Catalog No.S1802 Synonyms: NSC105823
Molecular Weight(MW): 258.23
AICAR (Acadesine), an AMPK activator, results in accumulation of ZMP, which mimics the stimulating effect of AMP on AMPK and AMPK kinase. Phase 3.
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Cultured hepatocytes were treated with 10 μM Compound C (Comp.C) for 30 min before treatment with 10 μM SAL, 1 mM AICAR for 3 h. Cell lysates were immunoblotted for the phosphorylation of AMPK, ACC, Akt and GSK3β. *P < 0.05, **P < 0.01 versus control; ##P < 0.01 versus SAL alone; †P < 0.05, ††P < 0.01 versus AICAR alone. Values are means ± SEM (n = 4).
British Journal of Pharmacology, 2015, 172(13):3284–3301.. AICAR (Acadesine) purchased from Selleck.
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|Description||AICAR (Acadesine), an AMPK activator, results in accumulation of ZMP, which mimics the stimulating effect of AMP on AMPK and AMPK kinase. Phase 3.|
|Features||A potential first-in-class adenosine regulating agent (ARA).|
Acadesine (500 μM) increases the ZMP content in extracts of isolated hepatocytes after up to 30-40 min treatment, then remains fairly constant at approximately 4 nmol/g. Acadesine (500 μM) causes a transient 12-fold activation of AMPK at 15 min in rat hepatocytes and 2-3 fold activation of AMPK in adipocytes, without affecting levels of ATP, ADP or AMP. Acadesine (500 μM) causes a dramatic inhibition of both fatty acid and sterol synthesis in rat hepatocytes. Acadesine (500 μM) also causes a dramatic inactivation of HMG-CoA reductase.  Acadesine induces apoptosis of B-CLL cells in a dose-dependent manner with EC50 of 380 μM. Acadesine (0.5 mM) decreases cell viability of B-CLL cells from 20 representative patients from 68% to 26%. Acadesine (0.5 mM) induces caspase activation and cytochrome crelease from mitochondria. Uptake and phosphorylation of Acadesine (0.5 mM) are required to induce apoptosis and activate AMPK in B-CLL cells. Acadesine (2-4 mM) only slightly affects the viability of T cells from B-CLL patients, Acadesine (0.5 mM) remarkedly reduces viability of B cells but not T cells.  Acadesine triggers loss of cell metabolism in K562, LAMA-84 and JURL-MK1 and is also effective in killing imatinib-resistant K562 cells and Ba/F3 cells carrying the T315I-BCR-ABL mutation. The effect of Acadesine is abrogated by GF109203X and Ro-32-0432, both inhibitor of classical and new PKCs and accordingly, Acadesine triggers relocation and activation of several PKC isoforms in K562 cells. Acadesine dose-dependently inhibits K562 colony formation at day 10, the growth inhibitory effect of acadesine is already detected at 0.25 mM and is maximal at 2.5 mM.  Acadesine causes a concentration-related reduction in CD18 expression on LPS-stimulated neutrophils in vitro.  Acadesine significantly (1 mM) inhibits N-formyl-methionyl-leucyl-phenylalanine-induced granulocyte CD11b up-regulation by a mean of 61% in blood. 
|In vivo||Acadesine (50 mg/kg) significantly reduces tumor formation in a mouse xenograft model of K562 cells.  Acadesine (10 mg/kg) results in higher fluid required to stabilize hemodynamics in pigs. Acadesine (10 mg/kg) inhibits LPS-induced protein permeability of pulmonary capillaries, peak inspiratory pressures on constant tidal volume and dead space ventilation in pigs. |
|In vitro||DMSO||51 mg/mL (197.49 mM)|
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Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT01813838||Terminated||SMD||Groupe Francophone des Myelodysplasies|Advancell - Advanced In Vitro Cell Technologies, S.A.||June 2013||Phase 1|Phase 2|
|NCT00872001||Terminated||Coronary Artery Bypass|Myocardial Infarction|Ventricular Dysfunction, Left|Stroke|Cardiopulmonary Bypass||Merck Sharp & Dohme Corp.|Duke Clinical Research Institute||April 2009||Phase 3|
|NCT00559624||Completed||Leukemia, B-Cell, Chronic||Advancell - Advanced In Vitro Cell Technologies, S.A.|Nexus Oncology Ltd||December 2007||Phase 1|Phase 2|
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