Acadesine - CAS 2627-69-2
Catalog number: 2627-69-2
Category: Inhibitor
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Acadesine is a 5-aminoimidazole-4-carboxamide (AICA) riboside, a purine nucleoside analog, and a nucleotide biosynthesis precursor with B cell pro-apoptotic activity. Following cellular uptake, acadesine is phosphorylated to AICA ribotide (ZMP), which mimics 5'-adenosine monophosphate (AMP). Acadesine-induced apoptosis also appears to require cytochrome c release from mitochondria and caspase activation and is p53-independent. However, the exact mechanism of acadesine-induced apoptosis is unknown.
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AICA riboside; AICAr ; AICA-riboside; Arasine; Protara; AIC-Riboside; Z-Riboside; AICA riboside; AICA; AICAR.
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PeriCor Therapeutics; Protherics PLC; Schering-Plough.
1.[High glucose promotes gap junctional communication in cultured neonatal cardiac fibroblasts via AMPK activation].
Chen F, Zhao WT, Chen FX, Fu GS, Mou Y, Hu SJ. Mol Biol (Mosk). 2014 Jul-Aug;48(4):687-95.
Cardiac fibroblasts are known to be essential for adaptiveresponses in the patho- genesis of cardiovascular diseases, and increased intercellular communication of myocardial cells and cardiac fibroblasts acts as a crucial factor in maintaining the functional integrity of the heart. AMP-activated kinase (AMPK) is a key stress signaling kinase, which plays an important role in promoting cell survival and improving cell function. However, the underlying link between AMPK and gap junctional communication (GJIC) is still poorly understood. In this study, a connection between AMPK and GJIC in high glucose-mediated neonatal cardiac fibroblasts was assessed using fibroblast migration, measurement of dye transfer and connexin43 (Cx43) expression. 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR) and Compound C (CC) were used to regulate AMPK activity. The levels of cell migration and Cx43 protein expression in neonatal cardiac fibroblasts increased during high glucose treatment, accompanied by developed dye transfer.
2.5-Aminoimidazole-4-carboxamide-1-β-d-ribofuranoside alleviated carbon tetrachloride-induced acute hepatitis in mice.
Yang C1, Gong X2, Ai Q3, Ge P4, Lin L4, Zhang L5. Int Immunopharmacol. 2015 Apr;25(2):393-9. doi: 10.1016/j.intimp.2015.02.018. Epub 2015 Feb 21.
AMP-activated protein kinase (AMPK) is one of the principal cellular energy sensors participating in maintenance of energy balance but recent evidences also suggested that AMPK might be involved in the regulation of inflammation. In the present study, the AMPK activator 5-aminoimidazole-4-carboxamide-1-β-d-ribofuranoside (AICAR) was used to investigate the potential roles of AMPK in carbon tetrachloride (CCl4)-induced acute hepatitis. The experimental data indicated that treatment with AICAR significantly decreased the elevation of plasma aminotransferases and alleviated hepatic histological abnormalities in CCl4-exposed mice. Treatment with AICAR also inhibited the increase of myeloperoxidase (MPO), the induction of TNF-α, IL-6, inducible nitric oxide synthase (iNOS), nitric oxide and the upregulation of matrix metalloproteinase 2 (MMP-2), MMP-3 and MMP-9 in mice exposed to CCl4. These effects were associated with suppressed nuclear accumulation of NF-κB p65.
3.Bcl-2high mantle cell lymphoma cells are sensitized to acadesine with ABT-199.
Montraveta A1, Xargay-Torrent S1, Rosich L1, López-Guerra M1,2, Roldán J1, Rodríguez V1, Lee-Vergés E1, de Frías M3, Campàs C3, Campo E2, Roué G1, Colomer D1,2. Oncotarget. 2015 Aug 28;6(25):21159-72.
Acadesine is a nucleoside analogue with known activity against B-cell malignancies. Herein, we showed that in mantle cell lymphoma (MCL) cells acadesine induced caspase-dependent apoptosis through turning on the mitochondrial apoptotic machinery. At the molecular level, the compound triggered the activation of the AMPK pathway, consequently modulating known downstream targets, such as mTOR and the cell motility-related vasodilator-stimulated phosphoprotein (VASP). VASP phosphorylation by acadesine was concomitant with a blockade of CXCL12-induced migration. The inhibition of the mTOR cascade by acadesine, committed MCL cells to enter in apoptosis by a translational downregulation of the antiapoptotic Mcl-1 protein. In contrast, Bcl-2 protein levels were unaffected by acadesine and MCL samples expressing high levels of Bcl-2 tended to have a reduced response to the drug. Targeting Bcl-2 with the selective BH3-mimetic agent ABT-199 sensitized Bcl-2high MCL cells to acadesine.
4.Predictors of contemporary coronary artery bypass grafting outcomes.
Weisel RD1, Nussmeier N2, Newman MF3, Pearl RG4, Wechsler AS5, Ambrosio G6, Pitt B7, Clare RM3, Pieper KS3, Mongero L8, Reece TL3, Yau TM9, Fremes S10, Menasché P11, Lira A12, Harrington RA4, Ferguson TB13; RED-CABG Executive and Steering Committees. J Thorac Cardiovasc Surg. 2014 Dec;148(6):2720-6.e1-2. doi: 10.1016/j.jtcvs.2014.08.018. Epub 2014 Aug 14.
OBJECTIVES: The study objective was to identify the predictors of outcomes in a contemporary cohort of patients from the Reduction in cardiovascular Events by acaDesine in patients undergoing CABG (RED-CABG) trial. Despite the increasing risk profile of patients who undergo coronary artery bypass grafting, morbidity and mortality have remained low, and identification of the current predictors of adverse outcomes may permit new treatments to further improve outcomes.
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CAS 2627-69-2 Acadesine

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