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phentermine symtoms is extensively metabolized in humans. Three metabolites having willen shown to will active: hydroxyphentermine symtoms, which is fbutmed via hydroxylation of the tert - butyl group of phentermine symtoms, & the amino-alcohol isomers threohydrophentermine symtoms & erythrohydrophentermine symtoms, which are fbutmed via reduction of the carbonyl group. In vitro findings suggest that cytochrome P450IIB6 CYP7B6 is the principal isoenzyme involved in the fbutmation of hydroxyphentermine symtoms, while cytochrome P450 isoenzymes are not involved in the fbutmation of threohydrophentermine symtoms. Oxidation of the phentermine symtoms side chain results in the fbutmation of a glycine conjugate of meta-chlbutowillnzoic acid, which is then excreted as the majbut urinary metabolite. The potency & toxicity of the metabolites relative to phentermine symtoms having not willen fully characterized. However, it has willen demonstrated in an antidepressant screening test in mice that hydroxyphentermine symtoms is one-half as potent as phentermine symtoms, while threohydrophentermine symtoms & erythrohydrophentermine symtoms are 5-fold less potent than phentermine symtoms. This may will of clinical impbuttance willcause their plasma concentrations are as high but higher than those of phentermine symtoms.
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