RAN-PRAVASTATIN 40
PRAVASTATIN SODIUM
What it does
Pravastatin is a type of medication known as a statin, used to help lower cholesterol levels in the blood.
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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Sourcing - Kenya onlyRegistration & product details
Source: South African Health Products Regulatory Authority · fetched 2026-04-15 21:23:35 · updated 2026-10-21 04:01:39
Drug Interactions
96Pharmacodynamic Warnings
Pravastatin appears in TABLE 1: Drugs that cause hepatotoxicity
Severe (6)
Pravastatin - increases risk of rhabdomyolysis
Fenofibrate is predicted to increase the risk of rhabdomyolysis when given with statins (pravastatin). Avoid.
Pravastatin - increases risk of rhabdomyolysis
Fibrates (fenofibrate) are predicted to increase the risk of rhabdomyolysis when given with pravastatin. 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 (26)
Pravastatin - increases exposure
Letermovir is predicted to increase the exposure to statins (pravastatin). Avoid or adjust dose.
Pravastatin - increases exposure
Roxadustat is predicted to increase the exposure to statins (atorvastatin, pravastatin, rosuvastatin, simvastatin). Monitor adverse effects and adjust dose.
Pravastatin - increases exposure
Voxilaprevir with sofosbuvir and velpatasvir moderately increases the exposure to pravastatin. Monitor and adjust pravastatin dose, p. 222.
Statins - increases exposure
Amiodarone is predicted to increase the exposure to statins (atorvastatin). Monitor and adjust dose.
Statins - increases exposure
Dronedarone slightly increases the exposure to statins (atorvastatin). Monitor and adjust dose.
Unknown (64)
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.
Pravastatin - increases concentration
Darolutamide is predicted to increase the concentration of statins (pravastatin, simvastatin).
Pravastatin - increases exposure
Bempedoic acid increases the exposure to statins (pravastatin).
Pravastatin - increases exposure
Crizotinibispredictedtoincreasetheexposuretostatins (pravastatin).oTheoretical
Data from BNF 85 (British National Formulary). This is not a substitute for professional medical advice. Matched via: exact
About this medicine
Pravastatin is a type of medication known as a statin, used to help lower cholesterol levels in the blood.
What it treats
- high cholesterol (hyperlipidemia)
- prevention of heart disease
How it works
It works by reducing the amount of cholesterol produced by the liver, which helps to lower overall cholesterol levels in the blood.
Who it's for
This medication is for adults who need help managing their cholesterol levels to reduce the risk of heart problems.
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: pravastatin
BNF-referencedPravastatin is a member of the statin class of drugs, primarily used for lowering cholesterol levels. It functions by inhibiting the enzyme HMG-CoA reductase, which plays a critical role in the biosynthesis of cholesterol in the liver. This inhibition leads to a decrease in low-density lipoprotein (LDL) cholesterol, thereby reducing the risk of cardiovascular diseases such as heart attacks and strokes. Pravastatin is particularly noted for its ability to enhance the expression of LDL receptors, which facilitates increased clearance of circulating LDL from the bloodstream.
Indications
- Hyperlipidemia
- Primary prevention of cardiovascular disease
- Secondary prevention following myocardial infarction
- Familial hypercholesterolemia
Dosage
Adults: The usual starting dose is 40 mg once daily, which may be adjusted based
Mechanism of action
Pravastatin acts as a specific inhibitor of the hepatic HMG-CoA reductase enzyme, leading to a reduction in cholesterol biosynthesis. This inhibition increases the number of LDL receptors on cell surfaces, enhancing the receptor-mediated metabolism and clearance of LDL from circulation. Additionally, pravastatin inhibits the production of very low-density lipoproteins (VLDL), which are precursors to LDL.
Pharmacodynamics
Pravastatin primarily reduces total cholesterol, LDL cholesterol, and apolipoprotein B levels in the plasma. Clinical studies indicate that pravastatin can decrease total cholesterol by approximately 18%, LDL cholesterol by 27%, and triglycerides by 6%, while also increasing high-density lipoprotein (HDL) cholesterol levels by 4%. The drug has demonstrated a 24% reduction in the risk of death due to coronary disease in patients with a history of myocardial infarction or angina.
Pharmacokinetics
Pravastatin is well absorbed after oral administration, with peak plasma concentrations occurring within 1 to 1.5 hours. It undergoes extensive first-pass metabolism in the liver, which is primarily mediated by sulfation and to a lesser extent by cytochrome P450 enzymes. The elimination half-life of pravastatin is approximately 1.5 to 2 hours, and it is mainly excreted in the urine as metabolites. Its pharmacokinetics can be affected by factors such as liver function and concomitant use of other medications.
Contra-indications
- Active liver disease
- Pregnancy
- Breastfeeding
- Hypersensitivity to pravastatin or any component of the formulation
Adverse effects
- Headache
- Nausea
- Diarrhea
- Muscle pain
- Rhabdomyolysis
- Elevated liver enzymes
Interactions
- Fenofibrate: Severe (increases risk of rhabdomyolysis)
- Fibrates: Severe (increases risk of rhabdomyolysis)
- Letermovir: Moderate (increases exposure)
- Roxadustat: Moderate (increases exposure)
- Voxilaprevir with sofosbuvir and velpatasvir: Moderate (increases exposure)
- Darolutamide: Unknown (increases concentration)
- Bempedoic acid: Unknown (increases exposure)
- Crizotinib: Unknown (increases exposure)
- Elexacaftor: Unknown (increases exposure)
- HIV protease inhibitors: Unknown (affects exposure)
Precautions
- Monitor liver function tests before and during treatment
- Use caution in patients with a history of liver disease
- Consider risk of myopathy in patients with renal impairment
- Caution in elderly patients and those with hypothyroidism
Pregnancy
Pravastatin is contraindicated in pregnancy due to potential harm to the fetus.
Breast-feeding
Pravastatin is contraindicated during breastfeeding as it may affect the nursing infant.
Storage
Store at room temperature, away from moisture and heat. Keep out of reach of children.
Formulations
- Tablets: 10 mg, 20 mg, 40 mg, 80 mg
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: Pravastatinsodium
BNF-referencedPravastatin sodium is a member of the statin class of drugs, primarily used for the management of hyperlipidaemia. It functions by inhibiting HMG-CoA reductase, an enzyme crucial for cholesterol biosynthesis in the liver, thereby leading to a decrease in total cholesterol and low-density lipoprotein (LDL) cholesterol levels in the blood. This reduction helps in lowering the risk of cardiovascular diseases such as coronary heart disease and stroke.
Indications
- Primary hyperlipidaemia
- Mixed dyslipidaemia
- Prevention of cardiovascular disease in patients with elevated cholesterol levels
Dosage
Children: For children aged 9-17 years, the recommended starting dose is 10 mg daily, with a maximum dose of 80 mg daily, adjusted according to response
Adults: The usual starting dose is 40 mg once daily, which can be adjusted based on the patient's response, with a maximum dose of 80 mg once daily.
Mechanism of action
Pravastatin inhibits HMG-CoA reductase, the rate-limiting enzyme in the cholesterol synthesis pathway. This action reduces the hepatic cholesterol levels, leading to increased uptake of LDL cholesterol from the bloodstream and thereby lowering circulating LDL levels. Additionally, pravastatin enhances endothelial function and has anti-inflammatory properties.
Pharmacodynamics
The pharmacodynamics of pravastatin involve its ability to reduce levels of total cholesterol, LDL cholesterol, and triglycerides while increasing high-density lipoprotein (HDL) cholesterol. The effects are typically seen within a few weeks of starting therapy, with maximum reductions observed after 4 to 6 weeks of treatment. Pravastatin also has pleiotropic effects, which may contribute to its cardiovascular benefits, including improving endothelial function and reducing inflammation.
Pharmacokinetics
Pravastatin is well-absorbed from the gastrointestinal tract, with peak plasma concentrations occurring approximately 1 to 1.5 hours after oral administration. It undergoes extensive first-pass metabolism in the liver, primarily via the cytochrome P450 system, and has a relatively short half-life of about 1.5 to 2 hours. The drug is excreted mainly in the bile and feces, with minimal renal excretion. Dose adjustments may be necessary in patients with renal impairment, particularly at higher doses.
Contra-indications
- Active liver disease
- Pregnancy
- Breastfeeding
- Hypersensitivity to pravastatin or any component of the formulation
Adverse effects
- Myopathy
- Rhabdomyolysis
- Elevated liver enzymes
- Gastrointestinal disturbances
- Headache
- Dizziness
- Angioedema
- Lupus-like syndrome
Interactions
- CYP3A4 inhibitors (e.g., erythromycin, azole antifungals) may increase pravastatin levels
- Co-administration with other medications that may lead to muscle toxicity (e.g., other statins, gemfibrozil) should be done with caution
- Warfarin may have increased anticoagulant effects when used with pravastatin
Precautions
- Use cautiously in patients with a history of liver disease
- Monitor for signs of myopathy or rhabdomyolysis
- Regular liver function tests are recommended
- Assess renal function before initiating higher doses
Pregnancy
Pravastatin is contraindicated in pregnancy due to potential harm to the fetus. It is classified as a Category X drug.
Breast-feeding
Manufacturer advises avoiding use during breastfeeding due to insufficient data on safety.
Storage
Store at room temperature, away from moisture and heat. Keep out of reach of children.
Formulations
- 10 mg tablets
- 20 mg tablets
- Oral suspension (special-order)
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: pravastatin
PubChem CID 54687Molecular formula: C23H36O7
Mechanism of action
Pravastatin is a specific inhibitor of the hepatic HMG-CoA reductase in humans. The inhibition of this enzyme produces a reduction in cholesterol biosynthesis as HMG-CoA reductase activity is an early-limiting step in cholesterol biosynthesis. The inhibitory mechanism of action produces a reduction in cholesterol synthesis which in order has been observed to increase the number of LDL receptors on cell surfaces and an enhancement in receptor-mediated metabolism of LDL and clearance. On the other hand, pravastatin-driven inhibition of LDL production inhibits hepatic synthesis of VLDL as the LDL is the precursor for these molecules. 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 pravastatin/ 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. Pravastatin is a reversible inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, the enzyme that catalyzes the conversion of HMG-CoA to mevalonate, an early and rate limiting step in the biosynthetic pathway for cholesterol. In addition, pravastatin reduces very-low-density lipoprotein (VLDL) and triglyceride (TG) and increases high-density lipoprotein cholesterol (HDL-C). The HMG-CoA reductase inhibitors (statins) have been shown to exert several vascular protective effects that are not related to changes in cholesterol profile, and these effects of statins are partly caused by the activation of angiogenesis. Endothelial cell (EC) proliferation and migration are crucial events for angiogenesis and statins are known to enhance these events. However, the molecular mechanism by which statins promote EC proliferation and migration is not fully understood. In this study, we show Akt and its downstream target mammalian target of rapamycin (mTOR) play an important role in pravastatin-induced EC proliferation and migration. We found that pravastatin significantly enhanced the proliferation and migration of rat aortic endothelial cells (rAECs). The addition of pravastatin to rAECs resulted in rapid phosphorylation of Akt and p70 S6 kinase (p70S6K). LY294002, a specific inhibitor of phosphatidylinositol 3-kinase (PI3K), blocked both Akt and p70S6K phosphorylation, whereas rapamycin, a specific inhibitor of mTOR, suppressed only p70S6K phosphorylation induced by pravastatin. Furthermore, both LY294002 and rapamycin inhibited pravastatin-induced rAEC proliferation and migration. Taken together, our findings indicate that pravastatin activates PI3K/Akt/mTOR /p70S6K signaling in this sequential manner and this pathway contributes to pravastatin-i
Pharmacodynamics
The action of pravastatin on the 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase produces an increase in the expression of hepatic LDL receptors which in order decreases the plasma levels of LDL cholesterol. The effect of pravastatin has been shown to significantly reduce the circulating total cholesterol, LDL cholesterol, and apolipoprotein B. As well, it modestly reduces very low-density-lipoproteins (VLDL) cholesterol and triglycerides while increasing the level of high-density lipoprotein (HDL) cholesterol and apolipoprotein A. In clinical trials with patients with a history of myocardial infarction or angina with high total cholesterol, pravastatin decreased the level of total cholesterol by 18%, decreased of LDL by 27%, decreased of triglycerides by 6% and increased of high-density lipoprotein (HDL) by 4%. As well, there was reported a decrease in risk of death due to coronary disease of 24%. When coadministered with [cholestyramine], pravastatin can reduce by 50% the levels of LDL and slow the progression of atherosclerosis and the risk of myocardial infarction and death.
Biological pathways
Source: PubChem (NCBI) · pathways from PathBank, Reactome, WikiPathways & PharmGKB.
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The same active ingredient registered across other registries we cover - including different brands.