Pravastatin !
A water-soluble statin that is not metabolized by CYP enzymes, so it has fewer drug interactions. It lowers LDL and prevents heart attacks.
Updated 2026-11-01
The figure shows compactin (mevastatin), the fungal statin from which pravastatin is derived, in the HMG-CoA pocket of human HMG-CoA reductase; pravastatin occupies the same site.
Mechanism of action
Pravastatin is an open-ring hydroxy acid that competitively inhibits HMG-CoA reductase in the liver. Less cholesterol synthesis activates SREBP-2, which raises LDL receptors on hepatocytes and increases LDL clearance from the blood. Being hydrophilic, it depends on active uptake into hepatocytes.
- Taken up into hepatocytes and blocks HMG-CoA reductase
- Liver cholesterol synthesis falls
- More LDL receptors clear LDL from the blood
- Fewer coronary events
Pharmacokinetics
- Absorption
- Oral, already in its active form; absolute bioavailability about 17% because of first-pass uptake by the liver.
- Metabolism
- Not metabolized to any appreciable extent by CYP enzymes; it is converted by isomerization and ring hydroxylation.
- Elimination
- Both routes: after an intravenous dose about half is cleared by the kidney and half by bile and biotransformation.
- Half-life
- Short: about 1.8 hours for the parent drug.
Indications
- High LDL cholesterol and prevention of coronary events Atherosclerosis and dyslipidaemia →
- Heterozygous familial hypercholesterolemia in children and adolescents Familial hypercholesterolemia →
- Secondary prevention after myocardial infarction Myocardial Infarction (Heart Attack) →
Adverse effects
Common
- Muscle aches
- Headache, nausea, diarrhea
- Raised liver transaminases
- Rises in HbA1c and fasting glucose
Contraindications
- Acute liver failure or decompensated cirrhosis
- Hypersensitivity to pravastatin or an excipient
Key interactions
- Gemfibrozil
- Increased myopathy risk; the combination is avoided.
- Cyclosporine
- Raises pravastatin exposure; the dose is restricted.
- Clarithromycin, erythromycin
- Raise pravastatin exposure (through transporters, not CYP3A4); the dose is limited.
- Other fibrates, niacin
- Add to the muscle risk; benefit is weighed against risk.
What is monitored
- Lipid panel before and some weeks after starting
- Liver enzymes at baseline and when clinically indicated
- Creatine kinase if there are muscle symptoms
Administration and safety
- Oral tablet once daily; its short half-life is why it was traditionally given in the evening.
- With a bile acid sequestrant, pravastatin is given at least 1 hour before or 4 hours after it.
- Lower starting doses are used in severe kidney impairment.
Nursing care
- Before: lipid panel, liver enzymes and a medication review.
- Ask about muscle pain, weakness or dark urine.
- Teach daily adherence alongside diet and exercise.
- Ask about pregnancy plans.
Pregnancy and breastfeeding
Stopped when pregnancy is recognized, with case-by-case weighing in very high-risk patients; not used while breastfeeding.
Test yourself
Think of the answer, then tap the question to see it.
Why does pravastatin have fewer CYP3A4 interactions than simvastatin?
It is not metabolized to any appreciable extent by CYP enzymes; it is cleared by isomerization, hydroxylation and excretion.
Why does clarithromycin still raise pravastatin levels?
Through transporters (OATP uptake), not CYP3A4, so the pravastatin dose is limited.
Which statin is used for heterozygous familial hypercholesterolemia from childhood?
Pravastatin is one of the statins labelled for children and adolescents with heterozygous FH.
Related drugs
Related conditions
Educational content on how drugs work; not a prescribing guide and no substitute for a health professional's advice. No doses are given.
Sources: Pravastatin: MedlinePlus Drug Information (MedlinePlus (U.S. National Library of Medicine), 2026); DailyMed - PRAVASTATIN SODIUM tablet (DailyMed (U.S. National Library of Medicine), 2026); COMPLEX OF THE CATALYTIC PORTION OF HUMAN HMG-COA REDUCTASE WITH COMPACTIN (ALSO KNOWN AS MEVASTATIN) (RCSB Protein Data Bank, 2001); Goodman & Gilman's The Pharmacological Basis of Therapeutics, 14th ed., ch. 37 (McGraw Hill, 2023).
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Representative model, for educational purposes only.