This page shows what was measured, who it was measured in, and what that does not settle.
What Abacavir does in the body
HIV treatment as part of a combination.
Abacavir is a counterfeit version of one of the four chemical letters DNA is built from. The cell modifies it into its active form, and the enzyme HIV uses to copy itself picks it up and stitches it into the growing chain, at which point the chain cannot be extended and the copy stops. Separately and by a completely unrelated route, in about one person in twenty the intact drug slips into a groove on an immune-presenting molecule and changes which of the body own proteins that molecule displays, which the immune system reads as foreign.
What happened in people
A genetic test reduced confirmed severe allergic reactions from 2.7 in 100 to none.
✓ 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
Evidence has disagreed for eighteen years on whether it raises heart attack risk.
Where it acts
Cytoplasm of CD4-positive T cells for the antiviral effect; the antigen-binding groove of an HLA molecule on the cell surface for the hypersensitivity reaction
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.
What the registries record it as
The substance registry classes this as chemical.
FDA substance registry · J220T4J9Q2 · read 2026-08-29
Where each sentence above came from
No recorded sentence describes the change this makes in a way that stands on its own. The page opens with what it is taken for instead, and the recorded explanation follows below.
Shown as the opening line on this page.
The limit a reviewer approved as the one that matters most here.
The four opening statements run to 120 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.
Immunologically confirmed hypersensitivity reaction to abacavir, prospective HLA-B*5701 screening against standard of care
0% versus 2.7% (p<0.001); negative predictive value 100%, positive predictive value 47.9%
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. Clinically diagnosed hypersensitivity was 3.4% against 7.8%, so clinical diagnosis over-called the confirmed reaction by more than two to one in both arms.
How far it carries. This study is recorded from the curated record, not from the registry match.
Form and route. Oral tablet and oral solution, single agent and in fixed-dose combinations
Interval reported. Not recorded in this summary
Written into the record, not signed off as a reviewed claim.
High stratum: hazard ratio 2.46 (95% CI 1.20 to 5.05) with efavirenz and 2.22 (1.19 to 4.14) with atazanavir-ritonavir, against abacavir. Low stratum: 1.23 (0.77 to 1.96) and 1.25 (0.76 to 2.05), no difference
Repeated elsewhere
Replicated
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. Blinded treatment in the high-viral-load stratum was stopped by the data and safety monitoring board. Time to regimen modification was also significantly shorter on abacavir in the low stratum with either third agent.
How far it carries. This study is recorded from the curated record, not from the registry match.
Form and route. Oral tablet and oral solution, single agent and in fixed-dose combinations
Interval reported. 95% CI 1
Written into the record, not signed off as a reviewed claim.
Recent abacavir use, relative rate 1.90 (95% CI 1.47 to 2.45) in 2008 and 1.98 (1.72 to 2.29) in 2016; no association for zidovudine, stavudine or lamivudine
Repeated elsewhere
Partially Replicated
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. This row records a harm signal, not a failed efficacy endpoint. Prescribing shifted away from higher cardiovascular-risk patients after 2008 and the association did not change (interaction p=0.74), which weakens but does not eliminate channelling bias as an explanation.
How far it carries. This study is recorded from the curated record, not from the registry match.
Form and route. Oral tablet and oral solution, single agent and in fixed-dose combinations
Interval reported. 95% CI 1
Written into the record, not signed off as a reviewed claim.
Risk difference for myocardial infarction between randomised abacavir-containing and abacavir-free regimens
✗ The study did not show it
Who was studied
FDA trial-level meta-analysis of 26 randomised trials
How many people
9868
Study design
Trial-level meta-analysis of randomised controlled trials, Mantel-Haenszel risk difference
Compared against
Not recorded for this study
Kind of result
A number that stands in for health
What was found
24 of 5,028 (0.48%) against 22 of 4,840 (0.46%), risk difference 0.008% (95% CI -0.26% to 0.27%)
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. Forty-six events in total across 26 trials, with mean follow-up of about 1.4 person-years per group. A null result at this event count does not exclude the doubling reported in the cohorts, and the analysis excluded trials conducted in Africa.
How far it carries. This study is recorded from the curated record, not from the registry match.
Form and route. Oral tablet and oral solution, single agent and in fixed-dose combinations
Interval reported. 95% CI -0
Written into the record, not signed off as a reviewed claim.
RNAWiki holds 4 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.
Start
Abacavir
What a person takes: Oral tablet and oral solution, single agent and in fixed-dose combinations.
The measurement behind this step
Taken with or without food. No renal dose adjustment is needed, because elimination is by alcohol dehydrogenase and glucuronidation rather than by the kidney. It must not be started without a documented HLA-B*5701 result.
Getting in
A genetic test comes before the first tablet
Before anyone takes abacavir, a blood test checks for one specific immune gene variant. Carriers are not given the drug at all. That test is part of the treatment, not an optional extra.
──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
HLA-B*5701 genotyping is required before initiation and is written into the labelling. Allele prevalence was 5.6% in the 1,956-patient PREDICT-1 population. The test has a negative predictive value of 100% against immunologically confirmed hypersensitivity and a positive predictive value of 47.9%, so roughly half of carriers excluded would not have reacted, which is a cost the strategy accepts deliberately.
Swallowed with or without food, and it does not touch the kidney
A tablet once or twice a day. Unlike its main competitor it is not filtered and concentrated by the kidney tubule, so it has no renal or bone effect and needs no dose change in kidney disease.
╌╌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
Oral bioavailability is around 83% and is unaffected by food. Elimination is by alcohol dehydrogenase and glucuronosyltransferase to inactive metabolites, with only about 2% excreted unchanged in urine, so no renal dose adjustment is required. It is not a cytochrome P450 substrate of consequence, so its interaction profile is short.
Inside the cell it is rebuilt into a counterfeit DNA letter
What is swallowed is not what works. Cellular enzymes convert it through several steps into a different molecule that looks like the DNA letter G, carrying the three phosphates a real building block would have.
╌╌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
Abacavir is phosphorylated by adenosine phosphotransferase to abacavir monophosphate, deaminated by a cytosolic deaminase to carbovir monophosphate, and then phosphorylated twice more to carbovir triphosphate, the active species. This activation route is independent of the kinases the other nucleoside analogues rely on, which is why abacavir retains activity in cells where thymidine analogue activation is limiting.
The copying enzyme inserts it and the chain ends there
Reverse transcriptase takes it for the real thing and stitches it in. The carbocyclic ring it is built on has no attachment point for the next letter, so the copy stops at that point.
╌╌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
Carbovir triphosphate competes with dGTP at the reverse transcriptase active site and is incorporated, after which the absence of a 3-prime hydroxyl on the cyclopentene ring enforces chain termination. The principal resistance substitutions are L74V, Y115F, K65R and M184V, and several of them impose replicative fitness costs, so accumulating clinically significant abacavir resistance generally requires more than one.
And in one person in twenty, a completely separate thing happens
None of the above has anything to do with the reaction. Intact abacavir slots into a groove on an immune-presenting molecule in carriers of one gene variant, changing which of the body own proteins get displayed there. The immune system sees a self it does not recognise and attacks.
╌╌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
Unmodified abacavir binds non-covalently in the F pocket of the HLA-B*57:01 antigen-binding cleft, where a C-terminal tryptophan normally anchors the peptide, altering cleft shape and chemistry and therefore the repertoire of endogenous peptides selected for presentation. The resulting altered self drives polyclonal CD8 T-cell activation and a systemic reaction. The relative risk in carriers exceeds 1,000. Rechallenge after a reaction can cause hypotension and death within hours and is prohibited regardless of genotype.
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 who test negative for HLA-B*5701 and who need a nucleoside backbone without renal or bone effects, commonly in the fixed-dose combination with dolutegravir and lamivudine.
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 abacavir have been established in pediatric patients aged 3 months and older.”
US prescribing information · 5676d391-f9a4-44be-9604-954b3d8d0e2b · read 2026-08-30
On older people, the label states: “Clinical trials of abacavir did not include sufficient numbers of subjects aged 65 and over to determine whether they respond differently from younger subjects.”
US prescribing information · 5676d391-f9a4-44be-9604-954b3d8d0e2b · read 2026-08-30
On people who are pregnant, the label states: “Exposure Registry There is a pregnancy exposure registry that monitors pregnancy outcomes in women exposed to abacavir during pregnancy.”
US prescribing information · 5676d391-f9a4-44be-9604-954b3d8d0e2b · read 2026-08-30
On people who are breastfeeding, the label states: “Risk Summary The Centers for Disease Control and Prevention recommends that HIV-1–infected mothers in the United States not breastfeed their infants to avoid risking postnatal transmission of HIV-1 infection.”
US prescribing information · 5676d391-f9a4-44be-9604-954b3d8d0e2b · read 2026-08-30
Where the result stopped carrying
Blinded treatment in the high-viral-load stratum of ACTG A5202 was stopped for excess virological failure on abacavir
The hypersensitivity reaction reached the market in 1998 as an unexplained idiosyncratic toxicity, was linked to an allele in 2002, prevented by screening from 2008, and only mechanistically explained in 2012
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 oral solution, single agent and in fixed-dose combinations
✎ 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: S6.
No source is stored against this line.
What is in the pack
Taken with or without food. No renal dose adjustment is needed, because elimination is by alcohol dehydrogenase and glucuronidation rather than by the kidney. It must not be started without a documented HLA-B*5701 result.
✎ 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
Serious and sometimes fatal hypersensitivity reactions are the boxed warning, strongly associated with HLA-B*5701 and characterised by fever, rash, gastrointestinal and respiratory symptoms. Rechallenge after a suspected reaction can cause hypotension and death within hours and is prohibited regardless of genotype. Lactic acidosis and severe hepatomegaly with steatosis are labelled class effects of nucleoside analogues. Immune reconstitution inflammatory syndrome can follow suppression. The myocardial infarction association reported in the D:A:D cohorts and not reproduced in pooled randomised trials is discussed in the audits and remains unresolved. Abacavir has no activity against hepatitis B.
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 oral solution, single agent and in fixed-dose combinations
✎ 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
No renal dose adjustment is needed, because elimination is by alcohol dehydrogenase and glucuronidation rather than by the kidney. It must not be started without a documented HLA-B*5701 result.
✎ 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
44 products list this as an active ingredient in the United States drug directory. 33 of them contain it and nothing else.
FDA National Drug Code directory · 61876-0718 · read 2026-08-29
They are sold as powder, solution, tablet and tablet, film coated, taken oral.
FDA National Drug Code directory · 61876-0718 · read 2026-08-29
The regulator's established pharmacologic class for it is cytochrome p450 1a1 inhibitors [moa], human immunodeficiency virus nucleoside analog reverse transcriptase inhibitor [epc] and nucleoside analog [ext].
FDA National Drug Code directory · 61876-0718 · read 2026-08-29
23 published labels name it as an active ingredient. 15 of them describe this substance alone, which is where its own label text on this page comes from.
US prescribing information · 5676d391-f9a4-44be-9604-954b3d8d0e2b · read 2026-08-29
Those labels are classed as human prescription drug.
US prescribing information · 5676d391-f9a4-44be-9604-954b3d8d0e2b · read 2026-08-29
Abacavir Sulfate is oral at 3 DOSAGE FORMS AND STRENGTHS Abacavir Tablets, USP are available containing abacavir sulfate, USP equivalent to 300 mg of abacavir. • The 300 mg tablets are peach, film-coated, capsule shaped, scored tablets debossed wi…, recorded as fda label in effect 2021-01-08 in the United States.
US prescribing information · 5676d391-f9a4-44be-9604-954b3d8d0e2b · read 2026-08-30
Recorded price in US: 0.53801 USD per one unit as the pricing file counts it — a tablet, capsule, patch or single item, across 12 priced products whose strengths and pack forms differ, as of 2026-08-26, paid by retail pharmacies buying the product, as surveyed by the Centers for Medicare & Medicaid Services. It is not a list price, an insurance price, or what anyone pays at a counter..
Recorded source · 2026-08-26 · read 2026-08-28
Evidence carries across two names for one substance. It does not carry across a salt, a mirror form or a mixture.
What it would be like to take◇Read from sources, not yet reviewed
What you could measure
This one is decided with a clinician, so this section holds questions to ask rather than a plan to run.
Self-experiment planning is not offered for a prescription or clinician-supervised medicine. The questions below are for a clinician or pharmacist.
Questions worth asking
Which of the trials of Abacavir 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 the randomised null result on myocardial infarction refutes the cohort association, when 46 events across 26 trials cannot detect a doubling
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 cohort association establishes causation, when no mechanism has been identified and unmeasured confounding cannot be excluded
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 absolute benefit of HLA-B*5701 screening measured in a predominantly white cohort describes its benefit where the allele is much rarer
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 negative HLA-B*5701 result makes continuation or rechallenge safe once symptoms have appeared
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 Abacavir 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.
PREDICT-1: a genetic test took immunologically confirmed reactions to zero
In plain words
In 1,956 patients randomised either to be genotyped before starting abacavir or to start it the usual way, confirmed hypersensitivity fell from 2.7% to zero. Nobody who tested negative had a confirmed reaction, in any patient, anywhere in the trial.
What was measured
Immunologically confirmed hypersensitivity reaction at six weeks: 0% against 2.7% (p<0.001), negative predictive value 100%, positive predictive value 47.9%
Effect estimate
No reviewed effect estimate exists for this record.
Limits
See the technical detail.
From the source
PREDICT-1 (NCT00340080) was a double-blind, prospective, randomised study across 19 countries in 1,956 abacavir-naive patients with HIV-1, comparing prospective HLA-B*5701 screening with exclusion of carriers against standard-of-care abacavir use without screening. All patients starting abacavir were observed for six weeks, and clinical diagnoses were confirmed immunologically by epicutaneous patch testing with abacavir. HLA-B*5701 prevalence was 5.6% (109 of 1,956). Immunologically confirmed hypersensitivity was 0% in the screening group against 2.7% in the control group (p<0.001), with a negative predictive value of 100% and a positive predictive value of 47.9%. Clinically diagnosed hypersensitivity, which is the less specific endpoint, fell from 7.8% to 3.4% (p<0.001). The gap between those two endpoints is itself informative: more than half of clinical diagnoses were not the reaction they were taken for.
Written into the record, not signed off as a reviewed claim
The mechanism arrived in 2012, fourteen years after the drug did
In plain words
For fourteen years the reaction was a statistical association with a gene. Two structural studies then showed that abacavir slots into the groove where that HLA molecule displays fragments of the body own proteins, changes the shape of the groove, and causes a different set of self-proteins to be displayed. The immune system attacks what looks like a new self.
What was measured
Non-covalent occupancy of the HLA-B*57:01 F pocket by unmodified abacavir, with mass-spectrometric identification of self-peptides presented only in the presence of drug
Effect estimate
No reviewed effect estimate exists for this record.
Limits
See the technical detail.
From the source
Illing and colleagues showed that unmodified abacavir binds non-covalently to HLA-B*57:01, lying across the bottom of the antigen-binding cleft and reaching into the F pocket, where a C-terminal tryptophan normally anchors bound peptides. Binding is specific to that allotype, changes the shape and chemistry of the cleft, and alters the repertoire of endogenous peptides that can be presented, producing a peptide-centric altered self that activates polyclonal CD8 T cells. Ostrov and colleagues independently demonstrated F-pocket binding and altered specificity, and identified specific self-peptides presented only in the presence of abacavir that were recognised by T cells from hypersensitive patients. The relative risk of the reaction in carriers exceeds 1,000. The same paper showed carbamazepine binding HLA-B*15:02 by the same principle, which converted an idiosyncratic single-drug curiosity into a general mechanism for HLA-linked drug hypersensitivity.
Written into the record, not signed off as a reviewed claim
ACTG A5202: inferior above 100,000 copies per millilitre, and the arm was stopped
In plain words
A blinded trial compared abacavir-lamivudine with tenofovir-emtricitabine in patients starting treatment. In those who began with a high viral load, abacavir failed significantly more often, and the data monitoring board stopped blinded treatment in that group. Below the threshold there was no difference.
What was measured
Time to virological failure by baseline viral load stratum: hazard ratio 2.46 (95% CI 1.20 to 5.05) and 2.22 (1.19 to 4.14) above 100,000 copies per millilitre
Effect estimate
No reviewed effect estimate exists for this record.
Limits
This entry records a failure.
From the source
ACTG A5202 (NCT00118898) randomised treatment-naive patients to blinded abacavir-lamivudine or tenofovir disoproxil-emtricitabine, each with open-label efavirenz or atazanavir-ritonavir, stratified by screening HIV RNA above or below 100,000 copies per millilitre. In the high stratum, before blinded treatment was stopped, time to virological failure was significantly shorter on abacavir-lamivudine with efavirenz (hazard ratio 2.46, 95% CI 1.20 to 5.05) and with atazanavir-ritonavir (2.22, 95% CI 1.19 to 4.14), and the data and safety monitoring board stopped blinded treatment in that stratum. In the low stratum, time to virological failure did not differ with atazanavir-ritonavir (1.25, 95% CI 0.76 to 2.05) or efavirenz (1.23, 95% CI 0.77 to 1.96), but time to regimen modification was significantly shorter on abacavir with either third agent, and time to a safety event was shorter with efavirenz. So the failure is confined to a stratum, it was detected by a blinded trial that stopped the arm, and it is the reason abacavir is not a first choice for someone presenting with a high viral load.
Written into the record, not signed off as a reviewed claim
Myocardial infarction: 1.90 in cohorts, no difference in randomised trials, and still unresolved after eighteen years
In plain words
A large observational study in 2008 found heart attacks nearly twice as common in people currently taking abacavir. The FDA then pooled 26 randomised trials and found no difference at all. The observational study kept following people and the association did not go away. Both bodies of evidence are still standing.
What was measured
That abacavir causes myocardial infarction, or alternatively that the randomised null result refutes the cohort finding — the trials are underpowered for the effect size in question and the cohorts cannot exclude unmeasured confounding
Effect estimate
No reviewed effect estimate exists for this record.
Limits
See the technical detail.
From the source
D:A:D reported in 2008 that among 33,347 patients over 157,912 person-years with 517 myocardial infarctions, recent but not cumulative abacavir use carried a relative rate of 1.90 (95% CI 1.47 to 2.45, p=0.0001), unchanged at 1.89 after adjusting for predicted ten-year coronary risk, with no excess beyond six months after stopping. The FDA then conducted a trial-level meta-analysis of 26 randomised controlled trials in which abacavir was randomised as part of a combination regimen, covering 9,868 subjects, 5,028 on abacavir and 4,840 not, with mean follow-up of about 1.4 person-years per group. Forty-six myocardial infarctions were reported, 24 (0.48%) against 22 (0.46%), risk difference 0.008% (95% CI -0.26% to 0.27%). D:A:D returned in 2016 with 49,717 participants, 941 events over 367,559 person-years, and current abacavir use associated with a 98% increase (relative rate 1.98, 95% CI 1.72 to 2.29), with no difference between the periods before and after the 2008 publication (interaction p=0.74) despite documented changes in prescribing away from higher-risk patients. That last point is the argument against channelling bias: prescribers changed behaviour and the association did not move. The argument on the other side is that 46 events across 26 randomised trials is too few to detect a doubling, and that the cohorts cannot exclude confounding they did not measure. Neither side has been refuted.
Written into the record, not signed off as a reviewed claim
The screening test was validated where the allele is common, and read across elsewhere
In plain words
PREDICT-1 was 84% white, and the allele it screens for is much less frequent in African and Asian populations. The test still works, because it detects the gene rather than the ancestry, but the trial that measured how much benefit it delivers was run in the population where the gene is most common.
What was measured
That the absolute benefit of HLA-B*5701 screening measured in a predominantly white cohort describes its benefit in populations where the allele is much rarer
Effect estimate
No reviewed effect estimate exists for this record.
Limits
See the technical detail.
From the source
Of the patients in PREDICT-1 who received abacavir, 84% were white, and the overall HLA-B*5701 prevalence in the trial was 5.6%. The paper states its own conclusion in population-restricted terms: in predominantly white populations similar to the one in this study, 94% of patients do not carry the allele. HLA-B*5701 frequency is substantially lower in most sub-Saharan African and East Asian populations, so the absolute number of reactions a screening programme prevents per thousand people tested is correspondingly lower, and the trial does not measure it in those populations. The negative predictive value of 100% is a property of the test and the reaction, not of the sampled group, so this is not an argument against screening; it is a note that the size of the benefit was established in one population and applied in all of them. The positive predictive value of 47.9% carries a second consequence: roughly half of carriers denied abacavir would never have reacted, and screening accepts that cost by design.
Written into the record, not signed off as a reviewed claim
It does nothing to hepatitis B, and that is a decision rather than a detail
In plain words
Both drugs abacavir competes with also treat hepatitis B. Abacavir does not. For a person carrying both viruses, choosing abacavir means the hepatitis B is left untreated, and stopping a hepatitis B drug in that situation causes a severe liver flare.
What was measured
Absence of hepatitis B polymerase activity, and absence of the hepatitis B discontinuation boxed warning that every competing nucleoside carries
Effect estimate
No reviewed effect estimate exists for this record.
Limits
See the technical detail.
From the source
Carbovir triphosphate is a deoxyguanosine analogue active against HIV-1 reverse transcriptase and has no useful activity against the hepatitis B polymerase. Tenofovir disoproxil, tenofovir alafenamide, lamivudine and emtricitabine all do have hepatitis B activity, and all four carry a boxed warning about severe acute exacerbation of hepatitis B on discontinuation. Abacavir carries no such warning because it was never suppressing the virus. Global hepatitis B and HIV co-infection prevalence is substantial in the regions where the fixed-dose combination containing abacavir is most used, which makes this a routine rather than an exotic consideration. It is listed as a measured audit rather than an inferred one because the absence of activity is a laboratory fact, not an extrapolation.
Written into the record, not signed off as a reviewed claim
A negative genetic test is not a licence to rechallenge after a reaction
In plain words
The screening test has a perfect record at ruling out the confirmed reaction, and that fact gets read as though a negative test made abacavir safe. It does not make rechallenge safe after a suspected reaction, because rechallenge has killed people and because more than half of clinically suspected reactions in the trial were something else.
What was measured
That a negative HLA-B*5701 result excludes hypersensitivity in an individual patient and makes continuation or rechallenge safe after symptoms appear
Effect estimate
No reviewed effect estimate exists for this record.
Limits
See the technical detail.
From the source
PREDICT-1 measured a negative predictive value of 100% against immunologically confirmed hypersensitivity in 1,956 patients over six weeks. That is a statement about the confirmed endpoint in that sample, not a guarantee of zero risk, and the trial also found that clinical diagnosis over-called the reaction by more than two to one: 7.8% clinically diagnosed against 2.7% confirmed in the control group. The labelling prohibits rechallenge after a suspected hypersensitivity reaction regardless of HLA status, because rechallenge has produced hypotension and death within hours. The inference being flagged is the everyday one: that a negative genotype means the reaction cannot be happening, and therefore that a patient with early symptoms can safely continue. Both halves of that are wrong, and the second half is the dangerous one.
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What is not here
7 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.
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How close this is to real life — found nothing in the sources checked.
Felt, measured, or meaningful — found nothing in the sources checked.
How long anything takes — found nothing in the sources checked.
What it may clash with — found nothing in the sources checked.
Other ways to the same goal — found nothing in the sources checked.
What changed on this page — found nothing in the sources checked.
The record as stored
The full record, for auditing
Everything above is built from what is below. This layer keeps the technical vocabulary, record identifiers and every stored row, so a reader who wants to check the page can.
The older medicine-wide conclusion held in this record
Written for a clinical reader, and about the medicine as a whole rather than about one indication, population and set of trials. RNAWiki does not treat it as a programme conclusion and no reviewer has signed it off in that form. It is here word for word because it is what the record holds.
A guanosine analogue that terminates the HIV DNA chain, and the drug that demonstrated a genetic test could abolish a specific toxicity: prospective HLA-B*5701 screening reduced immunologically confirmed hypersensitivity from 2.7% to 0% in 1,956 randomised patients, with a negative predictive value of 100%; it is nonetheless measurably inferior to tenofovir-emtricitabine above 100,000 copies per millilitre at baseline, and carries a cardiovascular association that observational and randomised evidence have disagreed about for eighteen years.
Recorded evidence blocks (10)
Q2
On the Abacavir label: indicated for what?
"Abacavir oral solution, in combination with other antiretroviral agents, is indicated for the treatment of human immunodeficiency virus (HIV-1) infection. Abacavir oral solution, a nucleoside analogue human immunodeficiency virus (HIV-1) reverse transcriptase inhibitor, is indicated in combination with other…": indications and usage on Abacavir's label. DailyMed label · e5cbf204-c10d-444b-aba0-180a30645d55 · 2026-08-13
Q3
133 registered trials of Abacavir — at which phases?
Registered studies posting no result
111 of 133
133 registered studies of Abacavir: 40 phase3, 33 phase2, 26 phase4, 18 phase1, 16 na, 4 na or unstated, 1 early phase1. CLINICALTRIALS_SNAPSHOT · 2026-09-01
420 with a PubMed record
Show the evidence
phase3
40
phase2
33
phase4
26
phase1
18
na
16
na or unstated
4
8 more recorded rows
early phase1
1
completed
113
unknown
7
terminated
4
withdrawn
4
not yet recruiting
2
recruiting
2
suspended
1
recorded 2026-09-01 · last checked 2026-09-04
Q4
4 of Abacavir's trials stopped: futility/efficacy, accrual/recruitment, other?
"No participants enrolled"; 4 of 133 registered studies
Show the evidence
Trial
NCT02470650
withdrawn; "No participants enrolled"
NCT02659761
terminated; "Sponsor decision due to slow recruitment rates and no future recruitment foreseen"
NCT02924389
terminated; "This study terminated early due to the ongoing covid-19 pandemic making it unsafe to recruit participants for in-person visits. Participants are living with HIV who are antiretroviral therapy-naive and are at high risk of COVID-19…"
NCT05193994
terminated; "A planned interim analysis resulted in the recommendation that the trial be stopped. The results showed no benefit of Triumeq for people with ALS compared with placebo on survival, the primary outcome measure."
recorded 2026-09-01 · last checked 2026-09-04
Q5
Human studies of Abacavir used Abacavir 600mg - Lamivudine 300mg — over how long?
studies of Abacavir used the recorded amount. ClinicalTrials.gov · 2026-09-01
6 recorded entries; human; also "Abacavir 600mg - Lamivudine 300mg", "abacavir (600 mg QD)", "Abacavir 600 mg"
1.54 ± 0.63 hours; Elimination: In single-dose trials, the observed elimination half-life (t ½ ) was 1.54 ± 0.63 hours.
bioavailabilitypharmacokinetics
83 %; The geometric mean absolute bioavailability of the tablet was 83%.
metabolismpharmacokinetics
Metabolism: In humans, abacavir is not significantly metabolized by cytochrome P450 enzymes.
recorded 2026-08-13 · last checked 2026-09-04
Q7
Which 59 trials of Abacavir posted no result?
Posted no result
59 of 59 completed trials
Registrations
NCT00000865, NCT00001086, NCT00000912, NCT00005018, NCT00001968 and NCT00000864, and 53 more
Completion dates
oldest 1998-04; newest 2024-03-11
Show the evidence
Trial
NCT00000865
1998-04
NCT00001086
1999-09
NCT00000912
2000-05
NCT00005018
2000-10
NCT00001968
2000-11
NCT00000864
2001-01
14 further recorded trials
NCT00001132
2001-04
NCT00006152
2002-08
NCT00011479
2002-08
NCT00000919
2002-11
NCT00043888
2003-05
NCT00000885
2003-06
NCT00001758
2003-08
NCT00046176
2004-05-17
NCT00044577
2004-05-25
NCT00270556
2004-10
NCT00087945
2004-12
NCT00000872
2005-01
NCT00028314
2005-03
NCT00004855
2005-04
Q8
At the median, Abacavir's trials enrolled 71 people — anything larger?
Median enrolment
71
Largest enrolment
1806
Registered trials counted
122
Q9
What do 8069 spontaneous reports say about Abacavir — 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.
Abacavir appears in spontaneous reports to regulators. Across the 10 most-reported reaction terms, 8069 reaction mentions were counted: virologic failure 1405; drug resistance 1364; viral mutation identified 1191; pathogen resistance 1089. FAERS via Open Targets · CHEMBL1380 · 2026-06-24
Show the evidence
virologic failure
1405
drug resistance
1364
viral mutation identified
1191
pathogen resistance
1089
abortion spontaneous
592
treatment failure
577
4 more recorded rows
anaemia
568
premature baby
481
immune reconstitution inflammatory syndrome
451
lipodystrophy acquired
351
recorded 2026-06-24 · last checked 2026-09-04
Q10
Which 10 reactions does Abacavir's label not list?
Metabolism: In humans, abacavir is not significantly metabolized by cytochrome P450 enzymes.
pharmacokinetics
In vitro experiments reveal that abacavir does not inhibit human CYP3A4, CYP2D6, or CYP2C9 activity at clinically relevant concentrations.
pharmacokinetics
Drug Interaction Studies Effect of Abacavir on the Pharmacokinetics of Other Agents: In vitro studies have shown that abacavir has potential to inhibit CYP1A1 and limited potential to inhibit metabolism mediated by CYP3A4.
pharmacokinetics
Abacavir did not inhibit or induce other CYP enzymes (such as CYP2C9, or CYP2D6).
pharmacokinetics
Based on in vitro study results, abacavir at therapeutic drug exposures is not expected to affect the pharmacokinetics of drugs that are substrates of the following transporters: organic anion transporter polypeptide (OATP)1B1/3, breast cancer resistance protein (BCRP) or P-glycoprotein (P-gp), organic cation transporter (OCT)1, OCT2, or multidrug and toxic extrusion protein (MATE)1 and MATE2-K.
pharmacokinetics
Riociguat: Coadministration of a single dose of riociguat (0.5 mg) to HIV-1-infected subjects receiving fixed-dose abacavir/dolutegravir/lamivudine is reported to increase riociguat AUC (∞) compared with riociguat AUC (∞) reported in healthy subjects due to CYP1A1 inhibition by abacavir.
2 more recorded rows
Interaction statementpharmacokinetics
Effect of Other Agents on the Pharmacokinetics of Abacavir: In vitro, abacavir is not a substrate of OATP1B1, OAP1B3, OCT1, OCT2, OAT1, MATE1, MATE2-K, multidrug resistance-associated protein (MRP)2 or MRP4; therefore, drugs that modulate these transporters are not expected to affect abacavir plasma concentrations.
Interaction statementpharmacokinetics
Abacavir is a substrate of BCRP and P-gp in vitro ; however, considering its absolute bioavailability (83%), modulators of these transporters are unlikely to result in a clinically relevant impact on abacavir concentrations.
ChEMBL 37 — CC BY-SA 3.0 Unported · ChEMBL ATC CC BY-SA · 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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