Isoxicam
(Synonyms: 伊索昔康) 目录号 : GC39534
Isoxicam 是一种口服有效的非甾体抗炎剂，可用于关节炎的研究。Isoxicam 是一种非选择性的 COX-1 和 COX-2 抑制剂。
Cas No.:34552-84-6
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Isoxicam is an orally active, long-acting, non-steroidal anti-inflammatory agent for the research of arthritis[1]. Isoxicam is a nonselective inhibitor of COX-1 and COX-2[2].
[1]. DiPasquale G, et al. The antiinflammatory properties of isoxicam (4-hydroxy-2methyl-N-(5-methyl-3isoxolyl-2H-1,2-benzothiazine-3-carboxamide 1,1-dioxide). Agents Actions. 1975 Aug;5(3):256-63. [2]. Xu S, et al. Oxicams bind in a novel mode to the cyclooxygenase active site via a two-water-mediated H-bonding Network. J Biol Chem. 2014 Mar 7;289(10):6799-808.
| Cas No. | 34552-84-6 | SDF | |
| 别名 | 伊索昔康 | ||
| Canonical SMILES | O=C(C1=C(O)C2=CC=CC=C2S(N1C)(=O)=O)NC3=NOC(C)=C3 | ||
| 分子式 | C14H13N3O5S | 分子量 | 335.34 |
| 溶解度 | DMSO: 5 mg/mL (14.91 mM) | 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 | 2.982 mL | 14.9102 mL | 29.8205 mL |
| 5 mM | 0.5964 mL | 2.982 mL | 5.9641 mL |
| 10 mM | 0.2982 mL | 1.491 mL | 2.982 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。
Evaluation of the safety of Isoxicam
Am J Med 1985 Oct 18;79(4B):28-32.PMID:3904436DOI:10.1016/0002-9343(85)90178-0.
Data collected from more than 1,800 patients with rheumatoid arthritis or degenerative joint disease in Phase 3 clinical studies of Isoxicam (Maxicam) indicated that the drug is well tolerated on both a short-term and a long-term basis. The most common type of adverse reaction to all medications (Isoxicam, aspirin, and indomethacin) was gastrointestinal: 22.6 percent with Isoxicam, at a dosage greater than 200 mg per day; 14.2 percent with Isoxicam at 200 mg per day; 31.6 percent with buffered aspirin at 3,600 to 4,800 mg per day; 24.6 percent with indomethacin at 150 mg per day; and 7.2 percent with placebo. The incidence of tinnitus and deafness was significantly greater with buffered aspirin than with Isoxicam, and the number of patients who had at least one episode of dizziness, vertigo, or headache was significantly greater with indomethacin than with Isoxicam. In open-label, long-term studies, in which approximately 70 percent of the patients participated, the types and frequencies of adverse effects were similar to those observed with Isoxicam during the controlled studies. The overall frequency of withdrawal for adverse reactions during the long-term studies was 11.5 percent, similar to that during the controlled studies. At the recommended dosage for Isoxicam of 200 mg per day, the incidence of gastrointestinal ulcers was 0.81 percent, well within the range expected among arthritic patients receiving nonsteroidal anti-inflammatory drugs. From the data collected in Phase 3 clinical studies, it may be concluded that Isoxicam is better tolerated than either aspirin or indomethacin and should not create unusual problems in the short-term or long-term treatment of rheumatoid arthritis or degenerative joint disease.
Interaction of Isoxicam with acetylsalicylic acid
Br J Clin Pharmacol 1984 Oct;18(4):567-71.PMID:6487496DOI:10.1111/j.1365-2125.1984.tb02505.x.
Ten healthy male volunteers were given 200 mg p.o. of Isoxicam after an overnight fast and the plasma concentrations over time followed for 96 h by h.p.l.c. Five days later enteric coated acetylsalicylic acid (ASA) 650 mg four times daily was started and continued for 10 days producing steady state trough plasma salicylate of 83 mg/l (range 21-133). A second 200 mg Isoxicam dose was given 5 days after starting ASA and the plasma concentration time-curve again followed. After ASA, there was no change in lag time (0.54 vs 0.51 h), time to peak concentration (10 vs 10 h), or disappearance t1/2 (28.7 vs 31.0 h) however the peak Isoxicam concentration and AUC were reduced 18 and 22% respectively (P less than 0.01). Plasma protein binding of Isoxicam studied by equilibrium dialysis was 96 +/- 1% in the absence and 86 +/- 5% in the presence of ASA. The reduction in binding was unrelated to plasma SA concentrations achieved or observed reductions in AUC for plasma Isoxicam. ASA decreased plasma Isoxicam binding, peak plasma Isoxicam concentrations and AUC without altering the apparent disappearance half-life of total plasma Isoxicam after a single oral dose.
The effect of administration of phenytoin on the pharmacokinetics of Isoxicam
Biopharm Drug Dispos 1987 Jan-Feb;8(1):57-61.PMID:3580513DOI:10.1002/bdd.2510080107.
This study was designed to determine whether the disposition of Isoxicam is influenced by the coadministration of another acidic drug, highly bound to plasma proteins and extensively metabolized, i.e., phenytoin. Ten healthy volunteers received an oral dose of 200 mg of Isoxicam prior to and following the oral administration of phenytoin (100 mg) twice a day for 10 days. Eleven blood samples were drawn during the period following each dose of Isoxicam. The area under the Isoxicam plasma concentration-time curve (AUC infinity) increased from 389 +/- 66 to 464 +/- 62 micrograms h ml-1 (+/- SEM) (p less than 0.05) after treatment with phenytoin. This increase was due to an increase in Isoxicam bioavailability; the absorption rate constant for Isoxicam increased correspondingly from 0.34 +/- 0.06 to 1.16 +/- 0.38 h-1 (p less than 0.05). Distribution and clearance of Isoxicam were probably not affected as its half-life was not changed, its plasma peak concentration increased, and the time to reach this peak decreased. It is concluded that phenytoin increases the rate and extent of absorption of Isoxicam.
In vivo metabolism of Isoxicam in rats, dogs, and monkeys
Drug Metab Dispos 1989 Nov-Dec;17(6):662-8.PMID:2575504doi
Isoxicam is a long half-life nonsteroidal anti-inflammatory agent which undergoes extensive metabolism prior to elimination in animals and man. The major route of Isoxicam transformation is hydroxylation of the methylisoxazole functionality to form hydroxymethylisoxicam, and cleavage of its benzothiazine moiety to give an oxoacetic acid metabolite. The metabolic pathway for scission of the benzothiazine moiety to the oxoacetic acid metabolite and to other potential metabolites is not known. To gain additional information on the metabolic fate of Isoxicam, 14C-isoxicam labeled on the N-methyl group was administered to rats, dogs, and monkeys with urine and feces collected for metabolic profiling and identification. Identified as new metabolites of Isoxicam were an open-ring sulfonamide, N-methylsaccharin, and saccharin. The formation of these metabolites suggests that Isoxicam undergoes direct oxidative scission of its benzothiazine ring at carbon atom 3 to generate the observed open-ring sulfonamide, N-methylsaccharin, and oxoacetic acid metabolites.
Painkiller Isoxicam and Its Copper Complex Can Form Inclusion Complexes with Different Cyclodextrins: A Fluorescence, Fourier Transform Infrared Spectroscopy, and Nuclear Magnetic Resonance Study
J Phys Chem B 2017 Sep 14;121(36):8454-8466.PMID:28806512DOI:10.1021/acs.jpcb.7b05649.
The interaction of a painkiller Isoxicam, belonging to the oxicam group of nonsteroidal anti-inflammatory drugs (NSAIDs) and its copper complex with different cyclodextrins (β-CD, γ-CD, HPβCD, and HPγCD), has been investigated in both solution and the solid state. Steady state and time-resolved fluorescence spectroscopy, fluorescence anisotropy, 1H NMR, and FTIR spectroscopy are used. Both the drug and its copper complex form a host-guest inclusion complex with all CDs. Fluorescence spectroscopy is used to determine binding constants and stoichiometries of the host-guest complex. The strongest binding is seen for γ-CD. 1H NMR study showed that Isoxicam penetrates into the CD cavity from the more accessible wider side. For β- and γ-CD, Isoxicam showed one type of binding, i.e., formation of an inclusion complex, whereas, for HPβCD and HPγCD, it showed two types of binding, i.e., inclusion in the CD cavities and interaction with the outer surface of the CD molecules mainly near the hydroxy propyl group. Deeper penetration occurred into the larger diameter cavity of γ-CD and HPγCD compared to β-CD and HPβCD. From FTIR and 1H NMR study, it is seen that predominantly the π-electron-rich benzene part of the drug and its complex penetrate into the host cavity.