AICAR phosphate - CAS 681006-28-0
Not Intended for Therapeutic Use. For research use only.
Category:
Inhibitor
Product Name:
AICAR phosphate
Catalog Number:
681006-28-0
Synonyms:
Acadesine phosphate; AICA Riboside phosphate
CAS Number:
681006-28-0
Description:
AICAR phosphate, is an AMP-activated protein kinase activator, which is used for the treatment of acute lymphoblastic leukemia and may have applications in treating other disorders such as diabetes. It stimulates glucose uptake and increases the activity of p38 mitogen-activated protein kinases α and β in skeletal muscle tissue, as well as suppressing apoptosis by reducing production of reactive oxygen compounds inside the cell.
Molecular Weight:
356.23
Molecular Formula:
C9H17N4O9P
COA:
Inquire
MSDS:
Inquire
Targets:
AMPK
Chemical Structure
CAS 681006-28-0 AICAR phosphate

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Reference Reading


1.Inactivation of AMPK mediates high phosphate-induced extracellular matrix accumulation via NOX4/TGFß-1 signaling in human mesangial cells.
Papadimitriou A1, Peixoto EB, Silva KC, Lopes de Faria JM, Lopes de Faria JB. Cell Physiol Biochem. 2014;34(4):1260-72. doi: 10.1159/000366336. Epub 2014 Sep 29.
BACKGROUND/AIMS: High phosphate (Pi) levels and extracellular matrix (ECM) accumulation are associated with chronic kidney disease progression. However, how high Pi levels contribute to ECM accumulation in mesangial cells is unknown. The present study investigated the role and mechanism of high Pi levels in ECM accumulation in immortalized human mesangial cells (iHMCs).
2.Uveal melanoma cell growth is inhibited by aminoimidazole carboxamide ribonucleotide (AICAR) partially through activation of AMP-dependent kinase.
Al-Moujahed A1, Nicolaou F2, Brodowska K1, Papakostas TD1, Marmalidou A1, Ksander BR3, Miller JW1, Gragoudas E1, Vavvas DG1. Invest Ophthalmol Vis Sci. 2014 Apr 29;55(7):4175-85. doi: 10.1167/iovs.13-12856.
PURPOSE: To evaluate the effects and mechanism of aminoimidazole carboxamide ribonucleotide (AICAR), an AMP-dependent kinase (AMPK) activator, on the growth of uveal melanoma cell lines.
3.Combined Treatment of MCF-7 Cells with AICAR and Methotrexate, Arrests Cell Cycle and Reverses Warburg Metabolism through AMP-Activated Protein Kinase (AMPK) and FOXO1.
Fodor T1, Szántó M1,2, Abdul-Rahman O1,2, Nagy L1,2, Dér Á3, Kiss B4, Bai P1,5,6. PLoS One. 2016 Feb 26;11(2):e0150232. doi: 10.1371/journal.pone.0150232. eCollection 2016.
Cancer cells are characterized by metabolic alterations, namely, depressed mitochondrial oxidation, enhanced glycolysis and pentose phosphate shunt flux to support rapid cell growth, which is called the Warburg effect. In our study we assessed the metabolic consequences of a joint treatment of MCF-7 breast cancer cells with AICAR, an inducer of AMP-activated kinase (AMPK) jointly with methotrexate (MTX), a folate-analog antimetabolite that blunts de novo nucleotide synthesis. MCF7 cells, a model of breast cancer cells, were resistant to the individual application of AICAR or MTX, however combined treatment of AICAR and MTX reduced cell proliferation. Prolonged joint application of AICAR and MTX induced AMPK and consequently enhanced mitochondrial oxidation and reduced the rate of glycolysis. These metabolic changes suggest an anti-Warburg rearrangement of metabolism that led to the block of the G1/S and the G2/M transition slowing down cell cycle.
4.Metabolomics Analysis Reveals that AICAR Affects Glycerolipid, Ceramide and Nucleotide Synthesis Pathways in INS-1 Cells.
ElAzzouny MA1, Evans CR2, Burant CF2, Kennedy RT3. PLoS One. 2015 Jun 24;10(6):e0129029. doi: 10.1371/journal.pone.0129029. eCollection 2015.
AMPK regulates many metabolic pathways including fatty acid and glucose metabolism, both of which are closely associated with insulin secretion in pancreatic β-cells. Insulin secretion is regulated by metabolic coupling factors such as ATP/ADP ratio and other metabolites generated by the metabolism of nutrients such as glucose, fatty acid and amino acids. However, the connection between AMPK activation and insulin secretion in β-cells has not yet been fully elucidated at a metabolic level. To study the effect of AMPK activation on glucose stimulated insulin secretion, we applied the pharmacological activator 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) to an INS-1 (832/13) β-cell line. We measured the change in 66 metabolites in the presence or absence of AICAR using different stable isotopic labeled nutrients to probe selected pathways. AMPK activation by AICAR increased basal insulin secretion and reduced the glucose stimulation index.