LESCOL CAPSULES 40MG
FLUVASTATIN SODIUM
What it does
Fluvastatin is a medication that helps lower cholesterol levels in the blood, reducing the risk of heart disease.
Commonly used for: high cholesterol (hyperlipidemia), prevention of heart disease
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 21:33:12 · updated 2026-07-20 11:07:22
Drug Interactions
98Pharmacodynamic Warnings
Fluvastatin appears in TABLE 1: Drugs that cause hepatotoxicity
Severe (6)
Fluvastatin - increases exposure
Darolutamide is predicted to increase the exposure to statins (atorvastatin, fluvastatin, rosuvastatin). Avoid.
Fluvastatin - 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 (30)
Fluvastatin - increases risk of rhabdomyolysis
Fenofibrate is predicted to increase the risk of rhabdomyolysis when given with statins (fluvastatin). Use with caution and adjust fenofibrate dose, p. 218.
Fluvastatin - increases exposure
Letermovir is predicted to increase the exposure to statins (fluvastatin). Monitor and adjust dose.
Fluvastatin - increases exposure
Etravirine is predicted to increase the exposure to statins (fluvastatin). Adjust dose.
Fluvastatin - decreases exposure
Rifampicin moderately decreases the exposure to statins (fluvastatin). Monitor and adjust dose.
Fluvastatin - increases exposure
Roxadustat might increase the exposure to statins (fluvastatin). Monitor adverse effects and adjust dose.
Unknown (62)
Daptomycin - increases risk of rhabdomyolysis
Statins are predicted to increase the risk of rhabdomyolysis when given with daptomycin. Daratumumab → see monoclonal antibodies Darbepoetin alfa → see TABLE 5 p. 1518 (thromboembolism), TABLE 16 p. 1
Daptomycin - increases risk of rhabdomyolysis e
Statins are predicted to increase the risk of rhabdomyolysis when given with daptomycin.
Fluvastatin - increases exposure
Amiodarone is predicted to increase the exposure to statins (fluvastatin).
Fluvastatin - increases exposure
Isavuconazole is predicted to increase the exposure to statins (fluvastatin, rosuvastatin).
Fluvastatin - increases exposure
Ciclosporin moderately increases the exposure to statins (fluvastatin).
Data from BNF 85 (British National Formulary). This is not a substitute for professional medical advice. Matched via: exact
About this medicine
Fluvastatin is a medication that helps lower cholesterol levels in the blood, reducing the risk of heart disease.
What it treats
- high cholesterol (hyperlipidemia)
- prevention of heart disease
How it works
Fluvastatin works by blocking a substance your body needs to make cholesterol, leading to lower cholesterol levels.
Who it's for
This medication is for adults who need help managing their cholesterol levels.
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: Fluvastatin
BNF-referencedFluvastatin is a synthetic lipid-lowering agent that belongs to the class of statins, specifically an HMG-CoA reductase inhibitor. It is primarily used to manage hyperlipidemia, notably primary hypercholesterolemia and mixed dyslipidemia. It functions by inhibiting the enzyme responsible for cholesterol synthesis in the liver, ultimately reducing plasma cholesterol levels. Fluvastatin is indicated for both the treatment of elevated cholesterol levels and the secondary prevention of cardiovascular events in patients with coronary heart disease.
Indications
- Primary hypercholesterolemia
- Mixed dyslipidemia
- Secondary prevention of coronary heart disease
Dosage
Children: Refer to
Adults: 40 mg to 80 mg once daily, to be taken at night. Doses may be adjusted at intervals of at least 4 weeks based on clinical response.
Mechanism of action
Fluvastatin selectively and competitively inhibits the hepatic enzyme hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase. This enzyme is crucial for converting HMG-CoA to mevalonate, which is the rate-limiting step in cholesterol biosynthesis. The inhibition of this enzyme leads to decreased hepatic cholesterol levels, which stimulates the synthesis of LDL receptors and enhances the hepatic uptake of LDL cholesterol, resulting in lowered levels of total and LDL cholesterol in the plasma.
Pharmacodynamics
Fluvastatin primarily lowers cholesterol and triglyceride levels in individuals with primary hypercholesterolemia and mixed dyslipidemia (Fredrickson types IIa and IIb). It has been shown to slow the progression of coronary atherosclerosis in patients with coronary heart disease (CHD) and serves as secondary prevention therapy to reduce the risk of requiring coronary revascularization procedures. Fluvastatin acts predominantly in the liver and is characterized by its extensive protein binding and minimal central nervous system penetration.
Pharmacokinetics
Fluvastatin has a relatively short half-life and is not associated with active metabolites. It undergoes extensive first-pass metabolism in the liver, which contributes to its pharmacological effects. The drug is primarily eliminated through hepatic metabolism and biliary excretion. Its absorption can be affected by food, and the drug is known to have high protein binding, which influences its distribution and elimination from the body.
Contra-indications
- Active liver disease
- Pregnancy
- Hypersensitivity to fluvastatin or any of its components
Adverse effects
- Myopathy
- Rhabdomyolysis
- Elevated liver enzymes
- Gastrointestinal disturbances (e.g. nausea, diarrhea)
- Headache
- Dizziness
- Fatigue
- Allergic reactions including rash and urticaria
Interactions
- Darolutamide: Severe (increases exposure)
- Tedizolid: Severe (increases exposure)
- Fenofibrate: Moderate (increases risk of rhabdomyolysis)
- Letermovir: Moderate (increases exposure)
- Etravirine: Moderate (increases exposure)
- Rifampicin: Moderate (decreases exposure)
- Roxadustat: Moderate (increases exposure)
- Fibrates: Moderate (increases risk of rhabdomyolysis)
- NNRTIs: Moderate (increases exposure)
- Amiodarone: Unknown (increases exposure)
Precautions
- Monitor liver function tests before and during treatment
- Use with caution in patients with a history of liver disease
- Assess renal function in patients with renal impairment
- Use with caution in patients at risk of myopathy or rhabdomyolysis
Pregnancy
Manufacturer advises against use during pregnancy due to potential risks.
Breast-feeding
Manufacturer advises avoiding use due to lack of information on safety.
Storage
Store below 25 degrees Celsius. Protect from light and moisture.
Formulations
- Fluvastatin 20 mg tablets
- Fluvastatin 40 mg tablets
- Fluvastatin oral suspension (sugar-free)
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: Fluvastatin
PubChem CID 1548972Molecular formula: C24H26FNO4
Mechanism of action
Fluvastatin selectively and competitively inhibits the hepatic enzyme hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase. HMG-CoA reductase is responsible for converting HMG-CoA to mevalonate, the rate-limiting step in cholesterol biosynthesis. Inhibition results in a decrease in hepatic cholesterol levels which stimulates the synthesis of LDL receptors and increases hepatic uptake of LDL cholesterol. The end result is decreased levels of plasma total and LDL cholesterol. Fluvastatin sodium is a competitive inhibitor of HMG-CoA reductase, the rate limiting enzyme that converts 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) to mevalonate, a precursor of sterols, including cholesterol. The inhibition of cholesterol biosynthesis reduces the cholesterol in hepatic cells, which stimulates the synthesis of LDL receptors and thereby increases the uptake of LDL particles. The end result of these biochemical processes is a reduction of the plasma cholesterol concentration. 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 fluvastatin/ 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 molecular dynamics simulation technique applied to the LOX-1 CTLD, considered in the entire receptor structure with or without a statin ligand inside the tunnel, indicates that the presence of a ligand largely increases the dimer stability. Electrophoretic separation and western blot confirm that different statins binding stabilize the dimer assembly of LOX-1 receptors in vivo. The simulative and experimental results allow us to propose a CTLD clamp motion, which enables the receptor-substrate coupling. These findings reveal a novel and significant functional effect of statins. Epidemiological studies suggest that statins (hydroxymethylglutaryl-CoA reductase inhibitors) could reduce the risk of Alzheimer disease. Although one possible explanation is through an effect on beta-amyloid (Abeta) metabolism, its effect remains to be elucidated. Here, we explored the molecular mechanisms of how statins influence Abeta metabolism. Fluvastatin at clinical doses significantly reduced Abeta and amyloid precursor protein C-terminal fragment (APP-CTF) levels among APP metabolites in the brain of C57BL/6 mice. Chronic intracerebroventricular infusion of lysosomal inhibitors blocked these effects, indicating that up-regulation of the lysosomal degradation of endogenous APP-CTFs is involved in reduced Abeta production. Biochemical analysis suggested that this was mediated by enhanced trafficking of APP-CTFs from endosomes to lysosomes, associated with marked changes of Rab proteins, which regulate endosomal function. In primary neurons, fluvastatin enhanced the degradation of APP-CTFs through an isoprenoid-dependent mechanism. Because our previous study suggests additive effects of fluvastatin on Abeta metabolism, we examined Abeta clearance rates by using the brain efflux index method and found its increased rates at high Abeta levels from brain. As LRP1 in brain microvessels was increased, up-regulation of LRP1-mediated Abeta clearance at the blood-brain barrier might be involved. In cultured brain microv
Pharmacodynamics
Fluvastatin, the first synthetically-derived HMG-CoA reductase inhibitor, is a hydrophilic, acidic, antilipemic agent used to lower cholesterol and triglyceride levels associated with primary hypercholesterolemia and mixed dyslipidemia (Fredrickson types IIa and IIb), to slow the progression of coronary atherosclerosis in patients with CHD and as secondary prevention therapy in patients with CHD to reduce the risk of requiring coronary revascularization procedures. Although similar to lovastatin, simvastatin, and pravastatin, fluvastatin has a shorter half-life, no active metabolites, extensive protein binding, and minimal CSF penetration. Fluvastatin acts primarily in the liver. It is prepared as a racemate of two erythro enantiomers of which the 3R,5S enantiomer exerts the pharmacologic effect.
Biological pathways
Source: PubChem (NCBI) · pathways from PathBank, Reactome, WikiPathways & PharmGKB.