AcipimoxCAS# 51037-30-0 |
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 51037-30-0 | SDF | Download SDF |
PubChem ID | 39880 | Appearance | Powder |
Formula | C6H6N2O3 | M.Wt | 154.12 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Synonyms | K-9321 | ||
Solubility | DMSO : ≥ 100 mg/mL (648.85 mM) H2O : 20 mg/mL (129.77 mM; Need ultrasonic) *"≥" means soluble, but saturation unknown. | ||
Chemical Name | 6-methyl-1-oxidopyrazin-1-ium-2-carboxylic acid | ||
SMILES | CC1=[N+](C(=CN=C1)C(=O)O)[O-] | ||
Standard InChIKey | DNRXJHATQULEHC-UHFFFAOYSA-N | ||
Standard InChI | InChI=1S/C6H6N2O3/c1-4-2-7-3-5(6(9)10)8(4)11/h2-3H,1H3,(H,9,10) | ||
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 | Antilipolytic agent; lowers plasma free fatty acid (FFA), triglyceride (TG), glucose and insulin levels and increases leptin levels. |
Acipimox Dilution Calculator
Acipimox Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 6.4885 mL | 32.4423 mL | 64.8845 mL | 129.769 mL | 162.2113 mL |
5 mM | 1.2977 mL | 6.4885 mL | 12.9769 mL | 25.9538 mL | 32.4423 mL |
10 mM | 0.6488 mL | 3.2442 mL | 6.4885 mL | 12.9769 mL | 16.2211 mL |
50 mM | 0.1298 mL | 0.6488 mL | 1.2977 mL | 2.5954 mL | 3.2442 mL |
100 mM | 0.0649 mL | 0.3244 mL | 0.6488 mL | 1.2977 mL | 1.6221 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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Kinetics and utilization of lipid sources during acute exercise and acipimox.[Pubmed:24895285]
Am J Physiol Endocrinol Metab. 2014 Jul 15;307(2):E199-208.
Overweight is associated with abnormalities of lipid metabolism, many of which are reversed by exercise. We investigated the impact of experimental antilipolysis and acute exercise on lipid kinetics and oxidation from VLDL-TG, plasma FFA, and "residual lipids" in overweight men (n = 8) using VLDL-TG and palmitate tracers in combination with muscle biopsies in a randomized, placebo-controlled design. Participants received placebo or Acipimox on each study day (4 h of rest, 90 min of exercise at 50% V(O(2 max))). Exercise suppressed VLDL-TG secretion significantly during placebo but not Acipimox (placebo-rest: 64.2 +/- 9.4; placebo-exercise: 48.3 +/- 8.0; Acipimox-rest: 55.2 +/- 13.4; Acipimox-exercise: 52.0 +/- 10.9). Resting oxidation of VLDL-TG FA and FFA was significantly reduced during Acipimox compared with placebo, whereas "residual lipid oxidation" increased significantly [VLDL-TG oxidation (placebo: 18 +/- 3 kcal/h; Acipimox: 11 +/- 2 kcal/h), FFA oxidation (placebo: 14 +/- 2 kcal/h; Acipimox: 4 +/- 0.5 kcal/h), and residual lipid oxidation (placebo: 3 +/- 5 kcal/h; Acipimox: 14 +/- 5 kcal/h)]. Additionally, during exercise on both placebo and Acipimox, oxidation of VLDL-TG and FFA increased, but the relative contribution to total lipid oxidation diminished, except for FFA, which remained unchanged during Acipimox. Residual lipid oxidation increased significantly during exercise in both absolute and relative terms. Changes in selected cellular enzymes and proteins provided no explanations for kinetic changes. In conclusion, suppressed FFA availability blunts the effect of exercise on VLDL-TG secretion and modifies the contribution of lipid sources for oxidation.
Effect of Dapagliflozin With and Without Acipimox on Insulin Sensitivity and Insulin Secretion in T2DM Males.[Pubmed:26765576]
J Clin Endocrinol Metab. 2016 Mar;101(3):1249-56.
AIM: To investigate the effect of lowering the plasma glucose and free fatty acid (FFA) concentrations with dapagliflozin and Acipimox, respectively, on insulin sensitivity and insulin secretion in T2DM individuals. METHODS: Fourteen male T2DM patients received an oral glucose tolerance test and euglycemic hyperinsulinemic clamp at baseline and were treated for 3 weeks with dapagliflozin (10 mg per day). During week 3, Acipimox (250 mg four times per day) treatment was added to dapagliflozin. The oral glucose tolerance test and insulin clamp were repeated at the end of weeks 2 and 3. RESULTS: Dapagliflozin caused glucosuria and significantly lowered the plasma glucose concentration (by 35 mg/dL; P < .01), whereas the fasting plasma FFA concentration was unaffected. Acipimox caused a further decrease in the fasting plasma glucose concentration (by 20 mg/dL; P < .01) and a significant decrease in the fasting plasma FFA concentration. Compared to baseline, insulin-mediated glucose disposal increased significantly at week 2 (from 4.48 +/- 0.50 to 5.30 +/- 0.50 mg/kg . min; P < .05). However, insulin-mediated glucose disposal at week 3 (after the addition of Acipimox) did not differ significantly from that at week 2. Glucose-stimulated insulin secretion at week 2 increased significantly compared to baseline, and it increased further and significantly at week 3 compared to week 2. CONCLUSION: Lowering the plasma glucose concentration with dapagliflozin improves both insulin sensitivity and beta-cell function, whereas lowering plasma FFA concentration by addition of Acipimox to dapagliflozin improves beta-cell function without significantly affecting insulin sensitivity.
Evidence for a direct effect of the NAD+ precursor acipimox on muscle mitochondrial function in humans.[Pubmed:25352640]
Diabetes. 2015 Apr;64(4):1193-201.
Recent preclinical studies showed the potential of nicotinamide adenine dinucleotide (NAD(+)) precursors to increase oxidative phosphorylation and improve metabolic health, but human data are lacking. We hypothesize that the nicotinic acid derivative Acipimox, an NAD(+) precursor, would directly affect mitochondrial function independent of reductions in nonesterified fatty acid (NEFA) concentrations. In a multicenter randomized crossover trial, 21 patients with type 2 diabetes (age 57.7 +/- 1.1 years, BMI 33.4 +/- 0.8 kg/m(2)) received either placebo or Acipimox 250 mg three times daily dosage for 2 weeks. Acipimox treatment increased plasma NEFA levels (759 +/- 44 vs. 1,135 +/- 97 mumol/L for placebo vs. Acipimox, P < 0.01) owing to a previously described rebound effect. As a result, skeletal muscle lipid content increased and insulin sensitivity decreased. Despite the elevated plasma NEFA levels, ex vivo mitochondrial respiration in skeletal muscle increased. Subsequently, we showed that Acipimox treatment resulted in a robust elevation in expression of nuclear-encoded mitochondrial gene sets and a mitonuclear protein imbalance, which may indicate activation of the mitochondrial unfolded protein response. Further studies in C2C12 myotubes confirmed a direct effect of Acipimox on NAD(+) levels, mitonuclear protein imbalance, and mitochondrial oxidative capacity. To the best of our knowledge, this study is the first to demonstrate that NAD(+) boosters can also directly affect skeletal muscle mitochondrial function in humans.
Metabolic Effects of Long-Term Reduction in Free Fatty Acids With Acipimox in Obesity: A Randomized Trial.[Pubmed:26691888]
J Clin Endocrinol Metab. 2016 Mar;101(3):1123-33.
CONTEXT: Increased circulating free fatty acids (FFAs) have been proposed to contribute to insulin resistance in obesity. Short-term studies have investigated the effects of Acipimox, an inhibitor of hormone-sensitive lipase, on glucose homeostasis, but longer-term studies have not been performed. OBJECTIVE: To test the hypothesis that long-term treatment with Acipimox would reduce FFA and improve insulin sensitivity among nondiabetic, insulin-resistant, obese subjects. DESIGN, SETTING, PATIENTS, AND INTERVENTION: At an academic medical center, 39 obese men and women were randomized to Acipimox 250 mg thrice-daily vs identical placebo for 6 months. MAIN OUTCOME MEASURES: Plasma lipids, insulin sensitivity, adiponectin, and mitochondrial function via assessment of the rate of post-exercise phosphocreatine recovery on (31)P-magnetic resonance spectroscopy as well as muscle mitochondrial density and relevant muscle gene expression. RESULTS: Fasting glucose decreased significantly in Acipimox-treated individuals (effect size, -6 mg/dL; P = .02), in parallel with trends for reduced fasting insulin (effect size, -6.8 muU/mL; P = .07) and HOMA-IR (effect size, -1.96; P = .06), and significantly increased adiponectin (effect size, +668 ng/mL; P = .02). Acipimox did not affect insulin-stimulated glucose uptake, as assessed by euglycemic, hyperinsulinemic clamp. Effects on muscle mitochondrial function and density and on relevant gene expression were not seen. CONCLUSION: These data shed light on the long-term effects of FFA reduction on insulin sensitivity, other metabolic parameters, and muscle mitochondrial function in obesity. Reduced FFA achieved by Acipimox improved fasting measures of glucose homeostasis, lipids, and adiponectin but had no effect on mitochondrial function, mitochondrial density, or muscle insulin sensitivity.
Acipimox stimulates leptin production from isolated rat adipocytes.[Pubmed:12176665]
J Endocrinol. 2002 Aug;174(2):267-72.
Acipimox is a nicotinic acid-derived antilipolytic drug devoid of major side effects, and has been used in a number of human trials. This work reports the effects of Acipimox on leptin production from isolated rat adipocytes, in comparison with nicotinic acid and insulin. For cells isolated from normal animals, all these three reagents stimulated leptin release to a similar extent. Acipimox and nicotinic acid were more potent than insulin in stimulating leptin release from cells isolated from diabetic animals, probably because of impaired insulin sensitivity in cells from these diseased animals. Co-incubation of Acipimox with norepinephrine or dibutyryl cAMP diminished its stimulatory effects on leptin release, in parallel with increased lipolysis, suggesting that intracellular free fatty acids play an important role in mediating leptin production in adipocytes.