A-1098 AICAR, Free Base, >99%

Synonyms : [Acadesine] [AICA-riboside] [AIC-Riboside] [5-Aminoimidazole-4-carboxamide riboside] [GP 1-110] [Z-Riboside]

Related Terms : [Arasine] [Protara]

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  • 25 mg
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  • 26
  • 22
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  • 50 mg
  • 47
  • 43
  • 37
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  • 100 mg
  • 79
  • 73
  • 62
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  • 200 mg
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  • 129
  • 109
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  • 250 mg
  • 158
  • 147
  • 124
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  • 500 mg
  • 285
  • 266
  • 225
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  • 1 g
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  • 496
  • 420
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  • 2 g
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  • 928
  • 785
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  • M.W. 258.23
  • C9H14N4O5
  • [2627-69-2]
  • M.I. 14: 2752

Storage: Store at or below -20 ºC. Solubility: Soluble in DMSO at 40 mg/mL; soluble in ethanol at 2 mg/mL with warming; soluble in water at 20 mg/mL with warming; buffers, serum, or other additives may increase or decrease the aqueous solubility. Disposal: A.

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  • AICAR, also known as acadesine, is an adenosine regulating agent and AMPK activator.
  • Treatment with AICAR before and during coronary artery bypass graft surgery in patients reduced early cardiac death, perioperative myocardial infarction, and combined adverse cardiovascular outcomes. Mangano, D.T. "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." J.A.M.A. 277: 325-332 (1997).
  • Perfusion of rat hindlimbs with medium containing AICAR was found to activate AMP-activated protein kinase (AMPK) in skeletal muscle, inhibit acetyl-CoA carboxylase, reduce malonyl-CoA, and increase fatty acid oxidation and glucose uptake. Merrill, G.F., et al. "AICA riboside increases AMP-activated protein kinase, fatty acid oxidation, and glucose uptake in rat muscle." Am. J. Physiol. 273: E1107-E1112 (1997).
  • After 45 minutes of blocking of a side branch of the left coronary artery in the dog, the ischemic area was reperfused for 3 hours and needle biopsies were taken for biochemical analysis. Adenine nucleotide de novo synthesis was shown to be very slow and it was doubled after ischemia. Adenine nucleotide synthesis was improved 5-fold by ribose (the basic substrate of the adenine nucleotide de novo synthesis), 9-fold by AICAR (an intermediate of the adenine nucleotide de novo synthesis), and 90-fold by adenosine (a substrate of the nucleotide salvage pathway). Mauser, M., et al. "Influence of ribose, adenosine, and "AICAR" on the rate of myocardial adenosine triphosphate synthesis during reperfusion after coronary artery occlusion in the dog." Circ. Res. 56: 220-230 (1985).
  • AICAR increased glucose uptake and the translocation of the glucose transporter likely by activating AMPK. Bergeron, R., et al. "Effect of AMPK activation on muscle glucose metabolism in conscious rats." Am. J. Physiol. 276: E938-E944 (1999).
  • Acute AICAR treatment inhibited hormone-sensitive lipase phosphorylation and activation, and had similar antilipolytic effects on both visceral and subcutaneous adipocytes. Anthony, N.M., et al. "Regulation of visceral and subcutaneous adipocyte lipolysis by acute AICAR-induced AMPK activation." Obesity 17: 1312-1317 (2009).
  • The effects of AICAR on insulin action were determined in insulin-resistant high-fat-fed rats. AICAR enhanced the glucose infusion rate during the clamp. Insulin-stimulated glucose uptake was improved by AICAR in white but not in red quadriceps, whereas glycogen synthesis was improved by AICAR in both red and white quadriceps. AICAR increased insulin suppressibility of hepatic glucose output. Thus, AICAR or similar compounds may have potential in treating insulin-resistant states and type 2 diabetes. Iglesias, M.A., et al. "AICAR administration causes an apparent enhancement of muscle and liver insulin action in insulin-resistant high-fat-fed rats." Diabetes 51: 2886-2894 (2002).
  • AICAR was found to be a proficient cytotoxic agent in acute lymphoblastic leukemia cells. The mechanisms of its anti-proliferative and apoptotic effect appeared to be through activation of p38-MAPK pathway, enhanced expression of cell cycle inhibitory proteins p27 and p53, and downstream effects on the mTOR pathway. Sengupta, T.K., et al. "Cytotoxic effect of 5-aminoimidazole-4-carboxamide-1-beta-4-ribofuranoside (AICAR) on childhood acute lymphoblastic leukemia (ALL) cells: implication for targeted therapy." Mol. Cancer 6: 46 (2007).
  • NOMENCLATURE: The names "AICAR" and "Acadesine" have been used by various vendors in conflicting ways, to describe either the non-phosphorylated compound or the 5'-phosphorylated compound. Our AICAR product is the non-phosphorylated compound, and we have chosen to use "AICAR" as our product name because that name has become the more widely used of the two names for the unphosphorylated compound.
  • AICAR was the active ingredient in drug formulations apparently prepared for human clinical trials and referred to under the trade names Arasine® and Protara®. NOTE: THE AICAR, FREE BASE RESEARCH COMPOUND SOLD BY LC LABORATORIES IS NOT ARASINE® NOR PROTARA®, AND IS NOT FOR HUMAN USE.
  • Sold for laboratory or manufacturing purposes only; not for human, veterinary, food, or household use.
  • This product is offered for R&D use in accordance with (i) 35 USC 271(e)+A13(1) in the U.S.; (ii) Section 69.1 of Japanese Patent Law in Japan; (iii) Section 11, No. 2 of the German Patent Act of 1981 in Germany; (iv) Section 60, Paragraph 5b of the U.K. Patents Act of 1977 in the U.K.; (v) Sections 55.2(1) and 55.2(6) and other common law exemptions of Canadian patent law; (vi) Section 68B of the Patents Act of 1953 in New Zealand together with the amendment of same by the Statutes Amendment Bill of 2002; (vii) such related legislation and/or case law as may be or become applicable in the aforementioned countries; and (viii) such similar laws and rules as may apply in various other countries.
  • Not available in some countries; not available to some institutions; not available for some uses.