N-desmethyl Eletriptan
(Synonyms: N-去甲基依曲普坦) 目录号 : GC49219
A metabolite of eletriptan
Cas No.:153525-55-4
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >95.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
N-desmethyl Eletriptan is a metabolite of eletriptan .1 It is formed from eletriptan primarily by the cytochrome P450 (CYP) isoform CYP3A4 in human liver microsomes.
1.Evans, D.C., O’Connor, D., Lake, B.G., et al.Eletriptan metabolism by human hepatic CYP450 enzymes and transport by human P-glycoproteinDrug Metab. Dispos.31(7)861-869(2003)
| Cas No. | 153525-55-4 | SDF | |
| 别名 | N-去甲基依曲普坦 | ||
| Canonical SMILES | O=S(CCC1=CC=C2C(C(C[C@H]3CCCN3)=CN2)=C1)(C4=CC=CC=C4)=O | ||
| 分子式 | C21H24N2O2S | 分子量 | 368.5 |
| 溶解度 | Acetonitrile: soluble,DMSO: soluble,Methanol: soluble | 储存条件 | -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 | 2.7137 mL | 13.5685 mL | 27.137 mL |
| 5 mM | 0.5427 mL | 2.7137 mL | 5.4274 mL |
| 10 mM | 0.2714 mL | 1.3569 mL | 2.7137 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。
Differential pharmacokinetic drug-drug interaction potential of eletriptan between oral and subcutaneous routes
Xenobiotica 2019 Oct;49(10):1202-1208.PMID:30588869DOI:10.1080/00498254.2018.1540805.
1. Pharmacokinetic drug-drug interaction (DDI) data is important from a label claim either in combination drug usage or in polypharmacy situation. 2. Eletriptan undergoes first pass related metabolism through CYP3A4 enzyme to form pharmacologically active N-desmethyl metabolite. 3. Differential DDI interaction of the concomitant oral dosing of ketoconazole (20.1 mg/kg), a CYP3A4 inhibitor, with oral (4.2 mg/kg) or subcutaneous dose (2.1 mg/kg) of eletriptan was evaluated in male Sprague Dawley rats. Serial pharmacokinetic samples were collected and simultaneously analysed for eletriptan/N-desmethyl Eletriptan using validated assay. Non-compartmentally derived pharmacokinetic parameters for various treatments were analysed statistically. 4. After oral eletriptan in presence of ketoconazole, Cmax (40 vs. 32 ng/mL alone) and AUCinf (81 vs. 24 ng.h/mL alone) of eletriptan increased; the formation of N-desmethyl Eletriptan decreased (Cmax=1.1 ng/mL, 3.9%) with ketoconazole as compared to without treatment (Cmax=3.7 ng/mL, 11.2%). After subcutaneous eletriptan in presence of ketoconazole, there was no change in Cmax (153 vs.152 ng/mL) or AUCinf (267 vs. 266 ng.h/mL) of eletriptan. Formation of N-desmethyl Eletriptan after the subcutaneous dose was determined at few intermittent time points with/without ketoconazole. 5. Preclinical data support differential DDI of eletriptan when dosed oral vs. subcutaneous, which need to be evaluated in a clinical setting.
Eletriptan metabolism by human hepatic CYP450 enzymes and transport by human P-glycoprotein
Drug Metab Dispos 2003 Jul;31(7):861-9.PMID:12814962DOI:10.1124/dmd.31.7.861.
"Reaction phenotyping" studies were performed with eletriptan (ETT) to determine its propensity to interact with coadministered medications. Its ability to serve as a substrate for human P-glycoprotein (P-gp) was also investigated since a central mechanism of action has been proposed for this "triptan" class of drug. In studies with a characterized bank of human liver microsome preparations, a good correlation (r2 = 0.932) was obtained between formation of N-desmethyl Eletriptan (DETT) and CYP3A4-catalyzed testosterone 6 beta-hydroxylation. DETT was selected to be monitored in our studies since it represents a significant ETT metabolite in humans, circulating at concentrations 10 to 20% of those observed for parent drug. ETT was metabolized to DETT by recombinant CYP2D6 (rCYP2D6) and rCYP3A4, and to a lesser extent by rCYP2C9 and rCYP2C19. The metabolism of ETT to DETT in human liver microsomes was markedly inhibited by troleandomycin, erythromycin, miconazole, and an inhibitory antibody to CYP3A4, but not by inhibitors of other major P450 enzymes. ETT had little inhibitory effect on any of the P450 enzymes investigated. ETT was determined to be a good substrate for human P-gp in vitro. In bidirectional transport studies across LLC-MDR1 and LLC-Mdr1a cell monolayers, ETT had a BA/AB transport ratio in the range 9 to 11. This finding had significance in vivo since brain exposure to ETT was reduced 40-fold in Mdr1a+/+ relative to Mdr1a-/- mice. ETT metabolism to DETT is therefore catalyzed primarily by CYP3A4, and plasma concentrations are expected to be increased when coadministered with inhibitors of CYP3A4 and P-gp activity.