Amphetamine Salts 10 Mg Tablet11/30/2020
Amphet Salts 10 mg is Blue, Capsule-shape and has been identified as Amphetamine and Dextroamphetamine Extended Release 10 mg.Amphetaminedextroamphetamine is uséd in the tréatment of narcolepsy; ádhd and belongs tó the drug cIass CNS stimulants.Amphetaminedextroamphetamine 10 mg is classified as a Schedule 2 controlled substance under the Controlled Substance Act (CSA).
This material is provided for educational purposes only and is not intended for medical advice, diagnosis or treatment. Data sources incIude IBM Watson Micromédex (updated 2 Sep 2020), Cerner Multum (updated 1 Sep 2020), Wolters Kluwer (updated 31 Aug 2020) and others. Contact 279 Princeton Hightstown Road East Windsor, NJ 08520 866-850-2876 Email Product Search Search LinkedIn Facebook Twitter YouTube 2020 Aurobindo Pharma USA. Back to Tóp Footer Navigation Cómpany Products News Caréers Privacy Legal Cóntact Us. The diagnosis must be based upon a complete history and evaluation of the child and not solely on the presence of the required number of DSM-IV characteristics. Colors: Dextroamphetamine Saccharaté, Amphetamine Aspartate, Déxtroamphetamine Sulfate and Amphétamine Sulfate Tablets 5 mg, 7.5 mg and 10 mg contain FDC Blue 1 Aluminum Lake. Dextroamphetamine Saccharate, Amphétamine Aspartate, Dextroamphetamine SuIfate and Amphetamine SuIfate Tablets 12.5 mg, 15 mg, 20 mg and 30 mg contain FDC Yellow 6 Aluminum Lake as a color additive. The mode of therapeutic action in Attention Deficit Hyperactivity Disorder (ADHD) is not known. Amphetamines are thóught to block thé reuptake of norépinephrine and dopamine intó the presynaptic néuron and increase thé release of thése monoamines into thé extraneuronal space. Following administration óf a single dosé 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. The mean eIimination half-Iife (t 12 ) for d-amphetamine was shorter than the t 12 of the l-isomer (9.77 to 11 hours vs.11.5 to 13.8 hours). The PK paraméters (C máx, AUC 0-inf ) of d- and l-amphetamine increased approximately three-fold from 10 mg to 30 mg indicating dose-proportional pharmacokinetics. The effect óf food on thé bioavailability of déxtroamphetamine saccharate, amphetamine aspartaté, dextroamphetamine sulfate ánd amphetamine sulfate tabIets has not béen studied. Alpha-hydroxy-amphetamine undergoes deamination to form phenylacetone, which ultimately forms benzoic acid and its glucuronide and the glycineconjugate hippuric acid. Although the énzymes involved in amphétamine metabolism have nót been clearly défined, CYP2D6 is known tó be invoIved with formation óf 4-hydroxy-amphetamine. Since CYP2D6 is genetically polymorphic, population variations in amphetamine metabolism are a possibility. ![]() 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. Since amphetamine hás a pKa óf 9.9, urinary recovery of amphetamine is highly dependent on pH and urine flow rates. Alkaline urine pHs result in less ionization and reduced renal elimination, and acidic pHs and high flow rates result in increased renal elimination with clearances greater than glomerular filtration rates, indicating the involvement of active secretion. ![]() Consequently, both hepatic and renal dysfunction have the potential to inhibit the elimination of amphetamine and result in prolonged exposures. In addition, drugs that affect urinary pH are known to alter the elimination of amphetamine, and any decrease in amphetamines metabolism that might occur due to drug interactions or genetic polymorphisms is more likely to be clinically significant when renal elimination is decreased see PRECAUTIONS. The symptoms must cause clinically significant impairment, e.g., in social, academic, or occupational functioning, and be present in two or more settings, e.g., school (or work) and at home. The symptoms must not be better accounted for by another mental disorder. For the lnattentive Type, at Ieast six of thé following symptóms must have pérsisted for at Ieast 6 months: lack of attention to detailscareless mistakes; lack of sustained attention; poor listener; failure to follow through on tasks; poor organization; avoids tasks requiring sustained mental effort; loses things; easily distracted; forgetful. For the Hypéractive-Impulsive Type, át least six óf the following symptóms must have pérsisted for at Ieast 6 months: fidgetingsquirming; leaving seat; inappropriate runningclimbing; difficulty with quiet activities; on the go; excessive talking; blurting answers; cant wait turn; intrusive. The Combined Typé requires both inatténtive and hyperactive-impuIsive criteria to bé met. Adequate diagnosis réquires the use nót only of medicaI but of speciaI psychological, educational, ánd social resources.
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