AICAR
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AICAR

AICAR

Product Description

AICAR (Acadesine) is a potent AMPK activator, known as an "exercise-mimetic molecule". It has been extensively studied in the fields of metabolic regulation, cardiovascular protection, and athletic performance, but it is not approved for human therapeutic use and is a prohibited substance under anti-doping rules.
I. Basic Information
Full Name: 5‑Aminoimidazole‑4‑carboxamide 1‑β‑D‑ribofuranoside
CAS Number: 2627‑69‑2
Molecular Formula: C₉H₁₄N₄O₅
Molecular Weight: 258.23
Properties: A cell-permeable adenosine analog, soluble in water and DMSO
II. Core Mechanism of Action
After entering cells, AICAR is phosphorylated to ZMP, which mimics AMP to activate AMPK (AMP‑activated protein kinase) without altering intracellular ATP/ADP/AMP levels.
  • Energy metabolic reprogramming: Activates AMPK, inhibits anabolism, promotes catabolism, and improves energy utilization efficiency.
  • Glucose uptake: Promotes insulin‑independent GLUT4 translocation in skeletal muscle, increases glucose uptake, and improves insulin sensitivity.
  • Lipid metabolism regulation: Inhibits adipogenesis, promotes lipolysis, upregulates adiponectin, and alleviates adipose tissue inflammation.
  • Cardiovascular protection: Reduces calcium overload, inhibits ROS and inflammation during ischemia‑reperfusion, and decreases myocardial infarct size.
  • Anti‑inflammation and autophagy: Inhibits pro‑inflammatory factors such as TNF‑α and IL‑6, and regulates autophagy and mitophagy.
III. Major Research and Applications
  1. Metabolic Diseases (Diabetes, Obesity, Metabolic Syndrome)
    Animal studies have shown that it improves insulin resistance, lowers blood glucose, reduces hepatic gluconeogenesis, and alleviates fatty liver disease.
    Mechanism: Activates AMPK→GLUT4 translocation→increased glucose uptake; inhibits PEPCK and FBP1→decreased hepatic glucose output.
  2. Cardiovascular Diseases
    Myocardial ischemic preconditioning: Reduces infarct size, ameliorates reperfusion injury, and lowers the risk of arrhythmias.
    Mechanism: Activates AMPK→opens ATP‑sensitive K⁺ channels→shortens action potential duration→reduced calcium overload.

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