Xarator (Atorvastatin) 20mg strip Pfizerအဆီကျဆေး
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Brand: Manufactured by Pfizer Puerto Rico and packed and released by Pfizer Germany
အဆီကျဆေး ဖြစ်ပြီးဆရာဝန် ညွှန်ကြားချက်ဖြင့်သာသောက်ရန်
Contents
Atorvastatin calcium.
Description
Each tablet contains atorvastatin calcium (as crystalline form) equivalent to atorvastatin 10, 20 or 40 mg.
Xarator also contains the following excipients: Calcium carbonate, microcrystalline cellulose, lactose monohydrate, croscarmellose sodium, polysorbate 80, hydroxypropyl cellulose, magnesium stearate, Opadry white YS-1-7040, antifoam AF emulsion medical, candelilla wax.
Atorvastatin calcium is a white to off-white crystalline powder, practically insoluble in aqueous solutions of pH≤4. It is very slightly soluble in distilled water, pH 7.4 phosphate buffer and acetonitrile, slightly soluble in ethanol and freely soluble in methanol.
Atorvastatin calcium is (C33H34FN2O5)2 Ca·3 H2O and its molecular weight is 1209.42.
Xarator also contains the following excipients: Calcium carbonate, microcrystalline cellulose, lactose monohydrate, croscarmellose sodium, polysorbate 80, hydroxypropyl cellulose, magnesium stearate, Opadry white YS-1-7040, antifoam AF emulsion medical, candelilla wax.
Atorvastatin calcium is a white to off-white crystalline powder, practically insoluble in aqueous solutions of pH≤4. It is very slightly soluble in distilled water, pH 7.4 phosphate buffer and acetonitrile, slightly soluble in ethanol and freely soluble in methanol.
Atorvastatin calcium is (C33H34FN2O5)2 Ca·3 H2O and its molecular weight is 1209.42.
Action
Pharmacology: Pharmacodynamics: Atorvastatin calcium is a synthetic lipid-lowering agent, which is an inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. This enzyme catalyzes the conversion of HMG-CoA to mevalonate, an early and rate-limiting step in cholesterol biosynthesis.
Mechanism of Action: Atorvastatin is a selective, competitive inhibitor of HMG-CoA reductase, the rate-limiting enzyme that converts 3-hydroxy-3-methylglutaryl-coenzyme A to mevalonate, a precursor of sterols, including cholesterol. In patients with homozygous and heterozygous familial hypercholesterolemia (FH), nonfamilial forms of hypercholesterolemia, and mixed dyslipidemia, atorvastatin reduces total cholesterol (total-C), low-density lipoprotein cholesterol (LDL-C) and apolipoprotein B (apo B). Atorvastatin also reduces very-low-density lipoprotein cholesterol (VLDL-C) and triglycerides (TG) and produces variable increases in high-density lipoprotein cholesterol (HDL-C).
Atorvastatin lowers plasma cholesterol and lipoprotein levels by inhibiting HMG-CoA reductase and cholesterol synthesis in the liver and by increasing the number of hepatic LDL receptors on the cell surface for enhanced uptake and catabolism of LDL.
Atorvastatin reduces LDL production and the number of LDL particles. Atorvastatin produces a profound and sustained increase in LDL receptor activity coupled with a beneficial change in the quality of circulating LDL particles. Atorvastatin is effective in reducing LDL in patients with homozygous familial hypercholesterolemia, a population that has not normally responded to lipid-lowering medication.
Atorvastatin and some of its metabolites are pharmacologically active in humans. The primary site of action of atorvastatin is the liver, which is the principal site of cholesterol synthesis and LDL clearance. Low-density lipoprotein cholesterol reduction correlates better with drug dose than it does with systemic drug concentration. Individualization of drug dosage should be based on therapeutic response (see Dosage & Administration).
In a dose-response study, atorvastatin (10-80 mg) reduced total-C (30-46%), LDL-C (41-61%), apo B (34-50%) and TG (14-33%). These results are consistent in patients with heterozygous familial hypercholesterolemia, nonfamilial forms of hypercholesterolemia and mixed hyperlipidemia, including patients with non-insulin-dependent diabetes mellitus.
In patients with isolated hypertriglyceridemia, atorvastatin reduces total-C, LDL-C, VLDL-C, apo B, TG and non-HDL-C and increases HDL-C. In patients with dysbetalipoproteinemia, atorvastatin reduces IDL-C (intermediate density lipoprotein cholesterol).
In patients with Fredrickson types IIa and IIb hyperlipoproteinemia pooled from 24 controlled trials, the median percent increases from baseline in HDL-C for atorvastatin (10-80 mg) were 5.1-8.7% in a non-dose-related manner. Additionally, analysis of this pooled data demonstrated significant dose related decreases in total-C/HDL-C and LDL-C/HDL-C ratios, ranging from -29 to -44% and -37 to -55%, respectively.
The effects of atorvastatin on ischemic events and total mortality were studied in the Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering study (MIRACL). This multicenter, randomized, double-blind, placebo-controlled study followed 3086 patients with acute coronary syndromes: Unstable angina or non-Q wave myocardial infarction (MI). Patients were treated with standard care, including diet, and either atorvastatin 80 mg daily or placebo for a median duration of 16 weeks. The final LDL-C, total-C, HDL-C and TG levels were 72, 147, 48, 139 mg/dL in the atorvastatin group, respectively, and 135, 217, 46, and 187 mg/dL, respectively, in the placebo group. Atorvastatin significantly reduced the risk of ischemic events and death by 16%. The risk of experiencing re-hospitalization for angina pectoris with documented evidence of myocardial ischemia was significantly reduced by 26%. Atorvastatin reduced the risk of ischemic events and death to a similar extent across the range of baseline LDL-C. In addition, atorvastatin reduced the risk of ischemic events and death to similar extents in patients with non-Q wave MI and unstable angina, as well as in males and females and in patients ≤65 years and >65 years.
Prevention of Cardiovascular Complications: In the Anglo-Scandinavian Cardiac Outcomes Trial Lipid Lowering Arm (ASCOT-LLA), the effect of atorvastatin on fatal and nonfatal coronary heart disease (CHD) was assessed in 10,305 hypertensive patients 40-80 years (mean of 63 years), without a previous myocardial infarction and with total cholesterol (TC) levels <6.5 mmol/L (251 mg/dL). Additionally all patients had at least 3 of the following cardiovascular risk factors: Male gender, age >55 years, smoking, diabetes, history of CHD in a 1st-degree relative, TC:HDL >6, peripheral vascular disease, left ventricular hypertrophy, prior cerebrovascular event, specific electrocardiogram (ECG) abnormality, proteinuria/albuminuria. In this double-blind, placebo-controlled study, patients were treated with antihypertensive therapy (goal BP <140/90 mmHg for nondiabetic patients, <130/80 mmHg for diabetic patients) and allocated to either atorvastatin 10 mg daily (n=5168) or placebo (n=5137). As the effect of atorvastatin treatment compared to placebo exceeded the significance threshold during an interim analysis, the ASCOT-LLA was terminated early at 3.3 years instead of 5 years. Additionally, blood pressure was well controlled and similar in patients assigned atorvastatin and placebo. These changes persisted throughout the treatment period
Mechanism of Action: Atorvastatin is a selective, competitive inhibitor of HMG-CoA reductase, the rate-limiting enzyme that converts 3-hydroxy-3-methylglutaryl-coenzyme A to mevalonate, a precursor of sterols, including cholesterol. In patients with homozygous and heterozygous familial hypercholesterolemia (FH), nonfamilial forms of hypercholesterolemia, and mixed dyslipidemia, atorvastatin reduces total cholesterol (total-C), low-density lipoprotein cholesterol (LDL-C) and apolipoprotein B (apo B). Atorvastatin also reduces very-low-density lipoprotein cholesterol (VLDL-C) and triglycerides (TG) and produces variable increases in high-density lipoprotein cholesterol (HDL-C).
Atorvastatin lowers plasma cholesterol and lipoprotein levels by inhibiting HMG-CoA reductase and cholesterol synthesis in the liver and by increasing the number of hepatic LDL receptors on the cell surface for enhanced uptake and catabolism of LDL.
Atorvastatin reduces LDL production and the number of LDL particles. Atorvastatin produces a profound and sustained increase in LDL receptor activity coupled with a beneficial change in the quality of circulating LDL particles. Atorvastatin is effective in reducing LDL in patients with homozygous familial hypercholesterolemia, a population that has not normally responded to lipid-lowering medication.
Atorvastatin and some of its metabolites are pharmacologically active in humans. The primary site of action of atorvastatin is the liver, which is the principal site of cholesterol synthesis and LDL clearance. Low-density lipoprotein cholesterol reduction correlates better with drug dose than it does with systemic drug concentration. Individualization of drug dosage should be based on therapeutic response (see Dosage & Administration).
In a dose-response study, atorvastatin (10-80 mg) reduced total-C (30-46%), LDL-C (41-61%), apo B (34-50%) and TG (14-33%). These results are consistent in patients with heterozygous familial hypercholesterolemia, nonfamilial forms of hypercholesterolemia and mixed hyperlipidemia, including patients with non-insulin-dependent diabetes mellitus.
In patients with isolated hypertriglyceridemia, atorvastatin reduces total-C, LDL-C, VLDL-C, apo B, TG and non-HDL-C and increases HDL-C. In patients with dysbetalipoproteinemia, atorvastatin reduces IDL-C (intermediate density lipoprotein cholesterol).
In patients with Fredrickson types IIa and IIb hyperlipoproteinemia pooled from 24 controlled trials, the median percent increases from baseline in HDL-C for atorvastatin (10-80 mg) were 5.1-8.7% in a non-dose-related manner. Additionally, analysis of this pooled data demonstrated significant dose related decreases in total-C/HDL-C and LDL-C/HDL-C ratios, ranging from -29 to -44% and -37 to -55%, respectively.
The effects of atorvastatin on ischemic events and total mortality were studied in the Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering study (MIRACL). This multicenter, randomized, double-blind, placebo-controlled study followed 3086 patients with acute coronary syndromes: Unstable angina or non-Q wave myocardial infarction (MI). Patients were treated with standard care, including diet, and either atorvastatin 80 mg daily or placebo for a median duration of 16 weeks. The final LDL-C, total-C, HDL-C and TG levels were 72, 147, 48, 139 mg/dL in the atorvastatin group, respectively, and 135, 217, 46, and 187 mg/dL, respectively, in the placebo group. Atorvastatin significantly reduced the risk of ischemic events and death by 16%. The risk of experiencing re-hospitalization for angina pectoris with documented evidence of myocardial ischemia was significantly reduced by 26%. Atorvastatin reduced the risk of ischemic events and death to a similar extent across the range of baseline LDL-C. In addition, atorvastatin reduced the risk of ischemic events and death to similar extents in patients with non-Q wave MI and unstable angina, as well as in males and females and in patients ≤65 years and >65 years.
Prevention of Cardiovascular Complications: In the Anglo-Scandinavian Cardiac Outcomes Trial Lipid Lowering Arm (ASCOT-LLA), the effect of atorvastatin on fatal and nonfatal coronary heart disease (CHD) was assessed in 10,305 hypertensive patients 40-80 years (mean of 63 years), without a previous myocardial infarction and with total cholesterol (TC) levels <6.5 mmol/L (251 mg/dL). Additionally all patients had at least 3 of the following cardiovascular risk factors: Male gender, age >55 years, smoking, diabetes, history of CHD in a 1st-degree relative, TC:HDL >6, peripheral vascular disease, left ventricular hypertrophy, prior cerebrovascular event, specific electrocardiogram (ECG) abnormality, proteinuria/albuminuria. In this double-blind, placebo-controlled study, patients were treated with antihypertensive therapy (goal BP <140/90 mmHg for nondiabetic patients, <130/80 mmHg for diabetic patients) and allocated to either atorvastatin 10 mg daily (n=5168) or placebo (n=5137). As the effect of atorvastatin treatment compared to placebo exceeded the significance threshold during an interim analysis, the ASCOT-LLA was terminated early at 3.3 years instead of 5 years. Additionally, blood pressure was well controlled and similar in patients assigned atorvastatin and placebo. These changes persisted throughout the treatment period
Xarator (Atorvastatin) 20mg strip Pfizerအဆီကျဆေး
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