Background:

APNEA is a potent, non-selective A3 adenosine receptor agonist.

APNEA is a non-selective agonist of the adenosine A3 receptors, at the subprotective dose of 1 mg/kg against electroconvulsions, significantly potentiates the anticonvulsive action of phenobarbital, diphenylhydantoin and valproate against maximal electroshock, being ineffective at lower doses. APNEA (0.0039-1 mg/kg) also enhances the protective activity of carbamazepine. APNEA at low doses potentiates the protective activity of Carbamazepine most likely through the A subtype of adenosine receptors. At higher doses, APNEA seems to enhance the anticonvulsive effect of other antiepileptics via adenosine A1 receptors[1].

APNEA (2-4 mg/kg) has no significant effect on seizure parameters (seizure severity, seizure duration and afterdischarge duration) in amygdala-kindled rats. N6-[2-(4-Aminophenyl)ethyl]adenosine is combined with antiepileptic drugs administered at doses ineffective in fully kindled rats[1].

[1]. Borowicz KK, et al. N6-2-(4-aminophenyl)ethyl-adenosine enhances the anticonvulsive activity of antiepileptic drugs. Eur J Pharmacol. 1997 May 30;327(2-3):125-133. [2]. Borowicz KK, et al. N(6)-2-(4-aminophenyl)ethyl-adenosine enhances the anticonvulsive action of conventional antiepileptic drugs in the kindling model of epilepsy in rats. Eur Neuropsychopharmacol. 2000 Jul;10(4):237-243.