Ajmaline
(Synonyms: NSC 15627) 目录号 : GC35273
Ajmaline是一种生物碱, 是一种Ia类的抗心律失常药。
Cas No.:4360-12-7
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Ajmaline is an alkaloid that is class Ia antiarrhythmic agent.
| Cas No. | 4360-12-7 | SDF | |
| 别名 | NSC 15627 | ||
| Canonical SMILES | CN1C2=CC=CC=C2[C@@]34[C@]1([H])[C@@](C[C@H]5[C@H](CC)[C@H]6O)([H])[N@]6[C@]([H])([C@H]5[C@H]4O)C3 | ||
| 分子式 | C20H26N2O2 | 分子量 | 326.43 |
| 溶解度 | DMSO: ≥ 100 mg/mL (306.34 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 | 3.0634 mL | 15.3172 mL | 30.6344 mL |
| 5 mM | 0.6127 mL | 3.0634 mL | 6.1269 mL |
| 10 mM | 0.3063 mL | 1.5317 mL | 3.0634 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。
Ajmaline Testing and the Brugada Syndrome
Am J Cardiol 2020 Nov 15;135:91-98.PMID:32861732DOI:10.1016/j.amjcard.2020.08.024.
Brugada syndrome (BrS) diagnosis requires the presence of a typical type 1 ECG pattern. Owing to the spontaneous ECG variability, the real BrS prevalence in the general population remains unclear. The aim of the present study was to evaluate the prevalence of positive Ajmaline challenge for BrS in a cohort of consecutive patients who underwent electrophysiological evaluation for different clinical reasons. All consecutive patients from 2008 to 2019 who underwent Ajmaline testing were prospectively included. A total of 2,456 patients underwent Ajmaline testing, 742 (30.2%) in the context of familial screening for BrS. In non-familial screening group (1,714) Ajmaline testing resulted positive in 186 (10.9%). Indications for Ajmaline testing were: suspicious BrS ECG in 23 cases (12.4%), palpitations in 27 (14.5%), syncope in 71 (38.2%), presyncope in 7 (3.8%), family history of sudden cardiac death in 18 (9.7%), documented ventricular arrhythmias in 12 (6.5%), unexplained cardiac arrest in 4 (2.2%), atrial fibrillation in 16 (8.5%), brady-arrhythmias in 1 (0.5%), and cerebrovascular accidents in 7 (3.7%). Compared with the overall population, Ajmaline testing positive patients were younger (42.8 ± 15.5 vs 48.9 ± 20.4; p <0.001) and more frequently male (65.1% vs 56.3%; p = 0.023). Implantable cardioverter defibrillator was implanted in 84 patients (45.2%). During a median follow-up of 42.4 months, 12 appropriate shocks and 13 implantable cardioverter defibrillator related complications were reported. In conclusion, the BrS was diagnosed in an unexpected high proportion of patients that underwent Ajmaline testing for a variety of cardiovascular symptoms. This can lead to an adequate counseling and clinical management in BrS patients.
Metabolic disposition of Ajmaline
Eur J Drug Metab Pharmacokinet 1989 Oct-Dec;14(4):309-16.PMID:2633926DOI:10.1007/BF03190117.
Urine was collected from six patients receiving a continuous infusion of 20 mg/h Ajmaline. Pooled urine was extracted with and without enzymatic conjugate cleavage or hydrolysis with concentrated hydrochloric acid. The extracts were analyzed by gas chromatography/mass spectrometry. Ajmaline and its metabolites in urine were identified in the form of their acetylated derivatives. Twenty two different acetylated derivatives of Ajmaline and its metabolites could be detected. Three of these derivatives were artifacts generated by acetylation and/or thermal decomposition. The major metabolic pathways were mono- and di-hydroxylation of the benzene ring with subsequent O-methylation, reduction of the C-21, oxidation of the C-17 and C-21-hydroxyl function, N-oxidation, and a combination of these metabolic steps. Ajmaline and its metabolites were mainly excreted in the form of their conjugates. Furthermore, the interference of sparteine, debrisoquine, quinidine, and nifedipine with Ajmaline metabolism was studied with semiquantitative thin-layer chromatography. Ajmaline metabolism was inhibited by co-administration of sparteine or quinidine, but not by debrisoquine or nifedipine. Sparteine most likely competed with Ajmaline metabolism. Quinidine probably bound competitively to ajmaline-metabolizing enzymes without being metabolized itself. Additionally, the metabolic ratio of hydroxyajmaline/Ajmaline in urine was determined in 9 extensive metabolizers and one poor metabolizer of dextromethorphan. The poor metabolizer had a significantly reduced metabolic ratio of hydroxyajmaline/Ajmaline, which indicates that Ajmaline metabolism probably co-segregates with polymorphic sparteine/debrisoquine/dextromethorphan metabolism.
Ajmaline attenuates electrocardiogram characteristics of inferolateral early repolarization
Heart Rhythm 2012 Feb;9(2):232-9.PMID:21914496DOI:10.1016/j.hrthm.2011.09.013.
Background: J waves are the hallmark of both inferolateral early repolarization (ER) and Brugada syndrome. While Ajmaline, a class 1a antiarrhythmic drug, accentuates the J wave in Brugada syndrome, its effect on ER is unreported. Objective: To describe the effect of Ajmaline on the electrocardiogram in ER. Methods: We analyzed electrocardiograms before and after the administration of intravenous Ajmaline (1 mg/kg) in 31 patients with ER, 21 patients with Brugada type 1 electrocardiogram (Br), and 22 controls. ER was defined as J-point elevation of ≥1 mm with QRS slurring or notching in ≥2 inferolateral leads (I, aVL, II, III, aVF, V4-V6). Results: Ajmaline decreased mean J-wave amplitude in the ER group from 0.2 ± 0.15 mV at baseline to 0.08 ± 0.09 mV (P < .001). The QRS width prolonged significantly in all 3 groups, but the prolongation was significantly less in the ER group (+21 ms) than in the Br group (+36 ms; P < .001) or controls (+28 ms; P = .010). Decrease in mean inferolateral R-wave amplitude was similar in all the groups (ER group -0.14 mV; Br group -0.11 mV; controls -0.13 mV; P = ns), but mean inferolateral S-wave amplitude increased significantly less in the ER group (ER group +0.14 mV; Br group +16 mV; controls +0.20 mV; P < .001). Conclusions: Ajmaline significantly decreases the J-wave amplitude in ER and prolongs the QRS width significantly less than in patients with Br. This indicates a different pathogenesis for both disorders. The altered terminal QRS vector probably is responsible for the decrease in the J-wave amplitude in ER, although a specific effect of Ajmaline on J waves cannot be excluded.
Ajmaline challenge for the diagnosis of Brugada syndrome: which protocol?
Arch Cardiovasc Dis 2010 Nov-Dec;103(11-12):570-8.PMID:21147441DOI:10.1016/j.acvd.2010.10.007.
Background: Ajmaline challenge is commonly used for the diagnosis of Brugada syndrome. A slow infusion rate has been recommended in view of the proarrhythmic risk, but the diagnostic value of various infusion rates has not been investigated. Aims: To compare rapid and slow Ajmaline infusion rates and to assess the proarrhythmic risk. Methods: The first part of this study prospectively compared rapid and slow infusion rates in terms of results and ventricular arrhythmias. Thirty-two patients (mean age 41±12 years; 26 men) received the two Ajmaline challenges on different days. According to randomization, Ajmaline (1 mg/kg) was infused at 1 mg/sec or over 10 minutes. The second part of the study retrospectively assessed the prevalence of ventricular arrhythmia during 386 challenges performed at a rapid infusion rate. Results: No differences were observed between rapid and slow tests. All patients diagnosed as positive or negative with one test obtained the same result with the other test. Ventricular premature beats were observed in five of 32 patients during the slow challenge and in four of 32 patients during the rapid challenge. No sustained ventricular arrhythmias were observed. Analysis of the 386 tests revealed four episodes of ventricular arrhythmia (two complex ventricular premature beats, one non-sustained ventricular tachycardia and one ventricular fibrillation). Conclusion: Slow and rapid infusions of Ajmaline have identical diagnostic performances on suspected Brugada electrocardiograms. Owing to the risk of severe proarrhythmia, a slow infusion rate, allowing early discontinuation, should be recommended.
Cholestatic hepatitis after diagnostic Ajmaline challenge
Acta Gastroenterol Belg 2017 Jul-Sep;80(3):425-426.PMID:29560676doi
We report a cholestatic hepatitis in an elderly woman after Ajmaline challenge during electrophysiological testing for Brugada syndrome. No other medication was reported in the previous 6 months of the onset of jaundice. Liver biopsy showed a cholestatic hepatitis with mild biliary damage. Liver enzymes normalized within 2 weeks as well as jaundice. To the best of our knowledge this is the second case of histologically proved cholestatic hepatitis induced by intravenous Ajmaline testing.