(atorvastatin · DailyMed)
CADUET
AMLODEPINE BESYLATE/ATORVASTATIN
What it does
Amlodipine is a medication used to treat certain heart and blood vessel conditions.
Commonly used for: high blood pressure (hypertension), angina (chest pain)
Read more in plain English ↓Plain-language summary for general understanding - not medical advice. Always follow your pharmacist/doctor.
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Source: Pharmacy and Poisons Board · fetched 2026-01-28 21:51:56 · updated 2026-03-23 04:37:02
Drug Interactions
127Pharmacodynamic Warnings
Atorvastatin appears in TABLE 1: Drugs that cause hepatotoxicity
Severe (7)
Atorvastatin - increases exposure
Darolutamide is predicted to increase the exposure to statins (atorvastatin, fluvastatin, rosuvastatin). Avoid.
Atorvastatin - increases exposure
Posaconazole is predicted to increase the exposure to statins (atorvastatin). Avoid.
Atorvastatin - increases exposure
Tedizolid is predicted to increase the exposure to statins (atorvastatin, fluvastatin, rosuvastatin). Avoid.
Statins - increases exposure
Darolutamide is predicted to increase the exposure to statins (atorvastatin, fluvastatin, rosuvastatin). Avoid.
Statins - increases exposure
Posaconazole is predicted to increase the exposure to statins (atorvastatin). Avoid.
Statins - increases exposure
Tedizolid is predicted to increase the exposure to statins (atorvastatin, fluvastatin, rosuvastatin). Avoid.
Statins - increases exposure
Voxilaprevir with sofosbuvir and velpatasvir markedly increases the exposure to statins (rosuvastatin). Avoid.
Moderate (40)
Atorvastatin - increases exposure
Amiodarone is predicted to increase the exposure to statins (atorvastatin). Monitor and adjust dose.
Atorvastatin - increases exposure
Dronedarone slightly increases the exposure to statins (atorvastatin). Monitor and adjust dose.
Atorvastatin - decreases exposure
Carbamazepine is predicted to decrease the exposure to statins (atorvastatin). Monitor and adjust dose. Also see TABLE 1 p. 1517.
Atorvastatin - decreases exposure
Eslicarbazepine is predicted to decrease the exposure to statins (atorvastatin). Monitor and adjust dose.
Atorvastatin - increases exposure
Fluconazole is predicted to increase the exposure to statins (atorvastatin, simvastatin). Monitor and adjust dose. Also see TABLE 1 p. 1517.
Unknown (80)
Aliskiren - increases exposure
Atorvastatin slightly to moderately increases the exposure to aliskiren.
Atorvastatin - decreases exposure
Apalutamide is predicted to decrease the exposure to statins (atorvastatin).
Atorvastatin - decreases exposure
Enzalutamide is predicted to decrease the exposure to statins (atorvastatin, simvastatin).
Atorvastatin - decreases exposure
Phenytoin moderately decreases the exposure to statins (atorvastatin).
Atorvastatin - decreases exposure
Oxcarbazepine is predicted to decrease the exposure to statins (atorvastatin, simvastatin).
Data from BNF 85 (British National Formulary). This is not a substitute for professional medical advice. Matched via: exact
About amlodepine
Amlodipine is a medication used to treat certain heart and blood vessel conditions.
What it treats
- high blood pressure (hypertension)
- angina (chest pain)
How it works
Amlodipine helps relax and widen blood vessels, making it easier for the heart to pump blood.
Who it's for
It is prescribed for adults who have high blood pressure or chest pain caused by angina.
AI-assisted summary grounded in BNF data - general information only, not medical advice. Always confirm with your pharmacist or doctor.
About atorvastatin
Atorvastatin is a medication used to lower cholesterol levels in the blood.
What it treats
- high cholesterol (hyperlipidemia)
- prevention of heart disease
- prevention of stroke
How it works
Atorvastatin works by blocking a substance your body needs to make cholesterol, which helps reduce the amount of cholesterol in your blood.
Who it's for
It is suitable for adults who have high cholesterol or are at risk of heart disease.
Drug class
Statins
Cautions
- • Be cautious if you are taking other medications that can harm the liver.
AI-assisted summary grounded in BNF data - general information only, not medical advice. Always confirm with your pharmacist or doctor.
Clinical monograph: amlodepine
Amlodipine is a long-acting dihydropyridine calcium channel blocker primarily used for the treatment of hypertension and angina pectoris. It works by relaxing blood vessels, thereby reducing blood pressure and decreasing the workload on the heart. Amlodipine is well-absorbed from the gastrointestinal tract, with a long half-life that allows for once-daily dosing.
Indications
- Hypertension
- Angina pectoris
- Chronic stable angina
- Vasospastic angina
Dosage
Children: Refer to the BNF for Children for specific paediatric dosing guidelines.
Adults: Refer to the BNF for specific adult dosing guidelines.
Mechanism of action
Amlodipine inhibits the influx of calcium ions into vascular smooth muscle and cardiac muscle by blocking L-type calcium channels. This results in vasodilation, decreased peripheral vascular resistance, and reduced myocardial oxygen demand, which helps in managing conditions like hypertension and angina.
Pharmacodynamics
The pharmacodynamic effects of amlodipine include a decrease in systemic vascular resistance and arterial pressure. It leads to significant reductions in both systolic and diastolic blood pressure without causing reflex tachycardia. Amlodipine also improves exercise tolerance in patients with chronic stable angina.
Pharmacokinetics
Amlodipine has a bioavailability of approximately 64-90% and reaches peak plasma concentrations within 6-12 hours after oral administration. It is extensively metabolized in the liver, primarily by cytochrome P450 3A4, and has a half-life of about 30-50 hours, allowing for once-daily dosing. The drug is excreted mainly in the urine as metabolites, with less than 10% excreted unchanged.
Contra-indications
- Severe hypotension
- Aortic stenosis
- Cardiogenic shock
- Severe hepatic impairment
- Hypersensitivity to amlodipine or any of its components
Adverse effects
- Peripheral edema
- Dizziness
- Fatigue
- Palpitations
- Nausea
- Flushing
- Abdominal pain
- Headache
Interactions
- CYP3A4 inhibitors (e.g., ketoconazole, itraconazole) may increase amlodipine levels
- CYP3A4 inducers (e.g., rifampicin, St. John's Wort) may decrease amlodipine levels
- Other antihypertensives may have additive effects when used concomitantly with amlodipine
Precautions
- Caution in patients with severe aortic stenosis
- Caution in patients with heart failure
- Monitor blood pressure regularly
- Use with caution in patients with hepatic impairment
Pregnancy
Amlodipine should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. Caution is advised.
Breast-feeding
Amlodipine is excreted in human breast milk. Caution is recommended when administered to nursing mothers.
Storage
Store at room temperature, away from moisture and heat. Keep out of reach of children.
Formulations
- Tablets (2.5 mg, 5 mg, 10 mg)
- Oral suspension (not widely available)
AI-synthesized from BNF references - general information only, not a substitute for professional medical advice or the current BNF. Verify doses with a pharmacist.
Clinical monograph: Atorvastatin
BNF-referencedAtorvastatin is a statin medication used to lower cholesterol levels and reduce the risk of cardiovascular disease. It works by inhibiting HMG-CoA reductase, an enzyme involved in the synthesis of cholesterol in the liver.
Indications
- Hyperlipidaemia
- Primary prevention of cardiovascular disease
- Secondary prevention of cardiovascular events
Dosage
Children: Refer to the BNF for Children for specific dosing information.
Adults: Initial dose is typically 10-20 mg once daily, which can be adjusted based on lipid levels and tolerability. Maximum dose is 80 mg once daily.
Mechanism of action
Atorvastatin competitively inhibits HMG-CoA reductase, leading to decreased cholesterol synthesis and increased uptake of LDL cholesterol from the blood.
Pharmacodynamics
Atorvastatin reduces total cholesterol, LDL cholesterol, and triglycerides while increasing HDL cholesterol. The effects are dose-dependent, and it may also provide vascular protection.
Pharmacokinetics
Atorvastatin is rapidly absorbed after oral administration, with peak plasma concentrations occurring within 1 to 2 hours. It undergoes extensive first-pass metabolism in the liver, primarily by CYP3A4. The elimination half-life is approximately 14 hours, and it is excreted mainly in bile.
Contra-indications
- Active liver disease
- Unexplained persistent elevations in serum transaminases
- Pregnancy
Adverse effects
- Myopathy
- Rhabdomyolysis
- Hepatotoxicity
- Severe cutaneous adverse reactions (SCARs)
- Hypoglycaemia
- Peripheral oedema
- Cough
- Dyspnoea
- Weight loss
Interactions
- darolutamide: Severe (increases exposure)
- posaconazole: Severe (increases exposure)
- tedizolid: Severe (increases exposure)
- amiodarone: Moderate (increases exposure)
- dronedarone: Moderate (increases exposure)
- carbamazepine: Moderate (decreases exposure)
- eslicarbazepine: Moderate (decreases exposure)
- fluconazole: Moderate (increases exposure)
- diltiazem: Moderate (increases exposure)
- cobicistat: Moderate (increases exposure)
Precautions
- Caution in patients with a history of haemorrhagic stroke
- Caution in hepatic impairment
- Patient counselling advised for muscle effects
Pregnancy
Manufacturer advises against use due to potential risk of fetal congenital anomalies.
Breast-feeding
Manufacturer advises to avoid; no information available.
Storage
Store in a cool, dry place away from direct sunlight.
Formulations
- Atorvastatin 10 mg tablets
- Atorvastatin 20 mg tablets
- Atorvastatin 30 mg tablets
- Atorvastatin 60 mg tablets
- Atorvastatin 80 mg tablets
AI-synthesized from BNF references - general information only, not a substitute for professional medical advice or the current BNF. Verify doses with a pharmacist.
Molecular reference: Atorvastatin
PubChem CID 60823Molecular formula: C33H35FN2O5
Mechanism of action
Atorvastatin is a statin medication and a competitive inhibitor of the enzyme HMG-CoA (3-hydroxy-3-methylglutaryl coenzyme A) reductase, which catalyzes the conversion of HMG-CoA to mevalonate, an early rate-limiting step in cholesterol biosynthesis. Atorvastatin acts primarily in the liver, where decreased hepatic cholesterol concentrations stimulate the upregulation of hepatic low-density lipoprotein (LDL) receptors, which increases hepatic uptake of LDL. Atorvastatin also reduces Very-Low-Density Lipoprotein-Cholesterol (VLDL-C), serum triglycerides (TG) and Intermediate Density Lipoproteins (IDL), as well as the number of apolipoprotein B (apo B) containing particles, but increases High-Density Lipoprotein Cholesterol (HDL-C). _In vitro_ and _in vivo_ animal studies also demonstrate that atorvastatin exerts vasculoprotective effects independent of its lipid-lowering properties, also known as the pleiotropic effects of statins. These effects include improvement in endothelial function, enhanced stability of atherosclerotic plaques, reduced oxidative stress and inflammation, and inhibition of the thrombogenic response. Statins were also found to bind allosterically to β2 integrin function-associated antigen-1 (LFA-1), which plays an essential role in leukocyte trafficking and T cell activation. In animal models, Lipitor lowers plasma cholesterol and lipoprotein levels by inhibiting 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase and cholesterol synthesis in the liver and by increasing the number of hepatic low-density lipoprotein (LDL) receptors on the cell surface to enhance uptake and catabolism of LDL; Lipitor also reduces LDL production and the number of LDL particles. Lipitor reduces LDL-cholesterol (LDL-C) in some patients with homozygous familial hypercholesterolemia (FH), a population that rarely responds to other lipid-lowering medication(s). Lipitor is a selective, competitive inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, the rate-limiting enzyme that converts 3-hydroxy-3-methylglutaryl-coenzyme A to mevalonate, a precursor of sterols, including cholesterol. Cholesterol and triglycerides circulate in the bloodstream as part of lipoprotein complexes. With ultracentrifugation, these complexes separate into HDL (high-density lipoprotein), IDL (intermediate-density lipoprotein), LDL (low-density lipoprotein), and VLDL (very-low-density lipoprotein) fractions. Triglycerides (TG) and cholesterol in the liver are incorporated into VLDL and released into the plasma for delivery to peripheral tissues. LDL is formed from VLDL and is catabolized primarily through the high-affinity LDL receptor. Clinical and pathologic studies show that elevated plasma levels of total cholesterol (total-C), LDL-cholesterol (LDL-C), and apolipoprotein B (apo B) promote human atherosclerosis and are risk factors for developing cardiovascular disease, while increased levels of HDL-C are associated with a decreased cardiovascular risk. Statins are largely used in clinics in the treatment of patients with cardiovascular diseases for their effect on lowering circulating cholesterol. Lectin-like oxidized low-density lipoprotein (LOX-1), the primary receptor for ox-LDL, plays a central role in the pathogenesis of atherosclerosis and cardiovascular disorders. We have recently shown that chronic exposure of cells to lovastatin disrupts LOX-1 receptor cluster distribution in plasma membranes, leading to a marked loss of LOX-1 function. Here we investigated the molecular mechanism of statin-mediated LOX-1 inhibition and we demonstrate that all tested statins /including atorvastatin/ are able to displace the binding of fluorescent ox-LDL to LOX-1 by a direct interaction with LOX-1 receptors in a cell-based binding assay. Molecular docking simulations confirm the interaction and indicate that statins completely fill the hydrophobic tunnel that crosses the C-type lectin-like (CTLD) recognition domain of LOX-1. Classical
Pharmacodynamics
Atorvastatin is an oral antilipemic agent that reversibly inhibits HMG-CoA reductase. It lowers total cholesterol, low-density lipoprotein-cholesterol (LDL-C), apolipoprotein B (apo B), non-high density lipoprotein-cholesterol (non-HDL-C), and triglyceride (TG) plasma concentrations while increasing HDL-C concentrations. High LDL-C, low HDL-C and high TG concentrations in the plasma are associated with increased risk of atherosclerosis and cardiovascular disease. The total cholesterol to HDL-C ratio is a strong predictor of coronary artery disease, and high ratios are associated with a higher risk of disease. Increased levels of HDL-C are associated with lower cardiovascular risk. By decreasing LDL-C and TG and increasing HDL-C, atorvastatin reduces the risk of cardiovascular morbidity and mortality. Elevated cholesterol levels (and high low-density lipoprotein (LDL) levels in particular) are an important risk factor for the development of CVD. Clinical studies have shown that atorvastatin reduces LDL-C and total cholesterol by 36-53%. In patients with dysbetalipoproteinemia, atorvastatin reduced the levels of intermediate-density lipoprotein cholesterol. It has also been suggested that atorvastatin can limit the extent of angiogenesis, which can be useful in the treatment of chronic subdural hematoma. **Myopathy/Rhabdomyolysis** Atorvastatin, like other HMG-CoA reductase inhibitors, is associated with a risk of drug-induced myopathy characterized by muscle pain, tenderness, or weakness in conjunction with elevated levels of creatine kinase (CK). Myopathy often manifests as rhabdomyolysis with or without acute renal failure secondary to myoglobinuria. The risk of statin-induced myopathy is dose-related, and the symptoms of myopathy are typically resolved upon drug discontinuation. Results from observational studies suggest that 10-15% of people taking statins may experience muscle aches at some point during treatment. **Liver Dysfunction** Statins, like some other lipid-lowering therapies, have been associated with biochemical abnormalities of liver function. Persistent elevations (> 3 times the upper limit of normal [ULN] occurring on two or more occasions) in serum transaminases occurred in 0.7% of patients who received atorvastatin in clinical trials. This effect appears to be dose-related. **Endocrine Effects** Statins are associated with a risk of increased serum HbA1c and glucose levels. An _in vitro_ study demonstrated a dose-dependent cytotoxic effect on human pancreatic islet β cells following treatment with atorvastatin. Moreover, insulin secretion rates decreased relative to control. HMG-CoA reductase inhibitors interfere with cholesterol synthesis and may theoretically interfere with the production of adrenal and/or gonadal steroids. Clinical studies with atorvastatin and other HMG-CoA reductase inhibitors have suggested that these agents do not affect plasma cortisol concentrations, basal plasma testosterone concentration, or adrenal reserve. However, the effect of statins on male fertility has not been fully investigated. The effects of statins on the pituitary-gonadal axis in premenopausal women are unknown. **Cardiovascular** Significant decreases in circulating ubiquinone levels in patients treated with atorvastatin and other statins have been observed. The clinical significance of a potential long-term statin-induced deficiency of ubiquinone has not been established. It has been reported that a decrease in myocardial ubiquinone levels could lead to impaired cardiac function in patients with borderline congestive heart failure. **Lipoprotein A** In some patients, the beneficial effect of lowered total cholesterol and LDL-C levels may be partly blunted by the concomitant increase in Lp(a) lipoprotein concentrations. Present knowledge suggests the importance of high Lp(a) levels as an emerging risk factor for coronary heart disease. Further studies have demonstrated statins affect Lp(a) levels diffe
Biological pathways
Source: PubChem (NCBI) · pathways from PathBank, Reactome, WikiPathways & PharmGKB.
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