AICAR
AICAR is a cell-permeable, allosteric activator of AMP-activated protein kinase (AMPK).
AMPK is a heterodimeric protein serine/threonine kinase that regulates the energy status of cells to protect cell from metabolic stress. AMPK phosphorylates various metabolic enzymes to activate catabolic pathways (e.g. ketogenesis) and block anabolic pathways (e.g. protein synthesis).
In rat primary astrocytes, microglia, and peritoneal macrophages, AICAR does-dependently inhibits the LPS-induced production of TNFα, IL-1β, and IL-6. AICAR treatment also blocks LPS-induced nitrite production and iNOS gene expression in those cells in a dose-dependent manner by activation of AMPK. Moreover, AICAR inhibits the LPS-induced C/EBP nuclear relocation via downregulating the expression of C/EBP-δ. [1]
In LPS-injected rats, AICAR treatment abolishes LPS-mediated increased levels of IL-1β and IFN-γ in serum. AICAR treatment also strongly inhibits the LPS-induced expression of iNOS in peritoneal macrophages isolated from these rats. Furthermore, the intraperitoneal injection of LPS significantly induces the expression of TNFα, IL-1β, and IFN-γ message in the rat spleen.
Reference:
1. Giri S, Nath N, Smith B et al. 5-aminoimidazole-4-carboxamide-1-beta-4-ribofuranoside inhibits proinflammatory response in glial cells: a possible role of AMP-activated protein kinase. J Neurosci. 2004 Jan 14;24(2):479-87.
- 1. Wei Q, Zhang B, et al. "Maslinic Acid Inhibits Colon Tumorigenesis by the AMPK-mTOR Signaling Pathway." J Agric Food Chem. 2019 Apr 17;67(15):4259-4272. PMID:30913881
- 2. Chen X, Han Y, et al. "Disulfide-bond A oxidoreductase-like protein protects against ectopic fat deposition and lipid-related kidney damage in diabetic nephropathy." Kidney Int. 2019 Feb 12.pii: S0085-2538(18)30899-8. PMID:30791996
- 3. Xu N, Wang Q, et al. "Fenofibrate improves vascular endothelial function and contractility in diabetic mice." Redox Biol. 2018 Oct 1;20:87-97. PMID:30296701
| Physical Appearance | A solid |
| Storage | Store at -20°C |
| M.Wt | 258.23 |
| Cas No. | 2627-69-2 |
| Formula | C9H14N4O5 |
| Synonyms | GP 1-110 |
| Solubility | ≥12.9 mg/mL in DMSO, ≥52.9 mg/mL in H2O, <1.2 mg/mL in EtOH |
| Chemical Name | 5-amino-1-[(2R,3R,4S,5R)-3,4-dihydroxy-5-(hydroxymethyl)oxolan-2-yl]imidazole-4-carboxamide |
| SDF | Download SDF |
| Canonical SMILES | CC(C=C(C)C=CC(=O)NO)C(=O)C1=CC=C(C=C1)N(C)C |
| Shipping Condition | Evaluation sample solution : ship with blue ice.All other available size: ship with RT , or blue ice upon request |
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. |
| Cell experiment [1]: | |
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Cell lines |
Rat primary astrocytes, microglia and peritoneal macrophages |
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Preparation method |
The solubility of this compound in DMSO is limited. General tips for obtaining a higher concentration: Please warm the tube at 37 °C for 10 minutes and/or shake it in the ultrasonic bath for a while. Stock solution can be stored below -20 °C for several months. |
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Reaction Conditions |
0.01 ~ 1 mM; 2 hrs |
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Applications |
In rat primary astrocytes, microglia and peritoneal macrophages, AICAR does-dependently inhibited the LPS-induced production of TNFα, IL-1β and IL-6. |
| Animal experiment [1]: | |
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Animal models |
LPS-injected rats |
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Dosage form |
100 mg/kg; i.p. |
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Applications |
In LPS-injected rats, AICAR abolished LPS-mediated increased levels of IL-1β and IFN-γ in serum. |
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Other notes |
Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal. |
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References: [1]. Giri S, Nath N, Smith B et al. 5-aminoimidazole-4-carboxamide-1-beta-4-ribofuranoside inhibits proinflammatory response in glial cells: a possible role of AMP-activated protein kinase. J Neurosci. 2004 Jan 14;24(2):479-87. |
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Quality Control & MSDS
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Chemical structure
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