Potent, highly selective α2-adrenoceptor agonist (Ki values are 1.08 and 1750 nM for α2- and α1-adrenoceptors respectively). Displays greater selectivity over α1-adrenoceptors than clonidine and UK 14,304 (1620-, 220- and 300-fold respectively). Inhibits twitch response in electrically stimulated mouse vas deferens (pD2 = 9.0). Active in vivo; displays hypotensive, bradycardic, sedative, anxiolytic, hypothermic and analgesic effects.
|Storage||Desiccate at RT|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
All Tocris products are intended for laboratory research use only.
References are publications that support the biological activity of the product.
Virtanen et al (1988) Characterization of the selectivity, specificity and potency of medetomidine as an α2-adrenoceptor agonist. Eur.J.Pharmacol. 150 9 PMID: 2900154
Savola et al (1986) Evidence for medetomidine as a selective and potent agonist at alpha 2-adrenoceptors. J.Aut.Pharmacol. 6 275
Scheinin et al (1989) Medetomidine - a novel α2-adrenoceptor agonist: a review of its pharmacodynamic effects. Prog.Neuro-Psychopharm.Biol.Psychiat. 13 635
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Major depressive disorder is characterized by depressed mood and a loss of interest and/or pleasure. Updated in 2015 this poster highlights presynaptic and postsynaptic targets for the potential treatment of major depressive disorder, as well as outlining the pharmacology of currently approved antidepressant drugs.
Peripheral sensitization is the reduction in the threshold of excitability of sensory neurons that results in an augmented response to a given external stimulus. This poster outlines the excitatory and inhibitory signaling pathways involved in modulation of peripheral sensitization. The role of ion channels, GPCRs, neurotrophins, and cytokines in sensory neurons are also described.
Parkinson's disease (PD) causes chronic disability and is the second most common neurodegenerative condition. This poster outlines the neurobiology of the disease, as well as highlighting current therapeutic treatments for symptomatic PD, and emerging therapeutic strategies to delay PD onset and progression.