Dexmethylphenidate 10mg modified-release capsules
Requires a prescription from a doctor or prescriber
Dexmethylphenidate is the dextrorotary form of methylphenidate introduced in 2002[A177181].
Strict controls: safe custody, register required
Legal requirements and restrictions
These are medicines with high potential for misuse but with accepted medical uses. Subject to the strictest controls.
Legal requirements
- Must be stored in a locked controlled drugs cabinet
- Pharmacy must keep a controlled drugs register
- Prescriptions valid for 28 days only
- Prescriptions must include specific details (dose, form, strength, total quantity)
- Cannot be emergency supplied by pharmacists
Other medicines in this category
Morphine, Oxycodone, Fentanyl, Methylphenidate (Ritalin), Amphetamines
Safety information for pregnancy and breastfeeding
Pregnancy
Breastfeeding
Always consult your doctor or midwife before taking any medicine during pregnancy or while breastfeeding. Source: DrugBank (CC BY-NC 4.0).
Official documents, adverse reaction reporting, and safety monitoring
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Data from the MHRA Yellow Card scheme. A reported reaction does not necessarily mean the medicine caused it. Contains public sector information licensed under the Open Government Licence v3.0.
EudraVigilance
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2 branded products available
WHO defined daily dose (DDD)
15 mg
Not a recommended dose. The DDD is the assumed average maintenance dose per day for a drug used for its main indication in adults. It is a statistical measure used for research and comparison purposes only.
Source: WHO Collaborating Centre for Drug Statistics Methodology, distributed via the NHS dm+d supplementary BNF/ATC mapping files (NHSBSA). Contains public sector information licensed under the Open Government Licence v3.0.
Therapeutically similar medicines
Similarity is based on WHO Anatomical Therapeutic Chemical (ATC) classification and on a factual NHS dm+d therapeutic-grouping code prefix. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
Check stock at pharmacies and supply information
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Search for this medicine at major UK pharmacy chains. These links open the retailer's own website — results depend on their current online catalogue.
Supply & safety information
Official UK regulator monitoring and safety alerts
Pharmacy links redirect to the retailer's own search and do not represent real-time stock levels. Shortage and safety information sourced from MHRA drug safety updates (gov.uk, Crown Copyright under OGL v3.0).
Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
Browse tools
SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. BNF code shown is the factual mapping value distributed by NHS Business Services Authority (NHSBSA) in the dm+d supplementary file under OGL v3.0; it is not affiliated with, nor licensed from, the publishers of the British National Formulary. ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Academic studies and reviews for this medicine's active substance
Showing the 50 most relevant studies.
Reviews & meta-analyses: 7 · Randomised trials: 3 · Trials: 6 · 2002–2026
Showing the 50 most relevant studies, sorted by most relevant.
Elyse E. Lower, Stewart B. Fleishman, Alyse Cooper, et al.
Journal of Pain and Symptom Management, 2009
- Central Nervous System Stimulants
- Antineoplastic Agents
- Fatigue
Elyse E. Lower, Stacy Harman, Robert P. Baughman
CHEST Journal, 2008
- Central Nervous System Stimulants
- Exercise Test
- Fatigue
Narong Maneeton, Pakapan Woottiluk, Sirijit Suttajit, et al.
Neuropsychiatric Disease and Treatment, 2015
BACKGROUND: The efficacy of dexmethylphenidate (d-MPH) has been proven in the treatment of children and adolescents with attention-deficit hyperactivity disorder (ADHD). OBJECTIVE: The aim of this systematic review is to determine the efficacy, acceptability, and tolerability of d-MPH in child and adolescent ADHD. METHODS: The searches of SCOPUS, MEDLINE, CINAHL, and Cochrane Controlled Trials Register were performed in February 2015. All randomized controlled trials of d-MPH versus placebo that were performed in children and adolescents with ADHD up to 18 years of age were included in the study. The efficacy was measured by using the pooled mean-endpoint or mean-changed scores of ADHD rating scales and the response rate. Acceptability and tolerability were measured by using the pooled rates of overall discontinuation and discontinuation due to adverse events, respectively. RESULTS: A total of 1,124 children and adolescents diagnosed as having ADHD were included in this review. In a laboratory school setting, the pooled mean-change and mean-endpoint scores in the d-MPH-treated group were significantly greater than those of the placebo-treated group with standardized mean difference (95% confidence interval [CI]) of -1.20 (-1.73, -0.67), I (2)=95%. Additionally, the pooled mean-changed scores of the ADHD rating scales for teachers and parents in the d-MPH-treated group were significantly greater than that of the placebo-treated group with weighted mean difference (95% CI) of -13.01 (-15.97, -10.05), I (2)=0% and (95% CI) of -12.99 (-15.57, -10.42), I (2)=0%, respectively. The pooled response rate in the d-MPH-treated groups had a significance higher than that of the placebo-treated group. The rates of pooled overall discontinuation and discontinuation due to adverse events between the two groups were not significantly different. CONCLUSION: Based on the findings in this review, it can be concluded that d-MPH medication is efficacious and tolerable in child and adolescent ADHD. However, the acceptability of d-MPH is no greater than that of the placebo. Further systematic studies may confirm these findings.
Abstract licence: CC BY-NC 3.0
Narong Maneeton, Benchalak Maneeton, Pakapan Woottiluk, et al.
European Neuropsychopharmacology, 2015
Gillian M. Keating, David P. Figgitt
Drugs, 2002
- Dexmethylphenidate Hydrochloride
- Absorption
- Attention Deficit Disorder with Hyperactivity
T. Spencer, L. Adler, J. McGough, et al.
Biological psychiatry, 2007
- Dexmethylphenidate Hydrochloride
- Central Nervous System Stimulants
- Attention Deficit Disorder with Hyperactivity
A. Raja Reddy, Lee Shepherd
International Journal of Innovative Science and Research Technology (IJISRT), 2024
Elyse E. Lower, Stacy Harman, Robert P. Baughman
CHEST Journal, 2007
Raul R. Silva, R. Muniz, K. Mccague, et al.
Psychopharmacology bulletin, 2025
- Dexmethylphenidate Hydrochloride
- Central Nervous System Stimulants
- Attention Deficit Disorder with Hyperactivity
Sharon B. Wigal, James M. Swanson, David Feifel, et al.
Journal of the American Academy of Child & Adolescent Psychiatry, 2004
- Central Nervous System Stimulants
- Attention Deficit Disorder with Hyperactivity
- Methylphenidate
Sources: aggregated from Europe PMC (EMBL-EBI), OpenAlex, Crossref, PubMed and other open scholarly databases. Retracted articles are excluded. Study information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
35 found
Half-life
2.2 hours
Mechanism
Methylphenidate inhibits dopamine and norepinephrine reuptake transporters in sy…
Food interactions
2 warnings
Human targets
3 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
90%
[A177187]…
Half-life
2.2 hours
Protein binding
12-15%
Volume of distribution
2.65L/kg
[A177187]
Metabolism
Elimination
48 hours
[A177187]
After 48 hours, 90% of the dose is collected in the urine and 3.3%…
Clearance
0.40L/h
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 1159 interactions
Animal studies in pregnant and lactating rats showed delayed fetal skeletal ossification, and reduced weight gain in male offspring[Label]. Due to these studies, caution must be exercised and the benefits and risks of taking this drug must be weighed[Label]. It is unlikely that dexmethylphenidate is carcinogenic but B6C3F1 mice, which are sensitive to the development of hepatic tumours, developed hepatoblastomas at 2 times the maximum recommended human dose[Label].
Methylpheidate was not found to be mutagenic but is weakly clastogenic in Chinese Hamster Ovary cells[Label]. Methylphenidate does not impair fertility in animal studies[Label].
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A177187]
90% of an oral dose is absorbed[Label] 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% .
[A177187]
Maximum concentration is generally reached in 1-1.5 hours[Label].
[A177187]
[A177187]
[A177187]
[A177187]
[A177187]
After 48 hours, 90% of the dose is collected in the urine and 3.3% is collected from feces.
[A177187]
Proteins and enzymes this drug interacts with in the body
PMID:10375632 PMID:11093780 PMID:1406597 PMID:15505207 PMID:19478460 PMID:39112701 PMID:39112703 PMID:39112705 PMID:8302271
Also mediates sodium- and chloride-dependent transport of norepinephrine (also known as noradrenaline) (By similarity). Regulator of light-dependent retinal hyaloid vessel regression, downstream of OPN5 signaling (By similarity)
PMID:2008212 PMID:8125921 PMID:38750358
Is responsible for norepinephrine re-uptake and clearance from the synaptic cleft, thus playing a crucial role in norepinephrine inactivation and homeostasis (By similarity). Can also mediate sodium- and chloride-dependent transport of dopamine PMID:11093780 PMID:8125921 PMID:39395208 PMID:39048818
PMID:10407194 PMID:12869649 PMID:21730057 PMID:27049939 PMID:27756841 PMID:34851672
Essential for serotonin homeostasis in the central nervous system. In the developing somatosensory cortex, acts in glutamatergic neurons to control serotonin uptake and its trophic functions accounting for proper spatial organization of cortical neurons and elaboration of sensory circuits.
In the mature cortex, acts primarily in brainstem raphe neurons to mediate serotonin uptake from the synaptic cleft back into the pre-synaptic terminal thus terminating serotonin signaling at the synapse (By similarity). Modulates mucosal serotonin levels in the gastrointestinal tract through uptake and clearance of serotonin in enterocytes. Required for enteric neurogenesis and gastrointestinal reflexes (By similarity).
Regulates blood serotonin levels by ensuring rapid high affinity uptake of serotonin from plasma to platelets, where it is further stored in dense granules via vesicular monoamine transporters and then released upon stimulation .
PMID:17506858 PMID:18317590
Mechanistically, the transport cycle starts with an outward-open conformation having Na1(+) and Cl(-) sites occupied. The binding of a second extracellular Na2(+) ion and serotonin substrate leads to structural changes to outward-occluded to inward-occluded to inward-open, where the Na2(+) ion and serotonin are released into the cytosol. Binding of intracellular K(+) ion induces conformational transitions to inward-occluded to outward-open and completes the cycle by releasing K(+) possibly together with a proton bound to Asp-98 into the extracellular compartment.
Na1(+) and Cl(-) ions remain bound throughout the transport cycle .
PMID:10407194 PMID:12869649 PMID:21730057 PMID:27049939 PMID:27756841 PMID:34851672
Additionally, displays serotonin-induced channel-like conductance for monovalent cations, mainly Na(+) ions. The channel activity is uncoupled from the transport cycle and may contribute to the membrane resting potential or excitability (By similarity)
Enzymes involved in drug metabolism — important for understanding drug interactions
ATC N06BA11
ATC N06BA15
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
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Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Dexmethylphenidate
Additional database identifiers
Drugs Product Database (DPD)
20243
ChemSpider
135807
BindingDB
50062915
PDB
A1D5U
ZINC
ZINC000000896711
HUGO Gene Nomenclature Committee (HGNC)
HGNC:11049
GenAtlas
SLC6A3
GeneCards
SLC6A3
GenBank Gene Database
M96670
GenBank Protein Database
553260
Guide to Pharmacology
927
UniProt Accession
SC6A3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:11048
GenAtlas
SLC6A2
GeneCards
SLC6A2
GenBank Gene Database
M65105
GenBank Protein Database
189258
Guide to Pharmacology
926
UniProt Accession
SC6A2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:11050
GenAtlas
SLC6A4
GeneCards
SLC6A4
GenBank Gene Database
X70697
GenBank Protein Database
36433
Guide to Pharmacology
928
UniProt Accession
SC6A4_HUMAN
UniProt Accession
Q6LAP9_HUMAN
DrugBank citations
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Structured knowledge from the free knowledge base
ATC classifications (Wikidata)
Linked open data from Wikidata (Q1207210), a free and open knowledge base operated by the Wikimedia Foundation. Data is available under the Creative Commons CC0 1.0 Public Domain Dedication. WHO INN from the World Health Organization.