Pempidine
(Synonyms: 五甲基哌啶,1,2,2,6,6-Pentamethylpiperidine) 目录号 : GC33726
Pempidine (Pyrilene, Perolysen, 1,2,2,6,6-Pentamethylpiperidine) is a long-acting ganglion-blocking compound.
Cas No.:79-55-0
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
Pempidine (Pyrilene, Perolysen, 1,2,2,6,6-Pentamethylpiperidine) is a long-acting ganglion-blocking compound.
| Cas No. | 79-55-0 | SDF | |
| 别名 | 五甲基哌啶,1,2,2,6,6-Pentamethylpiperidine | ||
| Canonical SMILES | CC1(C)CCCC(C)(C)N1C | ||
| 分子式 | C10H21N | 分子量 | 155.28 |
| 溶解度 | DMSO : ≥ 2.1 mg/mL (13.52 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 | 6.44 mL | 32.1999 mL | 64.3998 mL |
| 5 mM | 1.288 mL | 6.44 mL | 12.88 mL |
| 10 mM | 0.644 mL | 3.22 mL | 6.44 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。
Absorption, metabolism and elimination of Pempidine in the rat
Br J Pharmacol Chemother 1959 Jun;14(2):202-8.PMID:13662574DOI:10.1111/j.1476-5381.1959.tb01384.x.
Pempidine (1,2,2,6,6-pentamethylpiperidine) is a ganglion blocking agent introduced recently for the treatment of hypertension by oral administration of its hydrogen tartrate. It can be estimated colorimetrically by coupling with methyl orange, or fluorimetrically by reaction with eosin in xylene, the limits of sensitivity being 0.5 mug./ml. and 0.001 mug./ml. respectively. These methods, combined with appropriate extraction techniques, were suitable for estimating Pempidine in aqueous solutions of its salts, in biological fluids and the like, and for investigating the biochemical properties of the drug when given orally to rats in amounts similar to those used clinically.When administered orally to rats Pempidine was rapidly absorbed, the maximum concentration in plasma being attained after 30 min. The drug was preferentially taken up by erythrocytes and a red cell/plasma partition ratio of about 1.2 established with clinical doses. Pempidine was soon distributed throughout the body, including the cerebrospinal fluid, and the highest concentrations were found in kidney, spleen and liver. Pempidine also entered the foetus and passed thence into the amniotic fluid. Protein-binding of the drug occurred only to a very limited extent and there was little evidence that it was metabolized. Pempidine was excreted rapidly in urine during 24 hr. following oral administration.
The pharmacological actions of Pempidine and its ethyl homologue
Br J Pharmacol Chemother 1958 Dec;13(4):501-20.PMID:13618559DOI:10.1111/j.1476-5381.1958.tb00246.x.
Pempidine, and other highly active ganglion blocking agents of the polyalkylpiperidine series, were developed from tertiary alkylamines, themselves weakly active, on the hypothesis that high activity was conferred by the presence in the molecule of a sterically hindered secondary or tertiary nitrogen atom. Pempidine and its N-ethyl homologue (26539) resembled mecamylamine qualitatively. All three drugs blocked sympathetic and parasympathetic ganglia; this action was slow in onset and protracted. They blocked neuromuscular transmission, but only about one hundredth as powerfully as ganglionic transmission. They caused a fall in amplitude and rate of the isolated heart, and reduced coronary flow. They had local anaesthetic properties in one of four tests used. They caused tremor. All were well absorbed when administered orally. Pempidine was about twice as active as mecamylamine on ganglia, but only about one half to one quarter as toxic as judged by death, growth, induction of tremor, or cardiotoxicity. Compound 26539 was also quantitatively superior to mecamylamine in respect of these safety margins, but unlike Pempidine or mecamylamine damaged the pituitary gland and testis when administered daily for several months. The mode of action of the three drugs is discussed: the results give tentative support for the hypothesis that their action is intracellular.
Pharmacological evaluation of the antagonism of nicotine's central effects by mecamylamine and Pempidine
J Pharmacol Exp Ther 1990 Jul;254(1):45-51.PMID:2366189doi
The nature of mecamylamine's and Pempidine's antagonism of nicotine in the central nervous system has not been defined clearly. Although these compounds are thought to be noncompetitive antagonists in the brain due to the fact that they do not compete effectively for agonist binding to brain tissue in vitro, pharmacological evidence is lacking. The alteration of nicotine's dose-response curves for depression of spontaneous activity and antinociception was determined in the presence of increasing concentrations of Pempidine. Pempidine was found to increase the ED50 of nicotine (0.73 mg/kg) for depression of spontaneous activity in a dose-related manner. At a dose of 3 mg/kg, Pempidine increased nicotine's ED50 4.7-fold. The maximum effect of nicotine was achieved in the presence of the highest dose of Pempidine, suggesting competitive antagonism. However, Pempidine did decrease the maximum effect of nicotine in producing antinociception at doses that increased the ED50 13.7-fold which suggests a noncompetitive action. The structural requirements for mecamylamine's antagonism of these nicotine effects was also determined in order to address the question of whether the antagonists are interacting at a receptor site. The structure-activity relationships of the mecamylamine analogs revealed that the N-, 2- and 3-methyl groups were important for optimal potency. Optical isomerism was found to have little effect on potency. Addition of pyridinyl groups to the nitrogen abolished the activity of these compounds. The structural requirements for the agonists and antagonists therefore appear to be quite different. The alterations produced similar results for antagonism of both effects of nicotine. Mecamylamine and Pempidine therefore appear to exhibit both competitive and noncompetitive properties in antagonizing the central effects of nicotine.
Action of chlorothiazide on the distribution excretion and hypotensive effect of Pempidine in man
Br J Pharmacol Chemother 1961 Dec;17(3):488-506.PMID:13887050DOI:10.1111/j.1476-5381.1961.tb01136.x.
When chlorothiazide is given to hypertensive patients who are receiving Pempidine a rise in plasma Pempidine concentration occurs and this is proportionately greater than the additional fall in blood pressure. After Pempidine has been added to human whole blood in vitro or in vivo the ratio of the Pempidine concentration in the red cells to that in the plasma falls in the course of 1 hr from an initial value greater than 2 to about 1.2. If chlorothiazide is present also, however, the ratio remains constant at 0.7. Changes in the plasma Pempidine concentration in vivo probably result from the binding of Pempidine to plasma protein in the presence of chlorothiazide. This has been observed in vitro by a dialysis technique.
Antagonism of the nicotine-induced changes of the striatal dopamine metabolism in mice by mecamylamine and Pempidine
Naunyn Schmiedebergs Arch Pharmacol 1988 Aug;338(2):169-73.PMID:3185744DOI:10.1007/BF00174865.
The ability of nicotinic receptor blockers, mecamylamine and Pempidine, to antagonize the changes in striatal dopamine (DA) metabolism induced by repeated nicotine administration was studied. The contents of DA and its metabolites 3-methoxytyramine (3-MT), 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) were measured. Mice kept at 20-22 degrees C were given nicotine, 3 mg/kg, s.c., four times, at 30 min intervals, and sacrificed 20 min after the last dose. Hexamethonium, 10 mg/kg, i.p., was administered at 30 min before the first nicotine dose in order to prevent the peripheral effects of nicotine. Mecamylamine, 0.6 or 10 mg/kg, i.p., and Pempidine, 0.6 or 20 mg/kg, i.p., were given at 60 min before sacrifice. Mecamylamine and Pempidine decreased clearly the striatal 3-MT content, which suggests that the nigrostriatal dopaminergic neurons are physiologically controlled by a stimulatory nicotinic mechanism. The repeatedly administered nicotine caused deep hypothermia, and increased the striatal DOPAC content but decreased the 3-MT and HVA contents. The small dose of mecamylamine, which was the only dose found to effectively antagonize the nicotine-induced hypothermia, antagonized the decrease of HVA content. The large but not the small doses of mecamylamine and Pempidine antagonized the nicotine-induced increase of DOPAC content but none of the doses studied antagonized the decrease of 3-MT content. Thus it seems that nicotine decreases the 3-MT content by a mechanism distinct from the mechanism mediating the increase of the DOPAC content. The decreased 3-MT content most probably results from desensitization of nicotinic cholinergic receptors (nAChR) and following decrease of cholinergic regulation of nigrostriatal dopaminergic neurons.(ABSTRACT TRUNCATED AT 250 WORDS)