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TC 1698 dihydrochloride

CAS# 787587-06-8

TC 1698 dihydrochloride

Catalog No. BCC7394----Order now to get a substantial discount!

Product Name & Size Price Stock
TC 1698 dihydrochloride: 5mg $104 In Stock
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Chemical structure

TC 1698 dihydrochloride

3D structure

Chemical Properties of TC 1698 dihydrochloride

Cas No. 787587-06-8 SDF Download SDF
PubChem ID 21094258 Appearance Powder
Formula C13H20Cl2N2 M.Wt 275.22
Type of Compound N/A Storage Desiccate at -20°C
Solubility Soluble to 100 mM in water
Chemical Name 2-pyridin-3-yl-1-azabicyclo[3.2.2]nonane;dihydrochloride
SMILES C1CC(N2CCC1CC2)C3=CN=CC=C3.Cl.Cl
Standard InChIKey ZQUQBCHNSBJMCG-UHFFFAOYSA-N
Standard InChI InChI=1S/C13H18N2.2ClH/c1-2-12(10-14-7-1)13-4-3-11-5-8-15(13)9-6-11;;/h1-2,7,10-11,13H,3-6,8-9H2;2*1H
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Biological Activity of TC 1698 dihydrochloride

DescriptionSelective nicotinic α7 receptor agonist (EC50 = 440 nM). Also displays weak partial agonist/antagonist activity at β-subunit-containing receptors. Neuroprotective.

TC 1698 dihydrochloride Dilution Calculator

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TC 1698 dihydrochloride Molarity Calculator

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Preparing Stock Solutions of TC 1698 dihydrochloride

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 3.6335 mL 18.1673 mL 36.3346 mL 72.6691 mL 90.8364 mL
5 mM 0.7267 mL 3.6335 mL 7.2669 mL 14.5338 mL 18.1673 mL
10 mM 0.3633 mL 1.8167 mL 3.6335 mL 7.2669 mL 9.0836 mL
50 mM 0.0727 mL 0.3633 mL 0.7267 mL 1.4534 mL 1.8167 mL
100 mM 0.0363 mL 0.1817 mL 0.3633 mL 0.7267 mL 0.9084 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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References on TC 1698 dihydrochloride

Rhesus monkey alpha7 nicotinic acetylcholine receptors: comparisons to human alpha7 receptors expressed in Xenopus oocytes.[Pubmed:16266703]

Eur J Pharmacol. 2005 Nov 7;524(1-3):11-8.

An alpha7 nicotinic acetylcholine receptor sequence was cloned from Rhesus monkey (Macaca mulatta). This clone differs from the mature human alpha7 nicotinic acetylcholine receptor in only four amino acids, two of which are in the extracellular domain. The monkey alpha7 nicotinic receptor was characterized in regard to its functional responses to acetylcholine, choline, cytisine, and the experimental alpha7-selective agonists 4OH-GTS-21, TC-1698, and AR-R17779. For all of these agonists, the EC(50) for activation of monkey receptors was uniformly higher than for human receptors. In contrast, the potencies of mecamylamine and MLA for inhibiting monkey and human alpha7 were comparable. Acetylcholine and 4OH-GTS-21 were used to probe the significance of the single point differences in the extracellular domain. Mutants with the two different amino acids in the extracellular domain of the monkey receptor changed to the corresponding sequence of the human receptor had responses to these agonists that were not significantly different in EC(50) from wild-type human alpha7 nicotinic receptors. Monkey alpha7 nicotinic receptors have a serine at residue 171, while the human receptors have an asparagine at this site. Monkey S171N mutants were more like human alpha7 nicotinic receptors, while mutations at the other site (K186R) had relatively little effect. These experiments point toward the basic utility of the monkey receptor as a model for the human alpha7 nicotinic receptor, albeit with the caveat that these receptors will vary in their agonist concentration dependency. They also point to the potential importance of a newly identified sequence element for modeling the specific amino acids involved with receptor activation.

The neuroprotective effect of 2-(3-pyridyl)-1-azabicyclo[3.2.2]nonane (TC-1698), a novel alpha7 ligand, is prevented through angiotensin II activation of a tyrosine phosphatase.[Pubmed:14722323]

J Pharmacol Exp Ther. 2004 Apr;309(1):16-27.

We have recently provided evidence for nicotine-induced complex formation between the alpha7 nicotinic acetylcholine receptor (nAChR) and the tyrosine-phosphorylated enzyme Janus kinase 2 (JAK2) that results in subsequent activation of phosphatidylinositol-3-kinase (PI-3-K) and Akt. Nicotine interaction with the alpha7 nAChR inhibits Abeta (1-42) interaction with the same receptor, and the Abeta (1-42)-induced apoptosis is prevented through nicotine-induced activation of JAK2. These effects can be shown by measuring markers of cytotoxicity, including the cleavage of the nuclear protein poly(ADP-ribose) polymerase (PARP), the induction of caspase 3, or cell viability. In this study, we found that 2-(3-pyridyl)-1-azabicyclo[3.2.2]nonane (TC-1698), a novel alpha7-selective agonist, exerts neuroprotective effects via activation of the JAK2/PI-3K cascade, which can be neutralized through activation of the angiotensin II (Ang II) AT(2) receptor. Vanadate not only augmented the TC-1698-induced tyrosine phosphorylation of JAK2 but also blocked the Ang II neutralization of TC-1698-induced neuroprotection against Abeta (1-42)-induced cleavage of PARP. Furthermore, when SHP-1 was neutralized via antisense transfection, the Ang II inhibition of TC-1698-induced neuroprotection against Abeta (1-42) was prevented. These results support the main hypothesis that states that JAK2 plays a central role in the nicotinic alpha7 receptor-induced activation of the JAK2-PI-3K cascade in PC12 cells, which ultimately contribute to nAChR-mediated neuroprotection. Ang II inhibits this pathway through the AT(2) receptor activation of the protein tyrosine phosphatase SHP-1. This study supports central and opposite roles for JAK2 and SHP-1 in the control of apoptosis and alpha7-mediated neuroprotection in PC12 cells.

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