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A variety of appropriate [4-(benzyloxy) benzoyl]- and [4-(benzyloxy) benzyl] aminoalkanol derivatives [I-XVII] was synthesized and evaluated for anticonvulsant activity using the maximal electroshock (MES) and subcutaneous pentylenetetrazole (ScMet) tests in mice and rats. Neurotoxicity (TOX) was determined by the rotorod test. The most active compounds in the MES test in mice were the appropriate 4-(benzyloxy) benzyl derivatives of (R,S)- and S-(+)-2-amino-1-butanol [XI, XIII], 3-[4-(benzyloxy) benzyl] amino-3-methyl-1-butanol [XV], and S-(+)-2-[4-(benzyloxy) benzyl] amino-3-methyl-1-butanol [XVI]--all exhibiting 100% anti-MES protection (at 30 mg/kg, mice, i.p.) and non-toxic in the active doses. 4-[4-(Benzyloxy) benzyl] amino-1-butanol [X] exhibited activity in both MES and ScMet (100 mg/kg, mice, i.p., 100% anticonvulsant protection, 0.5 h and 4 h after administration, respectively).

Nine new N-acyl derivatives of 2-amino-1-alcohols and 1-amino-2-alcohols with a potential arrhythmic activity have been obtained. In the preliminary screening 2-[N-(7-theophyllineacetyl)-amino]-2-methyl-1-propanol, 5, was more active in the chloroform-induced arrhythmia than quinidine. Unlike to propranolol and quinidine, compound 5 in doses of 5-30 mg/kg, iv, did not prevent distortions of the cardiac rhythm evoked by adrenaline and strophanthine. When administered at the peak of arrhythmia, it did not abolish disturbances of the cardiac rhythm. Compound 5 had a low toxicity (LD50 = 3000 mg/kg, ip), did not change the control ECG curve, showed no cardiodepressive activity, and had weaker local anesthetic properties than lignocaine.