TC-2559 free base 

TC-2559 free base is a α4β2 nicotinic acetylcholine receptor (nAChR) agonists with an EC₅₀ of 0.18 μM. TC-2559 free base shows much weaker potencies on the group of b4-containing nAChR subtypes, α2β4, α4β4 and α3β4 receptors, with EC₅₀s in the range of 10-30 µM. TC-2559 free base can increase the discharge of dopamine cells in the ventral tegmental area (VTA) of rats in vitro, enhancing the excitability and aggressive behavior of VTA dopamine neurons. TC-2559 free base inhibits STAT3 to exert anti-inflammatory properties and relieves mice mechanical allodynia and improve rats cognitive deficits. TC-2559 free base can be used for the study of nerve pain^{[1][2][3][4][5]}.

TC-2559 free base (free base) competes effectively with [³H]-mocotine binding (K_i = 5 nM) ^[1].
TC-2559 free base (0-100 nM) enhances dopamine release in rat striatal synaptic vesicles (EC₅₀, E= 97%) and _{86Rb+ efflux in thalamic synaptic vesicles (EC50= 367 nM, E= 107%), while showing no activity in TE671/RD or PC12 cells at 1 mM^[1].
TC-2559 free base (10 μM, 2 h) can significantly reduce neuronal death in the brain cells of fetal mice^[1].
TC-2559 free base (200-500 μM, 3-6 h) suppresses the upregulation of CC-chemokine ligand 3 (CCL3) and interleukin-1b (IL-1b) in murine macrophages^[3].
TC-2559 free base (500 μM, 1-6 h) inhibits the phosphorylation of signal transducer and activator of transcription 3 (pSTAT3) in murine macrophages^[3].
TC-2559 free base (0.5 mM, 24 h) suppresses the upregulation of interleukin-1β (IL-1β) in the injured SCN after PSL in mice peritoneal macrophages^[4].
TC-2559 free base shows much weaker potencies on the group of β4-containing nAChR subtypes, α2β4, α4β4 and α3β4 receptors, with EC50s of 14, 12.5, >30, >100 and >100 μM, respectively^[5].}

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

TC-2559 free base (free base) (0.124-2.063 mg/kg, s.c., single dose) can dose-dependently reverse the memory impairment caused by cholinergic blockade in rats attenuation of scopolamine-induced amnesia^[1].
HC-2559 (0.124-2.063 mg/kg μmol/kg, s.c., single dose or for 5 days) significantly reduces errors in working memory, and sustainably improves working memory^[1].
HC-2559 (0.206-1.238 mg/kg, s.c., single dose or for 14 days) causes motor inhibition at a single administration and does not induce behavioral sensitization after continuous administration^[1].
TC-2559 free base (0.021-1.32 mg/kg, i.v., cumulative doses or single dose) activates VTA dopamine neurons through α4β2-like nAChRs^[2].
TC-2559 free base (0.47-4.70 mg/kg, s.c. or 20 nmol, perineural Injections, for 3 days) significantly relieves mechanical allodynia in mice behavioral model^[4].
TC-2559 free base (20 nmol, perineural Injections, for 3 days) suppresses microglial activation in the SDH induced by peripheral nerve injury in mice^[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

206.28

C₁₂H₁₈N₂O

189274-78-0

CNCC/C=C/C1=CN=CC(OCC)=C1

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. Bencherif M, et al. TC-2559: a novel orally active ligand selective at neuronal acetylcholine receptors. Eur J Pharmacol. 2000 Dec 1;409(1):45-55.  [Content Brief]

  [2]. Wang Y, et al. TC-2559 excites dopaminergic neurones in the ventral tegmental area by stimulating alpha4beta2-like nicotinic acetylcholine receptors in anaesthetised rats. Br J Pharmacol. 2006 Feb;147(4):379-90.  [Content Brief]

  [3]. Kiguchi N,et al. TC-2559, an α4β2 nicotinic acetylcholine receptor agonist, suppresses the expression of CCL3 and IL-1β through STAT3 inhibition in cultured murine macrophages. J Pharmacol Sci. 2015 Jun;128(2):83-6.  [Content Brief]

  [4]. Kiguchi N, et al. Inhibition of peripheral macrophages by nicotinic acetylcholine receptor agonists suppresses spinal microglial activation and neuropathic pain in mice with peripheral nerve injury. J Neuroinflammation. 2018 Mar 27;15(1):96.  [Content Brief]

  [5]. Chen Y, et al. The nicotinic alpha 4 beta 2 receptor selective agonist, TC-2559, increases dopamine neuronal activity in the ventral tegmental area of rat midbrain slices. Neuropharmacology. 2003 Sep;45(3):334-44.  [Content Brief]