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Dexmethylphenidate

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Collated from TripSit, Pharmacology, DrugCentral, DailyMed. Where sources differ (e.g. dosing), Compare shows them side by side.

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StimulantHabit-formingCommonTS

Also known as dexmethylphenidate, dextromethylphenidateTS

The psychoactive isomer of methylphenidate, mostly used to treat ADHD. Twice as potent as methylphenidate, and is said to have cleaner psychostimulant effects with fewer side effects.TS

Oral

Route dataTripSit

Dose
WeakerStronger
ThresholdLightCommonStrongHeavy
—10–20 mg20–30 mg30–40 mg40 mg+
050 mg
LightCommonStrongHeavy
Duration
ShorterLonger
Onset45–90 minutes
Total9–12 hours
After-effects1–12 hours
OnsetCome-upPeakOffset

🧬 Receptor activityPHDC

TargetActionAffinitySource
Sodium-dependent dopamine transporter—Ki 74.6 nMCHEMBL
Norepinephrine transporter—Ki 270 nMCHEMBL
Unchecked—Ki 10000 nMCHEMBL
Sodium-dependent dopamine transporter (SLC6A3)Inhibitor7.8 KiDRUGCENTRAL
Sodium-dependent noradrenaline transporter (SLC6A2)Inhibitor—DRUGCENTRAL
Dopamine receptor (Drd1)—7.08 IC50DRUGCENTRAL
Sodium-dependent dopamine transporter (Slc6a3)—7.13 KiDRUGCENTRAL
Transporter (Slc6a2)—6.57 KiDRUGCENTRAL
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Mechanism of actionPHDM

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.

PharmacodynamicsPHDM

Dexmethylphenidate is the d-enantiomer of methylphenidate. This enantiomer is more pharmacologically active than the racemic mixture and may block norepinephrine and dopamine reuptake in synapses.

Pharmacokinetics

Half-lifePH

The mean terminal half life is approximately 2.2 hours. However other studies have shown 3.8-3.9 hours, or 5.96 hours after intravenous administration and 5.69 hours following an oral dose.

AbsorptionPHDM

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.

MetabolismPH

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

Protein bindingPH

12-15% of dexmethylphenidate is protein bound. However, other studies have observed 15.2±5.2% protein binding in children and 16.2±1.1% in adults.

Plan when to take Dexmethylphenidate — see where onset, peak and comedown land on the clock

Fact-sheets from PsychonautWiki. Harm-reduction reference only — not medical advice.