AICAR
Acadesine
CAS: 2627-69-2
Molecular Formula: C9H14N4O5
AICAR - Names and Identifiers
| Name | Acadesine |
| Synonyms | AMPK AICAR Aicar Acadesine ACADESINE AIC-Riboside AICA-RIBOSIDE AICA-riboside 5-Aminoimidazole-4-carboxamide riboside 5-Amino-4-imidazolecarboxamide ribofuranoside 5-Aminoimidazole-4-carboxamide ribonucleoside 5-Aminomidazole-4-carboxamide-1-β-D-ribofuranoside 5-Aminoimidazole-4-carboxamide-1-§-D-Ribofuranoside 5-Amino-1beta-D-ribofuranosylimidazole-4-carboxamide 5-Amino-1-beta-ribofuranosyl-imidazole-4-carboxamide 5-amino-1-(beta-D-ribofuranosyl)-1H-imidazole-4-carboxamide 5-Aminoimidazole-4-carboxamide-1-beta-D-ribofuranosideAICAR 1-Deoxy-1-[(4-carbamoyl-5-amino-1H-imidazole)-1-yl]-β-D-ribofuranose |
| CAS | 2627-69-2 |
| EINECS | 220-097-5 |
| InChI | InChI=1/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 |
| InChIKey | RTRQQBHATOEIAF-UUOKFMHZSA-N |
AICAR - Physico-chemical Properties
| Molecular Formula | C9H14N4O5 |
| Molar Mass | 258.23 |
| Density | 2.06±0.1 g/cm3(Predicted) |
| Melting Point | 214-215 °C |
| Boling Point | 726.3±60.0 °C(Predicted) |
| Flash Point | 393.1°C |
| Water Solubility | Soluble in DMSO at 2mg/ml. Soluble in water or ethanol at less than 1mg/ml |
| Solubility | H2O: >10mg/mL |
| Vapor Presure | 3.83E-22mmHg at 25°C |
| Appearance | powder |
| Color | tan |
| Maximum wavelength(λmax) | 265nm(NaOH)(lit.) |
| Merck | 14,16 |
| pKa | 13.27±0.70(Predicted) |
| Storage Condition | -20°C |
| Stability | Stable for 2 years from date? of purchase as supplied. Solutions in DMSO or distilled water may be stored at -20°C for up to 3 months. |
| Refractive Index | 1.821 |
| MDL | MFCD00869751 |
| Physical and Chemical Properties | Melting Point: 215 - 216 ℃ |
| Use | Anti-platelet aggregation drugs |
| In vitro study | ZMP in ex vivo hepatocyte extracts was increased after 30-40 minutes of academic (500 μm) treatment and remained relatively stable at approximately 4 nmol/g. Academia (500 μm) caused transient AMPK activation (12-fold) in rat hepatocytes and AMPK activation (2-3-fold) in adipocytes at 15 min. Without affecting ATP,ADP or AMP levels. Academic INE (500 μm) significantly inhibited fatty acid and sterol synthesis in rat hepatocytes. Academic (500 μm) also caused significant HMG-CoA reductase inactivation. Academic Ine dose-dependently induced apoptosis in B- CLL cells with an EC50 of 380 μm. Academic INE (0.5 mM) reduced the cell viability of B- CLL cells from 20 typical patients from 68% to 26%. Academic INE (0.5 mM) induces caspase activation and cytochrome C release from mitochondria. Uptake and phosphorylation of academic INE (0.5 mM) is required for induction of apoptosis and activation of AMPK in B- CLL cells. While academic INE (2-4 mM) only slightly affected the activity of T cells from patients B- CLL, academic INE (0.5 mM) significantly reduced B cell activity with little effect on T cell activity. [2] Academic Ine caused a decrease in cellular metabolism in K562,LAMA-84 and JURL-MK1 and was effective in killing imatinib-resistant K562 cells and Ba/F3 cells carrying the T315I-BCR-ABL mutant. The effect of academic Ine would be abolished by GF109203X and Ro-32-0432, which are classical and novel PKCs inhibitors, respectively, and thus academic Ine causes rearrangement and activation of several PKC subtypes in K562 cells. Academic Ine dose-dependently inhibited K562 colony formation at day 10, with growth inhibition already detectable at 0.25 mM and maximal inhibition at 2.5 mM. In vitro, academia elicited a decrease in CD18 expression in LPS-stimulated neutrophils. Academic INE (1 mM) significantly inhibited N-formyl-methyldisulfonyl-leucine-phenylalanine-induced upregulation of granulocyte CD11b with an average inhibition rate of 61% in blood. |
| In vivo study | In a mouse K562 cell xenograft model, academia (50 mg/kg) significantly reduced tumor formation. Academic INE (10 mg/kg) caused an increase in the fluid required to stabilize hemodynamics in pigs. In pigs, academic INE (10 mg/kg) inhibited LPS-induced protein permeation in pulmonary capillaries, suppressed peak inspiratory pressure at constant respiratory volume, and increased ineffective ventilation chambers. |
AICAR - Risk and Safety
| Risk Codes | R36/37/38 - Irritating to eyes, respiratory system and skin. R61 - May cause harm to the unborn child |
| Safety Description | S26 - In case of contact with eyes, rinse immediately with plenty of water and seek medical advice. S36 - Wear suitable protective clothing. S45 - In case of accident or if you feel unwell, seek medical advice immediately (show the label whenever possible.) S53 - Avoid exposure - obtain special instructions before use. |
| WGK Germany | 3 |
| TSCA | Yes |
| HS Code | 29349990 |
AICAR - Preparation solution concentration reference
| 1mg | 5mg | 10mg | |
|---|---|---|---|
| 1 mM | 3.873 ml | 19.363 ml | 38.725 ml |
| 5 mM | 0.775 ml | 3.873 ml | 7.745 ml |
| 10 mM | 0.387 ml | 1.936 ml | 3.873 ml |
| 5 mM | 0.077 ml | 0.387 ml | 0.775 ml |
Last Update：2024-01-02 23:10:35
AICAR - Reference Information
| Use | AICAR is a nucleoside analog, and is able to significantly increase adenosine levels during ATP breakdown. Adenosine modulators (ARAs) have been suggested to have therapeutic potential in myocardial ischemia. Cardioprotection. |
| Definition | 1-ribosyl imidazole carboxamide, in which the formamide Group is located at the 4-position of the imidazole ring, and further substituted with an amino group at position 5. Purine nucleoside analogs and activators of AMP-activated protein kinase, used in the treatment of acute lymphoblastic leukemia, have been reported to have cardioprotective effects. |
| Adenosine modulator | acarbine is a prototype of a novel compound called adenosine modulator. Acarbine is a purine nucleoside analog that enters muscle cells and is immediately phosphorylated to ZMP(AICA ribonucleotide), which is further metabolized to inosine monophosphate (adenosine triphosphate (ATP)) and a synthetic intermediate of guanine triphosphate phosphonate). Some studies support and suggest that accidesin may be a substrate for ATP synthesis and lead to myocardial ATP Supplementation, supported by some studies, while others refute. Since serine may be a precursor of myocardial ATP synthesis, it has been proposed as a possible drug for Myocardial Protection during ischemia, especially since myocardial ATP depletion is associated with cell death. |
| biological activity | AICAR (academic, NSC105823, AICA Riboside) is an activator of AMPK, causing ZMP accumulation, the stimulation effect of AMP on AMPK and AMPKK was simulated. AICAR (academic) can induce mitochondrial autophagy. Phase 3. |
| Target | TargetValue AMPK (Cell-free assay) AMPK (Cell-free assay) |
| Target | Value |
| in vitro study | increased ZMP in ex vivo hepatocyte extracts after 30-40 minutes of treatment with academic (500 μm), it remained relatively stable at approximately 4 nmol/g. Academia (500 μm) caused transient AMPK activation (12-fold) in rat hepatocytes and AMPK activation (2-3-fold) in adipocytes at 15 min. Without affecting ATP,ADP or AMP levels. Academic INE (500 μm) significantly inhibited fatty acid and sterol synthesis in rat hepatocytes. Academic (500 μm) also caused significant HMG-CoA reductase inactivation. Academic Ine dose-dependently induced apoptosis in B- CLL cells with an EC50 of 380 μm. Academic INE (0.5 mM) reduced the cell viability of B- CLL cells from 20 typical patients from 68% to 26%. Academic INE (0.5 mM) induces caspase activation and cytochrome C release from mitochondria. Uptake and phosphorylation of academic INE (0.5 mM) is required for induction of apoptosis and activation of AMPK in B- CLL cells. While academic INE (2-4 mM) only slightly affected the activity of T cells from patients B- CLL, academic INE (0.5 mM) significantly reduced B cell activity with little effect on T cell activity. [2] Academic Ine caused a decrease in cellular metabolism in K562,LAMA-84 and JURL-MK1 and was effective in killing imatinib-resistant K562 cells and Ba/F3 cells carrying the T315I-BCR-ABL mutant. The effect of academic Ine would be abolished by GF109203X and Ro-32-0432, which are classical and novel PKCs inhibitors, respectively, and thus academic Ine causes rearrangement and activation of several PKC subtypes in K562 cells. Academic Ine dose-dependently inhibited K562 colony formation at day 10, with growth inhibition already detectable at 0.25 mM and maximal inhibition at 2.5 mM. In vitro, academia elicited a decrease in CD18 expression in LPS-stimulated neutrophils. Academic INE (1 mM) significantly inhibited N-formyl-methyldisulfonyl-leucine-phenylalanine-induced upregulation of granulocyte CD11b with an average inhibition rate of 61% in blood. |
| in vivo study | Academic (50 mg/kg) significantly reduced tumor formation in a mouse K562 cell xenograft model. Academic INE (10 mg/kg) caused an increase in the fluid required to stabilize hemodynamics in pigs. In pigs, academic INE (10 mg/kg) inhibited LPS-induced protein permeation in pulmonary capillaries, suppressed peak inspiratory pressure at constant respiratory volume, and increased ineffective ventilation chambers. |
| EPA chemical substance information | information is provided by: ofmpeb.epa.gov (external link) |
Last Update：2024-04-09 21:54:55
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Product Name: Inosine Impurity 4(Acadesine) Visit Supplier Webpage Request for quotationCAS: 2627-69-2
Tel: 0714-3999186
Email: 2853786052@qq.com
Mobile: 86+15671228036
QQ: 2853786052
Wechat: 15671228036
Spot supply
Product Name: Acadesine Visit Supplier Webpage Request for quotationCAS: 2627-69-2
Tel: 18301782025
Email: 3008007409@qq.com
Mobile: 18021002903
QQ: 3008007409
Wechat: 18301782025
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