AICAR 50mg

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AICAR 50mg

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5-Aminoimidazole-4-carboxamide ribonucleotide or AICAR is an analogue of adenosine monophosphate. The AICAR peptide is a cell penetrable activator of AMP-activated protein kinase (AMPK), a master regulator of metabolic rate that is switched on in times of limited energy availability and works to inhibit anabolic metabolism. Inside the body, activation of AMPK with AICAR imitates that the body is exercising and this triggers insulin-independent glucose uptake by muscle cells. This makes AICAR important for improving endurance and burning stored fat. AICAR was shown to stimulate fat breakdown decades ago and causes cells to move their fat stores into small organelles called mitochondria, where they are broken down to release their stored energy [1]. Animal studies have shown that AICAR can potently activate many metabolic genes to increase exercise endurance [2]. Interestingly, the compound also increased the exercise endurance in sedentary animals [2]. In animals, the compound has also been shown to reduce tissue inflammation and promote the healing of injured and damaged tissue [3]. The use of AICAR in human trials has shown that it can improve glucose regulation in diabetic patients by changing how their bodies respond to glucose, providing evidence that AICAR is useful in prevention and treatment of type II diabetes due to its glucose regulatory properties [4]. Additionally, AICAR has been shown to protecting against cardiac ischemic injury and to improve myocardial protection during heart bypass surgery [5]. Evidence has also shown that AICAR stimulation closely mimics the metabolic changes seen in contracting muscles, even without prior exercise [6]. AICAR also acts as an anti-inflammatory and reduces inflammation by disrupting signaling molecules that cause cells to become activated in mounting an immune response [7]. In conclusion, AICAR is useful for tissue healing, burning fat, stimulating muscle contraction and for reducing inflammation.

AICAR is fast acting, but has a short-half life and is rapidly eliminated by the body. AICAR can therefore be dosed daily. The recommended AICAR dose is 25 mg either once or twice per day. AICAR should be stored at -20°C and only reconstituted in bacteriostatic water just before use. Once dissolved, AICAR can be stored in the fridge, but it is not stable for more than 24 hours once dissolved and will lose activity after this time.

AICAR has been used safely in human studies up to concentrations of 25 mg/kg with minimal side effects [8]. AICAR may provide mild side effects at the recommended dosages of 50 mg per day, however, extreme overdose of AICAR can be dangerous since it can affect blood flow to the heart. 

References 

  1. Thomson, D.M. and W.W. Winder, AMPK Control of Fat Metabolism in Skeletal Muscle. Acta physiologica (Oxford, England), 2009. 196(1): p. 147-154.
  2. Narkar, V.A., et al., AMPK and PPARδ agonists are exercise mimetics. Cell, 2008. 134(3): p. 405-415.
  3. Idrovo, J.P., et al., AICAR attenuates organ injury and inflammatory response after intestinal ischemia and reperfusion. Mol Med, 2015. 20: p. 676-83.
  4. Winder, W.W., Can Patients with Type 2 Diabetes Be Treated with AMPK-Activators? Diabetologia, 2008. 51(10): p. 1761-1764.
  5. Drew, B.G. and B.A. Kingwell, Acadesine, an adenosine-regulating agent with the potential for widespread indications. Expert Opin Pharmacother, 2008. 9(12): p. 2137-44.
  6. Miyamoto, L., et al., AICAR stimulation metabolome widely mimics electrical contraction in isolated rat epitrochlearis muscle. American Journal of Physiology-Cell Physiology, 2013. 305(12): p. C1214-C1222.
  7. Kirchner, J., B. Brüne, and D. Namgaladze, AICAR inhibits NFκB DNA binding independently of AMPK to attenuate LPS-triggered inflammatory responses in human macrophages. Scientific Reports, 2018. 8(1): p. 7801.
  8. Babraj, J.A., et al., Blunting of AICAR-induced human skeletal muscle glucose uptake in type 2 diabetes is dependent on age rather than diabetic status. American Journal of Physiology-Endocrinology and Metabolism, 2009. 296(5): p. E1042-E1048.
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