Atipamezole (MPV 1248)
(Synonyms: 阿替美唑; MPV 1248) 目录号 : GC30791
An α2A-AR antagonist
Cas No.:104054-27-5
Sample solution is provided at 25 µL, 10mM.
;)
,-1-7$$$37316672.jpg');)
;)
;)
$$$36806353.jpg');)
;33(7)%EF%BC%9A546-561$$$37156877.jpg');)
;)
;)
;)
%201124-1138.$$$35908550.jpg');)
%20766-780.$$$37100057.jpg');)
%20418-432.$$$36893736.jpg');)
%EF%BC%9A-240-255.$$$35108512.jpg');)
533-545$$$36543525.jpg');)
%201-13.$$$36600053.jpg');)
;)
Quality Control & SDS
- View current batch:
- Purity: >99.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Atipamezole is an antagonist of α2A-adrenergic receptors (α2A-ARs; Ki = 1.86 nM).1,2 It is selective for α2A-ARs over α2B- and α1-ARs (Kis = 1,949.83 and 13,300 nM, respectively), as well as over 40 receptors, ion channels, and transporters (IC50s = 540->10,000 nM). Atipamezole (0.04, 0.08, and 1.2 mg/kg) reverses bradycardia and sedation induced by the α2-AR agonist medetomidine in dogs.3 It also prevents hypoalgesia induced by the non-steroidal anti-inflammatory drug (NSAID) ketoprofen in sheep.4 Atipamezole (0.3 mg/kg) enhances contralateral circling behavior induced by apomorphine or L-DOPA and prolongs the duration of action of L-DOPA in a rat model of Parkinson’s disease.5 Formulations containing atipamezole have been used to reverse the sedative and analgesic effects of dexmedetomidine or medetomidine in dogs.
1.Vacher, B., Funes, P., Chopin, P., et al.Rigid analogues of the α2-adrenergic blocker atipamezole: Small changes, big consequencesJ. Med. Chem.53(19)6986-6995(2010) 2.Pertovaara, A., Haapalinna, A., Sirvi?, J., et al.Pharmacological properties, central nervous system effects, and potential therapeutic applications of atipamezole, a selective α2-adrenoceptor antagonistCNS Drug Rev.11(3)273-288(2005) 3.Vainio, O., and V?h?-Vahe, T.Reversal of medetomidine sedation by atipamezole in dogsJ. Vet. Pharmacol. Ther.13(1)15-22(1990) 4.Lizarraga, I., and Chambers, J.P.Involvement of opioidergic and α2-adrenergic mechanisms in the central analgesic effects of non-steroidal anti-inflammatory drugs in sheepRes. Vet. Sci.80(2)194-200(2006) 5.Haapalinna, A., Leino, T., and Heinonen, E.The α2-adrenoceptor antagonist atipamezole potentiates anti-Parkinsonian effects and can reduce the adverse cardiovascular effects of dopaminergic drugs in ratsNaunyn Schmiedebergs Arch. Pharmacol.368(5)342-351(2003)
| Cas No. | 104054-27-5 | SDF | |
| 别名 | 阿替美唑; MPV 1248 | ||
| Canonical SMILES | CCC1(C2=CN=CN2)CC3=C(C=CC=C3)C1 | ||
| 分子式 | C14H16N2 | 分子量 | 212.29 |
| 溶解度 | DMSO : ≥ 30 mg/mL (141.32 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。 |
||
| 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 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 4.7105 mL | 23.5527 mL | 47.1054 mL |
| 5 mM | 0.9421 mL | 4.7105 mL | 9.4211 mL |
| 10 mM | 0.4711 mL | 2.3553 mL | 4.7105 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。
Atipamezole
Learn about the pharmacology, applications, and administration of this alpha2-adrenergic antagonist.
Ketamine-dexmedetomidine combined with local anesthesia, with or without different doses of atipamezole in the postoperative period, for orchiectomy in cats
Objective: To evaluate the anesthetic and cardiopulmonary effects of ketamine-dexmedetomidine combined with local anesthesia, associated or not in the postoperative period with different doses of atipamezole, for orchiectomy in cats.
Animals: 24 healthy cats.
Procedures: Cats received ketamine (7 mg/kg) combined with dexmedetomidine (10 ?g/kg) IM, and 1 mL of saline (group KDSAL), 25 ?g/kg (group KDAT25), or 50 ?g/kg (group KDAT50) of atipamezole IV, postoperatively. All cats received local anesthesia (2 mg/kg of lidocaine) intratesticular and SC. Physiologic variables were recorded at baseline and at time points during anesthesia. Ketamine rescue dose (1 mg/kg) was recorded. The quality of recovery, the degree of sedation, and side effects were evaluated postoperatively.
Results: 2 cats received a single additional bolus of ketamine to perform local anesthesia. Heart rate was lower in KDSAL, KDAT25, and KDAT50 during anesthesia, compared with baseline. Hypertension was observed intraoperatively in all groups. The time to head up, pedal reflex regained time, time to sternal recumbency, and time to standing were shorter in KDAT25 and KDAT50 compared to KDSAL. Lower sedation scores were assigned sooner to KDAT25 and KDAT50 than KDSAL. All groups resulted in low recovery quality scores and no side effects.
Clinical relevance: At the doses used, ketamine-dexmedetomidine combined with local anesthesia allowed the performance of orchiectomy. Rescue dose of ketamine for performing local anesthesia may be required. This combination can result in hypertension. Both atipamezole doses shortened the anesthetic recovery, without differences among them, and side effects.
Recommended doses of medetomidine-midazolam-butorphanol with atipamezole for preventing hypothermia in mice
A non-narcotic anesthetic combination (Me/Mi/Bu) of medetomidine (Me), midazolam (Mi), and butorphanol (Bu) has been recommended as the injectable anesthesia in mice. An original dose of Me/Mi/Bu (0.3/4.0/5.0 mg/kg) has provided sufficient anesthetic duration of 40-50 min in mice. In addition, atipamezole is available for reversal of Me/Mi/Bu anesthesia. As an adverse effect of Me/Mi/Bu anesthesia, however, severe hypothermia has been also observed in mice. In the present study, we investigated 1) the main agent in Me/Mi/Bu to cause of hypothermia, 2) the effects of the differential doses of atipamezole on hypothermia induced by Me/Mi/Bu anesthesia and on the plasma levels of creatinine phosphokinase and transaminases, and 3) those recommended doses for preventing hypothermia induced by Me/Mi/Bu anesthesia in mice. The results suggested that 1) the 汐2-agonist medetomidine is most likely to induce hypothermia in mice under Me/Mi/Bu anesthesia, 2) the antagonism of atipamezole within proper dose range is effective in promoting the recovery from Me/Mi/Bu-induced hypothermia, and 3) Me/Mi/Bu at the recommended dose of 0.2/6.0/10.0 mg/kg enable to provide anesthetic effects for 40 min and is more considerable to prevent the hypothermia than that at the original dose of 0.3/4.0/5.0 mg/kg.
Pharmacological properties, central nervous system effects, and potential therapeutic applications of atipamezole, a selective alpha2-adrenoceptor antagonist
Atipamezole is an alpha2-adrenoceptor antagonist with an imidazole structure. Receptor binding studies indicate that its affinity for alpha2-adrenoceptors and its alpha2/alpha1 selectivity ratio are considerably higher than those of yohimbine, the prototype alpha2-adrenoceptor antagonist. Atipamezole is not selective for subtypes of alpha2-adrenoceptors. Unlike many other alpha2-adrenoceptor antagonists, it has negligible affinity for 5-HT1A and I2 binding sites. Atipamezole is rapidly absorbed and distributed from the periphery to the central nervous system. In humans, atipamezole at doses up to 30 mg/subject produced no cardiovascular or subjective side effects, while at a high dose (100 mg/subject) it produced subjective symptoms, such as motor restlessness, and an increase in blood pressure. Atipamezole rapidly reverses sedation/anesthesia induced by alpha2-adrenoceptor agonists. Due to this property, atipamezole is commonly used by veterinarians to awaken animals from sedation/anesthesia induced by alpha2-adrenoceptor agonists alone or in combination with various anesthetics. Atipamezole increased sexual activity in rats and monkeys. In animals with sustained nociception, atipamezole increased pain-related responses by blocking the noradrenergic feedback inhibition of pain. In tests assessing cognitive functions, atipamezole at low doses has beneficial effects on alertness, selective attention, planning, learning, and recall in experimental animals, but not necessarily on short-term working memory. At higher doses atipamezole impaired performance in tests of cognitive functions, probably due to noradrenergic overactivity. Recent experimental animal studies suggest that atipamezole might have beneficial effects in the recovery from brain damage and might potentiate the anti-Parkinsonian effects of dopaminergic drugs. In phase I studies atipamezole has been well tolerated by human subjects.
Evaluation of atipamezole as a treatment for dexmedetomidine-induced cardiovascular depression in anesthetized cats
Objective: To evaluate the cardiovascular effects of atipamezole administered at half the volume or the same volume as dexmedetomidine to isoflurane-anesthetized cats.
Animals: 6 adult (1 to 2 years old) domestic shorthair cats (body weight, 3 to 6 kg).
Procedures: Each cat was anesthetized with isoflurane and rocuronium 3 times; there was a 1-week washout period between successive anesthetic procedures. For each anesthetic procedure, dexmedetomidine (5 米g/kg) was administered IV. Five minutes after dexmedetomidine was administered, atipamezole (25 or 50 米g/kg) or saline (0.9% NaCl) solution was administered IM. Pulse rate, mean arterial blood pressure (MAP), cardiac output (CO), and systemic vascular resistance (SVR) were measured during anesthesia before dexmedetomidine administration (baseline), after dexmedetomidine administration, and 15, 30, 60, and 120 minutes after administration of atipamezole or saline solution. Pulse rate and MAP were also recorded when MAP was at its lowest value. Hemodynamic variables were compared among treatments at baseline, after dexmedetomidine administration, and after administration of atipamezole or saline solution. Effects of treatment and time on all variables were assessed with mixed-effects models.
Results: Both doses of atipamezole resulted in a significantly lower MAP than did saline solution. Pulse rate, CO, and SVR were not significantly different among treatments after atipamezole or saline solution were administered.
Conclusions and clinical relevance: Atipamezole administered IM at half the volume or the same volume as dexmedetomidine was ineffective at increasing pulse rate or CO in anesthetized cats that received dexmedetomidine. However, atipamezole caused short-lasting but severe arterial hypotension.