oral: 0.025 g 2-4 times/day after the meal intramuscular or subcutaneous: 0.5-1 mL of 1% solution

It was studied the interaction of aprophen with nicotinic acetylcholine receptor (AChR) in BC3H-1 intact muscle cells and with receptor-enriched membranes of Torpedo californica. Aprophen diminished the maximal carbamylcholine-elicited sodium influx into muscle cells without shifting Kact (carbamylcholine concentration eliciting 50% of the maximal 22Na+ influx). Aprophen interacted with the AChR in its desensitized state in BC3H-1 cells without further enhancing agonist affinity. The affinity of aprophen for the allosterically coupled noncompetitive inhibitor site of the AChR in Torpedo was determined using [3H]phencyclidine as a probe. This compound was found to preferentially associate with the high affinity (desensitized) state rather than the resting state of Torpedo AChR. Thus, aprophen was the effective noncompetitive inhibitor of the AChR at concentrations of 1-50 microM, in either Torpedo or mammalian AChR.