Disease relevance of Brofaremine

• Is there a role for selective monoamine oxidase inhibitor therapy in bulimia nervosa? A placebo-controlled trial of brofaromine [1].
• Side effects more common with brofaromine than placebo included insomnia, dizziness, dry mouth, anorexia, tinnitus, and tremor [2].
• This study reports the effect of the MAO-A inhibitors, pirlindole (PIR), dehydropirlindole (DHP), brofaromine (BRO) and moclobemide (MCL) on primary-cultured brain cells exposed to iron-mediated toxicity [3].

Psychiatry related information on Brofaremine

• CONCLUSION: The results support the conclusion that the maladaptive personality traits characteristic of social phobia are at least as responsive to the monoamine oxidase inhibitor brofaromine as are the more circumscribed social anxiety responses [4].
• A double-blind comparative study of brofaromine and fluvoxamine in outpatients with panic disorder [5].
• The number of brofaromine patients who fulfilled the criteria for avoidant personality disorder had diminished from 15 (60%) to 5 (20%) [4].
• A double-blind, randomized, placebo-controlled, multi-center study of brofaromine in the treatment of post-traumatic stress disorder [6].
• In this study 30 patients with PD with or without agoraphobia (DSM-III-R) were treated with the selective and reversible MAO-A inhibitor brofaromine (150 mg daily) in a 12-week double-blind placebo controlled design [7].

High impact information on Brofaremine

• The data suggest that the selective reversible MAO-A inhibitor brofaromine has a larger therapeutic safety than phenelzine [8].
• Relative bioavailability of conjugated tyramine was elevated sixfold by brofaromine and 11.6-fold by phenelzine [8].
• Brofaromine for social phobia: a multicenter, placebo-controlled, double-blind study [2].
• A REM rebound occurred after withdrawal of brofaremine [9].
• Effects of brofaremine (CGP 11 305A), a short-acting, reversible, and selective inhibitor of MAO-A on sleep, nocturnal penile tumescence and nocturnal hormonal secretion in three healthy volunteers [9].

Chemical compound and disease context of Brofaremine

• Social phobia: the clinical efficacy and tolerability of the monoamine oxidase -A and serotonin uptake inhibitor brofaromine. A double-blind placebo-controlled study [10].
• Correlations of plasma and urinary phenylacetic acid and phenylethylamine concentrations with eating behavior and mood rating scores in brofaromine-treated women with bulimia nervosa [11].

Biological context of Brofaremine

• The specificity of brofaromine to inhibit deamination is limited to MAO-A, since no reduction in platelet MAO activity was measurable [12].
• Influence of age, frailty and liver function on the pharmacokinetics of brofaromine [13].
• Compared to EM, PM had significantly longer t1/2 (136%) and larger AUC(0-infinity) (110%) of the parent compound brofaromine and a lower Cmax (69%) and AUC (0-72 h) (40%) of its O-desmethyl metabolite [14].
• Five potential MAO-A inhibitors--harmine, N-methyl-harmine, harmaline, brofaromine, and clorgyline--were labelled with 11C and their brain kinetics evaluated in vivo in rhesus monkey using PET [15].

Anatomical context of Brofaremine

• Similar results were obtained when CGP 11305 A was preincubated with mitochondria or homogenates from rat liver in vitro, indicating an irreversible interaction [16].
• The effects of orally administered clomipramine, imipramine, citalopram, CGP 6085 A, fluoxetine and brofaromine on [3H]cyanoimipramine binding were similar to those obtained in the synaptosome ex vivo model in the absence of proadifen; ifoxetine seemed to be more potent in inhibiting [3H]cyanoimipramine binding [17].
• The effects of brofaromine, a reversible MAO-A inhibitor, on extracellular serotonin in the raphe nuclei and frontal cortex of freely moving rats [18].

Associations of Brofaremine with other chemical compounds

• Meta-analysis of the reversible inhibitors of monoamine oxidase type A moclobemide and brofaromine for the treatment of depression [19].
• The MAO-A inhibitors clorgyline and brofaromine also exhibit dopamine uptake inhibitory effects [20].
• These results indicate that brofaromine and cimoxatone are short-acting, reversible inhibitors of MAO-A activity in vivo [21].
• The effects of reversible inhibitors of monoamine oxidase-A (moclobemide, Ro 41-1049, both 20 mg/kg, i.p., and brofaromine, 10 mg/kg, i.p.) on the outflow of dopamine (DA) and its metabolites (3,4-dihydroxyphenylacetic acid and homovanillic acid) as well as of 5-hydroxyindoleacetic acid was investigated by trans-striatal microdialysis in rats [22].
• The aim of this study was to resolve the apparent discrepancy between the short duration of action of the MAO inhibitory effect of CGP 11305 A in vivo and its irreversible interaction with the enzyme in vitro [23].

Gene context of Brofaremine

• 3. Brofaromine inhibits MAO-A activities in a dose dependent manner in all brain regions examined [24].
• 5. Brofaromine does not inhibit MAO-B activities in the different regions examined [24].
• No such effect could be demonstrated for CGP 11305 A up to 150 mg/d. These results suggest that in man MAO A was inhibited by CGP 11305 A in daily dose of 40 mg or more, whereas it did not affect MAO B at up to 150 mg.(ABSTRACT TRUNCATED AT 250 WORDS)[25]
• CONCLUSION: Caffeine clearance, a simple, noninvasive test of CYP1A2 activity, is predictive of brofaromine clearance [13].
• Clinical, biochemical and psychometric findings with the new MAO-A-inhibitors moclobemide and brofaromine in patients with major depressive disorder [26].

Analytical, diagnostic and therapeutic context of Brofaremine

• Labeling experiments with radioactive brofaromine indicated that there was a high degree of non-specific binding but that no significant radioactivity remained associated with the enzyme on SDS-PAGE [27].
• The biologic assay, however, overestimated brofaromine by a factor of two in acute kinetic experiments with healthy volunteers as compared to a chromatographic technique, although both methods significantly correlated (r = 0.928) [28].
• The data of two control-group studies on brofaromine vs. imipramine were reanalyzed, the first, comprising 224 non-elderly and the second 195 elderly patients [29].
• Determination of the new monoamine oxidase inhibitor brofaromine and its major metabolite in biological material by gas chromatography with electron-capture detection [30].
• Brofaromine (CGP 11 305 A): estimation of plasma concentrations by a biologic technique as compared to liquid chromatography [28].

References