AICAR
It has no amino acids in it. None. It is sitting in the peptide aisle the way a golf cart sits in a bike rack, and the pharmacology is genuinely more interesting than the filing error.
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For research use only. Not for human or veterinary use.
What AICAR is
The plain-language version, first.
Not a peptide. Not close to a peptide. Filed here anyway.
AICAR (5-aminoimidazole-4-carboxamide riboside, INN acadesine) is a nucleoside analogue with molecular formula C9H14N4O5, molecular weight 258.23 and CAS 2627-69-2. It is taken up by adenosine transporters and phosphorylated by adenosine kinase to ZMP, an AMP mimetic that binds site 3 on the gamma subunit of AMP-activated protein kinase; it contains no amino acids and no peptide bonds, and it has never been approved by any regulatory authority.
Quick housekeeping before anything else.
This is not a peptide. There are no amino acids in it and there are no peptide bonds. It is a nucleoside.
It ended up in the peptide aisle the way a golf cart ends up in a bike rack. Roughly the right shape, wrong category entirely, nobody wants to be the one to move it.
What it actually is: a molecule your cells convert into something called ZMP, and ZMP happens to look enough like AMP that the cell's energy sensor responds to it.
That sensor is AMPK, and AMPK is essentially the low-battery warning for a cell.
A compound that does not raise the alarm so much as convince the alarm it should be going off.
What AICAR is
Mechanism studied, not outcome promised.
AICAR itself does very little. Adenosine kinase phosphorylates it inside the cell to ZMP, and ZMP is what binds site 3 on the AMPK gamma subunit. Uptake depends on adenosine transporters getting it through the membrane first.
Kim and colleagues (2016) state that as an AMP analogue, AICAR is able to activate many other AMP-dependent enzymes. Any effect attributed to AMPK on the basis of AICAR alone is under-evidenced.
Section S4.4.1 covers activators of AMP-activated protein kinase and gives AICAR and MOTS-c as its examples. S4.4 substances are non-Specified, which carries a harsher default sanction than Specified categories.
The cell has a low-battery light. This is a molecule that leans on the sensor.
Your phone shows a battery icon. The icon isn't the battery. It's a readout of the battery.
Now imagine leaning on the readout rather than the battery, so the phone starts behaving like it's running low whether or not it is.
That's AICAR. It doesn't drain the cell. It talks to the gauge.
Mechanically, the conversion product ZMP mimics AMP closely enough that AMPK responds as though energy is scarce. AMPK is a genuinely central switch, which is why this compound shows up across an enormous spread of unrelated laboratory literature.
And that spread is the reason to be careful reading it. A switch that broad has consequences that are broad too.
Here's the honest part. This is cell biology, done properly, over decades, in dishes and rodents.
A switch being real is not the same as knowing what happens when you lean on it in a person. Those are separate questions and only one has been answered.
The research so far for AICAR
Where the evidence is thin, we say so.
A well-described mechanism: adenosine transporter uptake, adenosine kinase phosphorylation to ZMP, and binding at site 3 of the AMPK gamma subunit. A widely cited 2008 Cell paper reporting 44% greater running endurance in sedentary mice. Two registered human trials in cardiac and haematological indications. A named entry on the WADA Prohibited List.
No approval anywhere. No human trial of any kind on endurance, fat loss or body composition. No replication of the mouse endurance result in people. No selectivity data supporting AICAR as a clean AMPK probe; the mechanistic literature says the opposite. RED-CABG failed for futility at 3,080 patients and a later study terminated at five for renal toxicity.
AICAR is the clearest example in this catalogue of a marketing story outrunning its evidence. One mouse paper in 2008 created the entire exercise-mimetic genre. The human record is two stopped trials and zero studies of endurance, fat loss or body composition.
Decades of clean laboratory work and a very short list of humans.
The laboratory file here is genuinely good, which makes the human gap more noticeable rather than less.
AICAR is a standard research tool. If you want AMPK activated in a dish, this is a thing people reach for and have reached for for a long time.
That is a real endorsement of the molecule as a reagent. It is not an endorsement of anything else.
The human side does not match. There is no controlled outcome trial in healthy adults for endurance, body composition or anything adjacent to why people search for it.
Worth knowing it is also prohibited in sport, and has been for a while, which tells you something about how it has been used regardless of what the file says.
A first-rate laboratory reagent with a reputation built somewhere the laboratory work never went.
Canadian stock, ships from BC. Research use only.
AICAR specs
The chemistry, exactly as released.
Who studies AICAR
Who tends to order this one, and why.
A research compound does not have one audience. It has a handful of rooms where the same question keeps coming up, and the question is a different question in each of them.
AMPK signalling researchers
AICAR is the standard pharmacological activator in this field, and understanding its limits matters as much as understanding its mechanism.
Metabolic enzymology labs
ZMP's promiscuity across AMP-dependent enzymes is a research question in its own right. If you study nucleotide sensing, that promiscuity is the point rather than the problem.
Anti-doping and analytical chemistry
AICAR is explicitly named on the WADA Prohibited List, so detection method development and endogenous baseline characterisation are active areas of work.
Purine metabolism researchers
AICAR ribotide accumulation defines AICA-ribosiduria, an inherited ATIC deficiency, and a trial in affected patients is currently recruiting.
Sold for laboratory research only. This is not guidance for personal use, and nothing here is a recommendation.
AICAR backstory
How it got here.
2008 is the year AICAR got famous and the reason it's still sold today. Narkar's group at Salk published in Cell that four weeks of AICAR in sedentary mice increased running endurance by 44%.
No treadmill. No wheel.
No training. The paper was called AMPK and PPARdelta agonists are exercise mimetics, and the phrase 'exercise in a pill' went around the world before most people read the methods section.
What the coverage skipped: the compound wasn't new in 2008. Acadesine had been in cardiac surgery development for years already, on the theory that AMPK activation protects ischaemic myocardium.
That theory got its answer in 2012. RED-CABG randomised 3,080 patients out of a projected 7,500 before it was stopped for futility.
Primary composite 5.1% versus 5.0%. Odds ratio 1.01.
Newman published it in JAMA. Then a myelodysplastic syndrome study opened in 2013 and terminated after five patients, with renal toxicity in the record.
Meanwhile the mouse paper kept getting cited on forums, and WADA put AICAR on the Prohibited List by name. The strangest footnote is that AICAR accumulation defines an inherited human disease.
AICA-ribosiduria, from ATIC deficiency, is counted in a handful of patients worldwide, and a trial in those patients is recruiting right now. One mouse study built the market.
Two human trials answered the question, and the market never noticed.
- 1
2008: 44% in untrained mice
Narkar and colleagues publish in Cell that four weeks of AICAR in sedentary mice with no training increased running endurance by 44%. The authors call the result unexpected. It becomes the origin of the exercise-in-a-pill phrase.
- 2
2012: RED-CABG stops for futility
Merck's phase 3 acadesine trial in coronary bypass surgery halts after 3,080 of a projected 7,500 patients. The primary composite is 5.1% versus 5.0% on placebo, odds ratio 1.01, published by Newman in JAMA.
- 3
2013: terminated at five patients
A phase 1-2 dose-escalation study in myelodysplastic syndromes (NCT01813838) is terminated with an actual enrolment of five. The recorded reason is renal toxicity.
Buying AICAR in Canada
What ships, how fast, and the paperwork.
The hard part of buying research material is almost never the compound. It is the logistics. What leaves the building, how fast it moves, and what is in the box beside the vial. Here is ours, plainly.
This is not a peptide
AICAR is a nucleoside analogue of 258.23 daltons with no amino acids and no peptide bonds. It is stocked and shipped as a small molecule, and any vendor selling it as a peptide has the chemistry wrong.
Named on the WADA Prohibited List
Section S4.4.1 lists AICAR by name among AMPK activators. S4.4 substances are non-Specified, which carries a harsher default sanction. There is no ambiguity in this one's anti-doping status at all.
The human record is two stopped trials
RED-CABG stopped for futility at 3,080 patients with an odds ratio of 1.01. A myelodysplastic syndrome study terminated at five patients with renal toxicity recorded. Never approved by any regulator. Research use only.
Stuff people ask about AICAR
If your question is not here, email us. Real human answers.
No. AICAR is 5-aminoimidazole-4-carboxamide riboside, a nucleoside analogue with the formula C9H14N4O5 and a molecular weight of 258.23. It contains no amino acids and no peptide bonds. Its INN is acadesine and its CAS number is 2627-69-2. It gets shelved with peptides by vendors, which is a marketing habit rather than a chemical fact.
One paper. Narkar and colleagues published in Cell in 2008 that four weeks of AICAR in sedentary mice, with no training at all, increased running endurance by 44%. The authors called the result unexpected. That single mouse experiment is the origin of essentially every AICAR performance claim, and it has never been replicated as a human endurance finding.
Yes, and the results were not good. RED-CABG was a phase 3 trial in coronary bypass surgery, stopped for futility after 3,080 of a projected 7,500 patients, with a primary composite of 5.1% versus 5.0% on placebo and an odds ratio of 1.01. A later myelodysplastic syndrome study terminated after five patients with renal toxicity recorded as the reason.
Yes, by name. WADA section S4.4.1 covers activators of AMP-activated protein kinase and gives AICAR and MOTS-c as its examples. S4.4 substances are non-Specified, which carries a harsher default sanction than Specified categories. This is one of the few compounds in this catalogue with a completely unambiguous anti-doping status.
Indirectly. Adenosine transporters carry AICAR into the cell, then adenosine kinase phosphorylates it to ZMP. ZMP resembles AMP closely enough to bind site 3 on the AMPK gamma subunit, so the enzyme behaves as if cellular energy is low. AICAR itself doesn't bind AMPK; the phosphorylated metabolite does the work.
No, and the mechanistic literature says so plainly. Kim and colleagues noted in a 2016 review that as an AMP analogue, AICAR is able to activate many other AMP-dependent enzymes. That means any observed effect could be AMPK or could be something else reading the same nucleotide signal. It's a useful tool with a real selectivity caveat.
Good pairing options with AICAR
What researchers stack alongside it.
Pairing is where research gets ahead of itself. These are the compounds researchers put in the same order as AICAR, which is a statement about ordering habits, not about evidence. Two things in one cart have not been studied together unless somebody studied them together.
Not a molecule. FSH and LH activity extracted from postmenopausal urine and standardised in international units. Still marketed in Canada in 2026, which makes it the rare extract with live approvals.
The unprocessed precursor, all 344 residues with the signal peptide still attached. The protein your body actually secretes is a different animal: 315 residues and 36 cysteines folded just so.
Order AICAR right now
One last look before you decide.
Freeze-dried, COA on the page, ships cold
If you are researching AICAR and you want a source you do not have to second-guess, start with the paperwork on this page. For research use only.
Not for human consumption. Not approved by Health Canada or any other regulatory body.
Page last updated August 19, 2026
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