(atorvastatin · DailyMed)
LIPITAS EZ-10MG
ATORVASTATIN+ EZETIMIBE
What it does
Atorvastatin is a medication used to lower cholesterol levels in the blood.
Commonly used for: high cholesterol (hyperlipidemia), prevention of heart disease, prevention of stroke
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Source: Pharmacy and Poisons Board · fetched 2026-01-28 21:23:39 · updated 2026-07-20 10:57:48
Drug Interactions
128Pharmacodynamic 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 (81)
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 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.
About ezetimibe
Ezetimibe is a medication that helps lower cholesterol levels in the blood.
What it treats
- high cholesterol (hyperlipidemia)
How it works
It works by reducing the amount of cholesterol your body absorbs from the food you eat.
Who it's for
This medication is for adults and children over the age of 10 who need help managing their cholesterol levels.
AI-assisted summary grounded in BNF data - general information only, not medical advice. Always confirm with your pharmacist or doctor.
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.
Clinical monograph: Ezetimibe
BNF-referencedEzetimibe is a cholesterol absorption inhibitor used primarily to lower lipid levels in the blood. It works by selectively inhibiting the intestinal absorption of cholesterol and phytosterols, leading to a decrease in the delivery of intestinal cholesterol to the liver, which in turn reduces hepatic cholesterol stores and increases clearance from the bloodstream. This medication is often used in conjunction with statins for enhanced lipid-lowering effects.
Indications
- Adjunct to dietary measures in primary hypercholesterolaemia
- Adjunct to dietary measures and statin treatment in homozygous familial hypercholesterolaemia
- Adjunct to dietary measures in homozygous sitosterolaemia
Dosage
Children: Refer to the BNF for Children for appropriate dosing information, as the
Adults: The typical adult dosage of ezetimibe is 10 mg once daily.
Mechanism of action
Ezetimibe mediates its cholesterol-lowering effects by selectively inhibiting the absorption of cholesterol and phytosterols in the small intestine. It primarily targets the Niemann-Pick C1-Like 1 (NPC1L1) protein, which is vital for the internalization of free cholesterol into enterocytes. By blocking this protein at the jejunal brush border, ezetimibe reduces intestinal cholesterol uptake, consequently lowering hepatic cholesterol levels and enhancing cholesterol clearance from the blood.
Pharmacodynamics
Ezetimibe effectively reduces levels of total cholesterol, low-density lipoprotein cholesterol (LDL-C), apoprotein B (Apo B), non-high-density lipoprotein cholesterol (non-HDL-C), and triglycerides while increasing high-density lipoprotein cholesterol (HDL-C) in patients with hyperlipidemia. Its lipid-lowering effects are significantly enhanced when used in combination with statins or fenofibrate, resulting in substantial reductions in LDL levels and modest increases in HDL-C.
Pharmacokinetics
Ezetimibe is absorbed in the gastrointestinal tract and undergoes extensive first-pass metabolism to its active form. The elimination half-life is approximately 22 hours, and it is primarily excreted in the bile. The pharmacokinetics may be affected by hepatic impairment, and its use is not recommended in patients with significant liver disease. Ezetimibe does not require exocrine pancreatic function for its activity.
Contra-indications
- Gall bladder disease
- Hypoalbuminaemia
- Nephrotic syndrome
- Severe hepatic impairment
Adverse effects
- Common or very common: Asthenia, gastrointestinal discomfort, decreased appetite, diarrhea, dizziness, headache, muscle complaints
- Uncommon: Acute kidney injury, alopecia, cholestasis, erectile dysfunction, nausea, photosensitivity reaction
- Rare or very rare: Cholelithiasis, depression, insomnia, interstitial lung disease, pancreatitis, pancytopenia, peripheral neuropathy, rhabdomyolysis
Interactions
- Ciclosporin: Increases exposure to ciclosporin when co-administered
- Bulevirtide: Unknown interaction affecting efficacy
Precautions
- Use with caution in patients with moderate to severe hepatic impairment
- Monitor for signs of muscle pain or weakness, especially if used concurrently with statins
Pregnancy
Manufacturer advises use only if potential benefit outweighs risk; no information available.
Breast-feeding
Manufacturer advises avoiding use; no information available.
Storage
Store at room temperature, away from moisture and heat.
Formulations
- Ezetimibe 10 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.
Molecular reference: Ezetimibe
PubChem CID 150311Molecular formula: C24H21F2NO3
Mechanism of action
Ezetimibe mediates its blood cholesterol-lowering effect via selectively inhibiting the absorption of cholesterol and phytosterol by the small intestine without altering the absorption of fat-soluble vitamins and nutrients. The primary target of ezetimibe is the cholesterol transport protein Niemann-Pick C1-Like 1 (NPC1L1) protein. NPC1L1 is expressed on enterocytes/gut lumen (apical) as well as the hepatobiliary (canalicular) interface and plays a role in facilitating internalization of free cholesterol into the enterocyte in conjunction with the adaptor protein 2 (AP2) complex and clathrin. Once cholesterol in the gut lumen or bile is incorporated into the cell membrane of enterocytes, it binds to the sterol-sensing domain of NPC1L1 and forms a NPC1L1/cholesterol complex. The complex is then internalized or endocytosed by joining to AP2 clathrin, forming a vesicle complex that is translocated for storage in the endocytic recycling compartment. Ezetimibe does not require exocrine pancreatic function for its pharmacological activity; rather, it localizes and appears to act at the brush border of the small intestine. Ezetimibe selectively blocks the NPC1L1 protein in the jejunal brush border, reducing the uptake of intestinal lumen micelles into the enterocyte. Overall, ezetimibe causes a decrease in the delivery of intestinal cholesterol to the liver and reduction of hepatic cholesterol stores and an increase in clearance of cholesterol from the blood. While the full mechanism of action of ezetimibe in reducing the entry of cholesterol into both enterocytes and hepatocytes is not fully understood, one study proposed that ezetimibe prevents the NPC1L1/sterol complex from interacting with AP2 in clathrin coated vesicles and induces a conformational change in NPC1L1, rendering it incapable of binding to sterols. Another study suggested that ezetimibe disrupts the function of other protein complexes involved in regulating cholesterol uptake, including the CAV1–annexin 2 heterocomplex. Niemann-Pick C1-like 1 (NPC1L1) is a polytopic transmembrane protein that plays a critical role in cholesterol absorption. Ezetimibe, a hypocholesterolemic drug, has been reported to bind NPC1L1 and block cholesterol absorption. However, the molecular mechanism of NPC1L1-mediated cholesterol uptake and how ezetimibe inhibits this process are poorly defined. Here we find that cholesterol specifically promotes the internalization of NPC1L1 and that this process requires microfilaments and the clathrin/AP2 complex. Blocking NPC1L1 endocytosis dramatically decreases cholesterol internalization, indicating that NPC1L1 mediates cholesterol uptake via its vesicular endocytosis. Ezetimibe prevents NPC1L1 from incorporating into clathrin-coated vesicles and thus inhibits cholesterol uptake. ... Niemann-Pick C1-like protein (NPC1L1) mediates the absorption of dietary cholesterol in the proximal region of the intestine, a process that is blocked by cholesterol absorption inhibitors (CAIs), including ezetimibe. Using a proteomic approach, /it is/ demonstrated that NPC1L1 is the protein to which ezetimibe and its analogs bind. Next, ... the site of interaction of ezetimibe analogs /was determined/ with NPC1L1 by exploiting the different binding affinities of mouse and dog NPC1L1 for the radioligand analog of ezetimibe, [(3)H]AS. Chimeric and mutational studies indicate that high-affinity binding of [(3)H]AS to dog NPC1L1 depends on molecular determinants present in a 61-aa region of a large extracellular domain (loop C), where Phe-532 and Met-543 appear to be key contributors. These data suggest that the [(3)H]AS-binding site resides in the intestinal lumen and are consistent with preclinical data demonstrating in vivo efficacy of a minimally bioavailable CAI. Furthermore, these determinants of [(3)H]AS binding lie immediately adjacent to a hotspot of human NPC1L1 polymorphisms correlated with hypoabsorption of cholesterol. These observations, taken together wit
Pharmacodynamics
Ezetimibe was shown to reduce the levels of total cholesterol (total-C), low-density lipoprotein cholesterol (LDL-C), apoprotein B (Apo B), non-high-density lipoprotein cholesterol (non-HDL-C), and triglycerides (TG), and increase high-density lipoprotein cholesterol (HDL-C) in patients with hyperlipidemia. This therapeutic effect was more profound when ezetimibe was co-administered with a statin or fenofibrate compared to either treatment alone. In clinical trials involving patients with homozygous and heterozygous familial hypercholesterolemia and in those with sitosterolemia, a recommended therapeutic dose of ezetimibe was effective in reducing the LDL levels by 15-20% while increasing HDL-C by 2.5-5%. The effects of increased exposure to ezetimibe secondary to moderate-severe hepatic impairment have not been assessed - patients meeting these criteria should avoid the use of ezetimibe. Post-marketing reports indicate the potential for myopathy and rhabdomyolysis in patients taking ezetimibe, and this risk appears to be exacerbated in patients concurrently receiving, or having recently received, statin therapy.
Biological pathways
Source: PubChem (NCBI) · pathways from PathBank, Reactome, WikiPathways & PharmGKB.
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