Reboxetine 4mg tablets
Requires a prescription from a doctor or prescriber
Reboxetine is an antidepressant drug used in the treatment of clinical depression, panic disorder and ADD/ADHD.
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Safety monitoring data
Yellow Card reports
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Suspected adverse reactions reported for Reboxetine
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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.
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Suspected adverse reactions reported for Reboxetine
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11 branded products available
MHRA licensed products
View all licensed products for Reboxetine on the MHRA register
Edronax 4mg tablets
Edronax 4mg tablets
Edronax 4mg tablets
Edronax 4mg tablets
This is the NHS Drug Tariff indicative price used for reimbursement purposes. It may not reflect the price paid by patients or pharmacies.
View full Drug TariffSource: NHS Drug Tariff via NHSBSA. Derived from dm+d VMPP (Virtual Medicinal Product Pack) pricing data. Contains public sector information licensed under the Open Government Licence v3.0.
WHO defined daily dose (DDD)
8 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 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
Guidelines from the National Institute for Health and Care Excellence
NICE clinical guidance(1)
Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
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Codes for healthcare professionals and prescribing systems
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SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. 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: 9 · Randomised trials: 5 · Trials: 2 · 1999–2026
Showing the 50 most relevant studies, sorted by most relevant.
Sarmiento LF, Ríos-Flórez JA, Rincón Uribe FA, et al.
2024
- Pituitary-Adrenal System
- Hypothalamo-Hypophyseal System
- Hydrocortisone
The hypothalamus-pituitary-adrenal axis (HPA axis) and the sympathetic-adrenal-medullary system (SAM system), two neuroendocrine systems associated with the stress response, have often been implicated to modulate decision-making in various domains. This systematic review summarizes the scientific evidence on the effects of pharmacological HPA axis and SAM system modulation on decision-making. We found 6375 references, of which 17 studies fulfilled our inclusion criteria. We quantified the risk of bias in our results with respect to missing outcome data, measurements, and selection of the reported results. The included studies administered hydrocortisone, fludrocortisone (HPA axis stimulants), yohimbine, reboxetine (SAM system stimulants), and/or propranolol (SAM system inhibitor). Integrating the evidence, we found that SAM system stimulation had no impact on risk aversion, loss aversion or intertemporal choice, while SAM system inhibition showed a tentative reduction in sensitivity to losses. HPA axis stimulation had no effect on loss aversion or reward anticipation but likely a time-dependent effect on decision under risk. Lastly, combined stimulation of both systems exhibited inconsistent results that could be explained by dose differences (loss aversion) and sex differences (risk aversion). Future research should address time-, dose-, and sex-dependencies of pharmacological effects on decision-making.
Abstract licence: CC BY
Rodoshi ZN, Shibu S, Omer O, et al.
2025
Post-stroke depression (PSD) is a common neuropsychiatric complication that adversely affects rehabilitation outcomes, cognitive recovery, and quality of life in stroke survivors. While selective serotonin reuptake inhibitors (SSRIs) are widely used as first-line treatment, serotonin-norepinephrine reuptake inhibitors (SNRIs) have emerged as potential alternatives with broader neurochemical targets. This systematic review aimed to compare the efficacy of SSRIs and SNRIs in the treatment and prevention of PSD. A comprehensive literature search was conducted across PubMed, Embase, Scopus, and Google Scholar in accordance with PRISMA guidelines, applying filters for English-language clinical trials. Five randomized controlled trials met the inclusion criteria and were analyzed. The findings revealed that both SSRIs and SNRIs significantly improved depressive symptoms, with escitalopram showing early and superior antidepressant effects compared to sertraline. SNRIs like duloxetine and reboxetine demonstrated added benefits in cognitive outcomes, prevention of PSD, and symptom subtype-specific efficacy, particularly in retarded depression. While the overall risk of bias was low in most studies, limitations such as small sample sizes and limited direct head-to-head comparisons were noted. These results support the clinical utility of both drug classes and emphasize the need for individualized pharmacologic strategies based on patient characteristics and symptom profiles.
Abstract licence: CC BY
Xia Y, Quednow BB, Bach DR
2026
- Propranolol
- Cycloserine
- Hydrocortisone
A large body of work has investigated the effect of various pharmacological compounds on aversive memory formation, retrieval, and modification in humans. A broad overview across signalling pathways and memory models is currently lacking. Here, we systematically review publications that tested the impact of acute pharmacological interventions on aversive memory in healthy humans, following PRISMA-2020. We identified 215 candidate compounds from 17 systems and searched PubMed, Web of Science and Scopus, until 14 June 2024. We identified 100 publications with 36 compounds targeting 13 systems. Three compounds were used by the majority of studies: hydrocortisone (n = 25), propranolol (n = 19), and D-cycloserine (n = 8), while many of the remaining 33 compounds were investigated in single studies only. We summarise the effect of each investigated compound across memory models, according to the targeted memory stage. Solid evidence emerges for an impact of propranolol on reconsolidation, and weak evidence for an impact of propranolol, 3,4-methylenedioxymethamphetamine (MDMA), benzodiazepines, yohimbine, reboxetine, and D-cycloserine on aversive memory encoding/consolidation, and valproic acid on extinction encoding/consolidation. Furthermore, 15 compounds showed significant effects in individual studies with no published replication attempts to date. We discuss potential research directions and suggest steps for greater comparability of findings between compounds, memory models, and laboratories.
Abstract licence: CC BY
Li Y, Yu M, Yang H, et al.
2025
- Antidepressive Agents
- Schizophrenia
- Duloxetine Hydrochloride
BackgroundThe treatment response for the negative symptoms of schizophrenia is not ideal, and the efficacy of antidepressant treatment remains a matter of considerable controversy. This systematic review and meta-analysis aimed to assess the efficacy of adjunctive antidepressant treatment for negative symptoms of schizophrenia under strict inclusion criteria.MethodsA systematic literature search (PubMed/Web of Science) was conducted to identify randomized, double-blind, effect-focused trials comparing adjuvant antidepressants with placebo for the treatment of negative symptoms of schizophrenia from database establishment to April 16, 2025. Negative symptoms were examined as the primary outcome. Data were extracted from published research reports, and the overall effect size was calculated using standardized mean differences (SMD).ResultsA total of 15 articles, involving 655 patients, were included in this review. Mirtazapine (N = 2, n = 48, SMD -1.73, CI -2.60, -0.87) and duloxetine (N = 1, n = 64, SMD -1.19, CI -2.17, -0.21) showed significantly better efficacy for negative symptoms compared to placebo. In direct comparisons between antidepressants, mirtazapine showed significant differences compared to reboxetine, escitalopram, and bupropion, but there were no significant differences between other antidepressants or between antidepressants and placebo. No publication bias for the prevalence of this condition was observed.ConclusionsThese findings suggest that adjunctive use of mirtazapine and duloxetine can effectively improve the negative symptoms of schizophrenia in patients who are stably receiving antipsychotic treatment. Therefore, incorporating antidepressants into future treatment plans for negative symptoms of schizophrenia is a promising strategy that warrants further exploration.
Abstract licence: CC BY
Xia Y, Quednow BB, Bach DR
2025
A large body of work has investigated the effect of various pharmacological compounds on aversive memory formation, retrieval, and modification in humans. A broad overview across signalling pathways and memory models is currently lacking. Here, we systematically review publications that tested the impact of acute pharmacological interventions on aversive memory in healthy humans, following PRISMA 2020. We identified 215 candidate compounds from 17 systems and searched Pubmed, Web of Science and Scopus, until 14 June 2024. In total, we identified 100 publications with 36 compounds targeting 13 systems. Three compounds were used by the majority of studies: hydrocortison (n=25), propranolol (n=19), and D-cycloserin (n=8), while many of the remaining 33 compounds were investigated in single studies only. We summarise the effect of each investigated compound across memory models, according to the targeted memory stage. Solid evidence emerges for an impact of propranolol on reconsolidation, and weak evidence for an impact of propranolol, 3,4-methylenedioxymethamphetamine (MDMA), benzodiazepines, yohimbine, reboxetine, and D-cycloserine on aversive memory encoding/consolidation, and valproic acid on extinction encoding/consolidation. Furthermore, 11 compounds showed significant effects in individual studies with no published replication attempts to date. We discuss potential research directions and suggest steps for greater comparability of findings between compounds, memory models, and laboratories.
Abstract licence: CC BY
Schiele MA, Fagan HA, Baldwin DS, et al.
2026
- Anti-Anxiety Agents
- Psychotherapy
- Generalized Anxiety Disorder
IntroductionTreatment resistance in anxiety disorders (TR-ADs) constitutes a major clinical challenge conferring a considerable burden regarding quality of life and societal health costs.MethodsThis systematic review provides an overview of pharmacological, psychotherapeutic, and neurostimulatory treatment options in adults with treatment-resistant generalized anxiety disorder (TR-GAD), panic disorder (TR-PD)/agoraphobia, and social anxiety disorder (TR-SAD).ResultsA total of 26 randomized controlled trials (RCTs) and 36 open label studies were identified, with, however, mostly small sample sizes and several methodological limitations. According to RCTs, selective serotonin reuptake inhibitors (SSRIs) or clomipramine are effective in TR-PD after failure to respond to cognitive behavioral therapy (CBT). In pharmacological TR-SAD, switching from one SSRI to another or to venlafaxine was found helpful in open label trials. RCTs further suggest augmentation with quetiapine, risperidone, olanzapine, or pregabalin in TR-GAD, pindolol in TR-PD, and clonazepam in TR-SAD. Open label studies in TR-AD provide preliminary evidence for ketamine or augmentation with nefazodone, reboxetine, buspirone, aripiprazole, olanzapine, quetiapine, risperidone, ziprasidone, divalproex sodium, levetiracetam, zonisamide, flumazenil, pregabalin, cannabidiol, and acamprosate. For pharmacological TR, CBT was effective in several RCTs. Following nonresponse to CBT, first evidence suggests effectiveness of Acceptance and Commitment Therapy and Mindfulness-Based Cognitive Therapy. Only inconclusive support was identified for repetitive transcranial magnetic stimulation in TR-AD.ConclusionIn summary, this integrative review may provide an evidence base for expert recommendations, inform clinical guidelines, and inspire further research into innovative, personalized treatment of TR-AD increasing response rates and lowering the considerable individual and public health burden of anxiety disorders.
Abstract licence: CC BY-NC
Hu X, Pan L, Li W
2023
- Attention Deficit Disorder with Hyperactivity
- Schizophrenia
- Norepinephrine
BackgroundNorepinephrine transporter inhibitors that can alter the level of neurotransmitter in the brain are used to treat neurological disorders. However, a number of studies have reported their limited significance as a result of their slow onset of action and moderate efficacy.ObjectivesTo determine the effects of norepinephrine reuptake inhibitors (NRIs), reboxetine and atomoxetine on schizophrenia and attention deficit hyperactivity disorder (ADHD).Material and methodsRelevant articles published between 2000 and 2022 were searched in the MEDLINE, CINAHL (via Ebsco), Web of Science and Scopus databases. Among the various NRIs, studies concerning the 2 potent drugs - reboxetine and atomoxetine - were selected for analysis. Odds ratios (ORs) with 95% confidence intervals (95% CIs) were estimated, along with the exploration of heterogeneity and publication bias, using RevMan software.ResultsA total of 14 eligible studies with a combined sample size of 970 patients were included. Using a random effects model, an OR of 0.55 (0.32-0.94), a Tau2 value of 0.23, a ÷2 value of 12.31, 8 degrees of freedom (df), an I2 of 35%, a Z value of 2.19, and a p-value of 0.03 were recorded for reboxetine. Atomoxetine had an OR of 0.35 (0.13-0.97), a Tau2 value of 0.58, a ÷2 value of 7.31, 4 df, an I2 of 45%, a Z value of 1.53, and a p-value of 0.04. All results were statistically significant with a low risk of publication bias, as was evident from the p-values >0.05 derived from the Egger's test and the Begg's test. These drugs provided comparable changes to control drugs in Hamilton Depression Rating Scale (HAM-D) scores, Positive and Negative Syndrome Scale (PANSS) scores and ADHD ratings. This confirms the efficacy of reboxetine for the treatment of schizophrenia and atomoxetine for the treatment of ADHD.ConclusionThe present meta-analysis suggests that NRIs are efficacious and therefore they are potential candidate drugs for the treatment of schizophrenia and ADHD.
Abstract licence: CC BY
Altree TJ, Aishah A, Loffler KA, et al.
2023
- Sleep Apnea, Obstructive
- Mandelic Acids
- Cross-Over Studies
Berger M, Solelhac G, Marchi NA, et al.
2023
- Sleep Apnea, Obstructive
- Oxygen
- Mandelic Acids
Tilaki EH, Hasanzadeh A, Shalbafan M, et al.
2023
- Fluoxetine
- Obsessive-Compulsive Disorder
- Reboxetine
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
1 found
Half-life
12.5 hours
Mechanism
Reboxetine is a selective inhibitor of noradrenaline reuptake.
Food interactions
None known
Human targets
1 target
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
Half-life
12.5 hours
Protein binding
98%
Metabolism
by glucuronide or sulphate conjugation.…
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 899 interactions
How the body processes this drug — absorption, distribution, metabolism, and elimination
by glucuronide or sulphate conjugation. It is metabolized by the cytochrome P450
CYP isoenzyme 3A4.
Proteins and enzymes this drug interacts with in the body
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
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that transport this drug across cell membranes
PMID:2897240 PMID:35970996 PMID:8898203 PMID:9038218 PMID:35507548
Catalyzes the flop of phospholipids from the cytoplasmic to the exoplasmic leaflet of the apical membrane. Participates mainly to the flop of phosphatidylcholine, phosphatidylethanolamine, beta-D-glucosylceramides and sphingomyelins .
PMID:8898203
Energy-dependent efflux pump responsible for decreased drug accumulation in multidrug-resistant cells PMID:2897240 PMID:35970996 PMID:9038218
ATC N06AX18
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)
Reboxetine
Additional database identifiers
ChemSpider
112870
BindingDB
388642
PDB
41X
ZINC
ZINC000003996032
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:2637
GenAtlas
CYP3A4
GeneCards
CYP3A4
GenBank Gene Database
M18907
Guide to Pharmacology
1337
UniProt Accession
CP3A4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2625
GenAtlas
CYP2D6
GeneCards
CYP2D6
GenBank Gene Database
M20403
GenBank Protein Database
181350
Guide to Pharmacology
1329
UniProt Accession
CP2D6_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:40
GenAtlas
ABCB1
GeneCards
ABCB1
GenBank Gene Database
M14758
GenBank Protein Database
307180
Guide to Pharmacology
768
UniProt Accession
MDR1_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite:
- DrugBank 6.02024Recommended citationKnox C., Wilson M., Klinger C.M., et alDrugBank 6.0: the DrugBank Knowledgebase for 2024Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
- DrugBank 5.02018Wishart D.S., Feunang Y.D., Guo A.C., et alDrugBank 5.0: a major update to the DrugBank database for 2018Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
- DrugBank 4.02014Law V., Knox C., Djoumbou Y., et alDrugBank 4.0: shedding new light on drug metabolismNucleic Acids Res. 2014 Jan 142(1):D1091-7
- DrugBank 3.02011Knox C., Law V., Jewison T., et alDrugBank 3.0: a comprehensive resource for 'omics' research on drugsNucleic Acids Res. 2011 Jan39(Database issue):D1035-41
- DrugBank 2.02008Wishart D.S., Knox C., Guo A.C., et alDrugBank: a knowledgebase for drugs, drug actions and drug targets.Nucleic Acids Research2008 Jan36(Database issue):D901-6
- DrugBank 1.02006Wishart D.S., Knox C., Guo A.C., et alDrugBank: a comprehensive resource for in silico drug discovery and exploration.Nucleic Acids Research2006 Jan 134(Database issue):D668-72