AICAR phosphateAMPK activator CAS# 681006-28-0 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 681006-28-0 | SDF | Download SDF |
PubChem ID | 78357776 | Appearance | Powder |
Formula | C9H17N4O9P | M.Wt | 356.23 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Synonyms | Acadesine phosphate; AICA Riboside phosphate | ||
Solubility | H2O : ≥ 180 mg/mL (505.29 mM) DMSO : ≥ 75 mg/mL (210.54 mM) *"≥" means soluble, but saturation unknown. | ||
Chemical Name | 5-amino-1-[(2R,3S,5R)-3,4-dihydroxy-5-(hydroxymethyl)oxolan-2-yl]imidazole-4-carboxamide;phosphoric acid | ||
SMILES | C1=NC(=C(N1C2C(C(C(O2)CO)O)O)N)C(=O)N.OP(=O)(O)O | ||
Standard InChIKey | BPVGMEHURDEDAZ-CODPYOKSSA-N | ||
Standard InChI | InChI=1S/C9H14N4O5.H3O4P/c10-7-4(8(11)17)12-2-13(7)9-6(16)5(15)3(1-14)18-9;1-5(2,3)4/h2-3,5-6,9,14-16H,1,10H2,(H2,11,17);(H3,1,2,3,4)/t3-,5?,6+,9-;/m1./s1 | ||
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. |
Description | AICAR phosphate is an activator of AMP-activated protein kinase (AMPK), down-regulates the insulin receptor expression in HepG2 cells.In Vitro:HepG2 cells are treated with various concentrations of AICAR (0.1-1.0 mM) for 12, 24, and 48 h, respectively. The expression level of IR-β significantly decreases with 0.25, 0.5, and 1.0 mM of AICAR at 48 h to 50%, 53%, and 46% of the control, respectively[1].In Vivo:Fourteen-week-old male, lean (L; 31.3 g body wt) wild-type andob/ob (O; 59.6 g body wt) mice are injected with the AMP-activated kinase (AMPK) activator AICAR (A) at 0.5 mg*g body wt-1*day-1 or saline control (C) for 14 days. At 24 h after the last injection (including a 12-h fast), all mice are killed, and the plantar flexor complex muscle (gastrocnemius, soleus, and plantaris) is excised for analysis. Muscle mass is lower in OC (159±12 mg) than LC, LA, and OA (176±10, 178±9, and 166±16 mg, respectively) mice, independent of a body weight change[2]. The kidney weight is significantly higher in the untreated group when compared with both the exercise and AICAR (0.5 mg/g body wt) groups. The heart weight is higher in the exercise group than in the other groups, whereas the liver weight is significantly higher in the AICAR-treated group when compared with the exercise and untreated groups[3]. References: |
AICAR phosphate Dilution Calculator
AICAR phosphate Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 2.8072 mL | 14.0359 mL | 28.0718 mL | 56.1435 mL | 70.1794 mL |
5 mM | 0.5614 mL | 2.8072 mL | 5.6144 mL | 11.2287 mL | 14.0359 mL |
10 mM | 0.2807 mL | 1.4036 mL | 2.8072 mL | 5.6144 mL | 7.0179 mL |
50 mM | 0.0561 mL | 0.2807 mL | 0.5614 mL | 1.1229 mL | 1.4036 mL |
100 mM | 0.0281 mL | 0.1404 mL | 0.2807 mL | 0.5614 mL | 0.7018 mL |
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. |
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AICAR phosphate (Acadesine)is an activator of AMPK [1].
AICAR phosphate has been reported to induce apoptosis in a dose-dependent fashion and that the EC50 value is 380±60μM on the viability assay of B-CLL cells. In addition, AICAR phosphate has been revealed to induce caspase activation and cytochrome c release from mitochondria in B-CLL cells. Furthermore, AICAR phosphate has shown that uptake and phosphorylation are required to induce apoptosis and activate AMPK. Apart from these, AICAR phosphate (2-4 mM) has shown to only slightly affects the viability of T cells from B-CLL patients, AICAR phosphate (0.5 mM) has been noted to remarkedly reduces viability of B cells but not T cells [1].
References:
[1] Campàs C1, Lopez JM, Santidrián AF, Barragán M, Bellosillo B, Colomer D, Gil J. Acadesine activates AMPK and induces apoptosis in B-cell chronic lymphocytic leukemia cells but not in T lymphocytes. Blood. 2003 May 1;101(9):3674-80. Epub 2003 Jan 9.
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Neuroprotective effect of activated 5'-adenosine monophosphate-activated protein kinase on cone system function during retinal inflammation.[Pubmed:27287531]
BMC Neurosci. 2016 Jun 10;17(1):32.
BACKGROUND: Retinal inflammation can cause retinal neural disorders. In particular, functional disorder in the cone photoreceptor system influences visual acuity. However, the underlying mechanism is not yet fully understood. In this study, we evaluated cone system function and the role of 5'-adenosine monophosphate-activated protein kinase (AMPK) during retinal inflammation. RESULTS: Six to eight-week-old male C57BL/6 mice received an intraperitoneal injection of lipopolysaccharide (LPS) to induce retinal inflammation, and were treated with an AMPK activator, 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR; 250 mg/kg body weight) or phosphate-buffered saline as vehicle 3 h before the LPS injection. The b-wave of the photopic electroretinogram, which represents cone system function, was decreased 24 h after LPS injection and this reduction was suppressed by AICAR treatment. At this time point, there was no remarkable morphological change in the cone photoreceptor cells. At 1.5 h after LPS injection, the retina mRNA levels of an inflammatory cytokine, Tnf-alpha, were increased, and those of a regulator of mitochondrial biogenesis, Pgc1-alpha, were decreased. However, AICAR treatment suppressed these changes in mRNA expression. Immunohistochemistry showed that induction of glial fibrillary acidic protein expression was also suppressed by AICAR 24 h after LPS injection. Furthermore, the mouse cone photoreceptor-derived cell line 661W was treated with AICAR to increase the level of phosphorylated and activated AMPK. After 3 h of AICAR incubation, 661W cells showed decreased Tnf-alpha mRNA levels and increased Pgc1-alpha mRNA levels. CONCLUSION: AMPK activation has a neuroprotective effect on cone system function during inflammation, and the effect may, at least in part, involve the regulation of inflammatory cytokines and mitochondrial condition.
Mogrol Derived from Siraitia grosvenorii Mogrosides Suppresses 3T3-L1 Adipocyte Differentiation by Reducing cAMP-Response Element-Binding Protein Phosphorylation and Increasing AMP-Activated Protein Kinase Phosphorylation.[Pubmed:27583359]
PLoS One. 2016 Sep 1;11(9):e0162252.
This study investigated the effects of mogrol, an aglycone of mogrosides from Siraitia grosvenorii, on adipogenesis in 3T3-L1 preadipocytes. Mogrol, but not mogrosides, suppressed triglyceride accumulation by affecting early (days 0-2) and late (days 4-8), but not middle (days 2-4), differentiation stages. At the late stage, mogrol increased AMP-activated protein kinase (AMPK) phosphorylation and reduced glycerol-3-phosphate dehydrogenase activity. At the early stage, mogrol promoted AMPK phosphorylation, inhibited the induction of CCAAT/enhancer-binding protein beta (C/EBPbeta; a master regulator of adipogenesis), and reduced 3T3-L1 cell contents (e.g., clonal expansion). In addition, mogrol, but not the AMPK activator AICAR, suppressed the phosphorylation and activity of the cAMP response element-binding protein (CREB), which regulates C/EBPbeta expression. These results indicated that mogrol suppressed adipogenesis by reducing CREB activation in the initial stage of cell differentiation and by activating AMPK signaling in both the early and late stages of this process.
GFAT1 phosphorylation by AMPK promotes VEGF-induced angiogenesis.[Pubmed:28008135]
Biochem J. 2017 Mar 7;474(6):983-1001.
Activation of AMP-activated protein kinase (AMPK) in endothelial cells regulates energy homeostasis, stress protection and angiogenesis, but the underlying mechanisms are incompletely understood. Using a label-free phosphoproteomic analysis, we identified glutamine:fructose-6-phosphate amidotransferase 1 (GFAT1) as an AMPK substrate. GFAT1 is the rate-limiting enzyme in the hexosamine biosynthesis pathway (HBP) and as such controls the modification of proteins by O-linked beta-N-acetylglucosamine (O-GlcNAc). In the present study, we tested the hypothesis that AMPK controls O-GlcNAc levels and function of endothelial cells via GFAT1 phosphorylation using biochemical, pharmacological, genetic and in vitro angiogenesis approaches. Activation of AMPK in primary human endothelial cells by 5-aminoimidazole-4-carboxamide riboside (AICAR) or by vascular endothelial growth factor (VEGF) led to GFAT1 phosphorylation at serine 243. This effect was not seen when AMPK was down-regulated by siRNA. Upon AMPK activation, diminished GFAT activity and reduced O-GlcNAc levels were observed in endothelial cells containing wild-type (WT)-GFAT1 but not in cells expressing non-phosphorylatable S243A-GFAT1. Pharmacological inhibition or siRNA-mediated down-regulation of GFAT1 potentiated VEGF-induced sprouting, indicating that GFAT1 acts as a negative regulator of angiogenesis. In cells expressing S243A-GFAT1, VEGF-induced sprouting was reduced, suggesting that VEGF relieves the inhibitory action of GFAT1/HBP on angiogenesis via AMPK-mediated GFAT1 phosphorylation. Activation of GFAT1/HBP by high glucose led to impairment of vascular sprouting, whereas GFAT1 inhibition improved sprouting even if glucose level was high. Our findings provide novel mechanistic insights into the role of HBP in angiogenesis. They suggest that targeting AMPK in endothelium might help to ameliorate hyperglycaemia-induced vascular dysfunction associated with metabolic disorders.
5-Aminoimidazole-4-carboxamide ribonucleoside-induced autophagy flux during differentiation of monocytic leukemia cells.[Pubmed:28975042]
Cell Death Discov. 2017 Oct 2;3:17066.
Pharmacological modulators of AMP-dependent kinase (AMPK) have been suggested in treatment of cancer. The biguanide metformin and 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR) have been reported to inhibit proliferation of solid tumors and hematological malignancies, but their role in differentiation is less explored. Our previous study demonstrated that AICAR alone induced AMPK-independent expression of differentiation markers in monocytic U937 leukemia cells, and no such effects were observed in response to metformin. The aim of this study was to determine the mechanism of AICAR-mediated effects and to test for the possible role of autophagy in differentiation of leukemia cells. The results showed that AICAR-mediated effects on the expression of differentiation markers were not mimicked by A769662, a more specific direct AMPK activator. Long-term incubation of U937 cells with AICAR and other differentiation agents, all-trans-retinoic acid (ATRA) and phorbol 12-myristate 13-acetate, increased the expression of the autophagy marker LC3B-II, and these effects were not observed in response to metformin. Western blot and immunofluorescence analyses of U937 cells treated with bafilomycin A1 or transfected with mRFP-GFP-LC3 proved that the increase in the expression of LC3B-II was due to an increase in autophagy flux, and not to a decrease in lysosomal degradation. 3-Methyladenine inhibited the expression of differentiation markers in response to all inducers, but had stimulatory effects on autophagy flux at dose that effectively inhibited the production of phosphatidylinositol 3-phosphate. The small inhibitory RNA-mediated down-modulation of Beclin 1 and hVPS34 had no effects on AICAR and ATRA-mediated increase in the expression of differentiation markers. These results show that AICAR and other differentiation agents induce autophagy flux in U937 cells and that the effects of AICAR and ATRA on the expression of differentiation markers do not depend on the normal levels of key proteins of the classical or canonical autophagy pathway.
AMP-Activated Kinase (AMPK) Activation by AICAR in Human White Adipocytes Derived from Pericardial White Adipose Tissue Stem Cells Induces a Partial Beige-Like Phenotype.[Pubmed:27322180]
PLoS One. 2016 Jun 20;11(6):e0157644.
Beige adipocytes are special cells situated in the white adipose tissue. Beige adipocytes, lacking thermogenic cues, morphologically look quite similar to regular white adipocytes, but with a markedly different response to adrenalin. White adipocytes respond to adrenergic stimuli by enhancing lipolysis, while in beige adipocytes adrenalin induces mitochondrial biogenesis too. A key step in the differentiation and function of beige adipocytes is the deacetylation of peroxisome proliferator-activated receptor (PPARgamma) by SIRT1 and the consequent mitochondrial biogenesis. AMP-activated protein kinase (AMPK) is an upstream activator of SIRT1, therefore we set out to investigate the role of AMPK in beige adipocyte differentiation using human adipose-derived mesenchymal stem cells (hADMSCs) from pericardial adipose tissue. hADMSCs were differentiated to white and beige adipocytes and the differentiation medium of the white adipocytes was supplemented with 100 muM [(2R,3S,4R,5R)-5-(4-Carbamoyl-5-aminoimidazol-1-yl)-3,4-dihydroxyoxolan-2-yl]meth yl dihydrogen phosphate (AICAR), a known activator of AMPK. The activation of AMPK with AICAR led to the appearance of beige-like morphological properties in differentiated white adipocytes. Namely, smaller lipid droplets appeared in AICAR-treated white adipocytes in a similar fashion as in beige cells. Moreover, in AICAR-treated white adipocytes the mitochondrial network was more fused than in white adipocytes; a fused mitochondrial system was characteristic to beige adipocytes. Despite the morphological similarities between AICAR-treated white adipocytes and beige cells, functionally AICAR-treated white adipocytes were similar to white adipocytes. We were unable to detect increases in basal or cAMP-induced oxygen consumption rate (a marker of mitochondrial biogenesis) when comparing control and AICAR-treated white adipocytes. Similarly, markers of beige adipocytes such as TBX1, UCP1, CIDEA, PRDM16 and TMEM26 remained the same when comparing control and AICAR-treated white adipocytes. Our data point out that in human pericardial hADMSCs the role of AMPK activation in controlling beige differentiation is restricted to morphological features, but not to actual metabolic changes.