Ionamin online research references
psych.ufl.edu
RATIONALE: We have shown previously that the anorectic effects of the catecholamine-releasing agent phentermine (PHEN) and the serotonin (5-HT)-releasing agent dexfenfluramine (DFEN) are greater than additive in rats. In the present study, we examined whether the norepinephrine-uptake inhibitors desmethylimipramine (DMI) and thionisoxetine (TNIX) have additive effects with either DFEN or with the 5-HT-uptake inhibitor fluoxetine (FLX). We also examined whether PHEN interacts with a postsynaptically acting 5-HT agonist. METHODS: Undeprived rats were trained to eat a daily sweet-milk dessert and on test days were systemically administered single or combination drugs and the intakes recorded. RESULTS: Both DMI and TNIX produced dose-related suppressions of food intake. However, by isobolographic analysis, they did not enhance the anorectic actions of either DFEN or FLX. In contrast, confirming and extending our previous work, PHEN had a greater potentiating effect on the anorectic actions of DFEN and FLX than TNIX. Further, the anorectic action of the 5-HT2c receptor agonist TFMPP was enhanced by PHEN. CONCLUSIONS: These and other data are consistent with the idea that 5-HT agents may work "upstream" of critical catecholaminergic synapses in the production of anorexia, and explain the diminished efficacy of norepinephrine-uptake inhibitors relative to PHEN. The implications for clinically useful anorectic agents are discussed briefly.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10789886&dopt=Abstract
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duke.edu
BACKGROUND: The combination of fenfluramine and phentermine was a widely used obesity treatment before the withdrawal of fenfluramine for an association with heart valve regurgitation. The prevalence and clinical significance of regurgitation among patients treated with these medications has yet to be fully established. METHODS AND RESULTS: To evaluate the potential association between the duration of treatment and the prevalence of heart valve abnormalities, we examined 1163 patients who had taken fenfluramine-phentermine and 672 control patients who had not taken the drug combination within 5 years. Mild or greater aortic regurgitation was present in 8.8% of treated patients and 3.6% of control patients (P<0.001). Moderate or greater mitral regurgitation was present in 2.6% of treated patients and 1.5% of control patients (P=0.18). The adjusted odds ratio compared with controls of aortic regurgitation of mild or greater severity increased according to duration of treatment: 90 to 180 days, 1.5 (P=0.23); 181 to 360 days, 2.4 (P=0.002); 361 to 720 days, 4.6 (P<0.001); >720 days, 6.2 (P<0.001). CONCLUSIONS: This is the largest study to demonstrate a relation between the length of treatment with fenfluramine-phentermine and the prevalence of valvular abnormalities. These findings suggest that valvular abnormalities in patients who took fenfluramine-phentermine primarily involve those who had taken these medications for >6 months and predominantly results in mild aortic regurgitation. The valve regurgitation identified by this study was not accompanied by significant differences in cardiovascular symptoms nor physical findings other than a higher prevalence of heart murmurs.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10790349&dopt=Abstract
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Biochem Pharmacol. 2000 Jun 15;59(12):1611-21.
Characterization of phentermine and related compounds as monoamine oxidase (MAO) inhibitors.
Ulus IH, Maher TJ, Wurtman RJ.
Department of Pharmacology and Clinical Pharmacology, Uludag University Medical School, Bursa, Turkey.
Phentermine was shown in the 1970s to inhibit the metabolism of serotonin by monoamine oxidase (MAO), but never was labeled as an MAO inhibitor; hence, it was widely used in combination with fenfluramine, and continues to be used, in violation of their labels, with other serotonin uptake blockers. We examined the effects of phentermine and several other unlabeled MAO inhibitors on MAO activities in rat lung, brain, and liver, and also the interactions of such drugs when administered together. Rat tissues were assayed for MAO-A and -B, using serotonin and beta-phenylethylamine as substrates. Phentermine inhibited serotonin-metabolizing (MAO-A) activity in all three tissues with K(i) values of 85-88 microM. These potencies were similar to those of the antidepressant MAO inhibitors iproniazid and moclobemide. When phentermine was mixed with other unlabeled reversible MAO inhibitors (e.g. pseudoephedrine, ephedrine, norephedrine; estradiol benzoate), the degree of MAO inhibition was additive. The cardiac valvular lesions and primary pulmonary hypertension that have been reported to be associated with fenfluramine-phentermine use may have resulted from the intermittent concurrent blockage of both serotonin uptake and metabolism.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10799660&dopt=Abstract
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