Atipamezole - CAS 104054-27-5
Catalog number: 104054-27-5
Category: Inhibitor
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
Molecular Weight:
Adrenergic Receptor
Atipamezole, a 4-substituted imidazole derivative, is an alpha2-adrenoceptor blocker which could be used for animals to recover from the anesthesia by lowering blood pressure and increasing heart rate and breathing rate.
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Off-white to light yellow crystal powder
DMSO: ≥ 30 mg/mL
-20ºC Freeze
Atipamezole is an alpha2-adrenoceptor blocker which could be used for animals to recover from the anesthesia by lowering blood pressure and increasing heart rate and breathing rate.
Shelf Life:
As supplied, 2 years from the QC date provided on the Certificate of Analysis, when stored properly
Boiling Point:
367.1ºC at 760 mmHg
1.115 g/cm3
Canonical SMILES:
1.Blood biochemical changes in mice after administration of a mixture of three anesthetic agents.
Ochiai Y1, Iwano H, Sakamoto T, Hirabayashi M, Kaneko E, Watanabe T, Yamashita K, Yokota H. J Vet Med Sci. 2016 Feb 19. [Epub ahead of print]
Currently, from the viewpoint of animal welfare, anesthesia or analgesia is required during experimental procedures in animals that are likely to cause pain. A part of these anesthetics have been reported to influence a blood biochemical level. It is important for us to understand the effect of the anesthetic on blood biochemistry when we choose the anesthetic agent to be used in experiments. In this study, we examined the blood biochemical changes in mice after administration of a new mixture of three anesthetic agents - medetomidine / midazolam / butorphanol (MMB). We subcutaneously administered two dose combinations of MMB (0.45 / 6 / 7.5 and 0.9 / 12 / 15 mg/kg) in mice, followed by administration of atipamezole, for reversal of anesthetic effects, after 1 hr. Thereafter, blood biochemistry was assessed at 1, 4 and 24 hr after MMB administration. We observed that MMB administration caused a transient increase in blood sugar, inorganic phosphorus, potassium and creatine kinase levels.
2.Dexmedetomidine Postconditioning Reduces Brain Injury after Brain Hypoxia-Ischemia in Neonatal Rats.
Ren X1,2, Ma H3, Zuo Z4. J Neuroimmune Pharmacol. 2016 Mar 2. [Epub ahead of print]
Perinatal asphyxia can lead to death and severe disability. Brain hypoxia-ischemia (HI) injury is the major pathophysiology contributing to death and severe disability after perinatal asphyxia. Here, seven-day old Sprague-Dawley rats were subjected to left brain HI. Dexmedetomidine was given intraperitoneally after the brain HI. Yohimbine or atipamezole, two α2 adrenergic receptor antagonists, were given 10 min before the dexmedetomidine injection. Neurological outcome was evaluated 7 or 28 days after the brain HI. Frontal cerebral cortex was harvested 6 h after the brain HI. Left brain HI reduced the left cerebral hemisphere weight assessed 7 days after the brain HI. This brain tissue loss was dose-dependently attenuated by dexmedetomidine. Dexmedetomidine applied within 1 h after the brain HI produced this effect. Dexmedetomidine attenuated the brain HI-induced brain tissue and cell loss as well as neurological and cognitive dysfunction assessed from 28 days after the brain HI.
Pon K, Caulkett N, Woodbury M. J Zoo Wildl Med. 2016 Mar;47(1):29-37. doi: 10.1638/2015-0121.1.
Alfaxalone is a neurosteroid that interacts with gamma-aminobutyric type A receptors to produce central nervous system depression and muscle relaxation. The effects of alfaxalone vary from sedation to general anesthesia. Alfaxalone is synergistic with other tranquilizers and sedatives and therefore has the potential to improve existing alpha-2 adrenergic agonist-based combinations used for wildlife immobilization. The objective of this study was to determine the efficacy and cardiopulmonary effects of a medetomidine-azaperone-alfaxalone (MAA) combination in captive white-tailed deer (Odocoileus virginianus). Eight captive white-tailed deer were restrained in a drop-floor chute; hand injected i.m. with 0.15 mg/kg medetomidine, 0.2 mg/kg azaperone, and 0.5 mg/kg alfaxalone; and released into a small enclosure for observation. The deer were maintained in lateral recumbency for a total time from postinjection (PI) of the drug of 60 min. At 60 min PI, atipamezole was administered i.
4.The adrenergic α2 antagonist atipamezole alters the behavioural effects of pramipexole and increases pramipexole concentration in blood plasma.
McCormick PN1, Fletcher PJ2, Wilson VS3, Remington GJ4. Life Sci. 2016 Mar 11. pii: S0024-3205(16)30165-5. doi: 10.1016/j.lfs.2016.03.017. [Epub ahead of print]
Pramipexole is a dopaminergic agonist used in Parkinson's disease treatment. It is thought to exert its therapeutic and side effects through actions on dopamine D3 receptors. In a recent study, we found that at doses occupying D3 but not D2 receptors pramipexole reduced locomotion and operant responding for primary and conditioned reinforcement. These effects, however, were not blocked by a D3 receptor antagonist and were present in D3 knockout mice, suggesting non-D3 receptor mechanisms. Among the next highest affinity binding sites of pramipexole are adrenergic α2 receptors. Here we explored α2 receptor involvement in the behavioural effects of pramipexole. We found that the α2 antagonist atipamezole, which was itself behaviourally silent, counteracted pramipexole's reduction of locomotion, but not operant responding for water or a conditioned reinforcer. The resulting behavioural profile was similar to that of a higher dose of pramipexole, leading to the hypothesize that atipamezole mediates its behavioural effects by increasing pramipexole effective dose.
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CAS 104054-27-5 Atipamezole

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