For research use only. Not for therapeutic Use.
Methyllycaconitine citrate is a specific antagonist of α7 neuronal nicotinic acetylcholine receptor (α7nAChR) with blood-brain barrier permeability.
Pretreatment with 5 and 10 μM Methyllycaconitine citrate (MLA) inhibits the decreased cell viability induced by Aβ25-35. Cell viability does not decrease after exposure to Methyllycaconitine citrate (2.5, 5, 10, 20 μM). Aβ25-35 treatment increases LC3-II levels, which is inhibited by administration of Methyllycaconitine citrate. Methyllycaconitine citrate also inhibits Aβ-induced autophagosome accumulation in SH-SY5Y cells. Flow cytometry also demonstrates decreased MDC-labeled vacuoles with Methyllycaconitine citrate treatment[1].
Methyllycaconitine citrate (MLA) (6 mg/kg) given alone intraperitoneally does not cause climbing behavior when compare with the saline group. Pretreatment with Methyllycaconitine citrate significantly inhibits methamphetamine (METH)-induced climbing behavior, by about 50%. Methyllycaconitine citrate does not modify either basal locomotor activity or METH-induced hyperlocomotion. The METH-induced depletion of dopamine neuron terminals is attenuated in mice pretreated with Methyllycaconitine citrate (250±43 fmol/mg, n=7). A direct effect of Methyllycaconitine citrate on body temperature is ruled out because Methyllycaconitine citrate does not affect basal body temperature (37.0±0.5°C, n=5) or reduce the METH-induced hyperthermia (38.2±0.4°C, n=6, MLA+METH group, n.s. versus METH group)[1].
| Catalog Number | R066968 |
| CAS Number | 351344-10-0 |
| Synonyms | [(2R,3R,4S,5R,6S,8R,13S,16S,17R,18S)-11-ethyl-8,9-dihydroxy-4,6,16,18-tetramethoxy-11-azahexacyclo[7.7.2.12,5.01,10.03,8.013,17]nonadecan-13-yl]methyl 2-[(3S)-3-methyl-2,5-dioxopyrrolidin-1-yl]benzoate;2-hydroxypropane-1,2,3-tricarboxylic acid |
| Molecular Formula | C43H58N2O17 |
| Purity | ≥95% |
| InChI | InChI=1S/C37H50N2O10.C6H8O7/c1-7-38-17-34(18-49-32(42)20-10-8-9-11-23(20)39-26(40)14-19(2)31(39)41)13-12-25(46-4)36-22-15-21-24(45-3)16-35(43,27(22)28(21)47-5)37(44,33(36)38)30(48-6)29(34)36;7-3(8)1-6(13,5(11)12)2-4(9)10/h8-11,19,21-22,24-25,27-30,33,43-44H,7,12-18H2,1-6H3;13H,1-2H2,(H,7,8)(H,9,10)(H,11,12)/t19-,21+,22+,24-,25-,27+,28-,29+,30-,33?,34-,35+,36?,37?;/m0./s1 |
| InChIKey | INBLZNJHDLEWPS-FOROPSOMSA-N |
| SMILES | CCN1CC2(CCC(C34C2C(C(C31)(C5(CC(C6CC4C5C6OC)OC)O)O)OC)OC)COC(=O)C7=CC=CC=C7N8C(=O)CC(C8=O)C.C(C(=O)O)C(CC(=O)O)(C(=O)O)O |
| Reference | [1]. Zheng X, et al. Methyllycaconitine alleviates amyloid-β peptides-induced cytotoxicity in SH-SY5Y cells. PLoS One. 2014 Oct 31;9(10):e111536. [2]. Escubedo E, et al. Methyllycaconitine prevents methamphetamine-induced effects in mouse striatum: involvement of alpha7 nicotinic receptors. J Pharmacol Exp Ther. 2005 Nov;315(2):658-67. [3]. Lockman PR, et al. Chronic nicotine exposure alters blood-brain barrier permeability and diminishes brain uptake of methyllycaconitine. J Neurochem. 2005 Jul;94(1):37-44. |
