AICAR: The "Metabolic Master" Simulating Energy Crises
I. Product Origin
AICAR (5-aminoimidazole-4-formamide ribonucleoside), also known as acadesine, was initially discovered as a key intermediate in the de novo synthesis pathway of purine nucleotides. Scientists, while studying cellular energy metabolism, discovered that this adenosine analog can penetrate cell membranes and be converted into ZMP within the cell. ZMP's structure is extremely similar to AMP, allowing it to "trick" cells into believing they are in a state of energy deficiency (such as hypoxia or glucose deficiency), thereby activating the cell's energy master switch-AMPK. This unique mechanism has transformed it from a mere biochemical intermediate into an indispensable star molecule in the field of metabolic research.
II. Product Parameters
Chemical Name: 5-Aminoimidazole-4-carboxamide 1-β-D-ribofuranoside
Synonyms: Acadesine, AICA Riboside, NSC105823
CAS No.: 2627-69-2
Molecular Formula: C₉H₁₄N₄O₅
Molecular Weight: 258.23 Da
Appearance: White or off-white powder
Purity: ≥98% or ≥99% (HPLC)
Solubility: Easily soluble in water (>7mg/ml), DMSO (20mg/ml), slightly soluble in ethanol.
Storage Conditions: Powder can be stored at -20℃ for 3 years; solution can be stored at -20℃ protected from light for up to 3 months.
III. Core Functions
Activation of the AMPK pathway: As a classic AMPK agonist, it does not alter ATP/ADP levels, but rather directly binds to and activates AMPK by mimicking AMP, initiating the cell's "energy-saving mode."
Regulation of glucose and lipid metabolism: Promotes non-insulin-dependent glucose uptake in skeletal muscle, increases fatty acid oxidation, and simultaneously inhibits hepatic gluconeogenesis and fatty acid synthesis.
Induction of autophagy and mitophagy: Relieves mTOR inhibition of autophagy through the AMPK/mTOR signaling axis, promoting cellular clearance of damaged proteins and organelles and maintaining homeostasis.
Anti-inflammatory and antioxidant effects: Inhibits the NF-κB pathway, reducing the release of pro-inflammatory factors such as TNF-α and IL-6; and enhances cellular antioxidant capacity through the p62/NRF2 pathway.
IV. Core Advantages
Dual regulatory mechanism: It can act through the classical AMPK pathway, and under specific conditions (such as protecting cardiomyocytes from doxorubicin toxicity), it exhibits a unique AMPK-independent protective effect.
Multi-target effects: In addition to AMPK, it can also affect YAP protein localization, regulate PPARα transcription, and even act as an autophagy inhibitor or agonist (depending on cell type and concentration), making it highly applicable.
High cell permeability: As a nucleoside analog, it can easily cross cell membranes and has a rapid onset of action in in vitro experiments without the need for transfection reagents.
**Broad Tool Value:** It is one of the "gold standard" drug tools for studying metabolic syndrome, cancer, inflammation, and autophagy mechanisms.
V. Applicable Scenarios
Metabolic Disease Research: Used to construct in vitro/in vivo models of type 2 diabetes, obesity, and fatty liver, and to explore the mechanisms of insulin resistance reversal.
Oncology Research: Investigates the inhibitory effects of the AMPK pathway on cancer cell proliferation, apoptosis, and metastasis, particularly widely used in leukemia, breast cancer, and prostate cancer research.
Cardiovascular and Pulmonary Diseases: Explores its tissue-protective effects in myocardial infarction, pulmonary fibrosis, and acute lung injury.
Exercise Physiology: Simulates metabolic adaptations induced by exercise training, studying the effects of "exercise mimics" on muscle endurance and glucose utilization.
VI. Precautions
Solution Preparation: Aqueous solutions are unstable and should be prepared and used immediately. If prepared as a DMSO stock solution, it should be aliquoted and frozen to avoid degradation due to repeated freeze-thaw cycles.
Concentration Optimization: Different cell lines show significant differences in sensitivity to AICAR (common range 0.5-5 mM). Literature review and preliminary experiments are necessary to determine the optimal concentration before use.
VII. Success Stories
In a study on silicosis, researchers induced a rat model of pulmonary fibrosis using bleomycin or silica. Results showed that AICAR treatment significantly reduced the degree of fibrosis in lung tissue and decreased the levels of inflammatory factors. Mechanistic studies revealed that AICAR inhibits NOX4-mediated reactive oxygen species production by activating the AMPK signaling pathway, thereby blocking the epithelial-mesenchymal transition. This study confirms the important value of AICAR as a potential anti-fibrotic agent in respiratory disease research.
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