Diethylpropion 75mg modified-release capsules
A appetite depressant considered to produce less central nervous system disturbance than most drugs in this therapeutic category.
Some safe custody exemptions; written records required
Legal requirements and restrictions
Medicines with lower misuse potential than Schedule 2. Subject to special prescription requirements but reduced record-keeping.
Legal requirements
- Safe custody requirements apply (locked storage)
- No controlled drugs register required
- Prescriptions valid for 28 days
- Can be emergency supplied by pharmacists
Other medicines in this category
Official documents, adverse reaction reporting, and safety monitoring
Report a side effect
Submit a Yellow Card report to the MHRA
Safety monitoring data
Yellow Card reports
The MHRA Yellow Card scheme collects reports of suspected side effects from healthcare professionals and patients. View the Drug Analysis Profile (iDAP) for real-world adverse reaction data.
View Drug Analysis Profile
Suspected adverse reactions reported for Diethylpropion
Browse all iDAP reports
Interactive Drug Analysis Profiles for all medicines
Report a side effect
Submit a Yellow Card report to the MHRA
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
The European Medicines Agency (EMA) collects suspected adverse reaction reports from across the EU/EEA through the EudraVigilance system. Search for safety data on this medicine.
Search EudraVigilance database
Browse substances A–Z in the European adverse reaction database
About EudraVigilance
Learn about EU pharmacovigilance and safety monitoring
EudraVigilance data is published by the European Medicines Agency (EMA). A suspected adverse reaction is not necessarily caused by the medicine.
1 branded products available
NHS prescribing volume and spending trends
Check stock at pharmacies and supply information
Pharmacy stock checkers
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
SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0.
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: 2 · Trials: 1 · 1961–2026
Showing the 50 most relevant studies, sorted by most relevant.
C. Cercato, V. A. Roizenblatt, C. C. Leança, et al.
International Journal of Obesity, 2004
H. Arias, A. Santamaría, Syed F. Ali
International review of neurobiology, 2009
M. Abramowicz, P. V. Haecke, M. Demedts, et al.
European Respiratory Journal, 2003
Hendricks EJ
2017
The global pandemic of obesity and overweight now affects between 2.8 and 3.5 billion of the world population and shows no signs of abatement. Treatment for what is now recognized as a chronic disease includes pharmacotherapy, considered an essential component of comprehensive therapy. New drug discovery is robust, but the pace of the US Food and Drug Administration approval for obesity drugs has been glacial, and only a handful of approved drugs are available for treating obesity. In the last 20 years, the US Food and Drug Administration has approved 208 drugs for cancer, 118 for cardiovascular diseases, 168 for neurological diseases, and 223 endocrinologic drugs, but only 6 for obesity, 2 of which have been taken off market. Currently, there are only 9 drugs approved by the FDA for obesity treatment. US physicians have turned to off-label drug use in their effort to care for increasing numbers of patients with excess adiposity. Phentermine is the most commonly used drug for treating obesity. Although approved only for short-term use, US physicians have used it successfully for long-term since its initial approval in 1959. This drug, used off-label for long-term, has proven to be safe and effective, far safer than the disease it is used to treat. Phentermine and diethylpropion, an equally safe but somewhat less effective drug, are both generic and therefore inexpensive. These drugs have been maligned inappropriately because their two-dimensional structure diagrams resemble amphetamine and also because of unproven presumptions about their potential adverse effects. In the face of an increasing epidemic, worldwide obese and overweight patients deserve effective treatment that prescribing these drugs could provide, if rehabilitated and used more frequently. US physicians will likely continue to use any drug proven useful off-label for this illness until such time as more effective drugs are approved.
Abstract licence: CC BY-NC
G. I. Nugraha, Fiki Amalia, Fata Imadudda'wah, et al.
Medicine, 2024
- Obesity
- Weight Loss
- Muscle, Skeletal
Lopez A, Gil-Lievana E, Gutierrez R
2025
This study investigated the sex-specific effects of commonly prescribed appetite suppressants on body weight and the manifestation of motor side effects, specifically stereotypy. Employing video recordings and DeepLabCut (DLC) for precise behavioral quantification, we analyzed stereotypy, defined as purposeless, repetitive motor behaviors, in male and female rats. Under control (saline) conditions, male rats exhibited a greater propensity for weight gain compared to females. However, in contrast, female rats demonstrated greater and more homogenous weight loss than males following the administration of diethylpropion and tesofensine. Phentermine and mazindol induced comparable weight loss in both sexes, whereas cathine elicited weight reduction exclusively in males. 5-HTP and d-amphetamine administration only prevented weight gain relative to controls. Analysis of motor side effects revealed that drugs primarily targeting dopamine pathways – specifically, phentermine, mazindol, diethylpropion, cathine, and d-amphetamine – induced pronounced stereotypies, particularly head-weaving, in both sexes. Interestingly, tesofensine elicited head-weaving behavior exclusively in female subjects, albeit to a lesser extent than that observed with other dopaminergic agents; conversely, tesofensine was most frequently associated with orolingual dyskinesia. Moreover, one of the most potent forms of stereotypy—backward locomotion, here referred to as “moonwalking”—was sporadically observed only following the administration of phentermine, diethylpropion, cathine, and mazindol, with diethylpropion inducing it most frequently. Male subjects treated with these same drugs exhibited an unexpected effect: spontaneous ejaculations, potentially attributable to the combined effects on dopamine and serotonin signaling in brain regions regulating sexual function. Network analysis and Markov transition matrices revealed distinct behavioral profiles associated with head-weaving, which emerged as the dominant attractor state, suggesting potential mechanistic differences among these drugs. Collectively, this study provides a valuable database characterizing the behavioral side effects of appetite suppressants.
Abstract licence: CC BY-NC
Fakhoury B, Sierra L, Rama K, et al.
2025
- Alcoholism
- Anti-Obesity Agents
- Bariatric Surgery
ImportancePatients who have undergone bariatric surgery have an elevated risk for alcohol use disorder (AUD). Incretin-based therapies (IBTs) may be associated with reward pathways in addition to weight loss.ObjectiveTo evaluate whether IBT after bariatric surgery is associated with a lower risk of new-onset AUD and initiation of medications for AUD (MAUDs) compared with non-IBT antiobesity medications (AOMs).Design, setting, and participantsThis retrospective cohort study included 15 382 adults who underwent bariatric surgery and subsequently received an AOM between January 1, 2020, and January 1, 2024, with outcomes assessed up to 2 years after AOM initiation. Data were derived from a multi-institutional US electronic health record network. Propensity score matching (1:1) balanced baseline covariates. Data were analyzed September 14, 2025.ExposuresPost-bariatric surgery treatment with an IBT (semaglutide, liraglutide, or tirzepatide) vs non-IBT AOMs (orlistat, phentermine, low-dose naltrexone, benzphetamine, phendimetrazine, or diethylpropion).Main outcomes and measuresOutcomes of interest were incidence rates (per 1000 person-years) and hazard ratios (HRs) of new-onset AUD and initiation of MAUDs, estimated using Kaplan-Meier and Cox proportional hazards regression models.ResultsThe study included 15 382 patients who underwent bariatric surgery and subsequently received AOMs (11 194 IBT [mean (SD) age, 51.4 (11.6) years; 8855 women (79.1%)]; and 4188 non-IBT [mean (SD) age, 45.1 (11.0) years; 3587 women (86.6%)]). After propensity score matching, 3990 patients were included in each group. Use of IBT was associated with a lower incidence of AUD (2.4 vs 5.2 per 1000 person-years) and a lower hazard of developing AUD (HR, 0.45; 95% CI, 0.25-0.81; P = .006) vs non-IBT use. Use of IBT was also associated with a lower incidence of initiating MAUDs (15.2 vs 25.6 per 1000 person-years) and a lower hazard of MAUD initiation (HR, 0.59; 95% CI, 0.46-0.75; P Conclusions and relevanceIn this cohort study of patients who underwent bariatric surgery, IBT was associated with a 55% lower risk of new-onset AUD and a 41% lower risk of initiation of MAUDs compared with non-IBT AOMs. These findings suggest potential neurobehavioral benefits associated with IBTs that may inform AOM selection in this high-risk population. Prospective studies are warranted to confirm these associations and examine long-term liver-related outcomes.
Abstract licence: CC BY
A. Sakinah, Rizky Abdullah, Izzah Faridh, et al.
Journal of World Science, 2026
Yan Kurniawan, Sisca Sisca, Monica Dwi Hartati, et al.
Jurnal Akta Trimedika, 2026
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
33 found
Half-life
4 to 6 hours
Mechanism
Diethylpropion is an amphetamine that stimulates neurons to release or maintain…
Food interactions
1 warning
Human targets
3 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
Half-life
4 to 6 hours
Metabolism
Elimination
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 1311 interactions
How the body processes this drug — absorption, distribution, metabolism, and elimination
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
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: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)
ATC A08AA03
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Show
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Diethylpropion
Additional database identifiers
Drugs Product Database (DPD)
9897
ChemSpider
6762
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: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:11050
GenAtlas
SLC6A4
GeneCards
SLC6A4
GenBank Gene Database
X70697
GenBank Protein Database
36433
Guide to Pharmacology
928
UniProt Accession
SC6A4_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