels. 1.6 Primary Prevention of Cardiovascular Disease In individuals without clinically evident coronary heart disease but with an increased risk of cardiovascular disease based on age ≥ 50 years old in men and ≥ 60 years old in women, hsCRP ≥ 2 mg/L, and the presence of at least one additional cardiovascular disease risk factor such as hypertension, low HDL-C, smoking, or a family history of premature coronary heart disease, CRESTOR is indicated to: ••reduce the risk of stroke ••reduce the risk of myocardial infarction ••reduce the risk of arterial revascularization procedures 1.7 Limitations of Use CRESTOR has not been studied in Fredrickson Type I and V dyslipidemias. Launch Date2003 |
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Primary | CRESTOR Approved UseCRESTOR is an HMG Co-A reductase inhibitor indicated for: ••patients with primary hyperlipidemia and mixed dyslipidemia as an adjunct to diet to reduce elevated total-C, LDL-C, ApoB, nonHDL-C, and TG levels and to increase HDL-C (1.1) ••patients with hypertriglyceridemia as an adjunct to diet (1.2) ••patients with primary dysbetalipoproteinemia (Type III hyperlipoproteinemia) as an adjunct to diet (1.3) ••patients with homozygous familial hypercholesterolemia (HoFH) to reduce LDL-C, total-C, and ApoB (1.4) ••slowing the progression of atherosclerosis as part of a treatment strategy to lower total-C and LDL-C as an adjunct to diet (1.5) ••pediatric patients 10 to 17 years of age with heterozygous familial hypercholesterolemia (HeFH) to reduce elevated total-C, LDL-C and ApoB after failing an adequate trial of diet therapy (1.1) ••risk reduction of MI, stroke, and arterial revascularization procedures in patients without clinically evident CHD, but with multiple risk factors (1.6) Limitations of use (1.7): ••CRESTOR has not been studied in Fredrickson Type I and V dyslipidemias. 1.1 Hyperlipidemia and Mixed Dyslipidemia CRESTOR is indicated as adjunctive therapy to diet to reduce elevated Total-C, LDL-C, ApoB, nonHDL-C, and triglycerides and to increase HDL-C in adult patients with primary hyperlipidemia or mixed dyslipidemia. Lipid-altering agents should be used in addition to a diet restricted in saturated fat and cholesterol when response to diet and nonpharmacological interventions alone has been inadequate. Pediatric Patients 10 to 17 years of age with Heterozygous Familial Hypercholesterolemia (HeFH) Adjunct to diet to reduce Total-C, LDL-C and ApoB levels in adolescent boys and girls, who are at least one year post-menarche, 10-17 years of age with heterozygous familial hypercholesterolemia if after an adequate trial of diet therapy the following findings are present: LDL-C > 190 mg/dL or > 160 mg/dL and there is a positive family history of premature cardiovascular disease (CVD) or two or more other CVD risk factors. 1.2 Hypertriglyceridemia CRESTOR is indicated as adjunctive therapy to diet for the treatment of adult patients with hypertriglyceridemia. 1.3 Primary Dysbetalipoproteinemia (Type III Hyperlipoproteinemia) CRESTOR is indicated as an adjunct to diet for the treatment of patients with primary dysbetalipoproteinemia (Type III Hyperlipoproteinemia). 1.4 Homozygous Familial Hypercholesterolemia CRESTOR is indicated as adjunctive therapy to other lipid-lowering treatments (e.g., LDL apheresis) or alone if such treatments are unavailable to reduce LDL-C, Total-C, and ApoB in adult patients with homozygous familial hypercholesterolemia. 1.5 Slowing of the Progression of Atherosclerosis CRESTOR is indicated as adjunctive therapy to diet to slow the progression of atherosclerosis in adult patients as part of a treatment strategy to lower Total-C and LDL-C to target levels. 1.6 Primary Prevention of Cardiovascular Disease In individuals without clinically evident coronary heart disease but with an increased risk of cardiovascular disease based on age ≥ 50 years old in men and ≥ 60 years old in women, hsCRP ≥ 2 mg/L, and the presence of at least one additional cardiovascular disease risk factor such as hypertension, low HDL-C, smoking, or a family history of premature coronary heart disease, CRESTOR is indicated to: ••reduce the risk of stroke ••reduce the risk of myocardial infarction ••reduce the risk of arterial revascularization procedures 1.7 Limitations of Use CRESTOR has not been studied in Fredrickson Type I and V dyslipidemias. Launch Date2003 |
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Primary | CRESTOR Approved UseCRESTOR is an HMG Co-A reductase inhibitor indicated for: ••patients with primary hyperlipidemia and mixed dyslipidemia as an adjunct to diet to reduce elevated total-C, LDL-C, ApoB, nonHDL-C, and TG levels and to increase HDL-C (1.1) ••patients with hypertriglyceridemia as an adjunct to diet (1.2) ••patients with primary dysbetalipoproteinemia (Type III hyperlipoproteinemia) as an adjunct to diet (1.3) ••patients with homozygous familial hypercholesterolemia (HoFH) to reduce LDL-C, total-C, and ApoB (1.4) ••slowing the progression of atherosclerosis as part of a treatment strategy to lower total-C and LDL-C as an adjunct to diet (1.5) ••pediatric patients 10 to 17 years of age with heterozygous familial hypercholesterolemia (HeFH) to reduce elevated total-C, LDL-C and ApoB after failing an adequate trial of diet therapy (1.1) ••risk reduction of MI, stroke, and arterial revascularization procedures in patients without clinically evident CHD, but with multiple risk factors (1.6) Limitations of use (1.7): ••CRESTOR has not been studied in Fredrickson Type I and V dyslipidemias. 1.1 Hyperlipidemia and Mixed Dyslipidemia CRESTOR is indicated as adjunctive therapy to diet to reduce elevated Total-C, LDL-C, ApoB, nonHDL-C, and triglycerides and to increase HDL-C in adult patients with primary hyperlipidemia or mixed dyslipidemia. Lipid-altering agents should be used in addition to a diet restricted in saturated fat and cholesterol when response to diet and nonpharmacological interventions alone has been inadequate. Pediatric Patients 10 to 17 years of age with Heterozygous Familial Hypercholesterolemia (HeFH) Adjunct to diet to reduce Total-C, LDL-C and ApoB levels in adolescent boys and girls, who are at least one year post-menarche, 10-17 years of age with heterozygous familial hypercholesterolemia if after an adequate trial of diet therapy the following findings are present: LDL-C > 190 mg/dL or > 160 mg/dL and there is a positive family history of premature cardiovascular disease (CVD) or two or more other CVD risk factors. 1.2 Hypertriglyceridemia CRESTOR is indicated as adjunctive therapy to diet for the treatment of adult patients with hypertriglyceridemia. 1.3 Primary Dysbetalipoproteinemia (Type III Hyperlipoproteinemia) CRESTOR is indicated as an adjunct to diet for the treatment of patients with primary dysbetalipoproteinemia (Type III Hyperlipoproteinemia). 1.4 Homozygous Familial Hypercholesterolemia CRESTOR is indicated as adjunctive therapy to other lipid-lowering treatments (e.g., LDL apheresis) or alone if such treatments are unavailable to reduce LDL-C, Total-C, and ApoB in adult patients with homozygous familial hypercholesterolemia. 1.5 Slowing of the Progression of Atherosclerosis CRESTOR is indicated as adjunctive therapy to diet to slow the progression of atherosclerosis in adult patients as part of a treatment strategy to lower Total-C and LDL-C to target levels. 1.6 Primary Prevention of Cardiovascular Disease In individuals without clinically evident coronary heart disease but with an increased risk of cardiovascular disease based on age ≥ 50 years old in men and ≥ 60 years old in women, hsCRP ≥ 2 mg/L, and the presence of at least one additional cardiovascular disease risk factor such as hypertension, low HDL-C, smoking, or a family history of premature coronary heart disease, CRESTOR is indicated to: ••reduce the risk of stroke ••reduce the risk of myocardial infarction ••reduce the risk of arterial revascularization procedures 1.7 Limitations of Use CRESTOR has not been studied in Fredrickson Type I and V dyslipidemias. Launch Date2003 |
|||
Primary | CRESTOR Approved UseCRESTOR is an HMG Co-A reductase inhibitor indicated for: ••patients with primary hyperlipidemia and mixed dyslipidemia as an adjunct to diet to reduce elevated total-C, LDL-C, ApoB, nonHDL-C, and TG levels and to increase HDL-C (1.1) ••patients with hypertriglyceridemia as an adjunct to diet (1.2) ••patients with primary dysbetalipoproteinemia (Type III hyperlipoproteinemia) as an adjunct to diet (1.3) ••patients with homozygous familial hypercholesterolemia (HoFH) to reduce LDL-C, total-C, and ApoB (1.4) ••slowing the progression of atherosclerosis as part of a treatment strategy to lower total-C and LDL-C as an adjunct to diet (1.5) ••pediatric patients 10 to 17 years of age with heterozygous familial hypercholesterolemia (HeFH) to reduce elevated total-C, LDL-C and ApoB after failing an adequate trial of diet therapy (1.1) ••risk reduction of MI, stroke, and arterial revascularization procedures in patients without clinically evident CHD, but with multiple risk factors (1.6) Limitations of use (1.7): ••CRESTOR has not been studied in Fredrickson Type I and V dyslipidemias. 1.1 Hyperlipidemia and Mixed Dyslipidemia CRESTOR is indicated as adjunctive therapy to diet to reduce elevated Total-C, LDL-C, ApoB, nonHDL-C, and triglycerides and to increase HDL-C in adult patients with primary hyperlipidemia or mixed dyslipidemia. Lipid-altering agents should be used in addition to a diet restricted in saturated fat and cholesterol when response to diet and nonpharmacological interventions alone has been inadequate. Pediatric Patients 10 to 17 years of age with Heterozygous Familial Hypercholesterolemia (HeFH) Adjunct to diet to reduce Total-C, LDL-C and ApoB levels in adolescent boys and girls, who are at least one year post-menarche, 10-17 years of age with heterozygous familial hypercholesterolemia if after an adequate trial of diet therapy the following findings are present: LDL-C > 190 mg/dL or > 160 mg/dL and there is a positive family history of premature cardiovascular disease (CVD) or two or more other CVD risk factors. 1.2 Hypertriglyceridemia CRESTOR is indicated as adjunctive therapy to diet for the treatment of adult patients with hypertriglyceridemia. 1.3 Primary Dysbetalipoproteinemia (Type III Hyperlipoproteinemia) CRESTOR is indicated as an adjunct to diet for the treatment of patients with primary dysbetalipoproteinemia (Type III Hyperlipoproteinemia). 1.4 Homozygous Familial Hypercholesterolemia CRESTOR is indicated as adjunctive therapy to other lipid-lowering treatments (e.g., LDL apheresis) or alone if such treatments are unavailable to reduce LDL-C, Total-C, and ApoB in adult patients with homozygous familial hypercholesterolemia. 1.5 Slowing of the Progression of Atherosclerosis CRESTOR is indicated as adjunctive therapy to diet to slow the progression of atherosclerosis in adult patients as part of a treatment strategy to lower Total-C and LDL-C to target levels. 1.6 Primary Prevention of Cardiovascular Disease In individuals without clinically evident coronary heart disease but with an increased risk of cardiovascular disease based on age ≥ 50 years old in men and ≥ 60 years old in women, hsCRP ≥ 2 mg/L, and the presence of at least one additional cardiovascular disease risk factor such as hypertension, low HDL-C, smoking, or a family history of premature coronary heart disease, CRESTOR is indicated to: ••reduce the risk of stroke ••reduce the risk of myocardial infarction ••reduce the risk of arterial revascularization procedures 1.7 Limitations of Use CRESTOR has not been studied in Fredrickson Type I and V dyslipidemias. Launch Date2003 |
Cmax
Value | Dose | Co-administered | Analyte | Population |
---|---|---|---|---|
25.86 ng/mL EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/18042475 |
10 mg single, oral dose: 10 mg route of administration: Oral experiment type: SINGLE co-administered: |
ROSUVASTATIN plasma | Homo sapiens population: HEALTHY age: ADULT sex: FEMALE / MALE food status: FASTED |
|
44.99 ng/mL EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/18042475 |
20 mg single, oral dose: 20 mg route of administration: Oral experiment type: SINGLE co-administered: |
ROSUVASTATIN plasma | Homo sapiens population: HEALTHY age: ADULT sex: FEMALE / MALE food status: FASTED |
|
10.22 ng/mL EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/18042475 |
5 mg single, oral dose: 5 mg route of administration: Oral experiment type: SINGLE co-administered: |
ROSUVASTATIN plasma | Homo sapiens population: HEALTHY age: ADULT sex: FEMALE / MALE food status: FASTED |
AUC
Value | Dose | Co-administered | Analyte | Population |
---|---|---|---|---|
216.77 ng × h/mL EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/18042475 |
10 mg single, oral dose: 10 mg route of administration: Oral experiment type: SINGLE co-administered: |
ROSUVASTATIN plasma | Homo sapiens population: HEALTHY age: ADULT sex: FEMALE / MALE food status: FASTED |
|
311.35 ng × h/mL EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/18042475 |
20 mg single, oral dose: 20 mg route of administration: Oral experiment type: SINGLE co-administered: |
ROSUVASTATIN plasma | Homo sapiens population: HEALTHY age: ADULT sex: FEMALE / MALE food status: FASTED |
|
75.93 ng × h/mL EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/18042475 |
5 mg single, oral dose: 5 mg route of administration: Oral experiment type: SINGLE co-administered: |
ROSUVASTATIN plasma | Homo sapiens population: HEALTHY age: ADULT sex: FEMALE / MALE food status: FASTED |
T1/2
Value | Dose | Co-administered | Analyte | Population |
---|---|---|---|---|
13.33 h EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/18042475 |
10 mg single, oral dose: 10 mg route of administration: Oral experiment type: SINGLE co-administered: |
ROSUVASTATIN plasma | Homo sapiens population: HEALTHY age: ADULT sex: FEMALE / MALE food status: FASTED |
|
15.4 h EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/18042475 |
20 mg single, oral dose: 20 mg route of administration: Oral experiment type: SINGLE co-administered: |
ROSUVASTATIN plasma | Homo sapiens population: HEALTHY age: ADULT sex: FEMALE / MALE food status: FASTED |
|
13.01 h EXPERIMENT https://pubmed.ncbi.nlm.nih.gov/18042475 |
5 mg single, oral dose: 5 mg route of administration: Oral experiment type: SINGLE co-administered: |
ROSUVASTATIN plasma | Homo sapiens population: HEALTHY age: ADULT sex: FEMALE / MALE food status: FASTED |
Funbound
Value | Dose | Co-administered | Analyte | Population |
---|---|---|---|---|
12% |
ROSUVASTATIN plasma | Homo sapiens population: UNKNOWN age: UNKNOWN sex: UNKNOWN food status: UNKNOWN |
Doses
Dose | Population | Adverse 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%) Sources: Page: p.2085Myocardial 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%) |
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
AE | Significance | Dose | Population |
---|---|---|---|
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
CYP3A4 | CYP2C9 | CYP2D6 | hERG |
---|---|---|---|
OverviewOther
Other Inhibitor | Other Substrate | Other Inducer |
---|---|---|
Drug as perpetrator
Target | Modality | Activity | Metabolite | Clinical evidence |
---|---|---|---|---|
Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2003/21-366_Crestor_Pharmr_P2.pdf#page=16 Page: 16.0 |
no | |||
Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2003/21-366_Crestor_Pharmr_P2.pdf#page=16 Page: 16.0 |
no | |||
Page: 11.0 |
no | |||
yes [Ki 15.4 uM] |
Drug as victim
Target | Modality | Activity | Metabolite | Clinical evidence |
---|---|---|---|---|
Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2003/21-366_Crestor_BioPharmr.pdf#page=51 Page: 51.0 |
major | no (co-administration study) Comment: fluconazole (inhibitor) had no statistically significant interaction with drug Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2003/21-366_Crestor_BioPharmr.pdf#page=51 Page: 51.0 |
||
Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2003/21-366_Crestor_BioPharmr.pdf#page=51 Page: 51.0 |
minor | |||
Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2003/21-366_Crestor_BioPharmr.pdf#page=51 Page: 51.0 |
minor | no (co-administration study) Comment: fluconazole (inhibitor) had no statistically significant interaction with drug Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2003/21-366_Crestor_BioPharmr.pdf#page=51 Page: 51.0 |
||
Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2003/21-366_Crestor_BioPharmr.pdf#page=51 Page: 51.0 |
minor | yes (co-administration study) Comment: Itraconazole increased exposure of rosuvastatin based on AUC by 39% and 28%; no significant effect of ketoconazole on rosuvastatin; Rosuvastatin exposure decreased in presence of erythromycin for 20% and 31% of AUC and Cmax, respectively; Cyclosporine increased rosuvastatin Cmax and AUC by ~10- and 7-fold, respectively; Sources: https://www.accessdata.fda.gov/drugsatfda_docs/nda/2003/21-366_Crestor_BioPharmr.pdf#page=51 Page: 51.0 |
||
yes | ||||
yes | ||||
yes | ||||
yes | ||||
yes | ||||
yes |
Tox targets
Target | Modality | Activity | Metabolite | Clinical evidence |
---|---|---|---|---|
PubMed
Title | Date | PubMed |
---|---|---|
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 |
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The statin wars: why AstraZeneca must retreat. | 2003 Oct 25 |
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Rosuvastatin alone or with extended-release niacin: a new therapeutic option for patients with combined hyperlipidemia. | 2004 Fall |
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Rosuvastatin-associated hepatitis with autoimmune features. | 2005 May |
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An overview of statin-associated proteinuria. | 2006 May |
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McArdle disease with rhabdomyolysis induced by rosuvastatin: case report. | 2007 Sep |
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Effect of rosuvastatin on cholestasis-induced hepatic injury in rat livers. | 2010 Mar-Apr |
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Rosuvastatin attenuates the elevation in blood pressure induced by overexpression of human C-reactive protein. | 2011 Jul |
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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
In Vitro Use Guide
Sources: https://www.ncbi.nlm.nih.gov/pubmed/27813604
HUVECs treated with 30 mM glucose were used to simulate high-glucose conditions, and rosuvastatin concentrations ranging from 0.1 to 10 nM were used.
Substance Class |
Chemical
Created
by
admin
on
Edited
Fri Dec 15 15:44:27 GMT 2023
by
admin
on
Fri Dec 15 15:44:27 GMT 2023
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Record UNII |
413KH5ZJ73
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Record Status |
Validated (UNII)
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Record Version |
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WHO-ATC |
C10BX09
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WHO-ATC |
C10BX14
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WHO-VATC |
QC10BX05
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WHO-ATC |
C10BX07
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WHO-ATC |
C10AA07
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NDF-RT |
N0000000121
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FDA ORPHAN DRUG |
420513
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WHO-ATC |
A10BH52
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WHO-ATC |
C10BA06
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WHO-VATC |
QC10AA07
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WHO-ATC |
C10BX10
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NCI_THESAURUS |
C1655
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WHO-ATC |
C10BX13
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LIVERTOX |
NBK548620
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WHO-ATC |
C10BX05
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NDF-RT |
N0000175589
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WHO-VATC |
QC10BA06
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Code System | Code | Type | Description | ||
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38545
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C66523
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100000088232
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DTXSID8048492
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ROSUVASTATIN
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446157
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C422923
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Rosuvastatin
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413KH5ZJ73
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413KH5ZJ73
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301542
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287714-41-4
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CHEMBL1496
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SUB20634
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DB01098
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m9672
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PRIMARY | Merck Index | ||
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2954
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8021
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7317
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Related Record | Type | Details | ||
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SALT/SOLVATE -> PARENT |
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EXCRETED UNCHANGED |
FECAL
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TARGET -> INHIBITOR |
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SALT/SOLVATE -> PARENT |
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TRANSPORTER -> SUBSTRATE |
Km
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TRANSPORTER -> SUBSTRATE | |||
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TRANSPORTER -> INHIBITOR | |||
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TRANSPORTER -> SUBSTRATE | |||
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METABOLIC ENZYME -> SUBSTRATE |
MAJOR
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BINDER->LIGAND |
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Related Record | Type | Details | ||
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METABOLITE LESS ACTIVE -> PARENT |
N-desmethyl rosuvastatin has approximately one-sixth to one-half the HMG-CoA reductase inhibitory activity of the parent compound.
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METABOLITE LESS ACTIVE -> PARENT |
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METABOLITE INACTIVE -> PARENT |
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Related Record | Type | Details | ||
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ACTIVE MOIETY |
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Name | Property Type | Amount | Referenced Substance | Defining | Parameters | References |
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Biological Half-life | PHARMACOKINETIC |
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ORAL BIOAVAILABILITY | PHARMACOKINETIC |
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Volume of Distribution | PHARMACOKINETIC |
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MAXIMUM TOLERATED DOSE | TOXICITY |
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Tmax | PHARMACOKINETIC |
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