덱스메틸페니데이트

DEA NFLIS-Drug Category -> Piperidines/PEA

DEA NFLIS-Drug Category -> Depressants and Tranquilizers

Methylphenidate blocks dopamine uptake in central adrenergic neurons by blocking dopamine transport or carrier proteins. Methylphenidate acts at the brain stem arousal system and the cerebral cortex and causes increased sympathomimetic activity in the central nervous system. Methylphenidate is a catecholamine reuptake inhibitor that indirectly increases catecholaminergic neurotransmission by inhibiting the dopamine transporter (DAT) and norepinephrine transporter (NET), which are responsible for clearing catecholamines from the synapse, particularly in the striatum and meso-limbic system.

Symptoms of overdose include vomiting, agitation, tremors, hyperreflexia, muscle twitching, convulsions (may be followed by coma), euphoria, confusion, hallucinations, delirium, sweating, flushing, headache, hyperpyrexia, tachycardia, palpitations, cardiac arrhythmias, hypertension, mydriasis, and dryness of mucous membranes.

Drug-Induced Liver Injury Severity and Toxicity (DILIst)

dexmethylphenidate

DILI Positive

Oral

DOI:10.1016/j.drudis.2019.09.022

N - Nervous system

QN - Nervous system

Methylphenidate inhibits dopamine and norepinephrine reuptake transporters in synapses, especially in the thalamus and striatum. One study shows no detectable difference in the caudal prefrontal cortex of treated or untreated monkeys, though multiple rat studies show activity on the prefrontal cortex. Imaging of human brains after administration of methylphenidate shows changes to blood flow of various regions of the brain including the striatum, supplementary motor area, and posterior parietal cortex.

Dexmethylphenidate is metabolised to the inactive metabolite ritalinic acid by carboxylesterase 1A1 in the liver. Other minor pathways metabolise dexmethylphenidate to the inactive metabolites 6-oxo-methylphenidate and p-hydroxy-methylphenidate which are de-esterified and conjugated into other unknown metabolites.

epatic, methylphenidate is metabolized primarily by de-esterification to ritalinic acid (α-phenyl-2-piperidine acetic acid, PPAA), which has little to no pharmacologic activity. Route of Elimination: Renal Half Life: 2-4 hours

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DEXMETHYLPHENIDATE

Established Pharmacologic Class [EPC] - Central Nervous System Stimulant

Physiologic Effects [PE] - Central Nervous System Stimulation

Dexmethylphenidate is a Central Nervous System Stimulant. The physiologic effect of dexmethylphenidate is by means of Central Nervous System Stimulation.

A loosely defined group of drugs that tend to increase behavioral alertness, agitation, or excitation. They work by a variety of mechanisms, but usually not by direct excitation of neurons. The many drugs that have such actions as side effects to their main therapeutic use are not included here.

Drugs that block the transport of DOPAMINE into axon terminals or into storage vesicles within terminals. Most of the ADRENERGIC UPTAKE INHIBITORS also inhibit dopamine uptake.

Taking dexmethylphenidate with or without food does not affect patients in a clinically relevant way. 90% of an oral dose is absorbed but as a result of hepatic first pass metabolism, oral bioavailability of dexmethylphenidate is 23% compared to l-methylphenidate with an oral bioavailability of 5%. Maximum concentration is generally reached in 1-1.5 hours.

Dexmethylphenidate is mainly eliminated renally. After 48 hours, 90% of the dose is collected in the urine and 3.3% is collected from feces.

2.65L/kg when administered intravenously.

0.40L/hr/kg following an intravenous dose and a renal clearance of 0.005L/hr/kg.