Procainamide
(Synonyms: 4-氨基-N-[2-(二乙基氨基)乙基]苯甲酰胺,Procaine amide; SP 100) 目录号 : GC64733
An Analytical Reference Standard
Cas No.:51-06-9
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
Procainamide (hydrochloride) is an analytical reference standard categorized as a local anesthetic.1 This product is intended for research and forensic applications.
1.Pietrzak, J., Butruk, E., and Ostrowski, J.Local anesthetics (benzyl alcohol, lidocaine, procainamide) inhibit aminopyrine accumulation in isolated rat parietal cellsPharmacology39(4)265-272(1989)
| Cas No. | 51-06-9 | SDF | Download SDF |
| 别名 | 4-氨基-N-[2-(二乙基氨基)乙基]苯甲酰胺,Procaine amide; SP 100 | ||
| 分子式 | C13H21N3O | 分子量 | 235.33 |
| 溶解度 | 储存条件 | 4°C, protect from light | |
| 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 | 4.2494 mL | 21.2468 mL | 42.4935 mL |
| 5 mM | 0.8499 mL | 4.2494 mL | 8.4987 mL |
| 10 mM | 0.4249 mL | 2.1247 mL | 4.2494 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。
Procainamide: a perspective on its value and danger
Heart Dis Stroke 1993 Nov-Dec;2(6):473-6.PMID:8137053doi
Procainamide remains one of the most widely used antiarrhythmic agents in clinical practice. Currently, it is widely used alone or in combination with class I agents (eg, mexiletine or tocainide) to prevent recurrent ventricular tachycardia or symptomatic nonsustained ventricular tachycardia. Procainamide is also used for short-term treatment of ventricular tachycardia and a variety of supraventricular tachycardias, primarily atrial flutter and atrial fibrillation. Long-term Procainamide therapy is limited by a number of systemic side effects, primarily lupus-like syndrome, gastrointestinal disturbances, and autoimmune blood dyscrasias. Procainamide levels can be useful in initial dose titrations; however, QRS and QT interval measurements help prevent drug toxicity. It is recommended that patients being started on antiarrhythmic therapy with Procainamide be admitted to the hospital for monitoring to ensure that their QT interval is not excessively prolonged.
Procainamide pharmacokinetics during extracorporeal membrane oxygenation
Perfusion 2023 Mar;38(2):409-413.PMID:34617854DOI:10.1177/02676591211050606.
Procainamide is a useful agent for management of ventricular arrhythmia, however its disposition and appropriate dosing during extracorporeal membrane oxygenation (ECMO) is unknown. We report experience with continuous Procainamide infusion in a critically ill adult requiring venoarterial ECMO for incessant ventricular tachycardia. Pharmacokinetic analysis of Procainamide and its metabolite, N-acetylprocainamide (NAPA), was performed using serum and urine specimens. Kidney function was preserved, and sequencing of the N-acetyltransferase 2 gene revealed the patient was a phenotypic slow acetylator. Procainamide volume of distribution and half-life were calculated and found to be similar to healthy individuals. However, despite elevated serum Procainamide concentrations, NAPA concentrations remained far lower in the serum and urine. The magnitude of Procainamide and NAPA discordance suggested alternative contributors to the deranged pharmacokinetic profile, and we hypothesized NAPA sequestration by the ECMO circuit. Ultimately, the patient received orthotopic cardiac transplantation and was discharged home in stable condition. Procainamide should be used cautiously during ECMO, with close therapeutic drug monitoring of serum Procainamide and NAPA concentrations. The achievement of therapeutic NAPA concentrations while maintaining safe serum Procainamide concentrations during ECMO support may be challenging.
Procainamide-induced psychosis: a case report and review of the literature
Ann Pharmacother 1999 Sep;33(9):948-51.PMID:10492498DOI:10.1345/aph.18378.
Objective: To describe a case of procainamide-induced psychosis in an adult treated for atrial fibrillation. Case summary: A 45-year-old Native American woman developed acute psychosis within 72 hours of initiating Procainamide for atrial fibrillation. Symptoms abated within 24 hours of discontinuing Procainamide. Serum Procainamide/N-acetylprocainamide concentrations were therapeutic throughout treatment. Sotalol was started without recurrence of symptoms. Discussion: Psychosis is a rare complication of treatment with Procainamide, but the exact mechanism for this adverse event is not fully understood. Seven cases implicating Procainamide as the cause of acute psychosis are reported in the literature. Cases of psychosis involving other antiarrhythmic agents have also been reported. Conclusions: Healthcare personnel should be aware of this adverse event related to Procainamide and other antiarrhythmic agents.
Clinical pharmacokinetics of Procainamide
Clin Pharmacokinet 1978 Mar-Apr;3(2):97-107.PMID:346289DOI:10.2165/00003088-197803020-00001.
Procainamide is almost completely absorbed after oral administration and peak plasma concentrations are generally reached within 1 to 2 hours. Upon intravenous administration there is a rapid initial distribution phase, which is completed after about 30 minutes. The pharmacokinetics can be described by a 2-compartment open model. The plasma half-life during the beta-phase averages 3 hours. The apparent volume of distribution is about 2L/kg body weight. At therapeutic plasma levels about 15% is bound to plasma proteins. Approximately 50% of administered Procainamide is eliminated as unchanged drug via the kidneys. N-Acetylprocainamide is the main metabolite and is the main metabolite and is pharmacologically active, with a recovery in urine of about 15% (range 7 to 34% in healthy subjects). The acetylation of Procainamide seems to be under the same monogenic control as that of isoniazid. At least 2 more metabolites have been found but are not yet identified. The renal clearance of Procainamide ranges from 179 to 660ml/min. Glomerular filtration and active tubular secretion seem to be the most important mechanisms. In patients with low-output cardiac and/or renal impairment, the absorption, distribution and elimination of the drug may be significantly altered. Determination of plasma levels is of particular value in these cases and will contribute to more safe and effective therapy in the majority of patients. As N-acetylprocainamide seems to have pharmacological effects comparable with those of Procainamide, both agents should be monitored simultaneously in order to optimise therapy.
Procainamide: clinical pharmacology and efficacy against ventricular arrhythmias
Ann N Y Acad Sci 1984;432:177-88.PMID:6084435DOI:10.1111/j.1749-6632.1984.tb14519.x.
Procainamide (PA) has been a mainstay of treatment against acute and chronic supraventricular and ventricular arrhythmias for more than 30 years. PA's clinical pharmacology has been studied extensively and its bioavailability (75-95%); volume of distribution (1.5-2.5 liters per kg), plasma protein-binding (15-25%), half-time for elimination (3-7 hours), and metabolism are known. PA's efficacy against acute ventricular arrhythmias and chronic stable VPDs is associated with plasma drug concentrations of 4 to 10 micrograms per ml; but much higher plasma concentrations may be required against sustained ventricular arrhythmias. From 30 to 60% of a PA dose is excreted as the metabolite, N-acetylprocainamide (NAPA), and PA's metabolism is determined genetically (fast or slow acetylation phenotype). Studies in patients with VPDs indicate that NAPA is also antiarrhythmic, although the contribution of NAPA to the antiarrhythmic effect after PA is not known. Studies in patients with the systemic lupus-like syndrome from PA show that NAPA is not associated with this. Investigations comparing efficacy and adverse effects of PA with those of new antiarrhythmic agents available for clinical trials are indicated in the future.