AICAR is a cell-permeable nucleoside analog. Once inside a cell it is phosphorylated to ZMP, a molecule that mimics AMP and switches on AMP-activated protein kinase (AMPK), the master energy sensor that shifts tissue toward fat oxidation, glucose uptake and mitochondrial biogenesis.
Researchers buy AICAR because it has been the reference pharmacological AMPK activator since the mid-1990s, with thousands of published studies behind it. Although it is technically a nucleoside rather than a peptide, it is stocked alongside our research peptides because labs use it in the same metabolic, endurance and recovery models. New to the field? Start with our complete guide to research peptides.
Whether you buy AICAR for a single cell-culture experiment or a multi-week rodent endurance protocol, the 50 mg vial format gives enough material for most pilot studies while keeping unopened stock sealed and frozen.
Detailed Mechanism of Action
AICAR (5-aminoimidazole-4-carboxamide-1-β-D-ribofuranoside, CAS 2627-69-2, MW 258.23 g/mol) enters cells through adenosine nucleoside transporters. Adenosine kinase then phosphorylates it to ZMP, also called AICAR monophosphate.
ZMP is a natural intermediate of de novo purine synthesis. When researchers buy AICAR and apply it at pharmacological concentrations, however, ZMP accumulates far above physiological levels and the cell reads that surplus as an energy deficit.
ZMP binds the cystathionine-β-synthase (CBS) domains of the AMPK γ-subunit, the same nucleotide-binding pockets normally occupied by AMP. Binding produces allosteric activation and shields Thr172 on the catalytic α-subunit from phosphatases, so the phosphorylation delivered by the upstream kinase LKB1 persists.
Unlike metformin or mitochondrial poisons, AICAR does not disturb the cellular AMP:ATP ratio. That is the main reason labs buy AICAR: it delivers the low-energy signal directly without depleting ATP or damaging the electron transport chain.
Downstream, activated AMPK phosphorylates and inhibits acetyl-CoA carboxylase (ACC). Malonyl-CoA falls, carnitine palmitoyltransferase-1 is released from inhibition, and fatty-acid oxidation rises. AMPK also drives GLUT4 translocation through TBC1D1 and AS160, increasing glucose uptake independently of insulin.
AMPK phosphorylates PGC-1α and raises NAD+ to engage SIRT1, which together stimulate mitochondrial biogenesis. In the liver, AMPK suppresses gluconeogenic gene expression and blocks lipogenesis through SREBP-1c, while phosphorylation of TSC2 and raptor restrains mTORC1 and anabolic protein synthesis.
AICAR is not perfectly specific. ZMP also inhibits fructose-1,6-bisphosphatase, activates glycogen phosphorylase, and raises extracellular adenosine by inhibiting adenosine kinase and AMP deaminase, which is the proposed basis for acadesine’s cardioprotective effects. Careful investigators who buy AICAR therefore pair it with AMPK-null models, dominant-negative constructs, or the inhibitor compound C to separate AMPK-dependent from AMPK-independent effects.
Published Research
The study that made researchers everywhere want to buy AICAR was published by Narkar and colleagues at the Salk Institute in Cell in 2008. Sedentary mice given AICAR at 500 mg/kg per day by intraperitoneal injection for four weeks ran 44% farther in a treadmill endurance test with no training at all, and their muscle showed an oxidative gene signature normally produced by exercise.
The paper coined the phrase “exercise mimetic” and directly prompted WADA to prohibit AICAR the following year. Read the abstract on PubMed (Narkar et al., 2008).
The molecular groundwork came earlier. Merrill and colleagues (1997) perfused rat hindlimb muscle with AICAR and recorded higher AMPK activity, inactivated ACC, a fall in malonyl-CoA, and increases in both fatty-acid oxidation and glucose uptake, demonstrating that AMPK activation alone reproduces the metabolic shift of contraction. See the 1997 American Journal of Physiology study.
Winder and colleagues (2000) then gave rats daily subcutaneous AICAR for four weeks and measured increases in citrate synthase, cytochrome c, δ-aminolevulinate synthase, hexokinase and GLUT4, the same adaptations produced by endurance training. That work is indexed here on PubMed.
Human data come from the clinical program that studied AICAR under the name acadesine. A 1997 JAMA meta-analysis of five randomized trials in coronary bypass surgery, covering roughly 4,000 patients, reported fewer perioperative myocardial infarctions, but the larger RED-CABG trial published in 2012 found no benefit on its composite endpoint and was stopped for futility.
Acadesine has also completed phase I/II testing in relapsed chronic lymphocytic leukemia, and infusion studies in healthy men have shown increased skeletal-muscle glucose uptake. Together these results explain why labs buy AICAR as a mechanistic tool compound rather than as a therapeutic candidate.
Tissue-Specific Effects in Research Models
Skeletal muscle. This is where most groups that buy AICAR focus. Acute exposure increases glucose transport and fatty-acid oxidation; chronic dosing raises mitochondrial enzyme content, GLUT4 protein, capillary density and the proportion of oxidative fibers, producing an endurance phenotype without contraction.
Liver. AICAR suppresses gluconeogenesis and lipogenesis in isolated hepatocytes, and chronic administration lowers blood glucose in ob/ob and db/db mouse models of insulin resistance. These hepatic effects are the basis for its use in diet-induced obesity and metabolic syndrome studies.
Heart. During ischemia, AMPK activation sustains glucose uptake and glycolytic ATP production, and the adenosine-raising action of AICAR adds a preconditioning-like layer of protection. This dual mechanism is why acadesine progressed to cardiac surgery trials.
Adipose tissue. AICAR restrains adipogenic differentiation of preadipocytes and modulates lipolysis, effects that researchers exploit in obesity and lipid-metabolism models.
Immune cells and brain. AICAR shifts macrophages toward an anti-inflammatory phenotype and reduces disease severity in experimental autoimmune encephalomyelitis, a mouse model of multiple sclerosis. Neuroscientists also buy AICAR to probe hypothalamic AMPK, where central administration increases feeding behavior, a reminder that AMPK effects are tissue dependent.
Cancer cell lines. Through AMPK-driven mTORC1 inhibition, AICAR slows proliferation across many tumor lines and triggers apoptosis in B-cell chronic lymphocytic leukemia cells while sparing normal T lymphocytes, the observation that launched the acadesine oncology program.
AICAR in Aging, Muscle Disease and Longevity Research
AMPK activity declines with age, and this decline is linked to reduced mitochondrial biogenesis, sarcopenia and insulin resistance. Longevity labs buy AICAR to test whether restoring the AMPK signal reverses these deficits, often alongside compounds covered in our guide to the best peptides for longevity research.
In mitochondrial-disease models, AICAR corrected cytochrome c oxidase deficiency and improved motor performance in Sco2-mutant mice (Viscomi et al., 2011). In the mdx mouse model of Duchenne muscular dystrophy, chronic AICAR stimulated autophagy and improved diaphragm structure and function (Pauly et al., 2012).
Because AMPK opposes mTORC1, AICAR is also used as the catabolic counterpoint in muscle-growth research. Groups studying hypertrophy pathways buy AICAR to switch anabolic signaling off on demand, and pair it with the compounds reviewed in our article on peptides for muscle growth and recovery.
AICAR vs Alternatives
| Feature | AICAR (This Product) | MOTS-c | Metformin |
|---|
| Compound class | Nucleoside analog (AICA riboside) | 16-amino-acid mitochondrial-derived peptide | Biguanide small molecule |
| Route to AMPK | Direct: ZMP mimics AMP at the γ-subunit | Indirect: folate-cycle inhibition raises endogenous AICAR | Indirect: mild complex I inhibition raises AMP:ATP |
| Exercise-mimetic evidence | +44% running endurance in sedentary mice (Narkar 2008) | Improved running capacity in young and aged mice (Reynolds 2021) | May blunt training adaptations in older adults (Konopka 2019) |
| Typical research route | Injection; oral bioavailability is very low | Injection | Oral |
| Plasma half-life | Short; intracellular ZMP persists longer | Short (rapid peptide clearance) | Roughly 4–9 hours |
| Known off-target notes | Other AMP-sensitive enzymes; adenosine accumulation | Nuclear translocation under stress; gene regulation | Gastrointestinal effects; complex I inhibition |
| WADA status | Prohibited since 2009 (S4 metabolic modulators) | Consult the current Prohibited List | Not prohibited |
| PSPeptides specification | 50 mg, 99%+ purity, COA included | See our MOTS-c research guide | Not a PSPeptides product |
The practical takeaway: buy AICAR when the question is “what does direct AMPK activation do in this system?”, choose MOTS-c when the question involves mitochondrial-nuclear signaling, and use metformin when a clinically relevant indirect activator is required.
Many labs that buy AICAR run it beside MOTS-c in the same protocol, since MOTS-c raises endogenous AICAR levels and the two make a natural dose-response pair. Our peptide stacking guide covers how to design those experimental arms.
Reconstitution & Handling
Each vial contains 50 mg of AICAR as a lyophilized powder. AICAR is freely water-soluble at working concentrations, which makes it easier to handle than most research peptides. Adding 2 mL of bacteriostatic water yields 25 mg/mL; adding 5 mL yields 10 mg/mL.
Let the vial reach room temperature, direct the diluent down the glass wall, and swirl gently until the solution is clear. Do not shake. For cell-culture work, dissolve in sterile PBS or medium and pass through a 0.22 µm filter. Published in vitro protocols most often use 0.5–2 mM AICAR for 1–24 hours.
Published rodent protocols, such as the Narkar and Winder studies above, used 250–500 mg/kg per day by intraperitoneal or subcutaneous injection. Researchers who buy AICAR for animal work should calculate vial requirements accordingly: a 25 g mouse at 500 mg/kg consumes 12.5 mg per day, so one 50 mg vial covers four mouse-days.
Our step-by-step reconstitution guide and the dosage calculator walkthrough apply directly to this product, and our subcutaneous vs intramuscular injection guide covers route selection for animal studies.
Experimental Design Tips
Because ZMP accumulation is dose- and time-dependent, pilot a concentration curve before committing an entire study. In cultured myotubes, 0.5 mM AICAR for 1 hour typically produces measurable ACC phosphorylation, while 2 mM for 16–24 hours is common for gene-expression endpoints. Confirm target engagement with phospho-AMPK (Thr172) and phospho-ACC (Ser79) western blots.
In animal work, inject at the same time each day, record body weight, and include vehicle controls injected with the same volume of saline. AICAR can lower blood glucose acutely, so check glucose within the first hour if the model is sensitive to hypoglycemia. Labs that buy AICAR for chronic studies often add an AMPK-null or compound C arm to attribute effects correctly.
Finally, remember that AICAR and exercise overlap but are not identical: AICAR does not raise heart rate, recruit motor units, or produce the mechanical signals that drive hypertrophy. Researchers buy AICAR to isolate the metabolic arm of exercise adaptation, not to replace training in a model.
Storage & Stability
Lyophilized AICAR is chemically robust because it has no peptide bonds to hydrolyze. Store sealed vials at −20°C for long-term stability of 24 months or more; 2–8°C is acceptable for several months, and the short time at room temperature during shipping does not affect purity.
Keep vials away from light and humidity, and allow a cold vial to warm before opening so condensation does not enter the powder. Once reconstituted, refrigerate at 2–8°C and use within four weeks.
For longer projects, divide the solution into single-use aliquots and freeze at −20°C, avoiding repeated freeze-thaw cycles. Discard any solution that turns yellow or cloudy. Our peptide storage guide and the guide to spotting degradation both apply. Researchers who buy AICAR in multi-vial quantities typically keep unopened stock frozen and reconstitute one vial at a time.
Certificate of Analysis
Every lot ships with a batch-specific COA reporting HPLC purity (99%+), mass-spectrometry identity confirmation against the expected molecular weight of 258.23 g/mol (C9H14N4O5), appearance, and lot number. Because AICAR is a small molecule rather than a peptide, the mass-spec peak is a clean single species, which makes identity verification simple.
If you are unsure how to interpret the chromatogram or the mass-spec trace, our guide on how to read a peptide COA walks through each section. We recommend that labs which buy AICAR keep the COA on file with their experimental records.
A Brief History of AICAR Research
AICAR was first developed as acadesine by Gensia Pharmaceuticals in the late 1980s as a cardioprotective agent for coronary bypass surgery. In 1995, Corton and colleagues showed that it activates AMPK in intact cells without changing nucleotide ratios, turning a failed cardiac drug into the most useful AMPK tool compound in the field.
Merrill’s hindlimb work in 1997 and Winder’s chronic-dosing study in 2000 established the metabolic and mitochondrial adaptations, and the 2008 Salk Institute exercise-mimetic paper brought AICAR to mainstream attention. WADA prohibited it in 2009, RED-CABG closed the cardiac chapter in 2012, and today labs buy AICAR mainly for metabolism, aging, immunology and oncology research.
Why Researchers Buy AICAR From PSPeptides
- US Manufactured: Every vial is produced in the United States under controlled conditions.
- Third-Party Tested: Independent HPLC and mass spectrometry on every batch, not just a representative lot.
- Fast Shipping: Free UPS 2nd Day Air over $150, same-day dispatch for orders placed before 2 PM EST.
- Flexible Payments: Credit cards, Afterpay, Klarna, Apple Pay and Google Pay.
- 7-Day Support: Reach us by email, phone or text any day of the week.
Choosing where to buy AICAR matters more than it does for most compounds, because purity problems in a nucleoside analog are invisible without a chromatogram. Our article on how to choose a research peptide supplier explains the questions to ask any vendor before you buy AICAR or any other research compound.
Frequently Asked Questions
Where can I buy AICAR online for research in 2026?
You can buy AICAR directly from PSPeptides in 50 mg vials. Each order ships from the United States with a batch-specific COA, and orders over $150 qualify for free UPS 2nd Day Air. Our guide to the legal status of research peptides in 2026 explains the research-use framework that applies to this product.
Is AICAR a peptide?
No. AICAR is a nucleoside analog, an imidazole carboxamide attached to a ribose sugar, with a molecular weight of 258 g/mol. Labs buy AICAR from peptide suppliers because it is used in the same metabolic, endurance and recovery research models as peptides such as MOTS-c, and because it requires the same cold-chain and COA standards.
What is the difference between AICAR and acadesine?
They are the same molecule. Acadesine is the international nonproprietary name used in the clinical trials for cardiac surgery and leukemia, while AICAR (or AICA riboside) is the name used in the basic-science literature. When you buy AICAR from PSPeptides you receive the identical compound described in both bodies of research.
How should I reconstitute and store AICAR?
Reconstitute the 50 mg vial with 2–5 mL of bacteriostatic water for a 25–10 mg/mL solution, swirling rather than shaking. Store the lyophilized powder at −20°C and the reconstituted solution at 2–8°C for up to four weeks. Researchers who buy AICAR for longer studies should freeze single-use aliquots to avoid repeated freeze-thaw cycles.
Can AICAR be given orally in research models?
Oral bioavailability of AICAR is very low because of first-pass metabolism and limited absorption, so nearly all published in vivo work uses intraperitoneal or subcutaneous injection. Groups that buy AICAR for oral-gavage studies should expect to use substantially higher doses and to confirm exposure with plasma or tissue ZMP measurements.
Why is AICAR banned by WADA?
WADA added AICAR to the Prohibited List in 2009 after the Salk Institute exercise-mimetic paper showed a 44% endurance gain in untrained mice. It currently sits in the S4 metabolic modulators category. That history is exactly why exercise physiologists and metabolism labs buy AICAR: it remains the cleanest pharmacological model of the AMPK arm of endurance adaptation.
Related Resources
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