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ABT 594 hydrochloride
Selective α4β2 nAChR agonist (EC50 = 140 nM for human α4β2 nAChRs, in vitro). Exhibits >900-fold selectivity for α4β2 nAChRs over other neurotransmitter receptors. Displays analgesic properties in various animal models of pain. Potentiates gabapentin mediated analgesia. Also demonstrates cognitive enhancement effects in rodent model of attention deficit.
|Storage||Store at -20°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 235.11. Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|1 mM||4.25 mL||21.27 mL||42.53 mL|
|5 mM||0.85 mL||4.25 mL||8.51 mL|
|10 mM||0.43 mL||2.13 mL||4.25 mL|
|50 mM||0.09 mL||0.43 mL||0.85 mL|
References are publications that support the biological activity of the product.
Donnelly-Roberts et al (1998) ABT-594 [(R)-5-(2-azetidinylmethoxy)-2-chloropyridine]: a novel, orally effective analgesic acting via neuronal nicotinic acetylcholine receptors: I. In vitro characterization. J.Pharmacol.Exp.Ther. 285 777 PMID: 9580626
Lynch et al (2005) ABT-594 (a nicotinic acetylcholine agonist): anti-allodynia in a rat chemotherapy-induced pain model. Eur.J.Pharmacol. 509 43 PMID: 15713428
Munro et al (2010) Selective potentiation of gabapentin-mediated antinociception in the rat formalin test by the nicotinic acetylcholine receptor agonist ABT-594. Neuropharmacology 59 208 PMID: 20562022
Mar et al (2017) MAM-E17 rat model impairments on a novel continuous performance task: effects of potential cognitive enhancing drugs. Psychopharmacology (Berl) 234 2837 PMID: 28744563
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Literature in this Area
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Alzheimer's disease (AD) is a degenerative brain disease and the most common cause of dementia, affecting approximately 47 million people worldwide. Updated in 2015, this poster summarizes the structural and functional changes observed in the progression of this neurodegenerative disease, as well as classic AD drug targets.
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.