![]() However, due to the probability of auto-inhibition and the lack of information on the concentration of these metabolites relative to in vivo concentrations, no predications regarding the potential for amphetamine or its metabolites to inhibit the metabolism of other drugs by CYP isozymes in vivo can be made. In vitro experiments with human microsomes indicate minor inhibition of CYP2D6 by amphetamine and minor inhibition of CYP1A2, 2D6, and 3A4 by one or more metabolites. Since CYP2D6 is genetically polymorphic, population variations in amphetamine metabolism are a possibility.Īmphetamine is known to inhibit monoamine oxidase, whereas the ability of amphetamine and its metabolites to inhibit various P450 isozymes and other enzymes has not been adequately elucidated. Although the enzymes involved in amphetamine metabolism have not been clearly defined, CYP2D6 is known to be involved with formation of 4-hydroxy-amphetamine. Alpha-hydroxy-amphetamine undergoes deamination to form phenylacetone, which ultimately forms benzoic acid and its glucuronide and the glycineconjugate hippuric acid. Norephedrine and 4-hydroxy-amphetamine are both active and each is subsequently oxidized to form4-hydroxy-norephedrine. The effect of food on the bioavailability of dextroamphetamine saccharate, amphetamine aspartate, dextroamphetamine sulfate and amphetamine sulfate tablets has not been studied.Īmphetamine is reported to be oxidized at the 4 position of the benzene ring to form 4-hydroxyamphetamine, or on the side chain α or β carbons to form alpha-hydroxy-amphetamine or norephedrine, respectively. The PK parameters (C max, AUC 0-inf) of d- and l-amphetamine increased approximately three-fold from 10 mg to 30 mg indicating dose-proportional pharmacokinetics. ![]() The mean elimination half-life (t 1/2) for d-amphetamine was shorter than the t 1/2 of the l-isomer (9.77 to 11 hours vs.11.5 to 13.8 hours). Following administration of a single dose 10 or 30 mg of dextroamphetamine saccharate, amphetamine aspartate, dextroamphetamine sulfate and amphetamine sulfate tablets to healthy volunteers under fasted conditions, peak plasma concentrations occurred approximately 3 hours post-dose for both d-amphetamine and l-amphetamine. ![]() Pharmacokineticsĭextroamphetamine saccharate, amphetamine aspartate, dextroamphetamine sulfate and amphetamine sulfate tablets contain d-amphetamine and l-amphetamine salts in the ratio of 3:1. Amphetamines are thought to block the reuptake of norepinephrine and dopamine into the presynaptic neuron and increase the release of these monoamines into the extraneuronal space. ![]() The mode of therapeutic action in Attention Deficit Hyperactivity Disorder (ADHD) is not known. Dextroamphetamine Saccharate, Amphetamine Aspartate, Dextroamphetamine Sulfate and Amphetamine Sulfate Tablets 12.5 mg, 15 mg, 20 mg and 30 mg contain FD&C Yellow #6 Aluminum Lake as a color additive.Īmphetamines are non-catecholamine sympathomimetic amines with CNS stimulant activity. Colors: Dextroamphetamine Saccharate, Amphetamine Aspartate, Dextroamphetamine Sulfate and Amphetamine Sulfate Tablets 5 mg, 7.5 mg and 10 mg contain FD&C Blue #1 Aluminum Lake. ![]() Inactive Ingredients: compressible sugar, magnesium stearate, maltodextrin, microcrystalline cellulose, sodium saccharin, and pregelatinized starch. ![]()
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