Abstract
This study was designed to examine the hypothesis that phenelzine is metabolized by polymorphic acetylation and that its effects are dependent on acetylator status. 30 depressed inpatients were given a 3-week course of phenelzine 30 mg t.i.d. The antidepressant effect, the degree of inhibition of monoamine oxidase and the amount of free phenelzine excreted in the urine were all significantly greater in slow acetylators than in fast. These findings strongly support the hypothesis.