This page shows what was measured, who it was measured in, and what that does not settle.
What Pravastatin does in the body
High cholesterol, and the prevention of heart attacks, strokes and cardiovascular death
Pravastatin blocks the enzyme the liver uses to build cholesterol, so the liver cell puts more LDL receptors on its surface and pulls cholesterol-carrying particles out of the bloodstream instead. What separates it from most statins is that it is water-soluble rather than fat-soluble: it cannot drift through cell membranes and has to be carried into the liver by a specific transporter. That makes it much more confined to the liver than its relatives, and it also means the body clears it by simple chemical rearrangement rather than through the busy CYP3A4 enzyme, so it collides with far fewer other drugs.
What happened in people
Fatal coronary events or non-fatal infarction 10.2% against 13.2% in post-infarction patients with average cholesterol (CARE, p=0.003)
✎ Source-linked record
Where this came from
A person wrote this into the record with the study named beside it. No reviewer has signed it off.
The recorded finding that sits closest to something a person would notice. Written into the record, not signed off, and it carries no population or interval.
That WOSCOPS demonstrated an all-cause mortality benefit in primary prevention — the result was 22% at p=0.051 with a confidence interval touching zero
Where it acts
Hepatocyte cytoplasm — reached almost exclusively through the OATP1B1 transporter, because this statin is water-soluble and cannot cross membranes unaided
Kind of result
A number that stands in for health
Supervision
Professional supervision is normally required. A regulator classifies this substance in a way that restricts how it is supplied.
What the registries record it as
The substance registry classes this as chemical.
FDA substance registry · KXO2KT9N0G · read 2026-08-29
Where each sentence above came from
No recorded sentence describes the change this makes in a way that stands on its own. The page opens with what it is taken for instead, and the recorded explanation follows below.
Shown as the opening line on this page.
A limit recorded against this substance. Not signed off as a reviewed claim.
The four opening statements run to 136 words.
Words this page uses
Four words worth knowing first
Chosen from what this page shows, with each one explained before the word it depends on.
Stand-in result
A stand-in result is a number measured because the real result takes too long.
A picture of it, and where the picture fails
It is like judging a journey by the speedometer rather than by arriving.
Where that stops being true. Speed does predict arrival. Many stand-in results do not predict the real one.
What people get wrong. A stand-in result is often reported as the result itself.
A surrogate endpoint substituted for a clinical endpoint, valid only where the substitution has been shown to hold.
Randomisation
Randomisation means chance decides who gets which treatment.
A picture of it, and where the picture fails
It is like a coin toss deciding the groups.
Where that stops being true. A coin toss is fair once. Fairness here comes from doing it for everyone.
What people get wrong. It is thought to make groups identical. It makes them similar on average, including on things nobody measured.
Allocation of participants to arms by a chance process, so that unmeasured factors are balanced in expectation.
Confidence interval
A confidence interval is the range the true answer is likely to sit in.
A picture of it, and where the picture fails
It is like a weather forecast giving a range rather than one number.
Where that stops being true. A forecast range covers tomorrow. This one covers what the study could resolve.
What people get wrong. The middle number is read as the answer. A range crossing zero means no change is still possible.
An interval estimate that would contain the true parameter in a stated proportion of repeated studies.
Pathway
A pathway is a chain of steps inside a cell, each one setting off the next.
A picture of it, and where the picture fails
A pathway is like a row of dominoes.
Where that stops being true. Dominoes fall one way. Pathways loop back and can switch themselves off.
What people get wrong. Changing one step is read as changing the outcome. Other steps often absorb it.
An ordered series of molecular interactions producing a defined cellular change.
What happened in people◇Read from sources, not yet reviewed
What was measured, goal by goal
One row for each goal a registered study measured something for. One column for each kind of thing that could be measured.
Registered studies list 40 outcome measures that RNAWiki could read. A registered study says what someone planned to measure. It does not say what they found. 0 of the matched studies tested this substance, and 0 posted a result.
There is no single score. A strong test result and a weak life result are different facts.
Goals down the side, kinds of measurement across the top. Each cell says what kind of thing was registered, not what was found.
Goal
Life outcome
What a body can do
How a person feels
A test result
A step in the body
Harms
How long
Who was studied
Cholesterol
∅Nothing in the sources checkedNo registered study lists a life outcome for this goal.
∅Nothing in the sources checkedNo registered study lists a performance measure for this goal.
∅Nothing in the sources checkedNo registered study lists a symptom measure for this goal.
△Only a number moved10 registered test measure.
∅Nothing in the sources checkedNo registered study lists a body-step measure for this goal.
—Not recordedHarms were not a registered measure for this goal.
—Not recordedNo finished study window is recorded.
…Waiting for a reviewerWho was studied is listed further down the page.
Blood sugar
∅Nothing in the sources checkedNo registered study lists a life outcome for this goal.
∅Nothing in the sources checkedNo registered study lists a performance measure for this goal.
∅Nothing in the sources checkedNo registered study lists a symptom measure for this goal.
△Only a number moved1 registered test measure.
∅Nothing in the sources checkedNo registered study lists a body-step measure for this goal.
—Not recordedHarms were not a registered measure for this goal.
—Not recordedNo finished study window is recorded.
…Waiting for a reviewerWho was studied is listed further down the page.
Healthy ageing
…Waiting for a reviewer1 registered study measure of this kind. No reviewed result yet.
∅Nothing in the sources checkedNo registered study lists a performance measure for this goal.
∅Nothing in the sources checkedNo registered study lists a symptom measure for this goal.
∅Nothing in the sources checkedNo registered study lists a test result for this goal.
∅Nothing in the sources checkedNo registered study lists a body-step measure for this goal.
—Not recordedHarms were not a registered measure for this goal.
—Not recordedNo finished study window is recorded.
…Waiting for a reviewerWho was studied is listed further down the page.
Which registered measures put each goal on this table
Cholesterol
ldl c; serum ldl c; fasting plasma low density lipoprotein cholesterol; low density lipoprotein cholesterol level after 8 weeks; low density lipoprotein cholesterol; hdl c level n; low density lipoprotein cholesterol from baseline to week 12; change from baseline in non hdl c
Blood sugar
glucose homeostasis; incident type 2 diabetes
Healthy ageing
all cause mortality
Sorted by fixed word lists, version v1. A name the rules do not recognise stays unsorted rather than moving to the nearest column.
What each mark on this table means
∅ Nothing in the sources checked
No registered study lists a life outcome for this goal.
△ Only a number moved
10 registered test measure.
— Not recorded
Harms were not a registered measure for this goal.
… Waiting for a reviewer
Who was studied is listed further down the page.
What happened in people◇Read from sources, not yet reviewed
What happened in people
Each card is one study: the exact question it asked, who was in it, and whether it showed what it set out to show.
Combined incidence of definite non-fatal myocardial infarction and death from coronary heart disease in men aged 45 to 64 with hypercholesterolaemia and no prior infarction
✓ The study showed what it set out to show
Who was studied
WOSCOPS — West of Scotland Coronary Prevention Study (N Engl J Med 1995;333:1301-1307)
174 definite coronary events against 248; 31% relative risk reduction (95% CI 17 to 43), p<0.001, over an average 4.9 years
Repeated elsewhere
Replicated
What this does not prove. Meeting one endpoint in one population does not carry to other goals or other people.
The limits of this study, and where it came from
Main limit. All-cause mortality fell 22% but with a 95% CI of 0 to 40 and p=0.051 — not significant, though the trial is routinely cited as though it were. Coronary death counting definite cases alone fell 28% at p=0.13. The population was men only, aged 45 to 64, with mean cholesterol 272 mg/dL, so nothing here transfers directly to women or to lower baseline cholesterol.
How far it carries. This study is recorded from the curated record, not from the registry match.
Form and route. Oral tablet at 10, 20, 40 and 80 mg, taken once daily, usually in the evening
Interval reported. 95% CI 17 to 43), p<0
Written into the record, not signed off as a reviewed claim.
10.2% against 13.2%; a 24% relative risk reduction (95% CI 9 to 36), p=0.003, on an absolute difference of three percentage points
Repeated elsewhere
Replicated
What this does not prove. Meeting one endpoint in one population does not carry to other goals or other people.
The limits of this study, and where it came from
Main limit. There were no significant differences in overall mortality or in non-cardiovascular mortality; the trial was not powered for either. The reported greater benefit in women rests on 576 women, and the greater benefit at higher pretreatment LDL is a subgroup analysis — both are hypothesis-generating rather than established.
How far it carries. This study is recorded from the curated record, not from the registry match.
Form and route. Oral tablet at 10, 20, 40 and 80 mg, taken once daily, usually in the evening
Interval reported. 95% CI 9 to 36), p=0
Written into the record, not signed off as a reviewed claim.
Mortality from coronary heart disease over a mean 6.1 years in patients with previous myocardial infarction or unstable angina and a broad range of cholesterol levels
6.4% against 8.3%; a 24% relative reduction (95% CI 12 to 35), p<0.001, with overall mortality 11.0% against 14.1% (22% reduction, 95% CI 13 to 31, p<0.001)
Repeated elsewhere
Replicated
What this does not prove. Meeting one endpoint in one population does not carry to other goals or other people.
The limits of this study, and where it came from
Main limit. The publication reports no clinically significant adverse effects of treatment. Stroke reduction was 19% at p=0.048, which is a real but marginal result and sits against PROSPER, where stroke was entirely unaffected.
How far it carries. This study is recorded from the curated record, not from the registry match.
Form and route. Oral tablet at 10, 20, 40 and 80 mg, taken once daily, usually in the evening
Interval reported. 95% CI 12 to 35), p<0
Written into the record, not signed off as a reviewed claim.
408 events against 473; hazard ratio 0.85 (95% CI 0.74 to 0.97), p=0.014, over an average 3.2 years
Repeated elsewhere
Partially Replicated
What this does not prove. Meeting one endpoint in one population does not carry to other goals or other people.
The limits of this study, and where it came from
Main limit. New cancer diagnoses were more frequent on pravastatin: HR 1.25 (95% CI 1.04 to 1.51), p=0.020. A meta-analysis of all pravastatin and all statin trials showed no overall increase. Stroke risk was unaffected (HR 1.03, p=0.8) despite stroke being part of the primary composite. There was no significant effect on cognitive function or disability.
How far it carries. This study is recorded from the curated record, not from the registry match.
Form and route. Oral tablet at 10, 20, 40 and 80 mg, taken once daily, usually in the evening
Interval reported. 95% CI 0
Written into the record, not signed off as a reviewed claim.
All-cause mortality with follow-up to eight years, pravastatin 40 mg daily against usual care, in hypertensive adults aged 55 or over with moderately elevated LDL cholesterol
Six-year mortality 14.9% against 15.3%; relative risk 0.99 (95% CI 0.89 to 1.11), p=0.88. Coronary events 9.3% against 10.4%, RR 0.91 (95% CI 0.79 to 1.04), p=0.16
Repeated elsewhere
Failed to Replicate
What this does not prove. A study that did not show an effect does not show that no effect exists anywhere.
The limits of this study, and where it came from
Main limit. During the trial 32% of usual-care participants with known coronary disease and 29% without started lipid-lowering drugs, leaving a differential of only 9.6% in total cholesterol and 16.7% in LDL. The trial is a demonstration of what happens to an unblinded active-control design when the control treatment becomes standard practice mid-trial, and the authors say so in their own conclusion.
How far it carries. This study is recorded from the curated record, not from the registry match.
Form and route. Oral tablet at 10, 20, 40 and 80 mg, taken once daily, usually in the evening
Interval reported. 95% CI 0
Written into the record, not signed off as a reviewed claim.
RNAWiki holds 5 written-up human studies for this substance, each with the question it asked.
How we know it
Each card names the study, the number of people and what the study set out to measure.
What this does not prove
These summaries were written by a person and have not been signed off as reviewed claims.
Why it matters
A study that failed is as informative as one that worked, and both are here.
What we still do not know
No reviewed claim exists, so no exact population, effect size or interval is published yet.
What happened in people◇Read from sources, not yet reviewed
How close this is to real life
The top step is something a person would feel or care about. The bottom is a guess from software. Filled steps are where evidence exists for this substance.
■Living longer, or avoiding a major eventEvidence recorded. Death, a heart attack, a stroke, a hospital stay.7 registered measures of this kind. No reviewed result.
□What a body can do day to dayNo evidence recorded. Walking, dressing, breathing, recovering.No registered study measures this.
□Measured performanceNo evidence recorded. How much was lifted, how far was run, how fast.No registered study measures this.
□Symptoms and quality of lifeNo evidence recorded. Pain, tiredness, mood, sleep, as the person rated it.No registered study measures this.
■A number that stands in for healthEvidence recorded. Cholesterol, blood sugar, bone density. A stand-in, not the thing itself.14 registered measures of this kind.
■A step measured inside a personEvidence recorded. Something measured in human tissue or human cells.A human record sits on the stored organism ladder.
■AnimalsEvidence recorded. Mice, rats, dogs. Useful for ideas, not proof about people.Stored records in Mouse, Rat. A result in animals says what to test next. It does not say what happens in people.
■Cells in a dishEvidence recorded. Cells or chemistry on a bench, far from a whole body.Stored mechanism abstracts describe steps measured in cells or tissue.
□A guess from softwareNo evidence recorded. Nobody measured it. RNAWiki never publishes one as a finding.RNAWiki stores no prediction for this record. Software can suggest a link. RNAWiki does not publish one as a finding.
Higher on these steps means closer to something a person would feel. It does not mean better done.
What it changes in the body◇Read from sources, not yet reviewed
The path through the body
From what a person takes to what changes. A solid line is a step measured in people. A dashed line is a step nobody has measured that way.
Start
Pravastatin
What a person takes: Oral tablet at 10, 20, 40 and 80 mg, taken once daily, usually in the evening.
The measurement behind this step
Given in the active acid form, so no metabolic activation is required. Peak plasma concentrations occur at 1 to 1.5 hours; average oral absorption is 34% and absolute bioavailability 17%, with a hepatic extraction ratio of 0.66. Systemic bioavailability after a bedtime dose is 60% lower than after a morning dose, and the evening dose was nonetheless marginally more effective — the drug is aimed at an organ whose cholesterol synthesis peaks overnight, not at the bloodstream. Food reduces systemic bioavailability without changing the lipid-lowering effect. Elimination half-life is about 1.8 hours; 20% of an oral dose appears in urine and 70% in faeces, and after intravenous dosing 47% of total body clearance is renal.
Getting in
It arrives already switched on
Unlike simvastatin and lovastatin, this tablet does not need the body to activate it. The molecule that inhibits the enzyme is the molecule you swallow.
──Measured in people. Written by a person from the study named beside the step. Not signed off as a reviewed claim.
The measurement behind this step
Pravastatin is administered orally in the active open-hydroxyacid form as the sodium salt, not as a lactone prodrug. Average oral absorption is 34% with absolute bioavailability 17%; peak plasma concentrations occur at 1 to 1.5 hours.
Fat-soluble statins slip through cell membranes anywhere in the body. This one cannot: it has to be carried into the liver cell by a specific transporter, and cells without that transporter barely see it.
──Measured in people. Written by a person from the study named beside the step. Not signed off as a reviewed claim.
The measurement behind this step
The 6β-hydroxyl makes pravastatin hydrophilic, so hepatic entry depends on OATP1B1 rather than on passive diffusion. Hepatic first-pass extraction ratio is 0.66. Plasma protein binding is approximately 50%, against roughly 95% for the lipophilic statins.
It jams the rate-limiting step of cholesterol synthesis
Inside the liver cell it blocks the enzyme that performs the slowest step in building cholesterol, and the whole pathway backs up behind it.
╌╌Described, with no measurement named. No measurement is named for this step, so it is drawn as an unconfirmed link.
The measurement behind this step
Reversible competitive inhibition of HMG-CoA reductase, the enzyme catalysing conversion of HMG-CoA to mevalonate — an early and rate-limiting step in cholesterol biosynthesis. VLDL and triglycerides fall and HDL cholesterol rises.
Deprived of the cholesterol it used to manufacture, the liver cell puts more receptors on its surface and pulls LDL particles out of the bloodstream. That is what lowers the number on the test.
╌╌Described, with no measurement named. No measurement is named for this step, so it is drawn as an unconfirmed link.
The measurement behind this step
Depletion of the intracellular sterol pool activates SREBP-2 and upregulates LDL receptor expression, increasing hepatic clearance of circulating LDL. Pravastatin 40 mg lowered LDL cholesterol by 26% in WOSCOPS and 34% in PROSPER.
Fewer coronary deaths, in three separate populations
Men with high cholesterol and no heart disease, people who had had a heart attack with normal cholesterol, and people with established coronary disease — all three groups had measurably fewer coronary events.
╌╌Described, with no measurement named. No measurement is named for this step, so it is drawn as an unconfirmed link.
The measurement behind this step
WOSCOPS: definite coronary events 174 against 248, a 31% reduction (p<0.001). CARE: 10.2% against 13.2%, a 24% reduction (p=0.003). LIPID: coronary death 6.4% against 8.3% and overall mortality 11.0% against 14.1%, both p<0.001.
The largest trial of the lot compared it against ordinary care rather than a dummy tablet, and found no difference in deaths. A third of the comparison group had started taking statins of their own.
──Measured in people. Written by a person from the study named beside the step. Not signed off as a reviewed claim.
The measurement behind this step
ALLHAT-LLT: all-cause mortality 14.9% against 15.3% at six years, RR 0.99 (95% CI 0.89 to 1.11), p=0.88, in 10,355 participants. Achieved separation was 9.6% in total cholesterol and 16.7% in LDL, against 26 to 35% in the placebo-controlled trials.
No suggested links are held for this record, so nothing is hidden from this path.
What we know
The record describes 6 steps from taking it to an effect in a person.
How we know it
Each step names the study behind it in the technical detail beside it.
What this does not prove
A change inside the body is a reason to look. It is not a result in a person.
Why it matters
A reader can see exactly where the chain stops being measured in people.
What we still do not know
No reviewed claim binds any of these steps to a named population.
What it would be like to take◇Read from sources, not yet reviewed
Felt, measured, or meaningful
Three different things that get called the same word. Registered studies measured all three, and mixing them is how a blood test becomes a health claim.
Felt
Things a person could notice without a test.
No registered study measured anything of this kind.
fasting plasma low density lipoprotein cholesterol
low density lipoprotein cholesterol level after 8 weeks
low density lipoprotein cholesterol
hdl c level n
cmax maximum observed concentration
low density lipoprotein cholesterol from baseline to week 12
glucose homeostasis
and 4 more.
Meaningful
Things that change how a life goes, not only a number.
survival
survival at 2 years
complete remission rate
all cause mortality
overall survival
composite of death from any cause
recurrent stroke
A registered study says what someone planned to measure. It does not say what they found. A number moving is not the same as a life going better. The two are shown apart here.
Felt, but not shown to help. A person notices a change. No study showed it leads anywhere good.
Measured, but not felt. A number moves. The person notices nothing. Both can be true.
Measured, but not shown to matter. A number moves in the good direction. Nobody showed that lives went better.
Matters, but takes years. The result that counts may take longer than anyone would keep watching.
Names that fit none of the three (19)
panss total
hiv rna
csf abeta levels
common carotid artery intima media thickness
brachial artery flow mediated vasodilatation
pharmacokinetics
bioequivalence
metabolic syndrome
general cardiovascular risk profile framingham heart study
bioequivalence based on cmax and auc
who stated that they had side effects
who took 90 of their doses
bioequivalence based on cmax and auc parameters
30 day maces after pci
time to radiologic progression
auc of simvastatin
adverse events as a measure of safety and tolerability
incident type 2 diabetes
hospitalized for acute kidney injury
These are harms, study-process measures, or names the rules did not recognise. They are shown rather than dropped.
What is missing or unclear◇Read from sources, not yet reviewed
Were people like you studied?
RNAWiki cannot tell whether a study fits you. It can show who was in it, and where the result stops carrying.
Who was studied
People similar to this profile were included.
Adults with high cholesterol and no known heart disease, adults with established coronary disease, children from age eight with familial hypercholesterolaemia, and — in practice — people taking drugs that collide with the CYP3A4-metabolised statins.
Who is missing from the studies
Which groups were under-represented in the studies has not been recorded for this substance. Pregnancy, breastfeeding, children, older adults, and people with liver or kidney conditions are commonly excluded from trials; nothing here says whether they were.
What the label states about particular groups
On pediatric, the label states: “The safety and effectiveness of pravastatin sodium have not been established in pediatric patients younger than 10 years of age with HeFH or in pediatric patients with other types of hyperlipidemia (other than HeFH).”
US prescribing information · 97f826f0-b5c5-410c-b1f0-523873981e8d · read 2026-08-30
On older people, the label states: “In clinical studies, 4,797 (36.4%) pravastatin sodium-treated patients were aged 65 and older and 110 (0.8%) were aged 75 and older.”
US prescribing information · 97f826f0-b5c5-410c-b1f0-523873981e8d · read 2026-08-30
On people who are pregnant, the label states: “Risk Summary Discontinue pravastatin sodium when pregnancy is recognized.”
US prescribing information · 97f826f0-b5c5-410c-b1f0-523873981e8d · read 2026-08-30
On people who are breastfeeding, the label states: “Risk Summary Based on one lactation study in published literature, pravastatin is present in human milk.”
US prescribing information · 97f826f0-b5c5-410c-b1f0-523873981e8d · read 2026-08-30
On people with reduced liver function, the label states: “Pravastatin sodium shows a large inter-subject variability in pharmacokinetics in patients with liver cirrhosis [ Clinical Pharmacology (12.3) ] .”
US prescribing information · 97f826f0-b5c5-410c-b1f0-523873981e8d · read 2026-08-30
On people with reduced kidney function, the label states: “is a risk factor for myopathy and rhabdomyolysis.”
US prescribing information · 97f826f0-b5c5-410c-b1f0-523873981e8d · read 2026-08-30
Where the result stopped carrying
ALLHAT-LLT: no significant reduction in all-cause mortality or coronary events against usual care
PROSPER: stroke entirely unaffected, hazard ratio 1.03, p=0.8
PROSPER: a statistically significant excess of new cancer diagnoses, which pooled analysis of the whole statin literature did not confirm
WOSCOPS: all-cause mortality missed the conventional significance threshold at p=0.051
This is a scope explorer, not a diagnosis engine.
It shows who was studied so you can see whether people similar to you were included.
RNAWiki cannot tell whether a study fits you. It can show who was in it.
What it would be like to take◇Read from sources, not yet reviewed
Why it might seem to do nothing
A real effect and a noticed effect are different things. These are the recorded reasons the two come apart.
It was studied for a different goal
The studies measured something else entirely.
On this record: Some registered studies measured things that match no goal on this page.
It was studied in different people
The people in the studies were not much like the reader.
On this record: Which groups were under-represented in the studies has not been recorded for this substance. Pregnancy, breastfeeding, children, older adults, and people with liver or kidney conditions are commonly excluded from trials; nothing here says whether they were.
The evidence may simply be wrong
Small early studies often do not hold up.
On this record: RNAWiki has not yet published a reviewed conclusion for this use.
Other reasons RNAWiki checked and found nothing for (10)
A different form was studied
The studied form is not the form on the shelf. Nothing in this record points to this reason.
There was nothing to correct
Where a level is already normal, topping it up may change nothing. Nothing in this record points to this reason.
Something else had to happen too
In the studies it was paired with training, a diet or another treatment. Nothing in this record points to this reason.
The change is too small to feel
A real change can still sit below what a person notices. Nothing in this record points to this reason.
Day-to-day swing hides it
Sleep, food, stress and time of day move most numbers more than this would. Nothing in this record points to this reason.
Not enough time yet
The studies ran longer than the person has waited. Nothing in this record points to this reason.
It was not taken as studied
Missed days change the result, and studies count them. Nothing in this record points to this reason.
Something else changed at the same time
Two changes at once cannot be told apart afterwards. Nothing in this record points to this reason.
The product may not be what it says
Contents of a sold product are not always what the label states. Nothing in this record points to this reason.
No recorded reason
RNAWiki has nothing stored that would explain it. Nothing in this record points to this reason.
None of these is a reason to take more. Taking more is not a step this page ever suggests.
What it would be like to take◇Read from sources, not yet reviewed
What taking it involves
The recorded facts about getting hold of it and using it. Nothing here is a suggestion about what you should do.
How it is supplied
Prescription only
❝ Quoted from a source
Where this came from
Copied from a source RNAWiki stored, with the source named.
Read from the recorded approval status.
No source is stored against this line.
Form and route
Oral tablet at 10, 20, 40 and 80 mg, taken once daily, usually in the evening
✎ Source-linked record
Where this came from
A person wrote this into the record with the study named beside it. No reviewer has signed it off.
The form and route recorded on this substance.
No source is stored against this line.
Who oversees it
Professional supervision is normally required. A regulator classifies this substance in a way that restricts how it is supplied.
❝ Quoted from a source
Where this came from
Copied from a source RNAWiki stored, with the source named.
Suppression classes recorded: S3.
No source is stored against this line.
What is in the pack
Given in the active acid form, so no metabolic activation is required. 66.
✎ Source-linked record
Where this came from
A person wrote this into the record with the study named beside it. No reviewer has signed it off.
Recorded notes on how this is sold. The rest of the recorded wording: Systemic bioavailability after a bedtime dose is 60% lower than after a morning dose, and the evening dose was nonetheless marginally more effective — the drug is aimed at an organ whose cholesterol synthesis peaks overnight, not at the bloodstream. Food reduces systemic bioavailability without changing the lipid-lowering effect. 8 hours; 20% of an oral dose appears in urine and 70% in faeces, and after intravenous dosing 47% of total body clearance is renal.
No source is stored against this line.
Where it is registered
Regulatory records are listed in the technical disclosure at the foot of this page.
# Counted from records
Where this came from
A count of rows RNAWiki holds. It describes our records, not your body.
Register entries are stored per jurisdiction and shown with their dates.
No source is stored against this line.
Why people stop
Not recorded.
∅ Nothing recorded
Where this came from
RNAWiki holds nothing here and says so rather than guessing.
No record of why people stopped taking it is stored for this substance.
No source is stored against this line.
What it would be like to take◇Read from sources, not yet reviewed
What can go wrong
Sorted by where each line came from. A regulator's label and a report somebody sent in are not the same kind of fact.
·Worth asking a clinician aboutWritten into the record from the studies named on this page
Contraindicated in hypersensitivity, in active liver disease or unexplained persistent transaminase elevation, in pregnancy and during breastfeeding. Myopathy with creatine kinase above ten times the upper limit of normal was rare, under 0.1%, in the trial programme; rare rhabdomyolysis with acute renal failure has been reported. Predisposing factors are age 65 and over, uncontrolled hypothyroidism and renal impairment. Immune-mediated necrotising myopathy is a separate rare entity that persists after the drug is stopped and carries anti-HMG-CoA reductase antibodies. Persistent transaminase elevations occur. Interactions are handled by dose limits rather than contraindications: 20 mg maximum with ciclosporin, 40 mg maximum with clarithromycin, avoid gemfibrozil, caution with other fibrates, colchicine and niacin at 1 g a day or more.
Nobody counted how many people took this and were fine, so this cannot be turned into a rate.
These are reports people sent to a regulator. They do not show the medicine caused the reaction.
Nobody counted how many people took the medicine and reported nothing.
The same event can be reported more than once, and many reports are incomplete.
News coverage, lawsuits and new warnings change how often people report.
A count is not a rate and not a risk.
Pravastatin appears in spontaneous reports to regulators. Across the 10 most-reported reaction terms, 27533 reaction mentions were counted. One report can name several reactions.
liver function test abnormal — 990 reaction mentions
myositis — 734 reaction mentions
immune-mediated myositis — 474 reaction mentions
open-targets-adr · recorded 2026-06-24 · a recorded source, not a stored snapshot
Over a long time. No completed tested study window is recorded, so long-term effects are not established by the registry record.
Groups the studies covered thinly. Which groups were under-represented in the studies has not been recorded for this substance. Pregnancy, breastfeeding, children, older adults, and people with liver or kidney conditions are commonly excluded from trials; nothing here says whether they were.
What is missing or unclear◇Read from sources, not yet reviewed
Does the exact form matter?
Evidence belongs to the exact thing that was tested. A different salt, a different mixture or a different preparation is a different question.
The form that was studied
Oral tablet at 10, 20, 40 and 80 mg, taken once daily, usually in the evening
✎ Source-linked record
Where this came from
A person wrote this into the record with the study named beside it. No reviewer has signed it off.
The form used in the studies cited on this page.
No source is stored against this line.
What is sold
66.
✎ Source-linked record
Where this came from
A person wrote this into the record with the study named beside it. No reviewer has signed it off.
Recorded notes on which forms are sold. The rest of the recorded wording: Systemic bioavailability after a bedtime dose is 60% lower than after a morning dose, and the evening dose was nonetheless marginally more effective — the drug is aimed at an organ whose cholesterol synthesis peaks overnight, not at the bloodstream. Food reduces systemic bioavailability without changing the lipid-lowering effect. 8 hours; 20% of an oral dose appears in urine and 70% in faeces, and after intravenous dosing 47% of total body clearance is renal.
No source is stored against this line.
What is recorded as being sold
200 products list this as an active ingredient in the United States drug directory. 200 of them contain it and nothing else.
FDA National Drug Code directory · 71610-884 · read 2026-08-29
They are sold as powder, tablet and tablet, film coated, taken oral.
FDA National Drug Code directory · 71610-884 · read 2026-08-29
The regulator's established pharmacologic class for it is hmg-coa reductase inhibitor [epc] and hydroxymethylglutaryl-coa reductase inhibitors [moa].
FDA National Drug Code directory · 71610-884 · read 2026-08-29
127 published labels name it as an active ingredient. 127 of them describe this substance alone, which is where its own label text on this page comes from.
US prescribing information · 97f826f0-b5c5-410c-b1f0-523873981e8d · read 2026-08-29
Those labels are classed as human prescription drug.
US prescribing information · 97f826f0-b5c5-410c-b1f0-523873981e8d · read 2026-08-29
PRAVASTATIN SODIUM is oral at 3 DOSAGE FORMS AND STRENGTHS Pravastatin Sodium Tablets, USP are supplied as: 10 mg of pravastatin sodium: Yellow colored, circular shaped, flat faced tablets with “G5” debossed on one side and “10” debossed on the othe…, recorded as fda label in effect 2026-06-17 in the United States.
US prescribing information · 97f826f0-b5c5-410c-b1f0-523873981e8d · read 2026-08-30
Recorded price in US: 0.05695–0.148 USD per one unit as the pricing file counts it — a tablet, capsule, patch or single item, across 86 priced products whose strengths and pack forms differ, as of 2026-08-26, paid by retail pharmacies buying the product, as surveyed by the Centers for Medicare & Medicaid Services. It is not a list price, an insurance price, or what anyone pays at a counter..
Recorded source · 2026-08-26 · read 2026-08-28
Evidence carries across two names for one substance. It does not carry across a salt, a mirror form or a mixture.
What it would be like to take◇Read from sources, not yet reviewed
What you could measure
This one is decided with a clinician, so this section holds questions to ask rather than a plan to run.
Self-experiment planning is not offered for a prescription or clinician-supervised medicine. The questions below are for a clinician or pharmacist.
Questions worth asking
Which of the trials of Pravastatin studied people like me?
What was measured, and for how long?
Was the result a laboratory value or a health outcome?
What would we watch for, and when would we stop?
Tracking can show whether something changed for you. It cannot show what caused it.
RNAWiki records evidence. It does not say whether this substance is right for you.
What is missing or unclear◇Read from sources, not yet reviewed
Claims that go past the evidence
Things said about this substance that sound reasonable, and the exact step that is missing between the evidence and the claim.
✗Goes past the evidence
That WOSCOPS demonstrated an all-cause mortality benefit in primary prevention — the result was 22% at p=0.051 with a confidence interval touching zero
Why it sounds right. It follows from something real on this page: a body step, an animal result or a related finding.
The missing step. Nobody measured this in people for this use, or the study that did measure it did not show it.
What would change this
A study in people, for this exact use, measuring this exact thing, that a reviewer signs off.
RNAWiki has not yet published a reviewed conclusion for this use.
✗Goes past the evidence
That the stroke reductions in CARE and LIPID are a property of the drug rather than of the population, when PROSPER found a hazard ratio of 1.03 at p=0.8
Why it sounds right. It follows from something real on this page: a body step, an animal result or a related finding.
The missing step. Nobody measured this in people for this use, or the study that did measure it did not show it.
What would change this
A study in people, for this exact use, measuring this exact thing, that a reviewer signs off.
RNAWiki has not yet published a reviewed conclusion for this use.
✗Goes past the evidence
That the greater benefit in women reported in CARE is established, when it rests on a subgroup of 576 women in a trial not powered for it
Why it sounds right. It follows from something real on this page: a body step, an animal result or a related finding.
The missing step. Nobody measured this in people for this use, or the study that did measure it did not show it.
What would change this
A study in people, for this exact use, measuring this exact thing, that a reviewer signs off.
RNAWiki has not yet published a reviewed conclusion for this use.
✗Goes past the evidence
That ALLHAT-LLT shows pravastatin does not work, when what it shows is a trial whose control arm adopted the treatment
Why it sounds right. It follows from something real on this page: a body step, an animal result or a related finding.
The missing step. Nobody measured this in people for this use, or the study that did measure it did not show it.
What would change this
A study in people, for this exact use, measuring this exact thing, that a reviewer signs off.
RNAWiki has not yet published a reviewed conclusion for this use.
What is missing or unclear◇Read from sources, not yet reviewed
What nobody knows yet
Open questions, each with why it is open and what would close it.
Missing populations
Which groups were under-represented in the studies has not been recorded.
Why it matters. Recorded by the evidence model as a gap on this record.
What would answer it
A study that measures it, and a reviewer to sign it off.
Last checked 2026-09-04. Searched: The sources listed in the receipts at the foot of this page.
Missing long-term data
No completed tested study window is recorded.
Why it matters. Recorded by the evidence model as a gap on this record.
What would answer it
A study that measures it, and a reviewer to sign it off.
Last checked 2026-09-04. Searched: The sources listed in the receipts at the foot of this page.
No reviewed conclusion
RNAWiki has not yet published a reviewed conclusion for this use.
Why it matters. Recorded by the evidence model as a gap on this record.
What would answer it
A study that measures it, and a reviewer to sign it off.
Last checked 2026-09-04. Searched: The sources listed in the receipts at the foot of this page.
Missing interaction studies
No interaction was found in the registers checked. Not finding one is not the same as showing there is none.
Why it matters. Recorded by the evidence model as a gap on this record.
What would answer it
A study that measures it, and a reviewer to sign it off.
Last checked 2026-09-04. Searched: The sources listed in the receipts at the foot of this page.
Formulation uncertainty
Several salts, forms or products of Pravastatin are recorded. Results from one form may not transfer to another.
Why it matters. Recorded by the evidence model as a gap on this record.
What would answer it
A study that measures it, and a reviewer to sign it off.
Last checked 2026-09-04. Searched: The sources listed in the receipts at the foot of this page.
Mechanism not reviewed
No reviewed mechanism story exists for this substance.
Why it matters. Recorded by the evidence model as a gap on this record.
What would answer it
A study that measures it, and a reviewer to sign it off.
Last checked 2026-09-04. Searched: The sources listed in the receipts at the foot of this page.
What happened in people◇Read from sources, not yet reviewed
Check any of this yourself
Every line above traced back to the study it came from. This is the technical layer, and the vocabulary changes here.
Every line above can be traced to the study named beside it. Follow the link and read it.
LIPID: overall mortality fell, not just coronary mortality
In plain words
Nine thousand people with previous heart attacks or unstable angina took pravastatin or placebo for six years. Eleven per cent of the drug group died against fourteen per cent on placebo.
What was measured
Coronary and all-cause mortality over a mean 6.1 years in 9,014 patients with established coronary disease
Effect estimate
No reviewed effect estimate exists for this record.
Limits
See the technical detail.
From the source
LIPID randomised 9,014 patients aged 31 to 75 with previous myocardial infarction or hospitalisation for unstable angina and total cholesterol 155 to 271 mg/dL to pravastatin 40 mg daily or placebo, mean follow-up 6.1 years. Death from coronary heart disease, the primary outcome, occurred in 6.4% against 8.3% — a 24% relative reduction (95% CI 12 to 35, p<0.001). Overall mortality was 11.0% against 14.1%, a 22% relative reduction (95% CI 13 to 31, p<0.001). Myocardial infarction fell 29% (p<0.001), stroke 19% (p=0.048) and coronary revascularisation 20% (p<0.001), with effects similar across all predefined subgroups. This is the trial that carries the label claim of reduced total mortality for this molecule.
Written into the record, not signed off as a reviewed claim
ALLHAT-LLT: nothing, in ten thousand people
In plain words
The largest pravastatin trial compared it not against a placebo but against whatever doctors would normally do. Deaths were identical. Coronary events were not significantly different. The reason is that a third of the comparison group started taking statins too.
What was measured
All-cause mortality at six years, pravastatin 40 mg against usual care, in 10,355 hypertensive adults
Effect estimate
No reviewed effect estimate exists for this record.
Limits
This entry records a failure.
From the source
ALLHAT-LLT randomised 10,355 ambulatory adults aged 55 or over with LDL cholesterol 120 to 189 mg/dL and hypertension plus at least one further coronary risk factor to open-label pravastatin 40 mg daily or usual care, with all-cause mortality as the primary outcome and follow-up to eight years. All-cause mortality was 14.9% against 15.3% at six years — relative risk 0.99 (95% CI 0.89 to 1.11), p=0.88. Coronary events were 9.3% against 10.4%, RR 0.91 (95% CI 0.79 to 1.04), p=0.16. The trial’s own explanation is arithmetic rather than pharmacological: 32% of usual-care participants with known coronary disease and 29% without started lipid-lowering drugs during the trial, so the achieved separation was only 9.6% in total cholesterol and 16.7% in LDL, against roughly 26 to 35% in the placebo-controlled trials. The lesson is not that pravastatin does not work. It is that a trial measures the difference between two arms, not the effect of a drug, and that an unblinded usual-care comparator in an era when the treatment is spreading will erase almost any effect.
Written into the record, not signed off as a reviewed claim
WOSCOPS is cited for a mortality benefit that missed significance
In plain words
The famous primary-prevention trial reduced heart attacks convincingly. Its reduction in deaths from any cause was 22% with a confidence interval that just touched zero, and a p value of 0.051. It is regularly described as though it had proved a survival benefit.
What was measured
That WOSCOPS demonstrated a reduction in all-cause mortality in primary prevention, when the result was 22% at p=0.051 with a confidence interval reaching zero
Effect estimate
No reviewed effect estimate exists for this record.
Limits
See the technical detail.
From the source
WOSCOPS randomised 6,595 men aged 45 to 64 with mean plasma cholesterol 272 mg/dL and no history of infarction to pravastatin 40 mg each evening or placebo, average follow-up 4.9 years. The primary endpoint — definite non-fatal myocardial infarction or coronary death — occurred 174 times against 248, a 31% relative reduction (95% CI 17 to 43, p<0.001). Death from all cardiovascular causes fell 32% (p=0.033). Death from any cause fell 22%, 95% CI 0 to 40, p=0.051 — on the wrong side of the conventional threshold, with a lower bound of exactly zero. Death from coronary heart disease counting definite cases alone fell 28% at p=0.13, and only reached p=0.042 when suspected cases were added. There was no excess of non-cardiovascular death, which was the specific reassurance the trial was designed to provide. All of that is a strong result. It is not a demonstrated all-cause mortality benefit, and the distinction matters most precisely in primary prevention, where the people being treated are well.
Written into the record, not signed off as a reviewed claim
PROSPER found more cancers, and the field decided it was noise
In plain words
In the trial of pravastatin in people aged seventy to eighty-two, new cancer diagnoses were 25% more common on the drug, and the difference was statistically significant. Pooling every statin trial afterwards showed no overall increase, and that pooled answer is the one medicine now works from.
What was measured
Incident cancer diagnoses on pravastatin against placebo in 5,804 people aged 70 to 82 (HR 1.25, 95% CI 1.04 to 1.51, p=0.020)
Effect estimate
No reviewed effect estimate exists for this record.
Limits
See the technical detail.
From the source
PROSPER randomised 5,804 men and women aged 70 to 82 with vascular disease or risk factors to pravastatin 40 mg daily or placebo for an average 3.2 years. The primary composite of coronary death, non-fatal myocardial infarction and fatal or non-fatal stroke fell from 473 to 408 events, hazard ratio 0.85 (95% CI 0.74 to 0.97, p=0.014), and coronary death fell 24% (p=0.043). New cancer diagnoses were more frequent on pravastatin: hazard ratio 1.25 (95% CI 1.04 to 1.51), p=0.020. The authors did the correct thing with their own inconvenient finding — they folded it into a meta-analysis of all pravastatin and all statin trials, which showed no overall increase in risk, and reported both. That is the shape of a genuine conclusion shift: a significant signal in one trial, examined against the whole evidence base, and set aside on the strength of it rather than ignored. A reader should note that the setting-aside is itself an inference, drawn from pooled data rather than from a trial designed to test carcinogenicity.
Written into the record, not signed off as a reviewed claim
PROSPER: no effect on stroke whatsoever
In plain words
The same elderly trial reduced heart attacks and coronary deaths and did absolutely nothing to stroke — a hazard ratio of 1.03 with a p value of 0.8.
What was measured
Fatal and non-fatal stroke on pravastatin against placebo in people aged 70 to 82 (HR 1.03, p=0.8)
Effect estimate
No reviewed effect estimate exists for this record.
Limits
This entry records a failure.
From the source
Stroke risk in PROSPER was unaffected: hazard ratio 1.03 (95% CI 0.81 to 1.31), p=0.8, over an average 3.2 years in people aged 70 to 82. The hazard ratio for transient ischaemic attack was 0.75 (95% CI 0.55 to 1.00, p=0.051). This sits against LIPID, where stroke fell 19% (p=0.048) in a younger secondary-prevention population, and CARE, where stroke fell 31% (p=0.03). The same molecule at the same dose produced a stroke benefit in two trials and none in a third, and the population that did not benefit is the one at highest absolute stroke risk. Three years may simply be too short for a lipid intervention to move stroke rates in the elderly; the honest statement is that the trial measured no effect and did not explain why.
Written into the record, not signed off as a reviewed claim
The interaction list is short because CYP3A4 is not involved
In plain words
Most statins are broken down by a liver enzyme that dozens of common drugs block. This one is not, and its official interaction list is correspondingly short — dose limits rather than outright bans.
What was measured
Metabolic route and the resulting drug-interaction constraints, from the label pharmacology and interactions sections
Effect estimate
No reviewed effect estimate exists for this record.
Limits
See the technical detail.
From the source
The label describes pravastatin’s major biotransformation pathways as isomerisation to 6-epi pravastatin and the 3α-hydroxyisomer SQ 31,906, and enzymatic ring hydroxylation to SQ 31,945. CYP3A4 is not the route. The consequences are visible in the interactions section: ciclosporin limits pravastatin to 20 mg once daily and clarithromycin to 40 mg once daily, gemfibrozil should be avoided, and fibrates, colchicine and lipid-modifying doses of niacin warrant caution. Every one of these is a dose limit or a caution. Simvastatin, by contrast, is outright contraindicated with strong CYP3A4 inhibitors, ciclosporin, danazol and gemfibrozil. That difference — not potency, in which pravastatin loses to everything modern — is the clinical reason to choose this molecule.
Source
Pravastatin sodium United States prescribing information, sections 7.1 to 7.5 and 12.3
Role in the trial
Not matched to a registered study
Identity check
no open identity hold
Audit mark
verified
Review state
Written into the record, not signed off as a reviewed claim
CARE: the benefit extended to people whose cholesterol was already normal
In plain words
Four thousand people who had had a heart attack but whose cholesterol was average took pravastatin or placebo. Coronary events fell by a quarter, in people no cholesterol guideline of the time would have treated.
What was measured
Fatal coronary events or non-fatal myocardial infarction over five years in post-infarction patients with average cholesterol
Effect estimate
No reviewed effect estimate exists for this record.
Limits
See the technical detail.
From the source
CARE randomised 4,159 post-infarction patients — 3,583 men and 576 women — with total cholesterol below 240 mg/dL (mean 209) and LDL 115 to 174 mg/dL (mean 139) to pravastatin 40 mg daily or placebo for five years. The primary endpoint of fatal coronary event or non-fatal myocardial infarction occurred in 10.2% against 13.2%: a 24% relative reduction (95% CI 9 to 36), p=0.003, on an absolute difference of three percentage points. Bypass surgery fell 26% (p=0.005), angioplasty 23% (p=0.01) and stroke 31% (p=0.03). There were no significant differences in overall mortality or in non-cardiovascular mortality — the trial was not powered for them. Two subgroup observations are worth keeping in view precisely because they are subgroup observations: the reduction was larger in women than in men, and larger in patients with higher pretreatment LDL.
This order is fixed in code and does not count clicks or time on the page.
What is not here
4 questions this page could not answer
These sections were prepared and left out because there was nothing to put in them. They are listed rather than hidden, so the gaps in this record are visible.
How long anything takes — found nothing in the sources checked.
What it may clash with — found nothing in the sources checked.
Other ways to the same goal — found nothing in the sources checked.
What changed on this page — found nothing in the sources checked.
The record as stored
The full record, for auditing
Everything above is built from what is below. This layer keeps the technical vocabulary, record identifiers and every stored row, so a reader who wants to check the page can.
The older medicine-wide conclusion held in this record
Written for a clinical reader, and about the medicine as a whole rather than about one indication, population and set of trials. RNAWiki does not treat it as a programme conclusion and no reviewer has signed it off in that form. It is here word for word because it is what the record holds.
The water-soluble statin with three placebo-controlled mortality trials — LIPID cut overall mortality from 14.1% to 11.0% in 9,014 patients (p<0.001) — and one trial against usual care, ALLHAT-LLT, in which it did nothing at all to all-cause mortality in 10,355 people (RR 0.99, p=0.88) because the control group started taking statins too.
Recorded evidence blocks (11)
Q2
What did Pravastatin's largest trial (2133900 people) and its longest (12 years) measure?
2133900 people in Pravastatin's largest registered study, 12 years in its longest registered window, measuring all cause mortality. ClinicalTrials.gov · 2026-09-01
36 phase1, 32 phase4, 28 phase2, 25 phase3, 10 na, 4 na or unstated, 1 early phase1; NCT00840177; 2021-10-21. Last human test completed 2025, NCT04284657.
Interpretation These counts include studies where Pravastatin was a comparison treatment, a background treatment or an exposure in an observational study, and the longest window may be a planned end date. Trial roles have not yet been classified for this record.
Show the evidence
phase1
36
phase4
32
phase2
28
phase3
25
na
10
na or unstated
4
2 more recorded rows
early phase1
1
Last recorded human testNCT04284657
2025-08-04
recorded 2026-09-01 · last checked 2026-09-04
Q3
From mouse to human: where has Pravastatin shown lifespan?
14 recorded entries; human; also "40 mg Pravastatin (Pravachol)", "Combination of Pravastatin 40 mg and Fenofibrate 160 mg", "Pravachol® 80 mg Tablets"
Show the evidence
human
NCT00330980
40 mg Pravastatin (Pravachol)
NCT00459745
Combination of Pravastatin 40 mg and Fenofibrate 160 mg
NCT00829309
Pravachol® 80 mg Tablets
NCT00830258
Pravastatin sodium 80 mg tablets
NCT00830258
Pravachol® 80 mg tablets
NCT01146093
Pravachol 80 mg tablets
8 more recorded rows
humanNCT01715714
Pravastatin 40 mg
humanNCT01856374
Pravastatin 20mg
humanNCT01872845
Pravastatin 40mg
humanNCT02155530
pravastatin 20 mg
humanNCT02155530
Pravastatin 20 mg (Homogeneous)
humanNCT04719481
Pravastatin Sodium 80 MG
humanNCT05251129
Pravastatin 40 Mg Oral Tablet
humanNCT06357104
Pravastatin Sodium 20 MG
recorded 2026-09-01 · last checked 2026-09-04
Q6
Which of 30 day maces after pci, adverse events as a measure of safety and tolerability and all cause mortality did Pravastatin's trials measure?
30 day maces after pci, adverse events as a measure of safety and tolerability and all cause mortality lead 40 outcome terms across Pravastatin's trials. ClinicalTrials.gov · 2026-09-01
ldl c, csf abeta levels, common carotid artery intima media thickness, brachial artery flow mediated vasodilatation, survival and survival at 2 years follow.
Change in Total Kidney Volume; evaluate the benefit on breast-related quality of life of systematic e-PROs; latest 2031-07-31
Show the evidence
Trial
NCT03273413
"Statin Therapy in Patients With Early Stage ADPKD"; n 150; "Change in Total Kidney Volume"; 2025-09-30
NCT04356209
"Improving Theempowerment in Patients With Severe Breast Fibrosis Radio-induced Treated by Pravastatin : Benefit of e-PROs (Electronic " Patient Reported Outcome ") on Breast-related Quality of Life"; n 105; "evaluate the benefit on breast-related quality of life of systematic e-PROs"; 2031-01-31
NCT06494111
"Systemic Therapy of Open-label Prophylactic Pravastatin or Pentoxifylline/Tocopherol Prevention of Lymphedema Advancing to Eventual Fibrosis: an Interventional Registry-embedded Bayesian Randomized Trial for Radiation Sequelae (STOP4-LATE-FIBROSE)"; n 295; "Safety and adverse events (AEs)"; 2031-03-01
NCT06912763
"Reversing External-beam Radiotherapy-associated Fibrosis Syndrome: an Interventional Bayesian Adaptive Randomized-controlled Orphan Drug Platform Trial for Orodental Sequelae (Reverse-fibrose)"; n 250; "Safety and adverse events"; 2031-07-31
NCT07098975
"Statin Intervention for Severe Early-Onset Placental Insufficiency. (STATIN-PRE Trial)"; n 154; "Days of prolongation of pregnancy between inclusion and delivery."; 2028-07
NCT07217938
"Novel Treatment of Radiation Associated Dysphagia With Statins"; n 48; "Feasibility of a 12 month trial investigating the use of pravastatin to treat radiation-associated dysphagia"; 2028-10-01
recorded 2026-09-01 · last checked 2026-09-04
Q8
Which 69 trials of Pravastatin posted no result?
Posted no result
69 of 69 completed trials
Registrations
NCT00000461, NCT01057654, NCT00000539, NCT00834379, NCT00834847 and NCT00380939, and 63 more
Completion dates
oldest 1992-11; newest 2024-03-20
Show the evidence
Trial
NCT00000461
1992-11
NCT01057654
1998-06
NCT00000539
1999-03
NCT00834379
2000-09
NCT00834847
2000-09
NCT00380939
2000-12
14 further recorded trials
NCT00000542
2002-03
NCT00000941
2002-03
NCT01146106
2002-12
NCT01146093
2003-03
NCT00006412
2003-05
NCT00648544
2003-07
NCT00650221
2003-07
NCT03073018
2003-11
NCT00382460
2003-12
NCT00005010
2004-03
NCT00221754
2004-03
NCT00330980
2004-03
NCT00227500
2004-10
NCT00654537
2004-10
Q9
At the median, Pravastatin's trials enrolled 70 people — anything larger?
Median enrolment
70
Largest enrolment
2133900
Registered trials counted
127
Q10
What do 27533 spontaneous reports say about Pravastatin — and not say?
These are reports people sent to a regulator. They do not show the medicine caused the reaction. Nobody counted how many people took the medicine and reported nothing. The same event can be reported more than once, and many reports are incomplete. News coverage, lawsuits and new warnings change how often people report. A count is not a rate and not a risk.
Pravastatin appears in spontaneous reports to regulators. Across the 10 most-reported reaction terms, 27533 reaction mentions were counted: myalgia 6968; rhabdomyolysis 6532; drug interaction 3617; blood creatine phosphokinase increased 3155. open-targets-adr · CHEMBL1144 · 2026-06-24
Show the evidence
myalgia
6968
rhabdomyolysis
6532
drug interaction
3617
blood creatine phosphokinase increased
3155
muscular weakness
2041
myopathy
1546
4 more recorded rows
renal failure acute
1476
liver function test abnormal
990
myositis
734
immune-mediated myositis
474
recorded 2026-06-24 · last checked 2026-09-04
Q11
Was Pravastatin studied with fasting?
fasting is named in Pravastatin's label sentences: "Individuals with elevated fasting low-density lipoprotein cholesterol levels were also randomized to pravastatin versus usual care." openfda-label+europepmc · 2026-08-21
1 recorded statement; fasting
Show the evidence
fasting
Individuals with elevated fasting low-density lipoprotein cholesterol levels were also randomized to pravastatin versus usual care.
recorded 2026-08-21 · last checked 2026-09-04
Q12
What is recorded about Pravastatin and NAD+?
"The effect of pravastatin was further investigated using the glucose metabolism assay, which showed that glucose consumption was inhibited both in non-senescent and senescent cells and intracellular nicotinamide adenine dinucleotide (NAD) was decreased in senescent cells." — where Pravastatin and NAD+ appear together. Europe PMC · pathway abstract search · 2023-07-04
"The effect of pravastatin was further investigated using the glucose metabolism assay, which showed that glucose consumption was inhibited both in non-senescent and senescent cells and intracellular nicotinamide adenine dinucleotide (NAD) was decreased in senescent cells."
PMID 35655385
"The results of this study suggest that pravastatin does not induce senolysis, but rather selectively inhibits the proliferation of senescent cells and that cellular senescence is enhanced by decreasing intracellular NAD and promoting IL-1β production."
autophagy
PMID 29686621
"This manuscript determines whether pravastatin protects against dexamethasone-induced avascular necrosis of the femoral head by activating endothelial progenitor cell autophagy."
PMID 29686621
"An autophagy inhibitor, 3-MA, reduced pravastatin protection in endothelial progenitor cells exposed to dexamethasone by attenuating pravastatin-induced autophagy."
mTORPMID 29686621
"We found that phosphorylation of AMPK was upregulated however phosphorylation of mTOR was downregulated in pravastatin-treated endothelial progenitor cells, which was attenuated by AMPK inhibitor compound C. Furthermore, liver kinase B1 (a phosphorylase of AMPK) knockdown eliminated pravastatin regulated autophagy protein LC3-II in endothelial progenitor cells <i>in vitro</i>."
AMPKPMID 29686621
"We found that phosphorylation of AMPK was upregulated however phosphorylation of mTOR was downregulated in pravastatin-treated endothelial progenitor cells, which was attenuated by AMPK inhibitor compound C. Furthermore, liver kinase B1 (a phosphorylase of AMPK) knockdown eliminated pravastatin regulated autophagy protein LC3-II in endothelial progenitor cells <i>in vitro</i>."
autophagyPMID 29686621
"We found that phosphorylation of AMPK was upregulated however phosphorylation of mTOR was downregulated in pravastatin-treated endothelial progenitor cells, which was attenuated by AMPK inhibitor compound C. Furthermore, liver kinase B1 (a phosphorylase of AMPK) knockdown eliminated pravastatin regulated autophagy protein LC3-II in endothelial progenitor cells <i>in vitro</i>."
mTORPMID 29686621
"We therefore demonstrated pravastatin rescued endothelial progenitor cells from dexamethasone-induced autophagy dysfunction through the AMPK-mTOR signaling pathway in a liver kinase B1-dependent manner."
AMPKPMID 29686621
"We therefore demonstrated pravastatin rescued endothelial progenitor cells from dexamethasone-induced autophagy dysfunction through the AMPK-mTOR signaling pathway in a liver kinase B1-dependent manner."
mTORPMID 37842233
"Mechanistic studies involved analysis of Rheb prenylation required for mTOR activation. <b>Results:</b> A strong synergy of CHR2863 with the statins simvastatin, fluvastatin, lovastatin, and pravastatin was demonstrated in U937 cells and two CHR2863-resistant sublines."
2 more recorded rows
AMPKPMID 19498441
"Pravastatin-induced phosphorylation of eNOS, one of the downstreams of AMPK, was inhibited by compound C, an AMPK antagonist."
NAD+PMID 20628008
"In addition, thrombin increased Rac1/p47(phox)-dependent NAD(P)H oxidase activities of rat aortas within 1 h, resulting in ROS generation, which was prevented by the coadministration of pravastatin."
recorded 2023-07-04 · last checked 2026-09-04
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