ABT 089 dihydrochloride
High affinity and selective α4β2 partial agonist (Ki = 16 nM). Exhibits >1000-fold and >10,000-fold selectivity for α4β2 over α1β1γ1 and α7 receptors respectively. Neuroprotective against glutamate-induced toxicity in rat cortical neurons in vitro. Enhances cognitive performance in vivo. Orally bioavailable and brain penetrant.
|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.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 265.18. Batch specific molecular weights may vary from batch to batch due to solvent 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||3.77 mL||18.86 mL||37.71 mL|
|5 mM||0.75 mL||3.77 mL||7.54 mL|
|10 mM||0.38 mL||1.89 mL||3.77 mL|
|50 mM||0.08 mL||0.38 mL||0.75 mL|
References are publications that support the products' biological activity.
Rueter et al (2004) ABT-089: pharmacological properties of a neuronal nicotinic acetylcholine receptor agonist for the potential treatment of cognitive disorders. CNS Drug Rev. 10 167 PMID: 15179445
Sullivan et al (1997) ABT-089 [2-methyl-3-(2-(S)-pyrrolidinylmethoxy)pyridine]: I. A potent and selective cholinergic channel modulator with neuroprotective properties. J.Pharmacol.Exp.Ther. 283 235 PMID: 9336329
Decker et al (1997) ABT-089 [2-methyl-3-(2-(S)-pyrrolidinylmethoxy)pyridine dihydrochloride]: II. A novel cholinergic channel modulator with effects on cognitive performance in rats and monkeys. J.Pharmacol.Exp.Ther. 283 247 PMID: 9336330
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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.