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TC 1698 dihydrochloride
Selective nicotinic α7 receptor agonist (EC50 = 440 nM). Also displays weak partial agonist/antagonist activity at β-subunit-containing receptors. Neuroprotective.
|Storage||Desiccate at RT|
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 275.22. 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||3.63 mL||18.17 mL||36.33 mL|
|5 mM||0.73 mL||3.63 mL||7.27 mL|
|10 mM||0.36 mL||1.82 mL||3.63 mL|
|50 mM||0.07 mL||0.36 mL||0.73 mL|
References are publications that support the biological activity of the product.
Marrero et al (2004) The neuroprotective effect of 2-(3-Pyridyl)-1-azabicyclo[3.2.2]nonane (TC-1698), a novel α7 ligand, is prevented through angiotensin II activation of a tyrosine phosphatase. J.Pharmacol.Exp.Ther. 309 16 PMID: 14722323
Papke et al (2005) Rhesus monkey α7 nicotinic acetylcholine receptors: comparisons to human α7 receptors expressed in Xenopus oocytes. Eur.J.Pharmacol. 524 11 PMID: 16266703
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Citations for TC 1698 dihydrochloride
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Literature in this Area
Tocris offers the following scientific literature in this area to showcase our products. We invite you to request* your copy today!
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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.
Learning & Memory Poster
Recognition memory enables us to make judgements about whether or not we have encountered a particular stimulus before. This poster outlines the cellular mechanisms underlying recognition memory and its links to long-term depression, as well as the use of pharmacological intervention to assess the role of neurotransmitters in recognition memory.
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.