Clonidine
(Synonyms: 可乐定) 目录号 : GC60717
Clonidine HCl(Kapvay) is a direct-acting α2 adrenergic agonist with an ED50 of 0.02±0.01 mg/kg.
Cas No.:4205-90-7
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
Clonidine HCl(Kapvay) is a direct-acting α2 adrenergic agonist with an ED50 of 0.02±0.01 mg/kg.
| Cas No. | 4205-90-7 | SDF | |
| 别名 | 可乐定 | ||
| Canonical SMILES | ClC1=C(NC2=NCCN2)C(Cl)=CC=C1 | ||
| 分子式 | C9H9Cl2N3 | 分子量 | 230.09 |
| 溶解度 | DMSO : 100 mg/mL (434.61 mM; Need ultrasonic) | 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 | 4.3461 mL | 21.7306 mL | 43.4613 mL |
| 5 mM | 0.8692 mL | 4.3461 mL | 8.6923 mL |
| 10 mM | 0.4346 mL | 2.1731 mL | 4.3461 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。
Clonidine hydrochloride
South Med J 1982 Jun;75(6):713-9.PMID:7046065DOI:10.1097/00007611-198206000-00022.
Clonidine hydrochloride (Catapres), a potent antihypertensive agent, has been in clinical use since 1974 in the United States. Clonidine, an alpha-adrenergic receptor agonist, stimulates central alpha receptors in the depressor site of the vasomotor center of the medulla oblongata and hypothalamus, which diminishes efferent sympathetic tone to the heart, kidneys, and peripheral vasculature with a concomitant increase in vagal activity. Hemodynamic and renal effects include reduction in supine and erect blood pressure, heart rate, total peripheral resistance, plasma renin activity, and urinary aldosterone and catecholamine excretion, with little effect on resting cardiac output, response to exercise, and preservation of renal function. Clonidine alone produces a significant reduction in mean arterial pressure in all degrees of hypertension during acute and chronic administration, with little or no tendency toward tolerance or postural hypotension. Its antihypertensive potency is enhanced with the concomitant use of a diuretic or vasodilator, and it may be used in place of a beta blocker with equal efficacy in the diuretic plus vasodilator combination. Serious adverse effects are uncommon, with more than 93% of patients tolerating the drug well. Sedation and dry mouth, the most common adverse effects, are usually related to dose and duration and are minimized by gradually increasing the dose and by taking the major portion of the twice-daily schedule at bedtime. Clonidine may be safely given to patients with congestive heart failure, ischemic heart disease, obstructive lung disease, chronic renal insufficiency, and diabetes mellitus. Clonidine is one of the most versatile and effective agents presently available for the treatment of hypertension.
Clonidine and alcohol withdrawal
Adv Alcohol Subst Abuse 1987;7(1):17-28.PMID:3327372doi
Clonidine attenuates opiate withdrawal syndrome, via reduction in catecholamine activity in the brain, most probably at the locus ceruleus. Clonidine and locus ceruleus lesions, in animals with alcohol dependency as with the opiates, modify alcohol withdrawal. Both alcohol loading and withdrawal from steady alcohol use alter catecholamines in man and animals. Clonidine's potential to treat alcoholics in withdrawal is reviewed. Several double blind studies showed Clonidine, or similar analogues, to be somewhat superior to placebo in acute alcohol withdrawal. Major improvements were in pulse, blood pressure and composite alcohol withdrawal scores. Side effects were minor and mainly included mild sedation, or postural hypotension. In the only available published study Clonidine compared reasonably well to a standard sedative in alcohol withdrawal, and greatly influential in plasma catecholamine levels. Other components of alcohol withdrawal, as seizures and hallucinations-delirium tremens have not been documented to change with Clonidine. The alpha-2-adrenergic agonists in alcohol treatment seemed modestly effective for treatment of some parts of alcohol withdrawal. They represent a promising, novel, but still investigational approach. Additional data, particularly comparing them to the benzodiazepines, are needed before their potential in therapeutics can be assessed.
Clonidine for smoking cessation
Cochrane Database Syst Rev 2004;2004(3):CD000058.PMID:15266422DOI:10.1002/14651858.CD000058.pub2.
Background: Clonidine was originally used to lower blood pressure. It acts on the central nervous system and may reduce withdrawal symptoms in various addictive behaviours, including tobacco use. Objectives: The aim of this review is to determine Clonidine's effectiveness in helping smokers to quit. Search strategy: We searched the Cochrane Tobacco Addiction Group trials register for trials of Clonidine. Date of the most recent search: May 2004. Selection criteria: We considered randomized trials of Clonidine versus placebo with a smoking cessation endpoint assessed at least 12 weeks following the end of treatment. Data collection and analysis: We extracted data in duplicate on the type of subjects, the dose and duration of Clonidine therapy, the outcome measures, method of randomization, and completeness of follow up. The main outcome measure was abstinence from smoking after at least 12 weeks follow up in patients smoking at baseline. We used the most rigorous definition of abstinence for each trial, and biochemically validated rates if available. Where appropriate, we performed meta-analysis using a fixed effect model. Main results: Six trials met the inclusion criteria. There were three trials of oral, and three of transdermal Clonidine. Some form of behavioural counselling was offered to all participants in five of the six trials. There was a statistically significant effect of Clonidine in one of these trials. The pooled odds ratio for success with Clonidine versus placebo was 1.89 (95% confidence interval 1.30 to 2.74). There was a high incidence of dose-dependent side-effects, particularly dry mouth and sedation. Reviewers' conclusions: Based on a small number of trials, in which there are potential sources of bias, Clonidine is effective in promoting smoking cessation. Prominent side-effects limit the usefulness of Clonidine for smoking cessation.
Clonidine for smoking cessation
Cochrane Database Syst Rev 2000;(2):CD000058.PMID:10796479DOI:10.1002/14651858.CD000058.
Background: Clonidine was originally used to lower blood pressure. It acts on the central nervous system and may reduce withdrawal symptoms in various addictive behaviours, including tobacco use. Objectives: The aim of this review is to determine Clonidine's effectiveness in helping smokers to quit. Search strategy: We searched the Cochrane Tobacco Addiction Group trials register. Date of the most recent search: October 1998. Selection criteria: We considered randomised trials of Clonidine versus placebo with a smoking cessation endpoint assessed at least 12 weeks following the end of treatment. Data collection and analysis: We extracted data in duplicate on the type of subjects, the dose and duration of Clonidine therapy, the outcome measures, method of randomisation, and completeness of follow-up. The main outcome measure was abstinence from smoking after at least twelve weeks follow-up in patients smoking at baseline. We used the most rigorous definition of abstinence for each trial, and biochemically validated rates if available. Where appropriate, we performed meta-analysis using a fixed effects model. Main results: Six trials met the inclusion criteria. There were three trials of oral, and three of transdermal Clonidine. Some form of behavioural counselling was offered to all participants in five of the six trials. There was a statistically significant effect of Clonidine in one of these trials. The pooled odds ratio for success with Clonidine vs placebo was 1.89 (95% confidence interval 1.30 to 2.74). There was a high incidence of dose-dependent side-effects, particularly dry mouth and sedation. Reviewer's conclusions: Based on a small number of trials, in which there are potential sources of bias, Clonidine is effective in promoting smoking cessation. Prominent side-effects limit the usefulness of Clonidine for smoking cessation.
Clonidine extended-release: in attention-deficit hyperactivity disorder
Paediatr Drugs 2011 Oct 1;13(5):329-36.PMID:21888447DOI:10.2165/11208100-000000000-00000.
Clonidine, an α(2)-adrenergic agonist, is approved in the US as an extended-release (XR) tablet for the treatment of attention-deficit hyperactivity disorder (ADHD) in children and adolescents (aged 6-17 years). In two, randomized, double-blind, multicenter, phase III trials of 8 weeks' duration, Clonidine XR improved the symptoms of ADHD in children and adolescents. Significantly greater reductions from baseline in ADHD rating scale IV (ADHD-RS-IV) total scores at week 5 (primary endpoint) were achieved by recipients of Clonidine XR 0.2 and 0.4 mg/day monotherapy than by recipients of placebo. When added to patients' normal stimulant regimen, significantly greater reductions from baseline in ADHD-RS-IV total scores at week 5 (primary endpoint) were achieved with a flexible dose of Clonidine XR 0.1-0.4 mg/day than with placebo. Symptomatic improvement of ADHD was achieved following 2 weeks' treatment with Clonidine XR. In both trials, significantly greater reductions from baseline in ADHD-RS-IV total scores were apparent at week 2 onwards for recipients of Clonidine XR than for recipients of placebo. Clonidine XR was generally well tolerated as monotherapy and as adjunctive therapy with stimulant regimens in clinical trials in children and adolescents.