This page shows what was measured, who it was measured in, and what that does not settle.
What Atorvastatin does in the body
Used to lower cholesterol and prevent heart attacks or strokes.
Cholesterol is manufactured inside liver cells by a chain of chemical steps, and atorvastatin jams the slowest step of that chain. The cell notices it is short of cholesterol and responds by putting more collection receptors on its surface, which pull LDL particles out of the bloodstream. The blood number falls mainly because the liver is now clearing more of it, not because less is being made.
What happened in people
A large study stopped early after atorvastatin reduced heart attacks and coronary deaths by about one third.
✓ Reviewed first-read answer
Where this came from
A person wrote this and a reviewer approved it against this exact record. It carries no effect size.
A reviewer approved this against this record. The reviewed-claim record carrying the exact population and effect size does not exist yet.
No source is stored against this line.
The limit that matters most
Studies have not separated cholesterol lowering from atorvastatin’s other possible effects.
Where it acts
Hepatocyte endoplasmic reticulum (liver)
Kind of result
The kind of result is not recorded
Supervision
Professional supervision is normally required. A regulator classifies this substance in a way that restricts how it is supplied.
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.
The limit a reviewer approved as the one that matters most here.
The four opening statements run to 96 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.
Formulation
A formulation is the exact made-up form a substance comes in.
A picture of it, and where the picture fails
It is like the difference between a whole bean and instant coffee.
Where that stops being true. Coffee tastes different. A formulation can change how much reaches the blood.
What people get wrong. Two products with the same name are assumed to behave the same. They often do not.
The specific composition and physical form of a product, including salt, excipients and release profile.
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 moved13 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.
Which registered measures put each goal on this table
Cholesterol
plasma lipid levels; ldl c from baseline to week 12; effects on bad cholesterol ldl c after 12 weeks; hdl c and ldl c; hdl c and non hdl c levels; lipid parameters at various timepoints over 12 months; ldl and hdl levels; low density lipoprotein cholesterol
Blood sugar
urinary protein/creatinine in type 1 or 2 diabetes
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
13 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.
Non-fatal myocardial infarction and fatal coronary heart disease
✓ The study showed what it set out to show
Who was studied
ASCOT-LLA
How many people
10305
Study design
Randomised double-blind placebo-controlled trial, stopped at median 3.3 years
Compared against
A dummy treatment
Kind of result
A number that stands in for health
What was found
HR 0.64 (95% CI 0.50-0.83), P = 0.0005
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 was 185 against 212, HR 0.87 (0.71-1.06), p=0.16 — not a significant difference, and often quoted as though it were.
How far it carries. This study is recorded from the curated record, not from the registry match.
Form and route. Oral tablet, four strengths
Interval reported. 95% CI 0
Written into the record, not signed off as a reviewed claim.
Time to first acute coronary heart disease event, coronary revascularisation or stroke
✓ The study showed what it set out to show
Who was studied
CARDS (NCT00327418)
How many people
2838
Study design
Randomised placebo-controlled trial, stopped 2 years early, median 3.9 years
Compared against
A dummy treatment
Kind of result
A number that stands in for health
What was found
Rate reduction 37% (95% CI -52 to -17), 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 death rate reduction of 27% did not reach significance (p=0.059) and the trial was stopped early, which inflates measured effect sizes.
How far it carries. This study is recorded from the curated record, not from the registry match.
Form and route. Oral tablet, four strengths
Interval reported. 95% CI -52 to -17), P = 0
Written into the record, not signed off as a reviewed claim.
Daily symptom intensity score in atorvastatin, placebo and no-tablet months
✓ The study showed what it set out to show
Who was studied
SAMSON (NCT02668016)
How many people
60
Study design
Randomised n-of-1 crossover trial, 12 monthly periods
Compared against
Not recorded for this study
Kind of result
A number that stands in for health
What was found
Statin 16.3 versus placebo 15.4, P = 0.388; both versus no-tablet 8.0, 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. Eleven of 60 did not complete the 12-month protocol. The finding is that symptoms are real and tablet-triggered, not that they are imagined.
How far it carries. This study is recorded from the curated record, not from the registry match.
Form and route. Oral tablet, four strengths
Interval reported. Not recorded in this summary
Written into the record, not signed off as a reviewed claim.
RNAWiki holds 6 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.1 registered measure of this kind. 1 written-up study measured this and did not show a benefit.
□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.16 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.
Where a source records it acting
Liver: The liver is the primary site of action and the principal site of cholesterol synthesis and LDL clearance
US prescribing information · 00afce9b-48c9-487a-a738-e359c005c707 · read 2026-08-27
Start
Atorvastatin
What a person takes: Oral tablet, four strengths.
The measurement behind this step
Taken once daily at any time of day; unlike the shorter-acting statins it does not need to be taken at night, because its active metabolites give it a long effective duration. Absorption is not meaningfully affected by food.
Getting in
Swallowed as the active drug, and mostly removed before it reaches the body
Unlike some statins, atorvastatin arrives already active. Most of a dose is captured by the liver on its first pass, which is convenient, because the liver is where it is meant to work.
╌╌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
Atorvastatin calcium is administered as the active hydroxy acid rather than as a lactone prodrug. Absorption is rapid but absolute systemic bioavailability is low because of extensive first-pass extraction by the liver, which concentrates drug at the site of action while limiting systemic exposure. Metabolism is by CYP3A4 to ortho- and para-hydroxylated metabolites that are themselves active inhibitors.
A pump on the surface of liver cells carries the drug inside. People who inherit a weaker version of that pump end up with more drug circulating in the rest of the body.
╌╌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
Organic anion transporting polypeptide 1B1 (OATP1B1, encoded by SLCO1B1) mediates hepatic uptake. The reduced-function c.521T>C variant increases systemic statin exposure and is the one genetic association with statin-related myopathy that has replicated across studies, which is the mechanistic reason hepatic uptake capacity and muscle exposure are inversely linked.
It plugs the substrate slot of the cholesterol-making enzyme
The drug slots into the space where the enzyme normally grips its raw material, so the raw material cannot get in and the assembly line stops at its slowest step.
──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 3,5-dihydroxyheptanoic acid arm mimics the HMG moiety of HMG-CoA and occupies that part of the reductase active site. Crystal structures of the human catalytic domain with six statins bound show that catalytically relevant residues near the carboxyl terminus become disordered to accommodate the bulky hydrophobic half of the drug; without that flexibility the statin could not bind at all.
The starved cell builds more LDL collection receptors
Sensing it is short of cholesterol, the cell switches on the gene for the receptor that catches LDL particles and puts more of those receptors on its surface.
╌╌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
Falling intracellular sterol releases SREBP-2 from the endoplasmic reticulum via SCAP and the site-1 and site-2 proteases; the cleaved transcription factor enters the nucleus and drives transcription of LDLR. Surface LDL receptor density rises and hepatic clearance of circulating LDL particles increases. The same programme also raises PCSK9, which degrades the receptor — the counter-regulation that the PCSK9 antibodies were designed to remove.
LDL in the blood falls, and over years fewer arteries block
The blood number drops within weeks. The reduction in heart attacks takes years to accumulate and is measured by counting events, not by measuring cholesterol.
──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
Across 26 randomised trials and 170,000 participants, each 1.0 mmol/L reduction in LDL cholesterol reduced the annual rate of major vascular events by just over a fifth, with no threshold detected across the range studied. In ASCOT-LLA the corresponding event count was 100 against 154 over a median 3.3 years.
No suggested links are held for this record, so nothing is hidden from this path.
What we know
The record describes 5 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.
Measured
Things only a test, a scale or a device shows.
plasma lipid levels
ldl c from baseline to week 12
effects on bad cholesterol ldl c after 12 weeks
hdl c and ldl c
hdl c and non hdl c levels
ldl and hdl levels
low density lipoprotein cholesterol
ldl c and non hdl c levels
brachial artery flow mediated dilation
ldl c lowering efficacy
and 6 more.
Meaningful
Things that change how a life goes, not only a number.
time to occurrence of fatal or non fatal 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 (23)
mean mean common carotid imt
statin toxicity
pefr
hip flexion
oxygen consumption and anaerobic threshold
muscle pathology
intima media thickness as measured by carotid ultrasound
time to complete healing
recurrence rate of foot ulcers
intima media thickness as measures by carotid ultrasound
lipid parameters at various timepoints over 12 months
vascular responses after treatment
tumor apoptosis
electron beam ct coronary artery calcification agatston
lvef
muscle sympathetic nerve activity
plaque volume
expression profile in atherosclerotic plaque
time of atrial fibrillation recurrence
decrease in incidence of deep vein thrombosis
These are harms, study-process measures, or names the rules did not recognise. They are shown rather than dropped.
What it would be like to take◇Read from sources, not yet reviewed
How long anything takes
Nine different lengths of time that get confused with each other. None of them is worked out from another.
Before anything is noticed.RNAWiki does not store this separately, and never works it out from another figure on this page.
Before a test result moves.RNAWiki does not store this separately, and never works it out from another figure on this page.
Before performance moves.RNAWiki does not store this separately, and never works it out from another figure on this page.
How long the result was watched.No finished study window is recorded for a study that tested this substance.
How long people took it.How long people actually took it is not stored. The study window is not the same thing.
How long people were followed.Follow-up length is not stored separately. It is never read off the study window, which would be a different thing.
How fast the body clears it. approximately 14 hours hours
Read from the label, which states: “Mean plasma elimination half-life of atorvastatin in humans is approximately 14 hours, but the half-life of inhibitory activity for HMG-CoA reductase is 20 to 30 hours due to the contribution of active metabolites.”
How long effects linger.RNAWiki does not store this separately, and never works it out from another figure on this page.
Beyond the studies. Nothing is recorded about the long term.
The longest finished study sets the edge of what anyone measured.
A study window is not how long people took it, and neither is how long they were followed. Where RNAWiki holds only one of the three, it shows one.
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 established cardiovascular disease, adults with diabetes and a risk factor, and adults whose calculated risk crosses a guideline threshold. It is on the WHO Model List of Essential Medicines and was the highest-grossing pharmaceutical product ever sold.
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 atorvastatin calcium have not been established in pediatric patients younger than 10 years of age with HeFH or HoFH, or in pediatric patients with other types of hyperlipidemia (other than HeFH or HoFH).”
US prescribing information · 09c6c750-ae05-459f-83e8-4a9e4fd85212 · read 2026-08-30
On older people, the label states: “Of the total number of atorvastatin calcium-treated patients in clinical trials, 15,813 (40%) were ≥65 years old and 2,800 (7%) were ≥75 years old.”
US prescribing information · 09c6c750-ae05-459f-83e8-4a9e4fd85212 · read 2026-08-30
On people who are pregnant, the label states: “Risk Summary Discontinue atorvastatin calcium when pregnancy is recognized.”
US prescribing information · 09c6c750-ae05-459f-83e8-4a9e4fd85212 · read 2026-08-30
On people who are breastfeeding, the label states: “Risk Summary There is no information about the presence of atorvastatin in human milk, the effects of the drug on the breastfed infant or the effects of the drug on milk production.”
US prescribing information · 09c6c750-ae05-459f-83e8-4a9e4fd85212 · read 2026-08-30
On people with reduced liver function, the label states: “In patients with chronic alcoholic liver disease, plasma concentrations of atorvastatin are markedly increased.”
US prescribing information · 09c6c750-ae05-459f-83e8-4a9e4fd85212 · read 2026-08-30
On people with reduced kidney function, the label states: “is a risk factor for myopathy and rhabdomyolysis.”
US prescribing information · 09c6c750-ae05-459f-83e8-4a9e4fd85212 · read 2026-08-30
Where the result stopped carrying
ASPEN missed its composite primary endpoint in 2,410 patients with type 2 diabetes despite a 29% LDL reduction
The 80 mg strength in TNT bought no survival advantage over 10 mg and produced six times the rate of persistent liver enzyme elevation
The class raises incident diabetes, and raises it further at intensive doses: OR 1.12 for diabetes against OR 0.84 for cardiovascular events in 32,752 participants
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.
A different form was studied
The studied form is not the form on the shelf.
On this record: This record is linked to 1 related forms. Evidence does not carry across all of them.
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 (9)
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, four strengths
✎ 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
Taken once daily at any time of day; unlike the shorter-acting statins it does not need to be taken at night, because its active metabolites give it a long effective duration.
✎ 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: Absorption is not meaningfully affected by food.
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
The commonest reported complaint is muscle ache, and the two randomised n-of-1 programmes above could not distinguish it from placebo. Rhabdomyolysis with acute renal failure is rare, real and distinguishable by markedly elevated creatine kinase. Persistent aminotransferase elevation occurred in 1.2% at 80 mg against 0.2% at 10 mg in TNT. The class raises incident diabetes by about 9%, more at intensive doses. CYP3A4 inhibitors raise exposure, which is the basis of the interaction warnings.
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.
Atorvastatin appears in spontaneous reports to regulators. Across the 10 most-reported reaction terms, 37541 reaction mentions were counted. One report can name several reactions.
liver function test abnormal — 1257 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, four strengths
✎ 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
Absorption is not meaningfully affected by food.
✎ 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 and how they compare.
No source is stored against this line.
What is recorded as being sold
445 products list this as an active ingredient in the United States drug directory. 364 of them contain it and nothing else.
FDA National Drug Code directory · 71335-2924 · read 2026-08-29
They are sold as granule, powder, suspension, tablet, tablet, coated and tablet, film coated, taken oral.
FDA National Drug Code directory · 71335-2924 · 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 · 71335-2924 · read 2026-08-29
272 published labels name it as an active ingredient. 257 of them describe this substance alone, which is where its own label text on this page comes from.
US prescribing information · 09c6c750-ae05-459f-83e8-4a9e4fd85212 · read 2026-08-29
Those labels are classed as human prescription drug.
US prescribing information · 09c6c750-ae05-459f-83e8-4a9e4fd85212 · read 2026-08-29
14 marketed supplement labels list this ingredient, classed as vitamin.
Those labels carry all other, nutrient and structure/function claims. A claim of that kind is written by the manufacturer and is not assessed by any regulator, so its presence says nothing about whether it is true.
Atorvastatin calcium is tablets (film-coated) at 10 mg; 20 mg; 40 mg; 80 mg of atorvastatin, recorded as prescription product; fda label in effect 2025-08-28 in the United States.
US prescribing information · 00afce9b-48c9-487a-a738-e359c005c707 · read 2026-08-27
Recorded price in US: 0.02325–0.06924 USD per one unit as the pricing file counts it — a tablet, capsule, patch or single item, across 265 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.
Evidence on this page does not automatically apply to this one.
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 Atorvastatin 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 atorvastatin reduces all-cause mortality — neither ASCOT-LLA (p=0.16) nor CARDS (p=0.059) reached significance for death, and TNT found no mortality difference between strengths
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 a given LDL reduction always delivers a proportional event reduction — ASPEN produced a 29% LDL fall and a hazard ratio of 0.90 that crossed 1
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 anti-inflammatory "pleiotropic" actions account for a measurable share of the benefit — plausible biochemistry, never isolated in a randomised trial
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 common muscle aches on a statin are pharmacological in origin, which is what both n-of-1 programmes were built to test and did not find
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 Atorvastatin 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.
ASCOT-LLA: 100 versus 154 primary events in 10,305 hypertensive patients
In plain words
Hypertensive patients with ordinary, not high, cholesterol were randomised to a low strength of atorvastatin or placebo. The trial was stopped early because the atorvastatin group was having a third fewer heart attacks and coronary deaths.
What was measured
Non-fatal myocardial infarction and fatal coronary heart disease over a median 3.3 years
Effect estimate
No reviewed effect estimate exists for this record.
Limits
See the technical detail.
From the source
Of 19,342 hypertensive patients aged 40 to 79 with at least three other cardiovascular risk factors, the 10,305 with non-fasting total cholesterol of 6.5 mmol/L or less were randomly assigned atorvastatin 10 mg or placebo. Treatment was stopped after a median follow-up of 3.3 years against a planned 5 years. The primary endpoint of non-fatal myocardial infarction plus fatal coronary heart disease occurred in 100 patients on atorvastatin against 154 on placebo, hazard ratio 0.64 (95% CI 0.50 to 0.83), p=0.0005; the separation appeared within the first year. Fatal and non-fatal stroke fell from 121 to 89 (HR 0.73, 0.56 to 0.96, p=0.024) and total cardiovascular events from 486 to 389 (HR 0.79, 0.69 to 0.90, p=0.0005). Total serum cholesterol was about 1.3 mmol/L lower than placebo at 12 months. All-cause deaths were 185 against 212, HR 0.87 (0.71 to 1.06), p=0.16, which is not a significant difference.
Written into the record, not signed off as a reviewed claim
CARDS: a 37% event reduction in type 2 diabetes without high LDL
In plain words
People with type 2 diabetes and no history of heart disease were given a low strength of atorvastatin or placebo. The trial was stopped two years early because the benefit had already crossed the prespecified stopping threshold.
What was measured
First acute coronary event, coronary revascularisation or stroke, over a median 3.9 years
Effect estimate
No reviewed effect estimate exists for this record.
Limits
See the technical detail.
From the source
A total of 2,838 patients aged 40 to 75 across 132 centres in the United Kingdom and Ireland were randomised to placebo (n=1,410) or atorvastatin 10 mg daily (n=1,428). Entrants had no documented cardiovascular disease, LDL cholesterol of 4.14 mmol/L or lower, and at least one of retinopathy, albuminuria, current smoking or hypertension. The trial stopped 2 years early on the prespecified efficacy rule. Over a median 3.9 years, 127 placebo patients (2.46 per 100 person-years) and 83 atorvastatin patients (1.54 per 100 person-years) had a major cardiovascular event, a rate reduction of 37% (95% CI -52 to -17), p=0.001. Stroke fell 48% (-69 to -11). The death rate fell 27% (-48 to 1), p=0.059, which does not reach significance.
Written into the record, not signed off as a reviewed claim
ASPEN: the LDL fell 29% and the composite endpoint did not move
In plain words
A fourth trial in type 2 diabetes gave the same drug at the same strength for four years. Cholesterol dropped just as much as in the successful trials. The count of cardiovascular events did not fall.
What was measured
Composite of cardiovascular death, non-fatal myocardial infarction, non-fatal stroke, revascularisation, resuscitated arrest and hospitalised angina over 4 years
Effect estimate
No reviewed effect estimate exists for this record.
Limits
This entry records a failure.
From the source
ASPEN randomised 2,410 subjects with type 2 diabetes to atorvastatin 10 mg or placebo in a 4-year double-blind parallel-group study. Mean LDL cholesterol reduction over 4 years was 29% against placebo (p<0.0001) — a surrogate effect equal to that in CARDS. Composite primary endpoint rates were 13.7% on atorvastatin against 15.0% on placebo, hazard ratio 0.90 (95% CI 0.73 to 1.12), which does not exclude no effect. In the 1,905 subjects without prior myocardial infarction or intervention the hazard ratio was 0.97 (0.74 to 1.28). Fatal and non-fatal myocardial infarction fell 27% overall, p=0.10. The investigators attributed the null result to study design, recruitment and protocol changes forced by evolving guidelines, and stated the trial "did not confirm the benefit of therapy".
Written into the record, not signed off as a reviewed claim
SAMSON: atorvastatin and placebo produced the same muscle symptoms
In plain words
Sixty people who had abandoned statins because of side effects took twelve monthly bottles: four with atorvastatin, four with placebo, four empty. Symptoms were about twice as bad in any month with a tablet, and identical whether the tablet contained the drug or not.
What was measured
Daily symptom intensity score in statin, placebo and no-tablet months
Effect estimate
No reviewed effect estimate exists for this record.
Limits
See the technical detail.
From the source
Participants received 12 one-month bottles — 4 atorvastatin 20 mg, 4 placebo, 4 empty — and recorded daily symptom intensity on a 1 to 100 scale by app. Sixty were randomised and 49 completed the 12-month protocol. Mean symptom score was 8.0 (95% CI 4.7 to 11.3) in no-tablet months, 16.3 (13.0 to 19.6) in statin months and 15.4 (12.1 to 18.7) in placebo months; both tablet conditions exceeded no-tablet at p<0.001, and statin did not differ from placebo (p=0.388). The nocebo ratio, the fraction of tablet-induced symptoms also induced by placebo, was 0.90. Neither symptom intensity on starting (OR 1.02, 0.98 to 1.06, p=0.28) nor relief on stopping (OR 1.01, 0.98 to 1.05, p=0.48) distinguished statin from placebo. Six months after the trial, 30 of 60 participants were back on statins.
Written into the record, not signed off as a reviewed claim
StatinWISE replicated it in 200 people in ordinary general practice
In plain words
A second, larger, independent set of n-of-1 trials recruited people who had already stopped or were about to stop statins because of muscle pain. Across six alternating two-month periods, the difference between drug and placebo was effectively zero.
What was measured
Mean difference in muscle symptom score, statin periods minus placebo periods
Effect estimate
No reviewed effect estimate exists for this record.
Limits
See the technical detail.
From the source
StatinWISE recruited 200 participants across 50 United Kingdom primary care sites between December 2016 and April 2018, each randomised to a sequence of six double-blind two-month periods of atorvastatin 20 mg daily or placebo, rating muscle symptoms on a 0-10 visual analogue scale at the end of each period. 151 provided scores for at least one statin and one placebo period and entered the primary analysis. The mean difference, statin minus placebo, was -0.11 (95% CI -0.36 to 0.14), p=0.40. Withdrawals for intolerable muscle symptoms were 18 (9%) during a statin period and 13 (7%) during a placebo period. Two thirds of those completing intended to restart long-term statin treatment.
Written into the record, not signed off as a reviewed claim
The diabetes signal is real, quantified, and small
In plain words
Statins raise the chance of being diagnosed with diabetes. Pooling thirteen trials, treating 255 people for four years produces one extra case.
What was measured
Odds ratio for incident diabetes on statin versus control, and number needed to harm
Effect estimate
No reviewed effect estimate exists for this record.
Limits
See the technical detail.
From the source
Sattar and colleagues pooled 13 statin trials with 91,140 participants, of whom 4,278 developed diabetes over a mean of 4 years — 2,226 on statin against 2,052 on control. Statin therapy carried a 9% increased odds of incident diabetes (OR 1.09, 95% CI 1.02 to 1.17) with little heterogeneity (I-squared 11%). Treating 255 patients (95% CI 150 to 852) for 4 years produced one extra case. Risk was highest in trials with older participants; neither baseline body-mass index nor the size of the LDL reduction explained the residual variation. Preiss and colleagues then compared intensive with moderate dosing across 5 trials and 32,752 participants: OR 1.12 (1.04 to 1.22) for new-onset diabetes against OR 0.84 (0.75 to 0.94) for cardiovascular events, a number needed to harm per year of 498 set against a number needed to treat per year of 155.
Written into the record, not signed off as a reviewed claim
TNT: more atorvastatin bought 2.2 percentage points and no extra survival
In plain words
Ten thousand patients with stable coronary disease took either 10 mg or 80 mg of the same drug for five years. The high strength prevented more events. It did not reduce deaths, and it produced six times as many liver enzyme abnormalities.
What was measured
First major cardiovascular event over a median 4.9 years, 80 mg versus 10 mg
Effect estimate
No reviewed effect estimate exists for this record.
Limits
See the technical detail.
From the source
TNT randomised 10,001 patients with clinically evident coronary heart disease and LDL below 130 mg/dL to double-blind atorvastatin 10 mg or 80 mg, followed for a median 4.9 years. Mean on-treatment LDL was 77 mg/dL on 80 mg against 101 mg/dL on 10 mg. A primary event occurred in 434 patients (8.7%) on 80 mg against 548 (10.9%) on 10 mg: an absolute reduction of 2.2 percentage points, a 22% relative reduction, hazard ratio 0.78 (95% CI 0.69 to 0.89), p<0.001. There was no difference between groups in overall mortality. Persistent elevations in liver aminotransferases occurred in 1.2% on 80 mg against 0.2% on 10 mg, p<0.001.
Written into the record, not signed off as a reviewed claim
The "pleiotropic effects" story is mechanism, not a tested endpoint
In plain words
Statins are often credited with anti-inflammatory and plaque-stabilising actions beyond cholesterol lowering. Those actions are real in the laboratory. No trial has separated them from the cholesterol lowering in people.
What was measured
That a measurable share of the clinical benefit comes from anti-inflammatory or plaque-stabilising actions independent of LDL lowering — biochemically plausible, never isolated in a randomised trial
Effect estimate
No reviewed effect estimate exists for this record.
Limits
See the technical detail.
From the source
Blocking HMG-CoA reductase depletes not only cholesterol but the isoprenoid intermediates farnesyl and geranylgeranyl pyrophosphate, which are required to anchor Rho, Rac and Ras to membranes; that biochemistry is well established and is the mechanistic basis of the pleiotropy claim. What does not exist is a randomised comparison isolating it. The strongest quantitative evidence runs the other way: the Cholesterol Treatment Trialists pooled individual data from 26 randomised trials and 170,000 participants and found benefit scaling with the size of the LDL reduction, each 1.0 mmol/L reduction cutting the annual rate of major vascular events by just over a fifth, with no threshold across the range studied. A benefit that scales with the LDL change is evidence for the LDL change, not against pleiotropy, but it leaves the pleiotropic contribution unmeasured.
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What is not here
3 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.
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 most-studied lipid-lowering drug there is: 100 versus 154 primary coronary events in 10,305 hypertensive patients in ASCOT-LLA and a 37% event reduction in 2,838 diabetic patients in CARDS, both statistically solid, alongside two independent n-of-1 trial programmes that found no difference at all between atorvastatin and placebo in muscle symptoms among people who had already reported them.
Recorded evidence blocks (14)
Q2
What did Atorvastatin's largest trial (2133900 people) and its longest (23 years) measure?
2133900 people in Atorvastatin's largest registered study, 23 years in its longest registered window, measuring mortality ; myocardial infarction ; stroke. ClinicalTrials.gov · 2026-09-01
214 phase4, 187 phase3, 172 phase2, 127 phase1, 86 na, 21 na or unstated, 9 early phase1; NCT03819101; 2042-03. Last human test completed 2026, NCT07717788.
Interpretation These counts include studies where Atorvastatin 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
phase4
214
phase3
187
phase2
172
phase1
127
na
86
na or unstated
21
2 more recorded rows
early phase1
9
Last recorded human testNCT07717788
2026-07-01
recorded 2026-09-01 · last checked 2026-09-04
Q3
From mouse to human: where has Atorvastatin shown lifespan?
"Very poor enrollment"; 71 of 780 registered studies
Show the evidence
Trial
NCT00004466
terminated; "Very poor enrollment"
NCT00127335
withdrawn; "Lack of funding"
NCT00181181
terminated; "Coronary flow by echo Doppler was obtainable in about 50% of subjects. The study was stopped early because of insufficient sample size to achieve adequate power"
NCT00243672
withdrawn; "The study chair changed his employment, the realization of the study was not possible"
NCT00249899
terminated; "Overall profile of the compound does not offer significant clinical advantage to patients over currently available lipid lowering agents"
NCT00252967
terminated; "Insufficient power to show therapy difference at interim analysis."
14 further recorded trials
NCT00292201
terminated; "Lack of funding to complete subject recruitment and testing"
NCT00343655
terminated; "The study was terminated on June 22, 2007 for inability to enroll patients within an appropriate timeframe. There were no efficacy/safety concerns."
NCT00344019
terminated; "slow recruitment"
NCT00427960
terminated; "Due to inadequate recruitment"
NCT00437892
terminated; "Competitive trials and slow recruitment rate"
NCT00491400
terminated; "Insufficient enrollment"
NCT00491751
terminated; "Insufficient enrollment"
NCT00532311
terminated; "Overall profile of the compound does not offer significant clinical advantage to patients over currently available lipid lowering agents"
NCT00585611
terminated; "Unable to recruit into the study"
NCT00587379
withdrawn; "Study closed per the request of PI due to lack of participant accrual"
NCT00590135
terminated; "Poor Reducibility - primary endpoint measure not obtainable"
NCT00640549
terminated; "See termination reason in detailed description."
20 recorded entries; human; also "Atorvastatin (10 mg or 80 mg)", "Atorvastatin (Lipitor, 40mg)", "Lipitor 20 mg"
Show the evidence
human
NCT00134550
Atorvastatin (10 mg or 80 mg)
NCT00172419
Atorvastatin (Lipitor, 40mg)
NCT00299884
Lipitor 20 mg
NCT00319449
Atorvastatin 10 mg
NCT00344019
Atorvastatin 80mg
NCT00474240
Atorvastatin 20 mg
14 more recorded rows
humanNCT00474240
AEGR-733 5 mg + atorvastatin 20 mg
humanNCT00474240
AEGR-733 10 mg + atorvastatin 20 mg
humanNCT00497016
atorvastatin 80 mg
humanNCT00535405
Atorvastatin 40 mg
humanNCT00572312
atorvastatin (Sortis) 40 mg
humanNCT00687271
Placebo for Atorvastatin 20 mg
humanNCT00736463
Atorvastatin 80 mg
humanNCT00782184
atorvastatin 40 mg
humanNCT00782184
atorvastatin 20 mg
humanNCT00973271
20 mg atorvastatin
humanNCT01185236
atorvastatin 20mg
humanNCT01218204
10mg atorvastatin
humanNCT01218204
80mg atorvastatin
humanNCT01228227
ATORVASTATIN 80 mg
recorded 2026-09-01 · last checked 2026-09-04
Q6
More Atorvastatin was worse in human: at what point?
Hormetic in human: "Hormetic dose responses were commonly reported, being induced by a broad range of chemicals, including pharmaceuticals (e.g., atorvastatin, isoproterenol, lithium, nicotine, ouabain), dietary supplements (e.g., curcumin, multiple ginsenosides, resveratrol), endogenous agents (e.g., estrogen, hydrogen peroxide,…" Europe PMC · dose-response search · 2026-04-14
5 recorded sentences naming Atorvastatin; Hormetic, Dose-response, dose-response
Show the evidence
HormeticPMID 34932953
"Hormetic dose responses were commonly reported, being induced by a broad range of chemicals, including pharmaceuticals (e.g., atorvastatin, isoproterenol, lithium, nicotine, ouabain), dietary supplements (e.g., curcumin, multiple ginsenosides, resveratrol), endogenous agents (e.g., estrogen, hydrogen peroxide, melatonin), and physical stressor agents (e.g., hypoxia, ionizing radiation)."
Dose-responsePMID 42182670
"Dose-response analysis revealed a more significant reduction in mortality rates with high-dose (>40 mg) atorvastatin."
dose-response
PMID 38385748
"In whole muscle homogenates from day 0 biopsies, atorvastatin inhibited complex III activity at midmicromolar concentrations, whereas complex IV activity was inhibited at low nanomolar concentrations.CONCLUSIONThese findings demonstrate that high-dose atorvastatin treatment elicits a striking progressive decline in skeletal muscle mitochondrial respiratory capacity, highlighting the need for…"
PMID 38737008
"We estimated ED<sub>50</sub> and E<sub>max</sub> for 3,033 unique individuals (atorvastatin: 1,632, simvastatin: 1,089, and rosuvastatin: 312) using a nonlinear, mixed effects dose-response model."
Dose-responsePMID 34448822
"Dose-response models predicted that combining bempedoic acid with the lowest statin dose of commonly used statins would achieve a similar degree of LDL-C lowering as quadrupling that statin dose; for example, the predicted LDL-C lowering was 54% with atorvastatin 80 mg compared with 54% with atorvastatin 20 mg + bempedoic acid 180 mg, and 42% with simvastatin 40 mg compared with 46% with…"
recorded 2026-04-14 · last checked 2026-09-04
Q7
Atorvastatin's half-life is approximately 14 hours — which schedules were studied?
approximately 14 hours, the half-life Atorvastatin's label states. openfda-label · 2e20a00c-b373-3a8c-e063-6294a90a637b · 2026-08-27
bioavailability approximately 14% %.
Show the evidence
half life
approximately 14 hours hours; Mean plasma elimination half-life of atorvastatin in humans is approximately 14 hours, but the half-life of inhibitory activity for HMG-CoA reductase is 20 to 30 hours due to the contribution of active metabolites.
bioavailability
approximately 14% %; The absolute bioavailability of atorvastatin (parent drug) is approximately 14% and the systemic availability of HMG-CoA reductase inhibitory activity is approximately 30%.
metabolism
Elimination Metabolism Atorvastatin calcium is extensively metabolized to ortho- and parahydroxylated derivatives and various beta-oxidation products.
recorded 2026-08-27 · last checked 2026-09-04
Q8
Which of brachial artery flow mediated dilation, changes in apob/apoa i levels and decrease in incidence of deep vein thrombosis did Atorvastatin's trials measure?
brachial artery flow mediated dilation, changes in apob/apoa i levels and decrease in incidence of deep vein thrombosis lead 40 outcome terms across Atorvastatin's trials. ClinicalTrials.gov · 2026-09-01
statin toxicity, pefr, hip flexion, oxygen consumption and anaerobic threshold, muscle pathology and effects on bad cholesterol ldl c after 12 weeks follow.
Show the evidence
plasma lipid levels
1
mean mean common carotid imt
1
ldl c from baseline to week 12
1
statin toxicity
1
pefr
1
hip flexion
1
14 more recorded rows
oxygen consumption and anaerobic threshold
1
muscle pathology
1
effects on bad cholesterol ldl c after 12 weeks
1
intima media thickness as measured by carotid ultrasound
1
hdl c and ldl c
1
hdl c and non hdl c levels
1
time to complete healing
1
recurrence rate of foot ulcers
1
intima media thickness as measures by carotid ultrasound
1
lipid parameters at various timepoints over 12 months
1
ldl and hdl levels
1
low density lipoprotein cholesterol
1
ldl c and non hdl c levels
1
time to occurrence of fatal or non fatal stroke
1
recorded 2026-09-01 · last checked 2026-09-04
Q9
Which of Atorvastatin's 81 ongoing trials reports first?
Disability free survival - death or development of dementia or development of persistent physical disability; 3-year cumulative incidence of recurrent HCC between the intervention group and control counterpart; latest 2042-03
Show the evidence
Trial
NCT02099123
"A Clinical Trial of STAtin Therapy for Reducing Events in the Elderly (STAREE)"; n 9971; "Disability free survival - death or development of dementia or development of persistent physical disability"; 2025-12
NCT03024684
"Statin for Preventing Hepatocellular Carcinoma Recurrence After Curative Treatment"; n 240; "3-year cumulative incidence of recurrent HCC between the intervention group and control counterpart"; 2027-01
NCT03560882
"A Pilot Trial of Atorvastatin in Tumor Protein 53 (p53) -Mutant and p53 Wild-Type Malignancies"; n 50; "Change in conformational mutant tumor protein 53 (p53)"; 2026-08-01
NCT03753555
"The Effect of InTensive Statin in Ischemic Stroke With inTracranial Atherosclerotic Plaques"; n 100; "Changes in remodeling index after the statin treatment"; 2027-11-30
NCT03819101
"Trial of Acetylsalicylic Acid and Atorvastatin in Patients With Castrate-resistant Prostate Cancer"; n 1210; "Overall Survival (OS)"; 2042-03
NCT04147286
"Atorvastatin to Reduce Inflammation After Tuberculosis Treatment Completion"; n 220; "Total lung glycolysis (TLG) on PET/CT imaging"; 2027-09-30
14 further recorded trials
NCT04262206
"Pragmatic Evaluation of Events And Benefits of Lipid-lowering in Older Adults"; n 20000; "Number of patients without diagnosis of new dementia"; 2026-12-31
NCT04347434
"Assessment of the Effects of Long-term Lipid-lowering Therapy in Patients With Primary STEMI or NSTEMI"; n 300; "Ventricular arrhythmias"; 2027-12-30
NCT04575857
"Role of Statins In Slowing Rheumatic Heart Disease (RHD) Progression"; n 100; "Enrollment rate"; 2040-02
NCT04601116
"The MASTER Study (MAmmary Cancer STatin ER Positive Study)"; n 3360; "Invasive disease-free survival"; 2035-01-01
NCT04679376
"Statins for the Treatment of NASH"; n 70; "Change in NASH as measured by improvement in NAS score Improvement in NAS score (≥ 2 points) with no worsening in fibrosis stage (≥1 point) OR improvement in fibrosis with no worsening of NASH (change in the NAS score of ≤ 0 points)."; 2026-12
NCT04735263
"Dark Adaptation as an Early Indicator of Response to Statin Therapy for Intermediate AMD"; n 21; "Change in Dark Adaptation recovery time measured by change in Rod Intercept time (RIT)"; 2028-01-01
NCT04765137
"Evaluate the Effect of Atorvastatin on Cerebrovascular Reactivity in Mild Cognitive Impairment (MCI)"; n 20; "Change of MRI whole brain cerebrovascular reactivity (wbCVR)"; 2027-12-31
NCT04767984
"Testing Atorvastatin to Lower Colon Cancer Risk in Longstanding Ulcerative Colitis"; n 42; "Reduction in mutant p53 staining in biopsy samples obtained during colonoscopies done before and after intervention"; 2026-11-30
NCT04789057
"Atorvastatin Effect on Reduction of COPD Exacerbations"; n 460; "COPD exacerbation rate"; 2027-05-31
NCT04847752
"Study of Predictive Factors Related to Prognosis of Patients With Ischemic Stroke Due to Large-artery Atherosclerosis"; n 1000; "all-cause mortality"; 2028-12-31
NCT04904536
"Statin TReatment for COVID-19 to Optimise NeuroloGical recovERy"; n 190; "Neurological Recovery"; 2025-07-30
NCT04915183
"Atorvastatin to Reduce Cisplatin-Induced Hearing Loss Among Individuals With Head and Neck Cancer"; n 224; "To determine the effectiveness of atorvastatin (20 mg) at reducing the incidence and severity of cisplatin-induced hearing loss in patients with head and neck squamous cell carcinoma (HNSCC)."; 2030-08-31
NCT05028829
"Safety and Efficacy of Atorvastatin v. Placebo on HCC Risk"; n 60; "Reduced magnitude of high-risk PLSec after treatment vs before treatment"; 2031-03-01
NCT05049603
"A Randomized Clinical Trial to Evaluate the Effects of Atorvastatin on Graves' Orbitopathy (GO): the STAGO-2 Study"; n 102; "Outcome of GO"; 2026-12-31
recorded 2026-09-01 · last checked 2026-09-04
Q10
Which running trial of Atorvastatin could settle lifespan?
NCT02099123 measures Disability free survival - death or development of dementia or development of persistent physical disability, reading out 2025-12.
8 open trials; n 9971; "A Clinical Trial of STAtin Therapy for Reducing Events in the Elderly (STAREE)"
Show the evidence
Trial
NCT02099123
"A Clinical Trial of STAtin Therapy for Reducing Events in the Elderly (STAREE)"; n 9971; "Disability free survival - death or development of dementia or development of persistent physical disability"; 2025-12
NCT06327451
"Evaluate the Efficacy and Safety of Atorvastatin Combined With Temozolomide in the Treatment of Glioblastoma"; n 50; "progression-free survival"; 2027-02-28
NCT05705804
"Effects of Pitavastatin or Combination of Pitavastatin and Ezetimibe on Glucose Metabolism Compared to AtoRvastatin in atheroscLerotic Cardiovascular Disease Patients With Metabolic Syndrome: The EZ-PEARL Randomized Trial"; n 250; "Change form baseline homeostatic model assessment for insulin resistance (HOMA-IR) at 24 weeks"; 2027-06-01
NCT04847752
"Study of Predictive Factors Related to Prognosis of Patients With Ischemic Stroke Due to Large-artery Atherosclerosis"; n 1000; "all-cause mortality"; 2028-12-31
NCT06157099
"Atorvastatin for Preventing Disease Metastasis in Patients With Resected High-Risk Stage IIA, IIB, or IIIA Melanoma"; n 150; "Recurrence-free survival (RFS)"; 2029-09-01
NCT05404139
"Duration of Androgen Receptor Pathway Inhibitor and ADT With Metastasis Directed Therapy in Oligometastatic Cancer of the Prostate (DIRECT)"; n 352; "Progression free survival"; 2031-02
2 further recorded trials
NCT04601116
"The MASTER Study (MAmmary Cancer STatin ER Positive Study)"; n 3360; "Invasive disease-free survival"; 2035-01-01
NCT03819101
"Trial of Acetylsalicylic Acid and Atorvastatin in Patients With Castrate-resistant Prostate Cancer"; n 1210; "Overall Survival (OS)"; 2042-03
Q11
Which 321 trials of Atorvastatin posted no result?
Posted no result
321 of 321 completed trials
Registrations
NCT00380939, NCT03884452, NCT03867110, NCT03867318, NCT00000941 and NCT00392717, and 315 more
Completion dates
oldest 2000-12; newest 2024-08-31
Show the evidence
Trial
NCT00380939
2000-12
NCT03884452
2001-05-24
NCT03867110
2001-07-27
NCT03867318
2001-11-16
NCT00000941
2002-03
NCT00392717
2002-03
14 further recorded trials
NCT02587416
2002-12
NCT03882996
2003-02-04
NCT02591836
2003-06
NCT03885921
2003-07-08
NCT00327418
2004-02
NCT00442325
2004-02
NCT00442845
2004-02
NCT00644670
2004-03
NCT00653744
2004-03
NCT00647543
2004-04
NCT00024531
2004-08
NCT00327691
2004-08
NCT00329173
2004-08
NCT00653796
2004-08-01
Q12
At the median, Atorvastatin's trials enrolled 90 people — anything larger?
Median enrolment
90
Largest enrolment
2133900
Registered trials counted
771
Q13
What do 37541 spontaneous reports say about Atorvastatin — 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.
Atorvastatin appears in spontaneous reports to regulators. Across the 10 most-reported reaction terms, 37541 reaction mentions were counted: myalgia 8663; rhabdomyolysis 7259; drug interaction 4270; drug hypersensitivity 4182. open-targets-adr · CHEMBL1487 · 2026-06-24
Show the evidence
myalgia
8663
rhabdomyolysis
7259
drug interaction
4270
drug hypersensitivity
4182
blood creatine phosphokinase increased
3872
muscular weakness
2469
4 more recorded rows
muscle spasms
2211
myopathy
1699
renal failure acute
1659
liver function test abnormal
1257
recorded 2026-06-24 · last checked 2026-09-04
Q14
Was Atorvastatin studied with fasting and exercise?
fasting and exercise are named in Atorvastatin's label sentences: "This randomised, placebo-controlled, double-blind, crossover study reveals that short-term high-dose atorvastatin treatment increases fasting and postprandial glucagon levels and alters amino acid and bile acid profiles without affecting glucose, insulin, or gut microbiota in healthy men." openfda-label+europepmc · 2026-08-30
2 recorded statements; fasting, exercise
Show the evidence
fasting
This randomised, placebo-controlled, double-blind, crossover study reveals that short-term high-dose atorvastatin treatment increases fasting and postprandial glucagon levels and alters amino acid and bile acid profiles without affecting glucose, insulin, or gut microbiota in healthy men.
exercise
Statin-naïve participants are randomized between three arms: (1) supervised exercise with atorvastatin (40 mg once daily) for three months, (2) supervised exercise without atorvastatin, or (3) unsupervised voluntary exercise.
recorded 2026-08-30 · last checked 2026-09-04
Q15
What is recorded about Atorvastatin and autophagy?
"Atorvastatin, primarily recognized for its cholesterol-lowering properties, has largely unexplored potential in modulating autophagy and safeguarding against age-related cognitive decline." — where Atorvastatin and autophagy appear together. Europe PMC · pathway abstract search · 2026-08-10
"Atorvastatin, primarily recognized for its cholesterol-lowering properties, has largely unexplored potential in modulating autophagy and safeguarding against age-related cognitive decline."
PMID 41108918
"In conclusion, atorvastatin showed neuroprotective impact in this aged rat model by reducing oxidative stress, inflammation, and apoptosis, while modulating autophagy markers."
senolyticPMID 42573875
"The 2024 randomized trials of middle meningeal artery embolization, the success of atorvastatin in the ATOCH trial, and emerging senolytic clinical translation collectively suggest that CSDH may be a tractable target for future mechanism-directed gerotherapeutic interventions."
mTORPMID 41871709
"Frequently studied drugs included niclosamide, metformin, atorvastatin, and doxazosin, targeting pathways such as PI3K/AKT/mTOR, apoptosis, and autophagy."
autophagyPMID 41871709
"Frequently studied drugs included niclosamide, metformin, atorvastatin, and doxazosin, targeting pathways such as PI3K/AKT/mTOR, apoptosis, and autophagy."
NAD+PMID 38927297
"It was found that the targeted binding compounds, such as NAD<sup>+</sup> and atorvastatin, could significantly induce and inhibit the larval settlement, respectively."
AMPK
PMID 40080393
"Compared with vehicle animals, i.v. atorvastatin inhibited RhoA membrane translocation, induced AMPK phosphorylation, prevented apoptosis execution, and improved cardiac remodelling in the infarcted heart of both groups, whereas innate immune cell infiltration was further reduced in i.v. atorvastatin-treated DCM animals."
PMID 37740286
"In this study, we developed liposome nanoparticles (Ato/CQ@L) for co-encapsulation of atorvastatin (Ato), an activator of AMP-activated protein kinase (AMPK), and chloroquine (CQ), an autophagy inhibitor."
PMID 38299233
"H&E and Oil red O staining were used to observe the improvement in MASLD, western blotting analysis was used to detect the expression of proteins related to fat metabolism and immunofluorescence was used to detect reactive oxygen species (ROS) levels. <i>In vitro</i>, donafenib and atorvastatin inhibited lipid accumulation in HepG2 cells. <i>In vivo</i>, donafenib and atorvastatin activated the…"
mTORPMID 33136767
"Further analysis revealed that atorvastatin promoted lipophagy by upregulating adenosine 5'-monophosphate-activated protein kinase (AMPK) phosphorylation, and downregulating mammalian target of rapamycin phosphorylation, whereas the AMPK inhibiter, compound C, attenuated these effects."
recorded 2026-08-10 · last checked 2026-09-04
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