Clinical Trial of Mebanazine—A New Monoamine Oxidase Inhibitor

1965 ◽  
Vol 111 (478) ◽  
pp. 899-902 ◽  
Author(s):  
S. J. G. Gilmour
Keyword(s):  
Clinical Trial ◽  
Side Effects ◽  
Monoamine Oxidase ◽  
Relapse Rate ◽  
Monoamine Oxidase Inhibitor ◽  
Oxidase Inhibitor ◽  
Monoamine Oxidase Inhibitors ◽  
Clinical Use ◽  
Clinical Toxicity

At the time when this investigation was being considered (June, 1961) the efficacy of the monoamine oxidase inhibitors in the treatment of depressive illnesses was already well recognized. It was also evident from a study of the published papers on this group of drugs that their use was accompanied by a number of side-effects which often raised problems in treatment. The clinical trial of a new drug of this class which, from the pre-clinical toxicity studies in animals, held promise of being less toxic than M.A.O. inhibitors already in clinical use was therefore considered worth while. Such a trial also seemed a useful opportunity to follow up previous observations with phenelzine (Gilmour, 1960) and the suggestion of Sargant (1961) that, given concurrently, M.A.O. inhibitors may potentiate the effect of E.C.T. and reduce the number of exposures necessary, and that their continuance after a course of E.C.T. has been completed may reduce the relapse rate.

Phase II trial of monoamine oxidase inhibitor phenelzine in biochemical recurrent prostate cancer.

2020 ◽  
Vol 38 (6_suppl) ◽  
pp. 94-94 ◽  
Author(s):  
Mitchell E. Gross ◽  
David B. Agus ◽  
Tanya B. Dorff ◽  
Jacek K. Pinski ◽  
David I. Quinn ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Clinical Trial ◽  
Monoamine Oxidase ◽  
Monoamine Oxidase Inhibitor ◽  
Depression Score ◽  
Oxidase Inhibitor ◽  
Monoamine Oxidase A ◽  
Recurrent Prostate Cancer ◽  
Open Label ◽  
Grade 3

94 Background: Monoamine oxidase A (MAOA) influences prostate cancer growth and metastasis in pre-clinical models. We examined effects of phenelzine (a monoamine oxidase inhibitor) in patients with biochemical recurrent castrate-sensitive prostate cancer. Methods: An open-label single arm clinical trial enrolled subjects with biochemical recurrent prostate cancer defined by: PSA ≥ 0.4 ng/ml (post-prostatectomy) or PSA ≥ 2 ng/ml above nadir (post-radiation therapy); no evidence of metastasis on imaging; and normal androgen levels. Subjects received phenelzine 30 mg orally twice daily. Mood symptoms were assessed with the hospital anxiety depression score (HADS) questionnaire. The primary endpoint was the proportion of patients who achieved a PSA decline of ≥50% from baseline. Results: Characteristics of the 20 eligible patients enrolled included: mean ± SD age 66.9 ± 4.8 years and PSA 4.7 ± 5.8 ng/dl. Maximal PSA declines ≥ 30% and ≥ 50% were observed in 25% (n=5/20) and 10% (n=2/20) of subjects, respectively. At 12 weeks, 17 subjects remained on treatment with PSA declines ≥ 30% and ≥ 50% of 24% (n=4/17) and 6% (n=1/17), respectively. Common toxicities observed included dizziness (grade 1 = 45%, grade 2= 35%), hypertension (grade ≥ 2 =30%), and edema (grade 1=25%, grade 2=10%). There was 1 episode of grade 4 hypertension (cycle 4) and 2 episodes of grade 3 syncope (cycle 12 and cycle 14) requiring treatment discontinuation. HADS questionnaires demonstrated a significant decrease in anxiety with no change in depressive symptoms on treatment. Conclusions: Phenelzine demonstrated efficacy in patients with biochemical recurrent castrate sensitive prostate cancer. Most treatment related toxicities were mild, but rare significant and reversible cardiovascular toxicities were observed. Therapies directed at MAOA may represent a new avenue for treatment in patients with recurrent prostate cancer. Clinical trial information: NCT02217709.

Sudden Death Associated with Switching Monoamine Oxidase Inhibitors

1986 ◽  
Vol 20 (12) ◽  
pp. 954-956 ◽  
Author(s):  
Stephen R. Bazire
Keyword(s):  
Sudden Death ◽  
Monoamine Oxidase ◽  
Abrupt Change ◽  
Monoamine Oxidase Inhibitor ◽  
Oxidase Inhibitor ◽  
Monoamine Oxidase Inhibitors ◽  
Free Interval ◽  
Drug Free

A drug-free interval is often recommended when switching monoamine oxidase inhibitors, although the evidence firmly supporting this caution has been minimal. A case is reported where an abrupt change in monoamine oxidase inhibitor was followed by the death of a patient.

A Controlled Study of the Effectiveness of Nialamide (“Niamid”) in Schizophrenia

1961 ◽  
Vol 107 (448) ◽  
pp. 572-574
Author(s):  
J. G. Hegarty ◽  
A. R. Dabbs ◽  
R. T. St. Blaize-Molony
Keyword(s):  
Side Effects ◽  
Monoamine Oxidase ◽  
Catalytic Oxidation ◽  
Monoamine Oxidase Inhibitor ◽  
Oxidase Inhibitor ◽  
Controlled Study ◽  
Enzyme Monoamine Oxidase

Nialamide is claimed to inhibit the activity of the enzyme monoamine oxidase which is known to be responsible for the breakdown by catalytic oxidation of various amines, e.g. serotonin and norepinephrine. It has been suggested that depression may be associated with inadequate levels of serotonin and/or norepinephrine and that the administration of a monoamine oxidase inhibitor should rationally help to relieve depression. No serious side-effects have been reported in the available literature except that agitated patients might become somewhat more agitated and overactive.

The blockade of serotonin uptake into synaptosomes: relationship to an interaction with monoamine oxidase inhibitors

1977 ◽  
Vol 55 (2) ◽  
pp. 180-187 ◽  
Author(s):  
John G. Sinclair ◽  
Grace F. Lo
Keyword(s):  
Monoamine Oxidase ◽  
Monoamine Oxidase Inhibitor ◽  
Oxidase Inhibitor ◽  
Monoamine Oxidase Inhibitors ◽  
Serotonin Uptake ◽  
Neuronal Uptake ◽  
5 Ht Uptake ◽  
Inhibition Of Neuronal Uptake ◽  
Depressant Drug

To test the hypothesis that the hyperpyrexia produced by meperidine and detromethorphan in rabbits pretreated with a monoamine oxidase inhibitor is related to inhibition of neuronal uptake of serotonin (5-hydroxytryptamine (5-HT)), fluoxetine (Lilly 110140) was studied. This potent and specific 5-HT neuronal uptake blocker was administered to phenelzine-pretreated rabbits and found to produce a lethal hyperpyrexia in doses equal to or greater than 2.5 mg/kg. The order of potency in blocking 5-[14C]HT uptake into synaptosomes prepared from rabbits was: fluoxetine > meperidine = dextromethorphan = levorphanol > anileridine > alphaprodine > morphine. Since fluoxetine, meperidine, and dextromethorphan produce hyperpyrexia in phenelzine-pretreated rabbits, whereas anileridine, alphaprodine, and morphine do not, there appears to be some correlation between the hyperpyrexic response and inhibition of 5-HT uptake. The exception is levorphanol, which is not hyperpyrexic despite being equipotent with meperidine and dextromethorphan in inhibiting 5-HT uptake. The ineffectiveness of levorphanol in producing hyperpyrexia may be due to its marked depressant properties, since the addition of another depressant drug (pentobarbital) antagonized the hyperpyrexic effect of meperidine.

Controlled Clinical Trial of Isocarboxazid (“Marplan”) in Hospital Psychiatry

1961 ◽  
Vol 107 (448) ◽  
pp. 567-571 ◽  
Author(s):  
Vasant G. Joshi
Keyword(s):  
Clinical Trial ◽  
Monoamine Oxidase ◽  
Monoamine Oxidase Inhibitor ◽  
Oxidase Inhibitor ◽  
Controlled Clinical Trial ◽  
Synthetic Drugs ◽  
Uncontrolled Trial ◽  
Treatment Of Depression ◽  
Hospital Psychiatry

A number of synthetic drugs have recently been introduced as specific antidepressants in psychiatry. Isocarboxazid (Marplan) is an analogue of iproniazid (Marsilid). Both belong to the monoamine oxidase inhibitor group of antidepressants. Isocarboxazid is said to be less toxic but of equal potency for a lesser dose than iproniazid. A controlled clinical trial of isocarboxazid was therefore undertaken to assess this drug in the treatment of depression. The results of this trial are reported in this paper together with the results of an uncontrolled trial in a further group of patients (group M) who received isocarboxazid only.

Possible antidepressant/mania-inducing effects of methionine: a reappraisal of the effects of methionine in chronic psychosis using modern diagnostic criteria

1989 ◽  
Vol 4 (3) ◽  
pp. 175-181
Author(s):  
J.F. Lipinski ◽  
R.C. Alexander
Keyword(s):  
Monoamine Oxidase ◽  
Diagnostic Criteria ◽  
Monoamine Oxidase Inhibitor ◽  
Manic Episode ◽  
Oxidase Inhibitor ◽  
Descriptive Data ◽  
Antidepressant Effects ◽  
Chronic Psychosis

SummaryThe authors have reviewed 13 published studies on methionine administration, usually in combination with a monoamine oxidase inhibitor (MAOI), to chronically psychotic patients, using modern (DSM-III) diagnostic criteria. Four of these studies contained sufficient descriptive data to allow reappraisal of the effects. The results of the review suggest that a proportion of the patients experienced the induction of a manic episode/antidepressant effects rather than the reported worsening of schizophrenia while treated with a methionine-MAOI combination. It is suggested that these observations are consistent with recent findings that S-adenosyl-L-methionine (SAMe) has antidepressant and mania-inducing effects.

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