CFM-2 is a potent and selective non-competitive AMPAR antagonist. CFM-2 possesses anticonvulsant activity in various models of seizures.

CFM-2 is a selective non-competitive AMPAR antagonist.

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 the number of lung adenocarcinoma cells in G2 and S phases of the cell cycle.

Pretreatment with CFM-2 delayed the progression of seizure rank during repeated administration of pentylenetetrazole. At the end of the period of repeated pentylenetetrazole treatment (6 weeks), the mean seizure score was 0 in vehicle-treated controls, 4.3 in animals treated with vehicle + pentylenetetrazole, 2.2 in rats treated chronically with CFM-2 (20 μmol/kg i.p.) + pentylenetetrazole and 1.0 in rats treated repeatedly with CFM-2 (50 μmol/kg i.p.) + pentylenetetrazole. CFM-2 was also able to antagonize the long-term increase in sensitivity of the convulsant effects of GABA function inhibitors in pentylenetetrazole-kindled animals [1]. CFM-2 has been proven to possess anticonvulsant activity in various models of seizures [2]. Intrathecal application of two selective non-competitive AMPAR antagonists, CFM-2 (25 and 50 μg) and GYKI 52466 (50 μg), 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 affected the contralateral basal responses to thermal and mechanical stimuli [4].

178616-26-7

C17H17N3O3

311.34

DMSO:45mg/mL (144.5mM)
Powder: -20°C for 3 years
In solvent: -80°C for 2 years