| Identification | Back Directory | [Name]
METHYLLYCACONITINE CITRATE | [CAS]
112825-05-5 | [Synonyms]
MLA
METHYLLYCACONITINE CITRATE
Methyllycaconitine citrate salt
MLA (Methyllycaconitine Citrate)
Cytotoxic T-Lymphocyte-Associated Antigen 8
INTERLEUKIN-17A; IL-17; IL-17A; CYTOTOXIC T-LYMPHOCYTE-ASSOCIATED ANTIGEN 8; CTLA-8; IL17A; CTLA8; IL17
[1A,4(S),6B,14A,16B]-20-ETHYL-1,6,14,16-TETRAMETHOXY-4-[[[2-(3-METHYL-2,5-DIOXO-1-PYRROLIDINYL)BENZOYL]OXY]METHYL]ACONITANE-7,8-DIOL CITRATE
[1α,4(S),6β,14α,16β]-20-Ethyl-1,6,14,16-tetramethoxy-4-[[[2-(3-methyl-2,5-dioxo-1-pyrrolidinyl)benzoyl]oxy]methyl]aconitane-7,8-diol citrate salt
[1ALPHA,4(S),6BETA,14ALPHA,16BETA]-20-ETHYL-1,6,14,16-TETRAMETHOXY-4[[[2-(3-METHYL-2,5-DIOXO-1-PYRROLIDINYL)BENZOYL]OXY]METHYL]-ACONITANE-7,8-DIOL CITRATE | [Molecular Formula]
C43H58N2O17 | [MDL Number]
MFCD00153837 | [MOL File]
112825-05-5.mol | [Molecular Weight]
874.92 |
| Chemical Properties | Back Directory | [storage temp. ]
−20°C | [solubility ]
H2O: 42 mg/mL | [form ]
solid | [color ]
white | [biological source]
Delphinium brownii seeds | [Water Solubility ]
H2O: 42mg/mL |
| Hazard Information | Back Directory | [Uses]
Methyllycaconitine citrate salt has been used as an α7 nicotinic acetylcholine receptor (α7 nAChR) antagonist:
- to study its effects on inflammatory response in rats post nicotine treatment
- to block the activity of galantamine
- to study its effects on the hepatic branch of the vagus nerve (hVNS) in rats
| [Biological Activity]
methyllycaconitine citrate(mla) is an antagonist of α7-containing neuronal nicotinic acetylcholine receptors (nachrs; ki = 1.4 nm)[1,2].mla inhibits the decreased cell viability induced by aβ25-35, pretreatment with 5 and 10 μm. aβ25-35 treatment increases lc3-ii levels, which is inhibited by administration of methyllycaconitine citrate. mla also inhibits aβ-induced autophagosome accumulation in sh-sy5y cells[3].mla inhibits methamphetamine(meth)-induced climbing behavior by 50%. mla prevents a decrease in striatal synaptosome dopamine (da) uptake, mla significantly attenuates meth-induced neurotoxicity at 72 h post-treatment. mla fully prevents microglial activation at 24 h post-treatment and tending to confirm its neuroprotective activity[4].[1]. kalappa b i, sun f, johnson s r, et al. a positive allosteric modulator of α7 nachrs augments neuroprotective effects of endogenous nicotinic agonists in cerebral ischaemia. brit.j.pharmacol, 2013, 169(8): 1862-1878.[2]. ward j m, cockcroft v b, lunt g g, et al. methyllycaconitine: a selective probe for neuronal α-bungarotoxin binding sites. febs lett, 1990, 270(1-2): 45-48 .[3]. zheng x, et al. methyllycaconitine alleviates amyloid-β peptides-induced cytotoxicity in sh-sy5y cells. plos one, 2014, 9(10): e111536.[4]. escubedo e, et al. methyllycaconitine prevents methamphetamine-induced effects in mouse striatum: involvement of alpha7 nicotinic receptors. j pharmacol exp ther, 2005, 315(2): 658-67. | [Biochem/physiol Actions]
Methyllycaconitine (MLA) is an α7 nicotinic acetylcholine receptor (α7 nAChR) antagonist. It is a norditerpenoid alkaloid synthesized by several species of Delphinium. MLA binds to the binding site of neuronal α-bungarotoxin. Low doses of MLA are associated with improvement of cognition in animals. |
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