Metamizole (sodium salt)
(Synonyms: 安乃近) 目录号 : GC44167
A nonopioid prodrug
Cas No.:68-89-3
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Metamizole (sodium salt) is a nonopioid prodrug that is rapidly hydrolyzed to the metabolites 4-methylaminoantipyrine (MAA) and 4-aminoantipyrine (AA), which have analgesic and antipyretic effects. MAA has been shown to inhibit COX activity 8-9-fold more potently than AA (COX-1: IC50s = 2.6 and 20.8 µM, respectively, and COX-2: IC50s = 4.7 and 41.8 µM, respectively). These metabolites can be further acylated with arachidonic acid to form compounds that can bind to central and peripheral cannabinoid (CB1 and CB2) receptors and TRPV1 receptors at low micromolar concentrations.
| Cas No. | 68-89-3 | SDF | |
| 别名 | 安乃近 | ||
| Canonical SMILES | CN(CS([O-])(=O)=O)C1=C(C)N(C)N(C2=CC=CC=C2)C1=O.[Na+] | ||
| 分子式 | C13H16N3O4S•Na | 分子量 | 333.3 |
| 溶解度 | DMF: 30 mg/ml,DMSO: 30 mg/ml,Ethanol: 20 mg/ml,PBS (pH 7.2): 10 mg/ml | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 3.0003 mL | 15.0015 mL | 30.003 mL |
| 5 mM | 0.6001 mL | 3.0003 mL | 6.0006 mL |
| 10 mM | 0.3 mL | 1.5002 mL | 3.0003 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Methanesulfonic acid sodium salt protects retina from acute light damage in mice
Chin Med J (Engl) 2012 Jul;125(13):2310-5.PMID:22882854doi
Background: Methanesulfonic acid sodium salt (Dipyrone), an antipyretic and analgesic drug, has been demonstrated to improve cerebral ischemia through the inhibition of mitochondrial cell death cascades. The aim of this study was to evaluate the potential photoprotective activity of methanesulfonic acid sodium salt in a model of light-induced retinopathy. Methods: One hundred mice were assigned randomly into vehicle (V), methanesulfonic acid sodium salt (D), light damage model plus vehicle (MV) and light damage model plus methanesulfonic acid sodium salt (MD) groups (n = 25 each). In the MD group, methanesulfonic acid sodium salt (100 mg/kg) was administered by intraperitoneal injection 30 minutes before light exposure. Twenty-four hours after light exposure, hematoxylin and eosin staining and transmission electron microscopy (TEM) were used for histological evaluation. The thickness of the outer plus inner-segment and outer nuclear layer was measured on sections parallel to the vertical meridian of the eye at a distance of 1000 mm from the optic nerve. Electroretinography (ERG) test was performed to assess the functional change. The morphology of mitochondria was also revealed by TEM. Finally, the expression of cytochrome c (CytC) and the relative apoptotic proteins were detected by Western blotting, and the interaction between mitochondrial proteins was investigated by co-immunoprecipitation. Results: The photoreceptor inner and outer segments of the MV group were significantly disorganized than the MD group. The thicknesses of the outer plus inner-segment layers and the outer nuclear layer, and the amplitudes of the a and b waves of the scotopic ERG response markedly decreased in the MV group compared to those in the MD group (P < 0.05). TEM examination revealed that the mitochondria of the MV group were distinctly swollen and contained disrupted cristae. In contrast, the morphology of mitochondria in the MD group was unaffected. Western blotting analysis showed that CytC, apoptosis proteinase activating factor-1 (Apaf-1), caspase 3, p53, p53-upregulated modulator of apoptosis (PUMA), Bax, and Bad were increased, whereas the anti-apoptotic proteins Bcl-2 and Bcl-X(L) were significantly decreased in the MV group than the MD group. Co-immunoprecipitation detection revealed that PUMA immunoreactivity precipitated by Bcl-X(L) decreased, whereas Bax immunoreactivity precipitated by Bcl-X(L) increased in the MD group compared to those in the MV group. Conclusion: Methanesulfonic acid sodium salt is an effective photoprotective agent against light-induced retinopathy through the inhibition of CytC-mediated mitochondrial impairment.
Comparative Effects of Metamizole (Dipyrone) and Naproxen on Renal Function and Prostacyclin Synthesis in Salt-Depleted Healthy Subjects - A Randomized Controlled Parallel Group Study
Front Pharmacol 2021 Sep 7;12:620635.PMID:34557087DOI:10.3389/fphar.2021.620635.
Aim: The objective was to investigate the effect of Metamizole on renal function in healthy, salt-depleted volunteers. In addition, the pharmacokinetics of the four major Metamizole metabolites were assessed and correlated with the pharmacodynamic effect using urinary excretion of the prostacyclin metabolite 6-keto-prostaglandin F1α. Methods: Fifteen healthy male volunteers were studied in an open-label randomized controlled parallel group study. Eight subjects received oral Metamizole 1,000 mg three times daily and seven subjects naproxen 500 mg twice daily for 7 days. All subjects were on a low sodium diet (50 mmol sodium/day) starting 1 week prior to dosing until the end of the study. Glomerular filtration rate was measured using inulin clearance. Urinary excretion of sodium, potassium, creatinine, 6-keto-prostaglandin F1α, and pharmacokinetic parameters of naproxen and Metamizole metabolites were assessed after the first and after repeated dosing. Results: In moderately sodium-depleted healthy subjects, single or multiple dose Metamizole or naproxen did not significantly affect inulin and creatinine clearance or sodium excretion. Both drugs reduced renal 6-keto-prostaglandin F1α excretion after single and repeated dosing. The effect started 2 h after intake, persisted for the entire dosing period and correlated with the concentration-profile of naproxen and the active Metamizole metabolite 4-methylaminoantipyrine (4-MAA). PKPD modelling indicated less potent COX-inhibition by 4-MAA (EC50 0.69 ± 0.27 µM) compared with naproxen (EC50 0.034 ± 0.033 µM). Conclusions: Short term treatment with Metamizole or naproxen has no significant effect on renal function in moderately sodium depleted healthy subjects. At clinically relevant doses, 4-MAA and naproxen both inhibit COX-mediated renal prostacyclin synthesis.
Metamizole-furosemide interaction study in healthy volunteers
Eur J Clin Pharmacol 1992;42(6):593-8.PMID:1623899DOI:10.1007/BF00265921.
The pharmacokinetic and pharmacodynamic interactions between Metamizole (dipyrone) and furosemide were investigated in 9 of 12 healthy female subjects able to complete the study. They received oral Metamizole 3 x 1 g for 3 days or placebo (cross-over) and on the last day of both study periods furosemide 20 mg IV. On the last two days a balanced sodium diet (120 mEq) and on Day 3 an oral water load (600 ml) were given. Metamizole significantly inhibited basal urine flow, whereas the fractional excretion of sodium and chloride and the 12 h-GFR remained unchanged. Metamizole significantly reduced furosemide clearance (175 vs 141 ml.min-1), furosemide-stimulated plasma renin activity (1.42 vs 0.79 ng AI.ml-1.h-1) and the urinary excretion of prostacyclin metabolites and of prostaglandin F2 alpha (by 70-81%). The renal clearance and terminal half-life of furosemide, peak renal chloride and volume excretion were unchanged. Thus, Metamizole did not interact with the renal excretion and the diuretic effect of furosemide, although prostaglandin synthesis was significantly reduced.
Study of DNA damage caused by dipyrone in presence of some transition metal ions
Saudi Pharm J 2017 Nov;25(7):961-966.PMID:29158701DOI:10.1016/j.jsps.2017.02.010.
The DNA damage in the presence of dipyrone (used as its sodium salt, NaDip) and some transition metal ions in an air saturated ([O2] ≈ 0.25 mM) non-buffered solution at T = (25.0 ± 0.5)°C was investigated by agarose gel electrophoresis. As metal ions Cu2+, Fe3+, Ni2+ and Mn3+ were selected and evaluated in the present study because of the important role they play in a biological system. pUC19 plasmid DNA damage-induced by NaDip (80-600 μM) was observed in the presence of 100 μM Cu2+. The damage was proportional to the NaDip concentration provided that the order of addition of reagents (pUC19 plasmid DNA + Cu2+ + NaDip) is obeyed. Addition in the reaction medium of ligands for Cu2+ and Cu+, respectively EDTA and neocuproine, promoted total inhibition or reduction of the pUC19 plasmid DNA damage suggesting the involvement of the Cu2+/Cu+ cycle. Besides, the decrease in the pUC19 plasmid DNA damage after addition of catalase (1.0 × 10-4 mg μL-1) in the same reaction medium indicates that H2O2 is also involved in the damage process. In NaDip concentration range (80-600 μM), and under same the experimental conditions, it was not possible to conclude whether there was pUC19 plasmid DNA damage caused by 10 μM Fe3+. No damage was observed in the presence of Mn3+ or Ni2+. Although the technique used in this study is sensitive to detect the pUC19 plasmid DNA damage it was not possible to identify in which DNA base this damage occurs. Further studies with other techniques should be made to unambiguously identify the oxidative intermediates that are responsible for the DNA damage. As far as we know, this is the first study dealing with the pUC19 plasmid DNA damage-induced by NaDip in presence of copper, iron, nickel and manganese ions.
Clinical and laboratory findings in 60 cows with type-3 abomasal ulcer
Schweiz Arch Tierheilkd 2019 Sep;161(9):523-531.PMID:31488393DOI:10.17236/sat00218.
This study involved 60 cows aged 1.9 to 13 years (mean 4.8 ± 2.3 years) with type-3 abomasal ulcer. The most common clinical signs were, in decreasing order of frequency, partial or complete anorexia (98%), obtunded demeanour (95%), decreased skin surface temperature (78%), congested scleral vessels (73%), abdominal guarding (61%), tachypnoea (58%), fever (58%) and tachycardia (55%). One or more concomitant disorders were diagnosed in 86% of the cows. The most common abnormal laboratory findings were hypokalaemia (75%), shortened glutaraldehyde test time (46%) and hyperfibrinogenaemia (43%). The diagnosis of type-3 abomasal ulcer was made in all cows during laparotomy and/or at postmortem examination. Forty-eight (80%) cows were euthanased immediately after the initial examination, during laparotomy or after unsuccessful treatment. Twelve (20%) cows were treated with a solution of sodium chloride and glucose administered via an indwelling jugular catheter, antibiotics, Metamizole or flunixin, and discharged from the clinic. Ten cows were still in production two years later.