About AICAR
Converted intracellularly to ZMP, a potent AMPK activator. AMPK activation increases fatty acid oxidation, glucose uptake, and mitochondrial biogenesis — the same metabolic pathways activated by sustained aerobic exercise.
AICAR (5-aminoimidazole-4-carboxamide ribonucleotide; acadesine) is a non-peptide, cell-permeable nucleoside analog and prodrug that is phosphorylated intracellularly to its monophosphate form (ZMP), which mimics AMP to activate AMP-activated protein kinase (AMPK) — the primary cellular energy sensor — producing metabolic effects that partially phenocopy those of exercise and caloric restriction. AMPK activation by AICAR upregulates GLUT4 expression and glucose uptake, stimulates fatty acid oxidation, increases mitochondrial biogenesis via PGC-1alpha, and suppresses hepatic gluconeogenesis; a landmark 2008 preclinical study demonstrated that AICAR administration in sedentary mice increased running endurance and activated exercise-related gene expression programs without physical training, generating significant research interest in its potential as an exercise mimetic. The only published human clinical trial involved intravenous AICAR administration in patients with type 2 diabetes, where it reduced hepatic glucose output and inhibited whole-body lipolysis via AMPK, validating the pathway pharmacology in humans; the exercise-mimetic effects observed in rodents have not been replicated or evaluated in any human study, and no oral or injectable form has been assessed for human performance use in published research. AICAR is not a peptide and has no FDA approval; it is prohibited in sport by WADA, available only as a research chemical, and all performance-related interest derives from preclinical rodent data that has not been translated to human investigation; the IV metabolic effects in diabetic patients should not be extrapolated to an athletic or performance context.
AICAR Benefits & Research Areas
Regulatory & Evidence
Risk Profile
Moderate risk profile in research contexts. Review contraindications and administration guidelines before use.
Regulatory Status
- Availability Status
- Research Only
Regulatory status reflects publicly available information and may change. This is not legal or medical advice.
Research Sources
6 sources cited · 6 moderate
1 RCT · 4 Cohorts · 1 Review
Berberine Regulates Hepatic Fatty Acid Metabolism via AMPK/SIRT1/PGC-1α Pathway.
Chin J Integr Med · 2026
# Summary Research found that berberine regulates hepatic fatty acid metabolism and reduces liver lipid accumulation through activation of the AMPK/SIRT1/PGC-1α signaling pathway. This study demonstrated that berberine's effects involve modulating the expression of proteins involved in fatty acid transport, synthesis, and breakdown, with results suggesting potential therapeutic relevance for non-alcoholic fatty liver disease concurrent with type 2 diabetes.
Pharmacological inhibition of TRPM4 channel stabilizes atherosclerotic plaque via inhibiting AMPK-Beclin1-mediated autophagy.
Eur J Pharmacol · 2026
# Summary Research found that AICAR, an AMPK agonist, reversed the protective effects of TRPM4 inhibition against excessive autophagy and apoptosis in endothelial cells exposed to oxidized low-density lipoprotein. This study demonstrated that AICAR's activation of the AMPK signaling pathway could counteract the beneficial cellular responses achieved through TRPM4 channel inhibition in the atherosclerotic disease model.
MiR-27b-3p suppresses proliferation and testosterone synthesis in goat Leydig cells by activating the AMPK pathway through PPARG targeting.
Anim Reprod Sci · 2026
# Summary Research found that miR-27b-3p suppresses Leydig cell proliferation and testosterone synthesis by targeting PPARG, which in turn regulates AMPK signaling. This study demonstrated that activating AMPK through this regulatory pathway can partially restore cellular functions impaired by PPARG suppression, revealing a molecular mechanism relevant to testicular development and reproductive function in male goats.
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Protective effects of adiponectin receptor agonists against equine lamellar endoplasmic reticulum stress.
Equine Vet J · 2026
# Summary Research found that adiponectin receptor agonists, including AICAR, reduced endoplasmic reticulum stress markers in equine lamellar cells exposed to chemical stressors. This study demonstrated that these compounds decreased expression of stress-response proteins and inflammatory markers, suggesting a potential protective mechanism relevant to laminitis pathophysiology.
Targeting AMPK Networks for Male Reproductive Health: Mechanisms and Emerging Therapies.
Cells · 2026
# Summary Research found that AMPK (AMP-activated protein kinase) functions as a key regulator connecting metabolic health to male reproductive processes, including sperm production and testosterone synthesis, with dysfunction linked to reduced sperm quality and fertility issues. This study demonstrated that pharmacological agents targeting AMPK signaling pathways, including AICAR among other approaches, show promise as potential therapeutic strategies for improving male reproductive outcomes in the context of metabolic dysfunction.
Intravenous AICAR administration reduces hepatic glucose output and inhibits whole body lipolysis in type 2 diabetic patients
Diabetologia · 2008
Research in a crossover clinical trial found that intravenous AICAR administration activated the AMPK pathway, reduced hepatic glucose output, and decreased circulating free fatty acids in male patients with type 2 diabetes, demonstrating in vivo AMPK activation as a metabolic regulatory mechanism.
Where to Buy AICAR — Providers & Availability
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Frequently Asked Questions — AICAR
AICAR (5-aminoimidazole-4-carboxamide ribonucleotide; acadesine) is a non-peptide, cell-permeable nucleoside analog and prodrug that is phosphorylated intracellularly to its monophosphate form (ZMP), which mimics AMP to activate AMP-activated protein kinase (AMPK) — the primary cellular energy sensor — producing metabolic effects that partially phenocopy those of exercise and caloric restriction. AMPK activation by AICAR upregulates GLUT4 expression and glucose uptake, stimulates fatty acid oxidation, increases mitochondrial biogenesis via PGC-1alpha, and suppresses hepatic gluconeogenesis; a landmark 2008 preclinical study demonstrated that AICAR administration in sedentary mice increased running endurance and activated exercise-related gene expression programs without physical training, generating significant research interest in its potential as an exercise mimetic.
endurance, fat oxidation, mitochondrial biogenesis, AMPK activation.
Research on AICAR primarily documents effects related to endurance and fat oxidation and mitochondrial biogenesis and AMPK activation. These are areas covered in preclinical and clinical literature — individual response varies and effects depend on context of use.
3 providers in the directory currently offer AICAR.
# Summary Research found that berberine regulates hepatic fatty acid metabolism and reduces liver lipid accumulation through activation of the AMPK/SIRT1/PGC-1α signaling pathway. This study demonstrated that berberine's effects involve modulating the expression of proteins involved in fatty acid transport, synthesis, and breakdown, with results suggesting potential therapeutic relevance for non-alcoholic fatty liver disease concurrent with type 2 diabetes.