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AICAR is a nucleotide molecule consisting of a ribose sugar, a phosphate group, and an adenine base. It is a precursor of adenosine monophosphate (AMP), a nucleotide that plays an important role in cellular energy metabolism. AICAR has been suggested to activate AMP-activated protein kinase (AMPK), an enzyme that regulates various metabolic processes. It has been studied for its potential applications, particularly in reducing reperfusion injury after tissue ischemia and mitigating metabolic disorders.
By activating AMPK, AICAR may increase glucose uptake in skeletal muscle, enhance insulin sensitivity, and improve glucose tolerance. AICAR has also been suggested by researchers to have anti-inflammatory potential and may improve exercise performance in animal studies.
Molecular formula: C9H15N4O8/P
Molecular Weight: 338.21 g/mol
Other known titles: AICA ribonucleotide
Research and Clinical Studies
AICAR Peptide and Organ Protection
AICAR may have organ-protective potential, especially against ischemia and reperfusion injury. The nucleotide has been suggested to reduce myocardial infarction size and improve cardiac function in an animal model of myocardial ischemia-reperfusion injury.(1) The likelihood of AICAR's potential to activate AMPK and reduce oxidative stress and inflammation is high, which are key contributors to reperfusion injury.
One meta-analysis aimed to investigate the potential of AICAR on cardiovascular and cerebrovascular complications following coronary artery bypass graft (CABG) surgery.(2) The data was collected from 5 randomized, placebo-controlled, double-blind clinical trials, including 4,043 subjects. From the results, AICAR was suggested to reduce perioperative myocardial infarction, cardiac death through postoperative day 4, and the combined outcome of myocardial infarction, stroke, or cardiac death. AICAR also appeared to reduce the use of ventricular-assistance devices for severe postoperative heart failure. The study concluded, "in [subjects] undergoing CABG surgery, treatment [...] before and during surgery can reduce early cardiac death, MI, and combined adverse cardiovascular outcomes."
AICAR may have protective action in other organs as well. One study investigated the potential of AICAR, an AMPK activator, on an experimental model of ethanol-induced hepatic steatosis in rats.(3) The study observed that chronic ethanol feeding appeared to result in a histologically and biochemically fatty liver; however, upon AICAR presentation, it appeared to attenuate the degree of change in the liver. AICAR also was reported to decrease the hepatic SREBP-1c and reduce FAS expression, leading to reduced triglyceride synthesis in rat livers.
AICAR Peptide and Insulin Sensitivity
Studies suggest that AICAR may lower blood sugar and improve insulin sensitivity due to its potential to activate the AMPK inside cells and make them draw in glucose. One animal study aimed to investigate whether giving AICAR could enhance glucose transport in equine skeletal muscle.(4) Upon presentation, AICAR appeared to decrease blood glucose and increase insulin concentration without affecting lactate concentration. AICAR also was reported to increase the ratio of phosphorylated to total AMPK in skeletal muscle and upregulated GLUT8 protein expression.
A clinical trial also aimed to determine whether AICAR may stimulate glucose uptake in muscle.(5) The study involved 29 male subjects. AICAR and exercise were used to stimulate muscle AMPK activity and glucose uptake. Results expressed the possibility that AICAR and exercise may increase glucose uptake in muscle, and AICAR may also increase whole-body glucose disposal. Researchers also suggested that AICAR could potentially increase the phosphorylation of extracellular signal-regulated kinase 1/2.
Another clinical trial in ten male subjects with type 2 diabetes observed that AICAR could potentially reduce hepatic glucose output, lower blood glucose concentrations, stimulate hepatic fatty acid oxidation, and inhibit whole-body lipolysis, thereby reducing plasma-free fatty acids concentration.(6) Although AMPK phosphorylation in skeletal muscle was not reported to be increased, the researchers reported acetyl-CoA carboxylase phosphorylation to be significantly increased.
AICAR Peptide and Endurance
Studies suggest that AICAR may potentially activate AMPK, glycogen phosphorylase, and fructose-1,6-bisphosphatase.(7) Some studies have reported these potential actions may contribute to enhanced oxidative metabolism and mitochondrial biogenesis.(8) Increasing the number and function of mitochondria may benefit muscle endurance. For example, one experiment suggested that AICAR may induce metabolic genes and enhance running endurance in sedentary mice by 44%.(9) The results suggest that peptides may target the AMPK-PPARdelta pathway to enhance training adaptation or even increase endurance without exercise.
Another animal experiment(10) also reported that "Mice treated with an agonist of the AMP-activated protein kinase showed an increase in endurance compared to exercise-trained controls." Furthermore, in a mouse model for Duchene muscular dystrophy, AICAR was reported by researchers to have the potential to enhance the impact of exercise and improve muscle function, probably by stimulating autophagy.(11) An infusion of AICA-riboside resulted in increment-correlated increases in forearm blood flow but did not appear to impact glucose uptake in skeletal muscle. The increase in blood flow appeared to be mediated by nitric oxide, as an inhibitor of endothelial NO synthase attenuated it. These findings suggest that AICAR may be beneficial for improving blood flow into muscle and acting as a NO-booster, which is also an important factor for improving performance during prolonged exercise.(12)
AICAR peptide is available for research and laboratory purposes only. Please review and adhere to our Terms and Conditions before ordering.
- Cieslik, K. A., Taffet, G. E., Crawford, J. R., Trial, J., Mejia Osuna, P., & Entman, M. L. (2013). AICAR-dependent AMPK activation improves scar formation in the aged heart in a murine model of reperfused myocardial infarction. Journal of molecular and cellular cardiology, 63, 26–36. https://doi.org/10.1016/j.yjmcc.2013.07.005
- Mangano D. T. (1997). Effects of acadesine on myocardial infarction, stroke, and death following surgery. A meta-analysis of the 5 international randomized trials. The Multicenter Study of Perioperative Ischemia (McSPI) Research Group. JAMA, 277(4), 325–332. https://doi.org/10.1001/jama.277.4.325
- Tomita, K., Tamiya, G., Ando, S., Kitamura, N., Koizumi, H., Kato, S., Horie, Y., Kaneko, T., Azuma, T., Nagata, H., Ishii, H., & Hibi, T. (2005). AICAR, an AMPK activator, has protective effects on alcohol-induced fatty liver in rats. Alcoholism, clinical and experimental research, 29(12 Suppl), 240S–5S. https://doi.org/10.1097/01.alc.0000191126.11479.69
- de Laat, M. A., Robinson, M. A., Gruntmeir, K. J., Liu, Y., Soma, L. R., & Lacombe, V. A. (2015). AICAR administration affects glucose metabolism by upregulating the novel glucose transporter, GLUT8, in equine skeletal muscle. Veterinary journal (London, England : 1997), 205(3), 381–386. https://doi.org/10.1016/j.tvjl.2015.05.018
- Cuthbertson, D. J., Babraj, J. A., Mustard, K. J., Towler, M. C., Green, K. A., Wackerhage, H., Leese, G. P., Baar, K., Thomason-Hughes, M., Sutherland, C., Hardie, D. G., & Rennie, M. J. (2007). 5-aminoimidazole-4-carboxamide 1-beta-D-ribofuranoside acutely stimulates skeletal muscle 2-deoxyglucose uptake in healthy men. Diabetes, 56(8), 2078–2084. https://doi.org/10.2337/db06-1716
- Boon, H., Bosselaar, M., Praet, S. F., Blaak, E. E., Saris, W. H., Wagenmakers, A. J., McGee, S. L., Tack, C. J., Smits, P., Hargreaves, M., & van Loon, L. J. (2008). Intravenous AICAR administration reduces hepatic glucose output and inhibits whole body lipolysis in type 2 diabetic patients. Diabetologia, 51(10), 1893–1900. https://doi.org/10.1007/s00125-008-1108-7
- Višnjić D, Lalić H, Dembitz V, Tomić B, Smoljo T. AICAr, a Widely Used AMPK Activator with Important AMPK-Independent Effects: A Systematic Review. Cells. 2021 May 4;10(5):1095. doi: 10.3390/cells10051095. PMID: 34064363; PMCID: PMC8147799.
- Hardie DG. AMP-activated protein kinase: an energy sensor that regulates all aspects of cell function. Genes Dev. 2011 Sep 15;25(18):1895-908. doi: 10.1101/gad.17420111. PMID: 21937710; PMCID: PMC3185962.
- Narkar, V. A., Downes, M., Yu, R. T., Embler, E., Wang, Y. X., Banayo, E., Mihaylova, M. M., Nelson, M. C., Zou, Y., Juguilon, H., Kang, H., Shaw, R. J., & Evans, R. M. (2008). AMPK and PPARdelta agonists are exercise mimetics. Cell, 134(3), 405–415. https://doi.org/10.1016/j.cell.2008.06.051
- Goodyear, L. J. (2008). The exercise pill—too good to be true?. New England Journal of Medicine, 359(17), 1842-1844.
- Bueno Júnior, C. R., Pantaleão, L. C., Voltarelli, V. A., Bozi, L. H., Brum, P. C., & Zatz, M. (2012). Combined effect of AMPK/PPAR agonists and exercise training in mdx mice functional performance. PloS one, 7(9), e45699. https://doi.org/10.1371/journal.pone.0045699
- Bosselaar, M., Boon, H., van Loon, L. J., van den Broek, P. H., Smits, P., & Tack, C. J. (2009). Intra-arterial AICA-riboside administration induces NO-dependent vasodilation in vivo in human skeletal muscle. American journal of physiology. Endocrinology and metabolism, 297(3), E759–E766. https://doi.org/10.1152/ajpendo.00141.2009
- Dixon, R., Gourzis, J., McDermott, D., Fujitaki, J., Dewland, P., & Gruber, H. (1991). AICA-riboside: safety, tolerance, and pharmacokinetics of a novel adenosine-regulating agent. Journal of clinical pharmacology, 31(4), 342–347. https://doi.org/10.1002/j.1552-4604.1991.tb03715.x