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Merck
CN

A8129

AICAR

Synonym(s):

5-Aminoimidazole-4-carboxamide 1-β-D-ribofuranoside, Acadesine, N1-(β-D-Ribofuranosyl)-5-aminoimidazole-4-carboxamide

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About This Item

Empirical Formula (Hill Notation):
C9H14N4O5
CAS Number:
Molecular Weight:
258.23
EC Number:
220-097-5
UNSPSC Code:
12352204
MDL number:
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InChI key

RTRQQBHATOEIAF-UUOKFMHZSA-N

InChI

1S/C9H14N4O5/c10-7-4(8(11)17)12-2-13(7)9-6(16)5(15)3(1-14)18-9/h2-3,5-6,9,14-16H,1,10H2,(H2,11,17)/t3-,5-,6-,9-/m1/s1

SMILES string

NC(=O)c1ncn([C@@H]2O[C@H](CO)[C@@H](O)[C@H]2O)c1N

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Biochem/physiol Actions

AICAR is a cell permeable activator of AMP-activated protein kinase (AMPK), a metabolic master regulator that is activated in times of reduced energy availability (high cellular AMP:ATP ratios) and serves to inhibit anabolic processes. In vivo, pharmacologic activation of AMPK with AICAR mimics exercise and triggers insulin-independent glucose uptake by skeletal muscle.
AICAR is a cell permeable activator of AMP-activated protein kinase (AMPK).

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Keiko Nagahara et al.
Journal of atherosclerosis and thrombosis, 23(12), 1345-1354 (2016-05-14)
The increase in monocyte chemoattractant protein-1 (MCP-1) and the decrease in adiponectin production from hypertrophic adipocytes are associated with adipose tissue inflammation and its metabolic complications. The aim of this study was to determine whether 5-aminoimidazole-4-carboxamide 1-β-D-ribofuranoside (AICAR), an adenosine
Elena Y Kochetkova et al.
Aging, 9(11), 2352-2375 (2017-11-16)
The Ras-Raf-MEK-ERK pathway plays a central role in tumorigenesis and is a target for anticancer therapy. The successful strategy based on the activation of cell death in Ras-expressing cells is associated with the suppression of kinases involved in Ras pathway.
Shigekazu Murakami et al.
Developmental cell, 51(1), 113-128 (2019-08-27)
Employing inducible genetically engineered and orthotopic mouse models, we demonstrate a key role for transcriptional regulator Yap in maintenance of Kras-mutant pancreatic tumors. Integrated transcriptional and metabolomics analysis reveals that Yap transcribes Myc and cooperates with Myc to maintain global
Ming Luo et al.
Cell metabolism, 28(1), 69-86 (2018-07-05)
Although breast cancer stem cells (BCSCs) display plasticity transitioning between quiescent mesenchymal-like (M) and proliferative epithelial-like (E) states, how this plasticity is regulated by metabolic or oxidative stress remains poorly understood. Here, we show that M- and E-BCSCs rely on

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