AMN082 free base 是一种选择性，具有口服活性，可透过血脑屏障的 mGluR7 激动剂，通过跨膜区的变构位点直接激活受体信号。在表达 mGluR7 的转染哺乳动物细胞上，AMN082 free base 有效抑制 cAMP 积累并刺激 GTPγS 结合 (EC50, 64-290 nM)。AMN082 free base 对其他 mGluR 亚型和选择性离子型谷氨酸受体具有选择性。具有抗抑郁作用。
货号:ajcx36624
CAS:83027-13-8
分子式:C28H28N2
分子量：392.54
溶解度:DMSO : 12.5 mg/mL (31.84 mM; ultrasonic and warming and heat to 60°C)
纯度：98%
存储：Store at -20°C
库存：现货

Background:

AMN082 free base, a selective, orally active, and brain penetrant mGluR7 agonist, directly activates receptor signaling via an allosteric site in the transmembrane domain. AMN082 free base potently inhibits cAMP accumulation and stimulates GTPγS binding (EC50 values, 64-290 nM) at transfected mammalian cells expressing mGluR7. AMN082 free base shows selectivity over other mGluR subtypes and selected ionotropic glutamate receptors. Antidepressant effects[1][2].

Preincubation of the synaptosomes with AMN082 (1 μM) for 10 min before 4-aminopyridine treatment efficiently inhibits the 4-aminopyridine-evoked release of glutamate, without altering the basal release of glutamate[2].

AMN082 (6 mg/kg; p.o.) induces stress hormone increases in an mGluR7-dependent fashion in mGluR7+/+ mice (C57BL/6 genetic background)[1].AMN082 (1.25-5.0 mg/kg, i.p.; 30 min before every Cocaine or Morphine injection during repeated drug administration or before Cocaine or Morphine challenge) dose-dependently attenuates the development, as well as the expression of Cocaine or Morphine locomotor sensitization[3].

[1]. Mitsukawa K, et al. A selective metabotropic glutamate receptor 7 agonist: activation of receptor signaling via an allosteric site modulates stress parameters in vivo. Proc Natl Acad Sci U S A. 2005;102(51):18712-18717.
[2]. Wang CC, et al. Metabotropic glutamate 7 receptor agonist AMN082 inhibits glutamate release in rat cerebral cortex nerve terminal. Eur J Pharmacol. 2018;823:11-18.
[3]. Jenda M, et al. AMN082, a metabotropic glutamate receptor 7 allosteric agonist, attenuates locomotor sensitization and cross-sensitization induced by cocaine and morphine in mice. Prog Neuropsychopharmacol Biol Psychiatry. 2015;57:166-175.