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CFM-2

CAS No. : 178616-26-7

MCE 国际站：CFM-2

产品活性：CFM-2 是一种有效的、选择性的、非竞争性的 AMPAR 拮抗剂。CFM-2 在不同的惊厥动物模型中均表现出抗惊厥活性。

研究领域：Membrane Transporter/Ion Channel  |  Neuronal Signaling

作用靶点：iGluR

In Vitro: CFM-2 inhibits the extracellular signal regulated kinase (ERK1/2) pathway, CFM-2 reduced phosphorylation of cAMP-responsive element binding protein (CREB), suppressed expression of cyclin D1, upregulated the cell cycle regulators and tumor suppressor proteins p21 and p53 and decreased number of lung adenocarcinoma cells in G2 and S phases of the cell cycle.

In Vivo: Pretreatment with CFM-2 delays the progression of seizure rank during repeated administration of pentylentetrazole. At the end of the period of repeated pentylentetrazole treatment (6 weeks) the mean seizure score was 0 in vehicle treated controls, 4.3 in animals treated with vehicle + pentylentetrazole, 2.2 in rats treated chronically with CFM-2 (20 μmol/kg; i.p.) + pentylentetrazole and 1.0 in rats treated repeatedly with CFM-2 (50 μmol/kg; i.p.) + pentylenetetrazole. CFM-2 is also able to antagonize the long-term increase in sensitivity of the convulsant effects of GABA function inhibitors in pentylentetrazole-kindled animals.
Intrathecal application of two selective non-competitive AMPAR antagonists, CFM-2 (25 and 50 μg) and GYKI 52466 (50μg), significantly attenuated mechanical and thermal hypersensitivities on the ipsilateral hind paw at 2 and 24 h post-CFA injection. Neither CFM-2 nor GYKI 52466 affects the contralateral basal responses to thermal and mechanical stimuli.

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