Acepromazine (maleate)
(Synonyms: 乙酰丙嗪马来酸酯,Acetopromazine maleate; Acetylpromazine maleate) 目录号 : GC45371
A phenothiazine antipsychotic
Cas No.:3598-37-6
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
Acepromazine is a phenothiazine antipsychotic, analog of chlorpromazine , and a dopamine receptor antagonist.1 It also binds to muscarinic receptors in rat brain (IC50 = 350 nM) and inhibits contractions of guinea pig ileum induced by acetylcholine .2 Acepromazine inhibits morphine-induced vomiting in dogs.3 It also inhibits development of a conditioned avoidance response, unconditioned escape response, and catalepsy in rats (ED50s = 0.98, 3.1, and 17 mg/kg, respectively).4 Formulations containing acepromazine have been used as tranquilizers and anesthetics premedicant in small and large animal veterinary care.
References
1. Monteiro, E.R., Teixeira Neto, F.J., Castro, V.B., et al. Effects of acepromazine on the cardiovascular actions of dopamine in anesthetized dogs. Vet. Anaesth. Analg. 34(5), 312-321 (2007).
2. Fjalland, B., Christensen, A.V., and Hyttel, J. Peripheral and central muscarinic receptor affinity of psychotropic drugs. Naunyn. Schmiedebergs. Arch. Pharmacol. 301(1), 5-9 (1977).
3. Koh, R.B., Isaza, N., Xie, H., et al. Effects of maropitant, acepromazine, and electroacupuncture on vomiting associated with administration of morphine in dogs. J. Am. Vet. Med. Assoc. 244(7), 820-829 (2014).
4. J., A. Pharmacological specificity of conditioned avoidance response inhibition in rats: Inhibition by neuroleptics and correlation to dopamine receptor blockade. Acta. Pharmacol. Toxicol. (Copenh). 51(4), 321-329 (1982).
| Cas No. | 3598-37-6 | SDF | |
| 别名 | 乙酰丙嗪马来酸酯,Acetopromazine maleate; Acetylpromazine maleate | ||
| Canonical SMILES | CN(C)CCCN1C2=C(C=CC(C(C)=O)=C2)SC3=CC=CC=C31.OC(/C=C\C(O)=O)=O | ||
| 分子式 | C19H22N2OS.C4H4O4 | 分子量 | 442.5 |
| 溶解度 | DMF: 1mg/mL,DMSO: 3mg/mL,Ethanol: 2mg/mL,PBS (pH 7.2): 2mg/mL | 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 | 2.2599 mL | 11.2994 mL | 22.5989 mL |
| 5 mM | 0.452 mL | 2.2599 mL | 4.5198 mL |
| 10 mM | 0.226 mL | 1.1299 mL | 2.2599 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 | ||||||||||
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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。
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Evaluation of whether Acepromazine maleate causes fentanyl to decrease the minimum alveolar concentration of isoflurane in cats
Am J Vet Res 2021 May;82(5):352-357.PMID:33904805DOI:10.2460/ajvr.82.5.352.
Objective: To determine whether isoflurane-anesthetized cats with demonstrated resistance to the immobilizing effects of fentanyl would exhibit naltrexone-reversible sparing of the minimum alveolar concentration (MAC) of isoflurane when fentanyl was coadministered with the centrally acting catecholamine receptor antagonist Acepromazine. Animals: 5 healthy male purpose-bred cats. Procedures: Anesthesia was induced and maintained with isoflurane in oxygen. Baseline isoflurane MAC was measured by use of a standard tail clamp stimulus and bracketing study design. Afterward, fentanyl was administered IV to achieve a plasma concentration of 100 ng/mL by means of target-controlled infusion, and isoflurane MAC was remeasured. Next, Acepromazine maleate (0.1 mg/kg) was administered IV, and isoflurane MAC was remeasured. Finally, isoflurane concentration was equilibrated at 70% of the baseline MAC. Movement of cats in response to tail clamping was tested before and after IV bolus administration of naltrexone. Physiologic responses were compared among treatment conditions. Results: Isoflurane MAC did not differ significantly between baseline and fentanyl infusion (mean ± SD, 1.944 ± 0.111% and 1.982 ± 0.126%, respectively). Acepromazine with fentanyl significantly decreased isoflurane MAC to 1.002 ± 0.056% of 1 atm pressure. When isoflurane was increased to 70% of the baseline MAC, no cats moved in response to tail clamping before naltrexone administration, but all cats moved after naltrexone administration. Conclusions and clinical relevance: Acepromazine caused fentanyl to decrease the isoflurane MAC in cats that otherwise did not exhibit altered isoflurane requirements with fentanyl alone. Results suggested that opioid-mediated increases in brain catecholamine concentrations in cats counteract the opioid MAC-sparing effect.
A retrospective study on the use of Acepromazine maleate in dogs with seizures
J Am Anim Hosp Assoc 2006 Jul-Aug;42(4):283-9.PMID:16822767DOI:10.5326/0420283.
Use of Acepromazine (i.e., acetylpromazine) maleate in dogs with a history of seizures is reportedly contraindicated because of the risk of decreasing the seizure threshold in these animals. In this retrospective study, Acepromazine was administered for tranquilization to 36 dogs with a prior history of seizures and to decrease seizure activity in 11 dogs. No seizures were seen within 16 hours of Acepromazine administration in the 36 dogs that received the drug for tranquilization during hospitalization. After Acepromazine administration, seizures abated for 1.5 to 8 hours (n=6) or did not recur (n=2) in eight of 10 dogs that were actively seizing. Excitement-induced seizure frequency was reduced for 2 months in one dog.
Acepromazine pharmacokinetics: a forensic perspective
Vet J 2012 Oct;194(1):48-54.PMID:22534188DOI:10.1016/j.tvjl.2012.03.017.
Acepromazine (ACP) is a useful therapeutic drug, but is a prohibited substance in competition horses. The illicit use of ACP is difficult to detect due to its rapid metabolism, so this study investigated the ACP metabolite 2-(1-hydroxyethyl)promazine sulphoxide (HEPS) as a potential forensic marker. Acepromazine maleate, equivalent to 30mg of ACP, was given IV to 12 racing-bred geldings. Blood and urine were collected for 7days post-administration and analysed for ACP and HEPS by liquid chromatography-mass spectrometry (LC-MS). Acepromazine was quantifiable in plasma for up to 3h with little reaching the urine unmodified. Similar to previous studies, there was wide variation in the distribution and metabolism of ACP. The metabolite HEPS was quantifiable for up to 24h in plasma and 144h in urine. The metabolism of ACP to HEPS was fast and erratic, so the early phase of the HEPS emergence could not be modelled directly, but was assumed to be similar to the rate of disappearance of ACP. However, the relationship between peak plasma HEPS and the y-intercept of the kinetic model was strong (P=0.001, r(2)=0.72), allowing accurate determination of the formation pharmacokinetics of HEPS. Due to its rapid metabolism, testing of forensic samples for the parent drug is redundant with IV administration. The relatively long half-life of HEPS and its stable behaviour beyond the initial phase make it a valuable indicator of ACP use, and by determining the urine-to-plasma concentration ratios for HEPS, the approximate dose of ACP administration may be estimated.
Hypotension in the horse induced by Acepromazine maleate
Aust Vet J 1982 Nov;59(5):148-52.PMID:6131662DOI:10.1111/j.1751-0813.1982.tb02761.x.
The hypotensive effect of Acepromazine maleate was related to both the dose and route of administration. The degree and duration of hypotension varied between individual horses. In general, intravenous administration produced a more rapid maximum effect than intramuscular injection and the larger the dose the longer blood pressure remained at low levels. Average systolic pressure (of 6 horses) remained significantly below control values for more than 6 h after an intramuscular injection of 0.05 mg Acepromazine maleate/kg body weight. Respiratory rate was markedly decreased, with the duration, but not the degree of bradypnoea related to the dose administered. A slight, transient decrease in body temperature was observed. Heart rate was not significantly influenced by administration of Acepromazine maleate.
Effects of Acepromazine maleate on platelet function assessed by use of adenosine diphosphate activated- and arachidonic acid- activated modified thromboelastography in healthy dogs
Am J Vet Res 2012 May;73(5):595-601.PMID:22533389DOI:10.2460/ajvr.73.5.595.
Objective: To evaluate the effect of Acepromazine maleate administered IV on platelet function assessed in healthy dogs by use of a modified thromboelastography assay. Animals: 6 healthy adult mixed-breed dogs. Procedures: Dogs received each of 3 treatments (saline [0.9% NaCl] solution [1 to 2 mL, IV] and Acepromazine maleate [0.05 and 0.1 mg/kg, IV]) in a randomized crossover study with a minimum 3-day washout period between treatments. From each dog, blood samples were collected via jugular venipuncture immediately before and 30 and 240 minutes after administration of each treatment. A modified thromboelastography assay, consisting of citrated kaolin-activated (baseline assessment), reptilase-ADP-activated (ADP-activated), and reptilase-arachidonic acid (AA)-activated (AA-activated) thromboelastography, was performed for each sample. Platelet inhibition was evaluated by assessing the percentage change in maximum amplitude for ADP-activated or AA-activated samples, compared with baseline values. Percentage change in maximum amplitude was analyzed by use of Skillings-Mack tests with significance accepted at a family-wise error rate of P < 0.05 by use of Bonferroni corrections for multiple comparisons. Results: No significant differences were found in the percentage change of maximum amplitude from baseline for ADP-activated or AA-activated samples among treatments at any time. Conclusions and clinical relevance: Platelet function in dogs, as assessed by use of a modified thromboelastography assay, was not inhibited by Acepromazine at doses of 0.05 or 0.1 mg/kg, IV. This was in contrast to previous reports in which it was suggested that Acepromazine may alter platelet function via inhibition of ADP and AA.