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AICAR

Gray market

Checked · 30 sources · 11 corrections on this page · No vendors · No affiliates · No one buys a word of it

0 human trials for this use

Limited Human Data for other uses · Animal only for this use · sedentary mice · Narkar 2008

Gray market · No FDA ruling — not on any list

Sold as a research chemical.

Bottom line

Real mouse endurance. No human trial has matched it. Actually running still wins on evidence.

Also called
  • Acadesine
  • AICA riboside
  • 5-Aminoimidazole-4-carboxamide-1-β-D-ribofuranoside
  • ZMP precursor
Category
Small Molecule — AMPK Activator / Exercise Mimetic
Class
Nucleoside analog / AMP mimetic
Molecular Weight
258.23 Da
Active Metabolite
ZMP (AICA ribotide)
Target
AMP-activated protein kinase (AMPK)
Route (studied)
IV (people) · SubQ (mice)
Route (sold)
SubQ or IV vials (research chemical)
FDA Status
Not approved
Human Trials
Cardiac surgery, CLL, small PK and metabolic studies
WADA Status
Banned S4 (Hormone & Metabolic Modulators)
Half-life
~1.5 h IV (parent); intracellular ZMP longer
Cost & Access
Research-only

Also for weight loss

The other four questions

What does it do? Tricks cells into thinking they're running low on energy: inside the cell it becomes ZMP, which copies AMP at the kinase (Corton et al., 1995). In rats, muscle pulled in glucose without insulin (Kurth-Kraczek et al., 1999; Hayashi et al., 1998) and four weeks of injections raised mitochondrial enzymes (Winder et al., 2000); in people, an IV infusion roughly doubled muscle glucose uptake in 29 healthy men (Cuthbertson et al., 2007) and lowered blood sugar and blood fat in 10 men with type 2 diabetes (Boon et al., 2008).
Who uses it? Metabolism labs, where it is the standard way to switch AMPK on in cells (Corton et al., 1995), and anti-doping labs, which measured it in the urine of 499 athletes to set reference values (Thomas et al., 2010) — despite WADA banning it as a performance enhancer and the high cost.
Does the evidence hold up? The famous 2008 paper showed untrained mice ran 44% farther after four weeks on AICAR (Narkar et al., 2008). Heart-surgery trials in the 1990s showed a mild heart-protection signal (Mangano, 1997); a larger 2009–2010 trial found none (Newman et al., 2012). No human endurance trial has been published.
Bottom line? Real mouse endurance. No human trial has matched it. Actually running still wins on evidence.

Dosing from the Literature

Published for fat loss: a mouse dose (500 mg/kg a day, intraperitoneally, for four weeks; Narkar et al., 2008) and the IV infusion of the 1990s heart-surgery trials (0.1 mg/kg a minute for 7 hours; Mangano, 1997). Not published: any human dose for fat loss.

Every figure below comes from the animal study or human trial named in its row. No FDA-approved dose exists for metabolic or performance use, and no published trial has given AICAR for fat loss or endurance in people.

ContextDoseRoute / ScheduleNotes
Mouse endurance (Narkar 2008)500 mg/kg/dayIntraperitoneal (IP) × 4 weeksTrial: sedentary adult C57BL/6J mice, which then ran about 23% longer and 44% farther than controls (Narkar et al., 2008). A mouse dose; no human equivalent has been published.
Rat muscle AMPK acute activation (Merrill 1997)0.5–2 mM AICAR in the perfusateHindlimb perfusionStudy: perfused rat hindlimb muscle; at 2 mM for 45 minutes, fatty-acid oxidation rose 2.8-fold and glucose uptake rose (Merrill et al., 1997). A bath concentration, not a dose given to an animal.
Human cardiac surgery (acadesine)~0.1 mg/kg/minIV continuous × 7 hoursTrials: 4,043 adults having coronary artery bypass surgery in five randomized trials, the drug also added to the cardioplegia solution (Mangano, 1997); the same infusion was used in RED-CABG (Newman et al., 2012).
Healthy volunteers (safety and kinetics study, Dixon 1991)10–100 mg/kgSingle IV and oral dosesTrial: healthy men given 10, 25, 50 or 100 mg/kg; well tolerated at every level, and under 5% of an oral dose reached the circulation (Dixon et al., 1991).
Dosing Disclaimer

In healthy men, under 5% of an oral dose reached the circulation and the plasma half-life was 1.4 hours (Dixon et al., 1991); every human study cited on this page gave AICAR as an IV infusion. No FDA-approved dose exists for metabolic or performance use. AICAR is prohibited at all times for WADA-tested athletes.

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What It Is

AICAR (5-aminoimidazole-4-carboxamide-1-β-D-ribofuranoside; also called AICA riboside or, as its pharmaceutical formulation, acadesine) is a small-molecule nucleoside analog in which an imidazole-carboxamide base is linked to a ribose sugar. It is a naturally occurring metabolic intermediate in the de novo purine biosynthesis pathway — cells routinely make and handle AICAR and its phosphorylated form as part of purine synthesis.

When AICAR is supplied exogenously (intravenously or subcutaneously), it is taken up by cells via nucleoside transporters and phosphorylated by adenosine kinase to its monophosphate form, ZMP (AICA ribotide). ZMP is a structural mimic of AMP (adenosine monophosphate) and is the pharmacologically active species: it binds the γ-subunit of AMP-activated protein kinase (AMPK) at the same allosteric site that AMP would, causing a conformational change that activates the kinase. From AMPK's perspective, ZMP accumulation looks like an energy crisis — a high AMP / ATP ratio — and it initiates the compensatory energy-generating program.

AICAR's rise to fame in the optimization space stems from a single influential paper: Narkar, Evans and colleagues published "AMPK and PPARδ (a gene switch for fat burning) Agonists Are Exercise Mimetics" in Cell in 2008 (PMID 18674809). That work reported that AICAR administration for four weeks increased running endurance in sedentary adult mice by roughly 44% — the "exercise in a pill" result. The underlying observation is physiologically real but has been frequently over-interpreted; AICAR was shown to reproduce a subset of endurance-training transcriptional (at the gene-switching level) adaptations without exercise in sedentary mice; the potentiation of exercise training the paper reports was for the PPARδ agonist GW501516, not AICAR. Translating these findings to trained adult humans, at non-ruinous cost and acceptable safety, has not succeeded.

AICAR also has a separate, older therapeutic history under the name acadesine. Large cardiac surgery trials in the 1990s investigated IV acadesine as a cardioprotective agent during coronary artery bypass grafting (CABG). The signal for reduction in myocardial infarction was consistent but modest (Mangano, JAMA 1997; PMID 9002496), and the drug ultimately did not obtain FDA approval for that indication. A later phase 3 trial in 3,080 patients was stopped early for futility (Newman et al., JAMA 2012; PMID 22782417). More recently, acadesine has been explored in chronic lymphocytic leukemia as a modulator of tumor-cell metabolism (Van Den Neste et al., Cancer Chemother Pharmacol 2013; PMID 23228986). Neither indication has yielded an approved product to date.

Mechanism of Action

  • Cellular uptake and ZMP formation — AICAR enters cells through nucleoside transporters and is phosphorylated by adenosine kinase to ZMP. In leukemic B cells, a nucleoside-transport inhibitor or an adenosine-kinase inhibitor blocked acadesine’s activation of AMPK, so both uptake and conversion to ZMP are required; T cells given the same concentration accumulated less ZMP and showed no AMPK phosphorylation (Campàs et al., Blood 2003; PMID 12522004).
  • AMPK activation by ZMP — In rat liver cells, ZMP reproduced both activating effects of AMP on AMPK, direct allosteric activation and promotion of its phosphorylation by an upstream kinase, and it did so without changing the cell's ATP, ADP or AMP (Corton et al., Eur J Biochem 1995; PMID 7744080).
  • Phosphorylation of ACC and lipogenic shutdown — In perfused rat hindlimb muscle, AICAR activated AMPK, inactivated acetyl-CoA carboxylase (ACC) and lowered malonyl-CoA, and fatty-acid oxidation rose 2.8-fold (Merrill et al., Am J Physiol 1997; PMID 9435525). In isolated rat fat cells, AICAR inhibited lipogenesis through the same phosphorylation of ACC (Sullivan et al., FEBS Lett 1994; PMID 7926017).
  • PGC-1α upregulation / mitochondrial biogenesis — In rats, 14 days of AICAR raised PGC-1α protein in the soleus and extensor digitorum longus muscles (Suwa et al., J Appl Physiol 2003; PMID 12777406), and 4 weeks of daily injections raised mitochondrial enzymes (citrate synthase, succinate and malate dehydrogenase) in white quadriceps and soleus but not in red quadriceps (Winder et al., J Appl Physiol 2000; PMID 10846039).
  • GLUT4 membrane translocation / insulin-independent glucose uptake — In perfused rat hindlimb muscle, AICAR increased AMPK activity, glucose uptake and GLUT4 translocation to the surface membrane (Kurth-Kraczek et al., Diabetes 1999; PMID 10426389), and in isolated rat muscle the PI3-kinase inhibitor wortmannin blocked insulin-stimulated glucose transport but not AICAR-stimulated transport, so the two work by different routes (Hayashi et al., Diabetes 1998; PMID 9703344). In people the two studies disagree: an infusion roughly doubled muscle glucose uptake in 29 healthy men (Cuthbertson et al., Diabetes 2007; PMID 17513706) but added nothing during an insulin clamp (Bosselaar et al., J Clin Pharmacol 2011; PMID 21148051).
  • mTORC1 suppression — In rats, AICAR injections cut muscle protein synthesis to 45% of control values, with lower phosphorylation of mTOR and of its downstream targets S6 kinase and 4E-BP1 (Bolster et al., J Biol Chem 2002; PMID 11997383).
  • PPARδ cross-talk — The Narkar / Evans 2008 paper found that AICAR and the PPARδ agonist GW501516 together induced several oxidative-metabolism genes in mouse muscle synergistically, an effect lost in muscle cells from PPARδ-null mice, where AICAR alone also failed to induce them; the endurance synergy it reported was between GW501516 and exercise training, and it did not test AICAR with exercise (Narkar et al., 2008).
  • Muscle fiber-type shift — In rats, 14 days of AICAR shifted fibers in the fast extensor digitorum longus muscle from type IIB toward type IIX, a more oxidative fast type (Suwa et al., J Appl Physiol 2003; PMID 12777406); the 2008 mouse endurance paper reported no fiber-type measurement for AICAR (five weeks of the PPARδ agonist alone changed neither fiber type nor endurance there), and we found no study showing a shift to slow-twitch type I fibers.
  • Autophagy (cellular self-cleanup) and mitophagy — Reviews of AMPK list autophagy and the disposal of mitochondria among the processes the kinase regulates, alongside mitochondrial biogenesis and cell growth (Hardie, Genes Dev 2011; PMID 21937710). No AICAR study cited on this page measured autophagy.
  • Cardioprotective adenosine-sparing mechanism (acadesine) — The cardiac-surgery trials called acadesine an adenosine-regulating agent (Newman et al., JAMA 2012; PMID 22782417). In dogs given AICA riboside before an hour of coronary occlusion, adenosine in venous blood from the ischemic area reached 1.79 µM against 0.22 µM with saline, collateral flow improved and arrhythmias were fewer (Gruber et al., Circulation 1989; PMID 2553298).

What the Research Shows

  • Narkar 2008 (Cell; PMID 18674809) — The definitive exercise-mimetic paper. Sedentary adult mice given 500 mg/kg a day intraperitoneally for 4 weeks ran about 23% longer and 44% farther on a treadmill than controls, carried less epididymal fat relative to body weight and used more oxygen, without a change in body weight. The synergy the paper reports is between the PPARδ agonist (GW501516) and exercise training, which together increased oxidative muscle fibers and running endurance. This paper established AICAR as an exercise-mimetic tool compound.
  • Merrill 1997 (Am J Physiol; PMID 9435525) — AICAR in the perfusate of rat hindlimb muscle increases AMPK activity, fatty-acid oxidation, and glucose uptake. Foundational mechanistic paper linking AMPK activation to muscle metabolic adaptations.
  • Insulin-independent glucose uptake in diabetic models — Multiple rodent models of type 2 diabetes and obesity show AICAR improves glucose tolerance and insulin sensitivity. In obese diabetic (ob/ob) mice, a week of daily AICAR injections corrected high blood glucose and improved glucose tolerance but worsened plasma fatty acids and triglycerides (Song et al., Diabetologia 2002; PMID 11845224); in insulin-resistant obese Zucker rats, 7 weeks normalized the oral glucose tolerance test, lowered triglycerides and free fatty acids and cut systolic blood pressure by 14.6 mmHg (Buhl et al., Diabetes 2002; PMID 12086950).
  • Cardiac surgery acadesine trials — In the 1990s, five randomized trials (4,043 patients) evaluated IV acadesine as a perioperative cardioprotective agent during CABG; pooled, they showed a modest, statistically significant reduction in perioperative MI and early cardiac death (Mangano, JAMA 1997; PMID 9002496). The phase 3 RED-CABG trial (2009–2010) found no benefit and was stopped for futility (Newman et al., JAMA 2012; PMID 22782417). The drug did not obtain FDA approval for cardioprotection.
  • AMP deaminase (AMPD1) deficiency — Myoadenylate deaminase deficiency disrupts the purine nucleotide cycle in muscle; in one study, affected patients fatigued after only 28% as much work as patients without it (Sabina et al., J Clin Invest 1984; PMID 6707201). We found no published human study of AICAR in this disorder; AICAR appears in its literature as a tool that blocks the same cycle and impairs rodent muscle (Swain et al., J Clin Invest 1984; PMID 6480832).
  • AICAR as a muscle-impairing tool (Swain et al., J Clin Invest 1984; PMID 6480832) — Earlier, AICAR was used for the opposite purpose: once phosphorylated in muscle it inhibits adenylosuccinate lyase, an enzyme of the purine nucleotide cycle, and in 28 mice infused with it, stimulated calf muscle developed 40% less tension than in 22 saline-treated mice.
  • Chronic lymphocytic leukemia (acadesine) — A 24-patient phase I/II study gave single IV doses of 50–315 mg/kg to patients with relapsed or refractory CLL and set 210 mg/kg as the maximum tolerated dose (Van Den Neste et al., Cancer Chemother Pharmacol 2013; PMID 23228986); in cells, acadesine induces apoptosis in leukemic B cells, a cell death later shown not to depend on AMPK (Santidrián et al., Blood 2010; PMID 20664053). Did not achieve approval.
  • Translational ceiling in trained humans — No randomized placebo-controlled trial of AICAR and endurance performance in trained adults has been published, at any dose. The mouse endurance result has not been tested in people.
  • Uric acid and blood-glucose signals — Uric acid is the main breakdown product of acadesine in people, serum uric acid rose transiently in the cardiac-surgery trials, and raised uric acid was common in the leukemia study (Dixon et al., 1993; Mangano, 1997; Van Den Neste et al., 2013). Blood glucose fell during an IV infusion in 10 men with type 2 diabetes (Boon et al., 2008).
Critical Context — Mouse vs Human

The 2008 result came from sedentary mice given 500 mg/kg a day for four weeks (Narkar et al., 2008). What is published in people is different: single IV doses of 10–100 mg/kg were well tolerated in healthy men, under 5% of an oral dose reached the circulation and the plasma half-life was 1.4 hours (Dixon et al., 1991); an infusion roughly doubled muscle glucose uptake in 29 healthy men but moved whole-body glucose disposal by 7% (Cuthbertson et al., 2007). No trial has measured endurance performance in people.

Human Data

  • Acadesine cardiac surgery program — Five randomized trials in the 1990s (4,043 CABG patients at 81 centers) compared an IV acadesine infusion with placebo. A meta-analysis of the five trials reported fewer perioperative myocardial infarctions (odds ratio 0.69) and cardiac deaths through day 4 (odds ratio 0.52) with acadesine (Mangano, JAMA 1997; PMID 9002496). The later phase 3 RED-CABG trial (300 sites, 2009–2010) gave the same infusion, 0.1 mg/kg per minute for 7 hours, to intermediate- to high-risk CABG patients and was stopped for futility after 3,080 of a planned 7,500 had been randomized: death, stroke or severe left ventricular dysfunction needing mechanical support by day 28 occurred in 5.1% on acadesine and 5.0% on placebo (Newman et al., JAMA 2012; PMID 22782417). The signal did not survive FDA scrutiny for approval; the drug was not granted marketing authorization for cardioprotection.
  • Muscle glucose uptake in healthy men — In 29 healthy men, an AICAR infusion roughly doubled muscle glucose uptake after 3 hours (bicycle exercise raised it 4.7-fold) but raised whole-body glucose disposal by only 7%, and AMPK activity in muscle did not change (Cuthbertson et al., Diabetes 2007; PMID 17513706). In a later study, a 67 mg/kg infusion given during high insulin added nothing to whole-body or forearm glucose uptake (Bosselaar et al., J Clin Pharmacol 2011; PMID 21148051).
  • Type 2 diabetes — In 10 men with type 2 diabetes, an IV AICAR infusion (0.75 mg/kg per minute) lowered blood glucose by cutting the liver’s glucose output while the rate at which glucose left the blood was unchanged, and lowered blood fatty acids by reducing their release (Boon et al., Diabetologia 2008; PMID 18709353).
  • Chronic lymphocytic leukemia Phase I/II — Exploration of acadesine as a metabolic tumor therapy in CLL. Did not yield an approved product. In the 24-patient phase I/II study, single IV doses up to 210 mg/kg (the maximum tolerated dose) were given; hyperuricemia was common and resolved with allopurinol, and renal impairment and clinically significant infusion-related hypotension occurred (Van Den Neste et al., Cancer Chemother Pharmacol 2013; PMID 23228986). In lab studies, acadesine killed leukemic B cells but largely spared T cells (Campàs et al., Blood 2003; PMID 12522004), and a later study from the same group found that this cell death does not depend on AMPK (Santidrián et al., Blood 2010; PMID 20664053).
  • Healthy-volunteer pharmacokinetic studies — Small healthy-volunteer IV PK studies document ~1.5 h plasma half-life and intracellular ZMP formation; plasma AICAR clearance is rapid. In healthy men given 10–100 mg/kg, the terminal half-life was 1.4 hours, red blood cells rapidly took up and phosphorylated the drug, and under 5% of an oral dose reached the circulation (Dixon et al., J Clin Pharmacol 1991; PMID 2037706); with radiolabeled drug, uric acid was its main breakdown product in plasma (Dixon et al., J Clin Pharmacol 1993; PMID 8227467).
  • Athletic use detection — AICAR detection methods (LC-MS/MS from urine) were developed by WADA-accredited laboratories around 2010 following the compound's S4 banning. Exogenous AICAR can be distinguished from endogenous AICAR by absolute concentration and pharmacokinetic signature.
  • No published endurance-performance RCT in trained humans — There is no Western peer-reviewed randomized placebo-controlled trial establishing AICAR's endurance-performance benefit in trained adult athletes.

Reconstitution & Storage

AICAR is not an approved drug, so no label sets a vial size, a water volume, a storage temperature or a shelf life for it, and no published study gives one. The rows below are arithmetic only.

Vial SizeBAC WaterConcentrationNotes
50 mg2 mL25 mg/mL0.1 mL (10 units on a U-100 syringe) holds 2.5 mg.
100 mg2 mL50 mg/mL0.1 mL (10 units) holds 5 mg.
500 mg (bulk research)10 mL50 mg/mLThe same concentration as the row above, in a larger volume.

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Side Effects & Risks

Important

Serum uric acid rose transiently in the acadesine cardiac-surgery trials (Mangano, 1997), and raised uric acid was common in the leukemia study, where it resolved with allopurinol (Van Den Neste et al., 2013). WADA-banned under S4. Consult a licensed healthcare provider.

Bloodwork & Monitoring

No trial, label or guideline sets monitoring for AICAR. The published human studies measured blood glucose and glucose kinetics (Cuthbertson et al., 2007; Boon et al., 2008), heart rate and blood pressure (Bosselaar et al., 2011), and serum uric acid, which rose transiently in the cardiac-surgery trials (Mangano, 1997) and was commonly raised in the leukemia study (Van Den Neste et al., 2013).

  • If athletic testing applies — Incompatible with tested sport. Detection methods are established.

Commonly Stacked With

No published study has combined AICAR with another compound in people.

GW501516 (Cardarine)

The PPARδ agonist given with AICAR in the Narkar / Evans 2008 mouse paper: six days of the pair (GW501516 5 mg/kg a day by gavage, AICAR 250 mg/kg a day intraperitoneally) induced several muscle oxidative genes more strongly than either drug alone, and the effect was absent in muscle cells from PPARδ-null mice (Narkar et al., 2008). GW501516 is itself WADA-banned.

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Legal Status

Current Status — April 2026

AICAR / acadesine is not FDA-approved for any indication. The historical cardiac-surgery development program did not reach approval; the CLL program did not advance. No active Phase III program exists for any indication as of April 2026.

AICAR is banned by WADA under category S4 (Hormone and Metabolic Modulators). It has been on the prohibited list since 2009. LC-MS/MS detection methods are established in WADA-accredited laboratories, and differentiation of exogenous from endogenous AICAR is feasible. USADA has issued athlete advisories against use. WADA’s 2026 List stays in force until 31 December 2026; the 2027 List, which replaces it on 1 January 2027, still names AICAR in S4.4.1 among the AMPK activators and adds two entries to that subsection: seladelpar, as a PPARδ agonist, and SLU-PP-332, SLU-PP-915 and related substances (Prohibited List 2027).

AICAR is not on any FDA 503A bulk-substance list. It was not among the 12 peptides FDA removed from Category 2 in April 2026 (FDA 503A categories list, April 22, 2026).

AICAR is available through research-chemical suppliers for laboratory use.

Cost & Access

AICAR is not approved for human use in the United States. It is available through research suppliers for laboratory research purposes only.

US 503A / 503B compounding pharmacies do not compound AICAR.

AICAR was not among the 12 peptides FDA removed from Category 2 in April 2026, and FDA’s 503A categories list, updated May 14, 2026, does not name it (FDA 503A categories list, April 22 and May 14, 2026). As a small molecule, any US regulatory pathway for AICAR would proceed through standard IND / NDA review — which no sponsor is currently pursuing in an obesity, diabetes, or performance indication.

Pricing and availability vary by vendor. Kalios does not sell compounds.

References

  1. Narkar VA, Downes M, Yu RT, Embler E, Wang YX, Banayo E, Mihaylova MM, Nelson MC, Zou Y, Juguilon H, Kang H, Shaw RJ, Evans RM. AMPK and PPARδ agonists are exercise mimetics. Cell. 2008;134(3):405-415. PMID: 18674809. (The definitive "exercise in a pill" mouse endurance paper.)
  2. Merrill GF, Kurth EJ, Hardie DG, Winder WW. AICA riboside increases AMP-activated protein kinase, fatty acid oxidation, and glucose uptake in rat muscle. Am J Physiol. 1997;273(6 Pt 1):E1107-E1112. PMID: 9435525. (Foundational AMPK-activation mechanistic paper.)
  3. Corton JM, Gillespie JG, Hawley SA, Hardie DG. 5-Aminoimidazole-4-carboxamide ribonucleoside. A specific method for activating AMP-activated protein kinase in intact cells? Eur J Biochem. 1995;229(2):558-565. PMID: 7744080. (Methodology establishing AICAR as the canonical AMPK-activator research tool.)
  4. Mangano DT; Multicenter Study of Perioperative Ischemia Research Group. Effects of acadesine on myocardial infarction, stroke, and death following surgery. A meta-analysis of the 5 international randomized trials. JAMA. 1997;277(4):325-332. PMID: 9002496. (Meta-analysis of acadesine cardiac surgery program.)
  5. Hardie DG. AMP-activated protein kinase: an energy sensor that regulates all aspects of cell function. Genes Dev. 2011;25(18):1895-1908. PMID: 21937710. (Authoritative AMPK review by a leading AMPK biochemist.)
  6. Sullivan JE, Brocklehurst KJ, Marley AE, Carey F, Carling D, Beri RK. Inhibition of lipolysis and lipogenesis in isolated rat adipocytes with AICAR, a cell-permeable activator of AMP-activated protein kinase. FEBS Lett. 1994;353(1):33-36. PMID: 7926017. (Early metabolic-effect characterization paper.)
  7. Kemp BE, Mitchelhill KI, Stapleton D, Michell BJ, Chen ZP, Witters LA. Dealing with energy demand: the AMP-activated protein kinase. Trends Biochem Sci. 1999;24(1):22-25. PMID: 10087918. (AMPK signaling framework reference.)
  8. Van Den Neste E, Cazin B, Janssens A, González-Barca E, Terol MJ, Levy V, Pérez de Oteyza J, Zachee P, Saunders A, de Frias M, Campàs C. Acadesine for patients with relapsed/refractory chronic lymphocytic leukemia (CLL): a multicenter phase I/II study. Cancer Chemother Pharmacol. 2013;71(3):581-591. PMID: 23228986.
  9. Sabina RL, Swain JL, Olanow CW, Bradley WG, Fishbein WN, DiMauro S, Holmes EW. Myoadenylate deaminase deficiency. Functional and metabolic abnormalities associated with disruption of the purine nucleotide cycle. J Clin Invest. 1984;73(3):720-730. PMID: 6707201. (AMP deaminase deficiency and the purine nucleotide cycle in muscle.)
  10. World Anti-Doping Agency. The 2009 Prohibited List: International Standard. WADA. 2009. (First inclusion of AICAR on the banned list under S4.)
  11. Thomas A, Beuck S, Eickhoff JC, Guddat S, Krug O, Kamber M, Schänzer W, Thevis M. Quantification of urinary AICAR concentrations as a matter of doping controls. Anal Bioanal Chem. 2010;396(8):2899-2908. PMID: 20225061. (AICAR doping detection methodology.)
  12. FDA. Bulk Drug Substances Nominated for Use in Compounding Under Section 503A of the FD&C Act (503A categories list), versions updated April 15, April 22 and May 14, 2026. fda.gov/media/94155/download. Read October 3, 2026. (Notice that 12 peptides would leave Category 2 because their nominations were withdrawn; their removal; GHK-Cu, except injectable, back in Category 1.)
  13. Newman MF, Ferguson TB, White JA, Ambrosio G, Koglin J, Nussmeier NA, Pearl RG, Pitt B, Wechsler AS, Weisel RD, Reece TL, Lira A, Harrington RA. Effect of adenosine-regulating agent acadesine on morbidity and mortality associated with coronary artery bypass grafting: the RED-CABG randomized controlled trial. JAMA. 2012;308(2):157-164. PMID: 22782417. (NCT00872001.)
  14. Dixon R, Gourzis J, McDermott D, Fujitaki J, Dewland P, Gruber H. AICA-riboside: safety, tolerance, and pharmacokinetics of a novel adenosine-regulating agent. J Clin Pharmacol. 1991;31(4):342-347. PMID: 2037706.
  15. Dixon R, Fujitaki J, Sandoval T, Kisicki J. Acadesine (AICA-riboside): disposition and metabolism of an adenosine-regulating agent. J Clin Pharmacol. 1993;33(10):955-958. PMID: 8227467.
  16. Cuthbertson DJ, Babraj JA, Mustard KJ, Towler MC, Green KA, Wackerhage H, Leese GP, Baar K, Thomason-Hughes M, Sutherland C, Hardie DG, Rennie MJ. 5-aminoimidazole-4-carboxamide 1-beta-D-ribofuranoside acutely stimulates skeletal muscle 2-deoxyglucose uptake in healthy men. Diabetes. 2007;56(8):2078-2084. PMID: 17513706.
  17. Boon H, Bosselaar M, Praet SF, Blaak EE, Saris WH, Wagenmakers AJ, McGee SL, Tack CJ, Smits P, Hargreaves M, van Loon LJ. Intravenous AICAR administration reduces hepatic glucose output and inhibits whole body lipolysis in type 2 diabetic patients. Diabetologia. 2008;51(10):1893-1900. PMID: 18709353.
  18. Bosselaar M, Smits P, van Loon LJ, Tack CJ. Intravenous AICAR during hyperinsulinemia induces systemic hemodynamic changes but has no local metabolic effect. J Clin Pharmacol. 2011;51(10):1449-1458. PMID: 21148051.
  19. Kurth-Kraczek EJ, Hirshman MF, Goodyear LJ, Winder WW. 5' AMP-activated protein kinase activation causes GLUT4 translocation in skeletal muscle. Diabetes. 1999;48(8):1667-1671. PMID: 10426389.
  20. Hayashi T, Hirshman MF, Kurth EJ, Winder WW, Goodyear LJ. Evidence for 5' AMP-activated protein kinase mediation of the effect of muscle contraction on glucose transport. Diabetes. 1998;47(8):1369-1373. PMID: 9703344.
  21. Winder WW, Holmes BF, Rubink DS, Jensen EB, Chen M, Holloszy JO. Activation of AMP-activated protein kinase increases mitochondrial enzymes in skeletal muscle. J Appl Physiol (1985). 2000;88(6):2219-2226. PMID: 10846039.
  22. Suwa M, Nakano H, Kumagai S. Effects of chronic AICAR treatment on fiber composition, enzyme activity, UCP3, and PGC-1 in rat muscles. J Appl Physiol (1985). 2003;95(3):960-968. PMID: 12777406.
  23. Bolster DR, Crozier SJ, Kimball SR, Jefferson LS. AMP-activated protein kinase suppresses protein synthesis in rat skeletal muscle through down-regulated mammalian target of rapamycin (mTOR) signaling. J Biol Chem. 2002;277(27):23977-23980. PMID: 11997383.
  24. Song XM, Fiedler M, Galuska D, Ryder JW, Fernström M, Chibalin AV, Wallberg-Henriksson H, Zierath JR. 5-Aminoimidazole-4-carboxamide ribonucleoside treatment improves glucose homeostasis in insulin-resistant diabetic (ob/ob) mice. Diabetologia. 2002;45(1):56-65. PMID: 11845224.
  25. Buhl ES, Jessen N, Pold R, Ledet T, Flyvbjerg A, Pedersen SB, Pedersen O, Schmitz O, Lund S. Long-term AICAR administration reduces metabolic disturbances and lowers blood pressure in rats displaying features of the insulin resistance syndrome. Diabetes. 2002;51(7):2199-2206. PMID: 12086950.
  26. Gruber HE, Hoffer ME, McAllister DR, Laikind PK, Lane TA, Schmid-Schoenbein GW, Engler RL. Increased adenosine concentration in blood from ischemic myocardium by AICA riboside. Effects on flow, granulocytes, and injury. Circulation. 1989;80(5):1400-1411. PMID: 2553298.
  27. Swain JL, Hines JJ, Sabina RL, Harbury OL, Holmes EW. Disruption of the purine nucleotide cycle by inhibition of adenylosuccinate lyase produces skeletal muscle dysfunction. J Clin Invest. 1984;74(4):1422-1427. PMID: 6480832.
  28. Campàs C, Lopez JM, Santidrián AF, Barragán M, Bellosillo B, Colomer D, Gil J. Acadesine activates AMPK and induces apoptosis in B-cell chronic lymphocytic leukemia cells but not in T lymphocytes. Blood. 2003;101(9):3674-3680. PMID: 12522004.
  29. Santidrián AF, González-Gironès DM, Iglesias-Serret D, Coll-Mulet L, Cosialls AM, de Frias M, Campàs C, González-Barca E, Alonso E, Labi V, Viollet B, Benito A, Pons G, Villunger A, Gil J. AICAR induces apoptosis independently of AMPK and p53 through up-regulation of the BH3-only proteins BIM and NOXA in chronic lymphocytic leukemia cells. Blood. 2010;116(16):3023-3032. PMID: 20664053.
  30. World Anti-Doping Agency. Prohibited List 2027 (in effect January 1, 2027), French edition with track changes, August 26, 2026, and Summary of Major Modifications and Explanatory Notes, 2027 Prohibited List, August 17, 2026: wada-ama.org/sites/default/files/2026-09/2027list_final_fr_track_changes_26_august_2026.pdf and 2027_list_explanatory_note_en_final_17_august_2026_1.pdf, read October 12, 2026 in the Internet Archive’s copies captured October 9, 2026 (web.archive.org). The List’s English edition was not available there and was not read.

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Checked 18 Oct 2026