Ionamin online research references
ufl.edu
RATIONALE: Studies of the effect of anorectic drugs such as fenfluramine in mice have indicated the desirability of using experimental protocols that do not involve deprivation. OBJECTIVE: We have developed a non-deprivation or "dessert" protocol for use in mice that are maintained in standard housing conditions, and examine the effects of a serotonergic agent dexfenfluramine (DFEN), a dopaminergic agent phentermine (PHEN), and a selective norepinephrine uptake inhibitor thionisoxetine (TNIX) alone and in combination. METHODS: Female C57BL/6J mice were adapted to 30 min daily presentation of a gelatinized form of sweetened milk using a holder that hooks over the side of the cage during tests; food spillage and contamination are minimal. Dose-inhibition curves were determined for DFEN, PHEN, and TNIX alone and for fixed ratio combinations of DFEN with either PHEN or TNIX. RESULTS: Each drug produced a near linear dose-inhibition curve with the 50% inhibitory doses (DI50) of 5.6, 3.2 and 12.2 mg/kg, respectively. By isobolographic analysis, the effects of the drug combinations were strictly additive. CONCLUSION: The procedure described is highly suitable for testing anorectic drugs in mice and is adaptable to a variety of housing conditions and diets. The DFEN+ PHEN combination was additive, which contrasts with its reported supra-additive effect in rats.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11594445&dopt=Abstract
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Int J Obes Relat Metab Disord. 2001 Oct;25(10):1450-3.
Additive effects on rat brain 5HT release of combining phentermine with dexfenfluramine.
Prow MR, Lancashire B, Aspley S, Heal DJ, Kilpatrick IC.
Knoll Limited, Research and Development, Nottingham, UK.
OBJECTIVE AND DESIGN: This study examined the effects of the anti-obesity agents, phentermine and dexfenfluramine given alone or in combination, on in vitro and in vivo 5HT release from rat brain tissue. RESULTS: In vitro, phentermine was without effect on basal [3H]5HT efflux from hypothalamic slices whereas dexfenfluramine (10 microM) evoked a 131% increase in [3H]5HT release. In combination, the two drugs did not alter [3H]5HT release beyond that caused by dexfenfluramine alone. At pharmacologically equivalent doses, phentermine (5.7 mg/kg, i.p.) caused a rapid, modest elevation, and dexfenfluramine (3 mg/kg, i.p.) a larger but equally rapid elevation of extracellular 5HT in the microdialysates from the rat anterior hypothalamus. In combination, the increase in extracellular 5HT evoked by these drugs was not significantly greater than the sum of their individual effects. CONCLUSIONS: This study provides evidence that phentermine's actions are not restricted to catecholamine systems and indicates that combining phentermine with dexfenfluramine results in an additive increase in neuronal 5HT release.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11673764&dopt=Abstract
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knoll.co.uk
OBJECTIVE AND DESIGN: It has been proposed that the anti-obesity agent, phentermine, may act in part via inhibition of monoamine oxidase (MAO). The ability of phentermine to inhibit both MAO(A) and MAO(B) in vitro has been examined along with that of the fenfluramine isomers, a range of selective serotonin reuptake inhibitors and sibutramine and its active metabolites. RESULTS: In rat brain, harmaline and lazabemide showed potent and selective inhibition of MAO(A) and MAO(B), their respective target enzymes, with IC(50) values of 2.3 and 18 nM. In contrast, all other drugs examined were only weak inhibitors of MAO(A) and MAO(B) with IC(50) values for each enzyme in the moderate to high micromolar range. For MAO(A), the IC(50) for phentermine was estimated to be 143 microM, that for S(+)-fenfluramine, 265 microM and that for sertraline, 31 microM. For MAO(B), example IC(50)s were as follows: phentermine (285 microM), S(+)-fenfluramine (800 microM) and paroxetine (16 microM). Sibutramine was unable to inhibit either enzyme, even at its limit of solubility. CONCLUSION: We therefore suggest that MAO inhibition is unlikely to play a role in the pharmacodynamic properties of any of the tested drugs, including phentermine. Instead, the lack of potency of these drugs as MAO inhibitors is contrasted with their powerful ability either to inhibit the uptake of one or more monoamines (fluoxetine, paroxetine, sertraline, sibutramine's active metabolites) or to evoke the release of one or more monoamines (S(+)-fenfluramine, S(+)-norfenfluramine, phentermine). These differences in mode of action may be linked to the adverse cardiovascular events experienced with some of the releasing agents.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11673765&dopt=Abstract
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