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AICARAMPK activator

AICAR

Catalog No. A8184
Size Price Stock Qty
10mM (in 1mL DMSO) $55.00 In stock
50mg $40.00 In stock
200mg $120.00 In stock
1g $350.00 In stock

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Sample solution is provided at 25 µL, 10mM.

Quality Control

Chemical structure

AICAR

Protocol

Cell experiment [1]:

Cell lines

Rat primary astrocytes, microglia and peritoneal macrophages

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.

Reaction Conditions

0.01 ~ 1 mM; 2 hrs

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]:

Animal models

LPS-injected rats

Dosage form

100 mg/kg; i.p.

Applications

In LPS-injected rats, AICAR abolished LPS-mediated increased levels of IL-1β and IFN-γ in serum.

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.

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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Chemical Properties

Cas No. 2627-69-2 SDF Download SDF
Synonyms GP 1-110
Chemical Name 5-amino-1-[(2R,3R,4S,5R)-3,4-dihydroxy-5-(hydroxymethyl)oxolan-2-yl]imidazole-4-carboxamide
Canonical SMILES CC(C=C(C)C=CC(=O)NO)C(=O)C1=CC=C(C=C1)N(C)C
Formula C9H14N4O5 M.Wt 258.23
Solubility Limited solubility Storage Store at -20°C
General tips No
Shipping Condition No

Background

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.