This page shows what was measured, who it was measured in, and what that does not settle.
What Clopidogrel does in the body
Used to prevent clots after a heart attack, stent or stroke.
Platelets recruit each other using a chemical signal that lands on a specific receptor. Clopidogrel arrives as an inactive molecule, is converted by liver enzymes into a reactive form, and that form permanently welds itself to the receptor. The platelet can never respond to that signal again, so the effect lasts the platelet's whole ten-day life and only fades as new platelets are made.
What happened in people
Added to aspirin, it prevented about two events and caused about one extra major bleed per 100 people.
✓ 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
Genetic or blood-test guided dosing has not clearly improved outcomes.
Where it acts
Platelet surface membrane, after activation in the liver
Kind of result
The kind of result is not recorded
Supervision
RNAWiki has not recorded a supervision or regulatory status for this substance.
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 95 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.
Comparator
A comparator is whatever the treatment was measured against.
A picture of it, and where the picture fails
It is like the other runner in a race.
Where that stops being true. A race has one winner. A study can show both arms improved.
What people get wrong. Results are read without asking what the other group got. Beating nothing is not beating a treatment.
The control condition against which the experimental intervention is assessed.
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.
Absolute difference
An absolute difference is how many more people in a hundred were affected.
A picture of it, and where the picture fails
It is like counting heads in two rooms of a hundred.
Where that stops being true. Heads are easy to count. Study results carry a margin of error too.
What people get wrong. It is confused with a percentage change, which can look far larger.
The arithmetic difference in event rates between arms.
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.
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.
Composite of cardiovascular death, non-fatal myocardial infarction or stroke, added to aspirin
✓ The study showed what it set out to show
Who was studied
CURE
How many people
12562
Study design
Randomised double-blind placebo-controlled trial, 3 to 12 months
Compared against
A dummy treatment
Kind of result
Living longer, or avoiding a major event
What was found
RR 0.80 (95% CI 0.72-0.90), P < 0.001; absolute difference 2.1 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. Major bleeding rose from 2.7% to 3.7% (RR 1.38, p=0.001), an absolute increase of 1.0 point against an absolute event reduction of 2.1.
How far it carries. This study is recorded from the curated record, not from the registry match.
Form and route. Oral tablet, and a fixed combination with aspirin
Interval reported. 95% CI 0
Written into the record, not signed off as a reviewed claim.
Composite of myocardial infarction, stroke or cardiovascular death on clopidogrel plus aspirin
✗ The study did not show it
Who was studied
CHARISMA (NCT00050817)
How many people
15603
Study design
Randomised double-blind placebo-controlled trial, median 28 months
Compared against
A dummy treatment
Kind of result
Living longer, or avoiding a major event
What was found
RR 0.93 (95% CI 0.83-1.05), P = 0.22
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. In the multiple-risk-factor subgroup without established disease, cardiovascular death was 3.9% on clopidogrel against 2.2% on placebo, p=0.01.
How far it carries. This study is recorded from the curated record, not from the registry match.
Form and route. Oral tablet, and a fixed combination with aspirin
Interval reported. 95% CI 0
Written into the record, not signed off as a reviewed claim.
Composite of cardiovascular death, myocardial infarction, stroke, stent thrombosis and severe recurrent ischaemia in CYP2C19 loss-of-function carriers
✗ The study did not show it
Who was studied
TAILOR-PCI (NCT01742117)
How many people
5302
Study design
Randomised open-label strategy trial, 12 months
Compared against
Not recorded for this study
Kind of result
Living longer, or avoiding a major event
What was found
HR 0.66 (95% CI 0.43-1.02), P = 0.06
Repeated elsewhere
Unreplicated
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. The trial was powered at 85% to detect a hazard ratio of 0.50, a large effect. None of 11 prespecified secondary endpoints differed significantly.
How far it carries. This study is recorded from the curated record, not from the registry match.
Form and route. Oral tablet, and a fixed combination with aspirin
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 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
Blood and vessels: The active metabolite binds irreversibly to platelet receptors, inhibiting platelet aggregation (as recorded)
US prescribing information · 0078fb3d-3595-4ae1-a059-1d5e81c879cf · read 2026-08-27
Start
Clopidogrel
What a person takes: Oral tablet, and a fixed combination with aspirin.
The measurement behind this step
Once daily, usually preceded by a loading dose because only a small fraction of each dose becomes active drug and steady-state platelet inhibition otherwise takes several days. Food does not meaningfully affect it. Effect persists for days after stopping because the receptor block is irreversible and recovery requires new platelets.
Getting in
Absorbed well, and then mostly thrown away
Most of the tablet that gets absorbed is immediately broken down into a useless form. Only about one part in seven ever goes down the route that makes the active drug.
╌╌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
Absorption is at least 50%, and roughly 85% of absorbed drug is hydrolysed by hepatic carboxylesterase-1 to an inactive carboxylic acid. The remaining 15% is available for oxidative activation. This is why the loading dose exists and why the drug takes days to reach steady-state effect without one.
Two liver oxidations, mostly by one variable enzyme, make the active form
The liver has to modify the molecule twice to produce the reactive species that works. The main enzyme doing this varies widely between people for genetic reasons.
╌╌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
Clopidogrel is oxidised to 2-oxo-clopidogrel and then to the thiol active metabolite, with CYP2C19 contributing substantially to both steps alongside CYP1A2, CYP2B6 and CYP3A4. CYP2C19*2 and *3 are loss-of-function alleles present in roughly a quarter to a third of people depending on ancestry, and *17 is a gain-of-function allele. The active metabolite has a half-life of minutes.
A reactive thiol welds itself onto the platelet receptor
The active form makes a permanent chemical bond with the receptor. That platelet is finished for the rest of its life; there is no undoing 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
The thiol metabolite forms a disulphide bridge with extracellular cysteine residues, principally Cys17 and Cys270, on the P2Y12 receptor. The bond is covalent and irreversible, so recovery requires production of new platelets rather than clearance of drug — which is why effect persists for days after the last dose and why surgery requires several days of withdrawal.
Platelets can no longer recruit each other with their main chemical signal, so a small clot does not snowball into an occluding one.
╌╌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
Blocking P2Y12 removes Gi-mediated inhibition of adenylate cyclase, so cyclic AMP stays high and VASP remains phosphorylated. Glycoprotein IIb/IIIa activation, dense granule release and the sustained phase of aggregation are all suppressed. Aspirin blocks a parallel amplification loop through thromboxane A2, which is why the two are additive and why their bleeding risks are additive too.
Two fewer events per hundred, one more major bleed per hundred
Added to aspirin after an acute coronary syndrome, it prevented about two cardiovascular events per hundred people and caused about one extra major bleed per hundred.
╌╌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
In CURE the primary composite was 9.3% against 11.4% (relative risk 0.80, p<0.001) with major bleeding 3.7% against 2.7% (relative risk 1.38, p=0.001). Life-threatening bleeding and haemorrhagic stroke did not differ significantly. In CAPRIE, against aspirin alone, the annual event rate was 5.32% against 5.83%.
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 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.
People after coronary stenting, after acute coronary syndrome, after ischaemic stroke and with peripheral arterial disease. It is on the WHO Model List of Essential Medicines and generic almost everywhere.
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: “Safety and effectiveness in pediatric populations have not been established.”
US prescribing information · 4cd07a3c-9673-4aa0-b76a-d79df2399ee1 · read 2026-08-30
On older people, the label states: “Of the total number of subjects in the CAPRIE and CURE controlled clinical studies, approximately 50% of patients treated with clopidogrel were 65 years of age and older, and 15% were 75 years and older.”
US prescribing information · 4cd07a3c-9673-4aa0-b76a-d79df2399ee1 · read 2026-08-30
On people who are pregnant, the label states: “Risk Summary Available data from cases reported in published literature and postmarketing surveillance with clopidogrel use in pregnant women have not identified any drug-associated risks for major birth defects or miscarriage [see Data] .”
US prescribing information · 4cd07a3c-9673-4aa0-b76a-d79df2399ee1 · read 2026-08-30
On people who are breastfeeding, the label states: “Risk Summary There are no data on the presence of clopidogrel in human milk or the effects on milk production.”
US prescribing information · 4cd07a3c-9673-4aa0-b76a-d79df2399ee1 · read 2026-08-30
On people with reduced liver function, the label states: “No dosage adjustment is necessary in patients with hepatic impairment [see Clinical Pharmacology ( 12.2 )] .”
US prescribing information · 4cd07a3c-9673-4aa0-b76a-d79df2399ee1 · read 2026-08-30
On people with reduced kidney function, the label states: “Experience is limited in patients with severe and moderate renal impairment [see Clinical Pharmacology ( 12.2 )] .”
US prescribing information · 4cd07a3c-9673-4aa0-b76a-d79df2399ee1 · read 2026-08-30
Where the result stopped carrying
CHARISMA missed its primary endpoint and showed a mortality signal against clopidogrel in primary prevention
GRAVITAS moved the surrogate 22 percentage points and the clinical endpoint not at all
TAILOR-PCI, the definitive test of pharmacogenomic antiplatelet selection, did not reach significance
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 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 (11)
It was studied for a different goal
The studies measured something else entirely. Nothing in this record points to this reason.
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, and a fixed combination with aspirin
✎ 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
RNAWiki has not recorded a supervision or regulatory status for this substance.
❝ Quoted from a source
Where this came from
Copied from a source RNAWiki stored, with the source named.
No register row and no identity class settled the question.
No source is stored against this line.
What is in the pack
Once daily, usually preceded by a loading dose because only a small fraction of each dose becomes active drug and steady-state platelet inhibition otherwise takes several days. Food does not meaningfully affect it. Effect persists for days after stopping because the receptor block is irreversible and recovery requires new platelets.
✎ 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 and what that means for what is in the pack.
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 US label carries a boxed warning about diminished antiplatelet effect in CYP2C19 poor metabolisers. Bleeding is the principal risk and rises when combined with aspirin: major bleeding 3.7% against 2.7% in CURE. Thrombotic thrombocytopenic purpura is rare and can occur within the first two weeks. Omeprazole and esomeprazole inhibit CYP2C19 and are specifically discouraged in the label. Elective surgery generally requires withdrawal several days in advance because the effect cannot be reversed pharmacologically.
Nobody counted how many people took this and were fine, so this cannot be turned into a rate.
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, and a fixed combination with aspirin
✎ 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
Food does not meaningfully affect it. Effect persists for days after stopping because the receptor block is irreversible and recovery requires new platelets.
✎ 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
3 products list this as an active ingredient in the United States drug directory. 3 of them contain it and nothing else.
FDA National Drug Code directory · 31722-758 · read 2026-08-29
They are sold as powder and tablet, taken oral.
FDA National Drug Code directory · 31722-758 · read 2026-08-29
The regulator's established pharmacologic class for it is cytochrome p450 2c8 inhibitors [moa], decreased platelet aggregation [pe] and p2y12 platelet inhibitor [epc].
FDA National Drug Code directory · 31722-758 · read 2026-08-29
16 published labels name it as an active ingredient. 16 of them describe this substance alone, which is where its own label text on this page comes from.
US prescribing information · 3aef6fd4-7160-4678-9362-ca76174bfd0e · read 2026-08-29
Those labels are classed as human prescription drug.
US prescribing information · 3aef6fd4-7160-4678-9362-ca76174bfd0e · read 2026-08-29
19 marketed supplement labels list this ingredient, classed as fat/fatty acid, multi-vitamin and mineral (mvm), other combinations and 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.
Clopidogrel is film-coated tablets at Film-coated tablets: 75 mg, recorded as prescription product; fda label in effect 2024-05-17 in the United States.
US prescribing information · 0078fb3d-3595-4ae1-a059-1d5e81c879cf · read 2026-08-27
Recorded price in US: 0.04704 USD per one unit as the pricing file counts it — a tablet, capsule, patch or single item, across 42 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.
RNAWiki could not confidently classify this substance, so no self-experiment plan is offered.
Questions worth asking
Which of the trials of Clopidogrel 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 correcting high on-treatment platelet reactivity prevents events — GRAVITAS corrected it and produced a hazard ratio of 1.01
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 CYP2C19 genotype-guided drug selection improves outcomes — TAILOR-PCI gave 0.66 with p=0.06 against a trial powered for 0.50
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 dual antiplatelet therapy benefits people with risk factors but no established disease — CHARISMA found higher cardiovascular death in that subgroup
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 CAPRIE advantage over aspirin is substantial — its confidence interval runs from 0.3% to 16.5%
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 Clopidogrel 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.
CURE: 2.1 percentage points fewer events, 1.0 point more major bleeding
In plain words
Adding clopidogrel to aspirin after an acute coronary syndrome prevented about two events per hundred patients and caused about one extra major bleed per hundred.
What was measured
Composite of cardiovascular death, non-fatal myocardial infarction or stroke, and major bleeding, over 3 to 12 months
Effect estimate
No reviewed effect estimate exists for this record.
Limits
See the technical detail.
From the source
CURE randomised 12,562 patients presenting within 24 hours of an acute coronary syndrome without ST-segment elevation to clopidogrel 300 mg then 75 mg daily (n=6,259) or placebo (n=6,303), both on aspirin, for 3 to 12 months. The first primary composite of cardiovascular death, non-fatal myocardial infarction or stroke occurred in 9.3% against 11.4%: relative risk 0.80 (95% CI 0.72 to 0.90), p<0.001, an absolute difference of 2.1 percentage points. The second primary outcome adding refractory ischaemia was 16.5% against 18.8% (0.86, 0.79 to 0.94, p<0.001). In-hospital refractory or severe ischaemia, heart failure and revascularisation were also lower. Major bleeding was higher on clopidogrel: 3.7% against 2.7%, relative risk 1.38, p=0.001. Life-threatening bleeding (2.2% against 1.8%, p=0.13) and haemorrhagic stroke (0.1% against 0.1%) did not differ significantly.
Written into the record, not signed off as a reviewed claim
CAPRIE: better than aspirin by 8.7% relative, with a lower bound of 0.3%
In plain words
The trial that established the drug compared it directly with aspirin in more than nineteen thousand patients. Clopidogrel won, narrowly, and the statistical margin was thin.
What was measured
Annual risk of ischaemic stroke, myocardial infarction or vascular death, clopidogrel versus aspirin
Effect estimate
No reviewed effect estimate exists for this record.
Limits
See the technical detail.
From the source
CAPRIE randomised 19,185 patients with atherosclerotic vascular disease manifest as recent ischaemic stroke, recent myocardial infarction or symptomatic peripheral arterial disease, with more than 6,300 in each subgroup, to clopidogrel 75 mg or aspirin 325 mg once daily, mean follow-up 1.91 years. There were 1,960 first events. Annual risk of ischaemic stroke, myocardial infarction or vascular death was 5.32% on clopidogrel against 5.83% on aspirin: a relative risk reduction of 8.7% (95% CI 0.3 to 16.5), p=0.043. The on-treatment analysis gave 9.4%. Severe adverse events were comparable: rash 0.26% against 0.10%, diarrhoea 0.23% against 0.11%, upper gastrointestinal discomfort 0.97% against 1.22%, intracranial haemorrhage 0.33% against 0.47%, gastrointestinal haemorrhage 0.52% against 0.72%. A confidence interval whose lower bound is 0.3% is compatible with a benefit close to nothing.
Written into the record, not signed off as a reviewed claim
CHARISMA: missed overall, and higher cardiovascular death in primary prevention
In plain words
Extending dual antiplatelet therapy to a broad high-risk population did not reduce events. In the subgroup who had risk factors but no established disease, more people died of cardiovascular causes on clopidogrel.
What was measured
Composite of myocardial infarction, stroke or cardiovascular death over a median 28 months, and subgroup cardiovascular death
Effect estimate
No reviewed effect estimate exists for this record.
Limits
This entry records a failure.
From the source
CHARISMA randomised 15,603 patients with clinically evident cardiovascular disease or multiple risk factors to clopidogrel 75 mg plus low-dose aspirin or placebo plus aspirin, median follow-up 28 months. The primary composite of myocardial infarction, stroke or cardiovascular death occurred in 6.8% against 7.3%: relative risk 0.93 (95% CI 0.83 to 1.05), p=0.22. The principal secondary endpoint including hospitalisation for ischaemic events was 16.7% against 17.9% (0.92, 0.86 to 0.995, p=0.04) and severe bleeding 1.7% against 1.3% (1.25, 0.97 to 1.61, p=0.09). In the multiple-risk-factor subgroup without established disease the primary rate was 6.6% on clopidogrel against 5.5% on placebo (1.2, 0.91 to 1.59, p=0.20), and cardiovascular death was higher on clopidogrel: 3.9% against 2.2%, p=0.01. In the established-atherothrombosis subgroup the rate was 6.9% against 7.9% (0.88, 0.77 to 0.998, p=0.046).
Written into the record, not signed off as a reviewed claim
GRAVITAS: the platelet test moved 22 points and the outcome moved zero
In plain words
Patients whose platelets were still reactive on standard-dose clopidogrel were randomised to a double dose. The laboratory measurement improved substantially. The event rate was identical to the second decimal place.
No reviewed effect estimate exists for this record.
Limits
See the technical detail.
From the source
GRAVITAS randomised 2,214 patients found to have high on-treatment platelet reactivity 12 to 24 hours after percutaneous intervention with drug-eluting stents, at 83 North American centres, to high-dose clopidogrel (600 mg load then 150 mg daily) or standard dose (no additional load, 75 mg daily) for 6 months. At 6 months the primary endpoint of cardiovascular death, non-fatal myocardial infarction or stent thrombosis occurred in 25 of 1,109 (2.3%) on high dose against 25 of 1,105 (2.3%): hazard ratio 1.01 (95% CI 0.58 to 1.76), p=0.97. Severe or moderate bleeding was not increased (1.4% against 2.3%; 0.59, 0.31 to 1.11, p=0.10). The pharmacodynamic endpoint moved decisively: high-dose clopidogrel produced a 22 absolute percentage-point reduction in persistently high on-treatment reactivity at 30 days (40% against 62%, p<0.001). A large surrogate change with an identical clinical result is the cleanest possible demonstration that the surrogate was not the mechanism of risk.
Written into the record, not signed off as a reviewed claim
TAILOR-PCI: genotype-guided drug selection missed its endpoint at p=0.06
In plain words
More than five thousand patients were randomised to point-of-care genotyping with a switch to a different drug for those carrying reduced-function variants, or to standard clopidogrel. The difference did not reach significance.
What was measured
Twelve-month composite of cardiovascular death, infarction, stroke, stent thrombosis and severe recurrent ischaemia in CYP2C19 loss-of-function carriers
Effect estimate
No reviewed effect estimate exists for this record.
Limits
This entry records a failure.
From the source
TAILOR-PCI randomised 5,302 patients undergoing percutaneous coronary intervention (median age 62, 25% women, 82% acute coronary syndrome) to genotype-guided therapy with point-of-care CYP2C19 testing, prescribing ticagrelor to loss-of-function carriers and clopidogrel to non-carriers, or to conventional clopidogrel with genotyping deferred 12 months. Among 1,849 loss-of-function carriers, the 12-month primary composite of cardiovascular death, myocardial infarction, stroke, stent thrombosis and severe recurrent ischaemia occurred in 35 of 903 (4.0%) on the genotype-guided strategy against 54 of 946 (5.9%) on conventional therapy: hazard ratio 0.66 (95% CI 0.43 to 1.02), p=0.06. The trial was powered at 85% to detect a hazard ratio of 0.50. None of the 11 prespecified secondary endpoints differed significantly, including major or minor bleeding (1.9% against 1.6%; 1.22, 0.60 to 2.51, p=0.58). Across all randomised patients the primary endpoint occurred in 4.4% against 5.3% (0.84, 0.65 to 1.07, p=0.16).
Written into the record, not signed off as a reviewed claim
The genotype is real, the pharmacology is real, and the clinical payoff is not established
In plain words
CYP2C19 variants genuinely reduce how much active drug is made, and that is measurable. Two randomised trials designed to turn that knowledge into fewer events did not succeed.
What was measured
That testing CYP2C19 genotype or platelet reactivity and acting on the result reduces cardiovascular events — tested twice in randomised trials, and neither reached its endpoint
Effect estimate
No reviewed effect estimate exists for this record.
Limits
See the technical detail.
From the source
The pharmacology is not in dispute: roughly 15% of absorbed clopidogrel is converted to the active thiol metabolite, largely by CYP2C19, and reduced-function alleles lower both metabolite formation and measured platelet inhibition. Two randomised strategies were built on that. GRAVITAS corrected the platelet phenotype directly, achieving a 22 percentage-point absolute improvement in on-treatment reactivity, and produced a hazard ratio of 1.01. TAILOR-PCI acted on the genotype by switching carriers to ticagrelor and produced 0.66 with p=0.06, against a trial powered to detect 0.50. Neither established a clinical benefit. The consistent reading is that reduced metabolite formation is a real biochemical fact that has not been shown to be a modifiable cause of events at the population level, which is a different conclusion from either "genotyping works" or "the genotype does not matter".
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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.
An irreversible P2Y12 blocker with a 2.1 percentage-point absolute event reduction added to aspirin in 12,562 acute coronary syndrome patients, offset by a 1.0 point increase in major bleeding — and the drug on which both platelet-function-guided and genotype-guided dosing were tested in randomised trials and neither changed outcomes.
Recorded evidence blocks (11)
Q1
On the Clopidogrel label: indicated for what?
"Clopidogrel tablets are a P2Y 12 platelet inhibitor indicated for: • Acute coronary syndrome – For patients with non–ST-segment elevation ACS (unstable angina [UA]/non–ST-elevation myocardial infarction [NSTEMI]), clopidogrel tablets has been shown to reduce the rate of myocardial infarction (MI) and stroke. ( 1.1 ) –…": indications and usage on Clopidogrel's label. DailyMed label · c9928956-bb7b-4ec2-bc38-d3c9c4199cae · 2026-07-24
Q2
561 registered trials of Clopidogrel — at which phases?
Registered studies posting no result
447 of 561
561 registered studies of Clopidogrel: 221 phase4, 133 phase3, 74 phase2, 73 phase1, 43 na, 37 na or unstated, 3 early phase1. CLINICALTRIALS_SNAPSHOT · 2026-09-01
"Stopped due to low percentage of patients with detectable CTCs at baseline."; 45 of 561 registered studies
Show the evidence
Trial
NCT00263211
terminated; "Stopped due to low percentage of patients with detectable CTCs at baseline."
NCT00305162
terminated; "Insufficient evidence of the clinical effectiveness of cangrelor"
NCT00385138
terminated; "Insufficient evidence of the clinical effectiveness of cangrelor"
NCT00421252
terminated; "Difficult to enroll patients; limited resources available"
NCT00589862
withdrawn; "Failure to secure adequate funding"
NCT00638326
terminated; "Greater differences between randomized patients than previously anticipated"
14 further recorded trials
NCT00640679
terminated; "Due to slow enrollment the study was stopped prematurely."
NCT00910299
terminated; "Due to the low rate of primary endpoint events experienced in the study to date"
NCT00940784
withdrawn; "Could not get drug"
NCT00944333
terminated; "STOP due to recent data in literature questioning the need to continue DAP beyond six months in patients with stable coronary artery stenting with DES."
NCT00991029
terminated; "The trial was halted by the DSMB."
NCT01011257
withdrawn; "No funding secured."
NCT01107899
terminated; "Terminated due to Enrollment futility"
NCT01158703
terminated; "poor recruitment and reduction in CT surgery support"
NCT01339026
terminated; "Change in guidelines favouring newer antiplatelet drugs in ACS"
NCT01452152
terminated; "Terminated by study sponsor."
NCT01612884
terminated; "Slow enrollment"
NCT01661322
terminated; "Trial reached a definitive answer ahead of full recruitment."
NCT01826175
withdrawn; "Study terminated mutually by sponsor \& PI due to no enrollment"
NCT02034292
terminated; "Sponsor Decision"
recorded 2026-09-01 · last checked 2026-09-04
Q4
Human studies of Clopidogrel used Iscover 75 mg filmtablets — over how long?
Human studies of Clopidogrel used "Iscover 75 mg filmtablets". ClinicalTrials.gov · 2026-09-01
20 recorded entries; human; also "Plavix 75 mg filmtablets", "clopidogrel 600 mg", "Plavix 600 mg"
Show the evidence
human
NCT00372216
Iscover 75 mg filmtablets
NCT00372216
Plavix 75 mg filmtablets
NCT00421252
clopidogrel 600 mg
NCT00421252
Plavix 600 mg
NCT00648947
Clopidogrel Bisulfate Tablets 75 mg
NCT00648947
Plavix® Tablets 75 mg
14 more recorded rows
humanNCT00817999
Clopidogrel 75 mg/day
humanNCT00817999
Clopidogrel 300 mg
humanNCT00882739
Clopidogrel 600 mg
humanNCT00882739
Clopidogrel 900 mg
humanNCT01097343
clopidogrel 75 mg
humanNCT01097343
Clopidogrel 150 mg
humanNCT01228214
clopidogrel(75mg/daily for 12 months)
humanNCT01349777
clopidogrel 75mg
humanNCT01381185
Aspirin 200mg qd, Clopidogrel 2x75mg qd
humanNCT01630642
Torrent's Clopidogrel Tablets USP 75 mg
humanNCT01757262
75mg Clopidogrel
humanNCT01758614
Aspirin 100mg per day or clopidogrel 75mg per day
humanNCT01779401
Clopidogrel 75mg
humanNCT01779401
Clopidogrel 150mg
recorded 2026-09-01 · last checked 2026-09-04
Q5
Clopidogrel's half-life is 6 hours — which schedules were studied?
6 hours; After a single, oral dose of 75 mg, clopidogrel has a half-life of approximately 6 hours.
metabolismpharmacokinetics
Clopidogrel is a prodrug and is metabolized to a pharmacologically active metabolite and inactive metabolites.
recorded 2026-07-24 · last checked 2026-09-04
Q6
Which running trial of Clopidogrel could settle lifespan?
NCT02735707 measures All-cause mortality, reading out 2028-02.
2 open trials; n 20000; "Randomized, Embedded, Multifactorial Adaptive Platform Trial for Community- Acquired Pneumonia"
Show the evidence
Trial
NCT02735707
"Randomized, Embedded, Multifactorial Adaptive Platform Trial for Community- Acquired Pneumonia"; n 20000; "All-cause mortality"; 2028-02
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
Q7
Which 230 trials of Clopidogrel posted no result?
Posted no result
230 of 230 completed trials
Registrations
NCT00105209, NCT00648453, NCT00020189, NCT00648947, NCT00650169 and NCT00714961, and 224 more
Completion dates
oldest 2003-12; newest 2024-08-01
Show the evidence
Trial
NCT00105209
2003-12
NCT00648453
2004-04
NCT00020189
2004-08
NCT00648947
2004-12
NCT00650169
2005-01
NCT00714961
2005-01
14 further recorded trials
NCT00360386
2005-02
NCT00140465
2005-07
NCT00050817
2005-08
NCT00406991
2006-03
NCT00115375
2006-04
NCT00433784
2006-04
NCT00693069
2006-04
NCT00368238
2006-07
NCT00296803
2006-08
NCT01506713
2006-09
NCT01512485
2006-10
NCT00343876
2006-11
NCT00404053
2006-11
NCT00109382
2007-02
Q8
At the median, Clopidogrel's trials enrolled 135 people — anything larger?
Median enrolment
135
Largest enrolment
377753
Registered trials counted
553
Q9
What do 11410 spontaneous reports say about Clopidogrel — 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.
Clopidogrel appears in spontaneous reports to regulators. Across the 10 most-reported reaction terms, 11410 reaction mentions were counted: anaemia 2276; gastrointestinal haemorrhage 2031; drug interaction 1368; melaena 1012. FAERS via Open Targets · CHEMBL1083385 · 2026-06-24
Show the evidence
anaemia
2276
gastrointestinal haemorrhage
2031
drug interaction
1368
melaena
1012
haemoglobin decreased
919
haematochezia
862
4 more recorded rows
haemorrhage
841
rectal haemorrhage
739
epistaxis
698
haematemesis
664
recorded 2026-06-24 · last checked 2026-09-04
Q10
Which 10 reactions does Clopidogrel's label not list?
7.5 Warfarin (CYP2C9 Substrates) Although the administration of clopidogrel 75 mg per day did not modify the pharmacokinetics of S-warfarin (a CYP2C9 substrate) or INR in patients receiving long-term warfarin therapy, coadministration of clopidogrel with warfarin increases the risk of bleeding because of independent effects on hemostasis.
drug_interactions
However, at high concentrations in vitro , clopidogrel inhibits CYP2C9.
drug_interactions
7.8 Repaglinide (CYP2C8 Substrates) The acyl-β-glucuronide metabolite of clopidogrel is a strong inhibitor of CYP2C8.
drug_interactions
Clopidogrel can increase the systemic exposure to drugs that are primarily cleared by CYP2C8, thereby needing dose adjustment and appropriate monitoring.
pharmacokinetics
Metabolism Clopidogrel is extensively metabolized by two main metabolic pathways: one mediated by esterases and leading to hydrolysis into an inactive carboxylic acid derivative (85% of circulating metabolites) and one mediated by multiple cytochrome P450 enzymes.
2 more recorded rows
Interaction statementpharmacokinetics
The active metabolite is formed mostly by CYP2C19 with contributions from several other CYP enzymes, including CYP1A2, CYP2B6 and CYP3A.
Interaction statementpharmacokinetics
Effect of clopidogrel on other drugs In vitro studies have shown that the glucuronide metabolite of clopidogrel is a strong inhibitor of CYP2C8.
ChEMBL 37 — CC BY-SA 3.0 Unported · ClinicalTrials.gov — US Government work · Open Targets 26.06 — CC0 · mixed register set; per-register licences in docs/specs/corpus-20k-sources.md · openFDA / DailyMed — US Government work
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