Orlistat 27mg chewable tablets
The global prevalence of obesity is increasing rapidly.
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Yellow Card reports
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Suspected adverse reactions reported for Orlistat
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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 Orlistat
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1 branded products available
WHO defined daily dose (DDD)
360 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
Guidelines from the National Institute for Health and Care Excellence
NICE clinical guidance(7)
Naltrexone–bupropion for managing overweight and obesity (TA494)
Type 2 diabetes: prevention in people at high risk (PH38)
Liraglutide for managing overweight and obesity (TA664)
Semaglutide for managing overweight and obesity (TA875)
Setmelanotide for treating obesity caused by LEPR or POMC deficiency (HST21)
Overweight and obesity management (QS212)
Overweight and obesity management (NG246)
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
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: 25 · Randomised trials: 12 · 1998–2026
Showing the 50 most relevant studies, sorted by most relevant.
L. Sjöström, A. Rissanen, T. Andersen, et al.
The Lancet, 1998
Michael Davidson, J. Hauptman, M. Digirolamo, et al.
JAMA, 1999
A. Sahebkar, L. Simental‐Mendía, Ž. Reiner, et al.
Pharmacological Research, 2017
A. Avenell, C. Robertson, Z. Skea, et al.
Health technology assessment, 2018
Hu Wang, Li Wang, Yujia Cheng, et al.
Biomedical reports, 2018
McGowan B, Ciudin A, Baker JL, et al.
2025
- Obesity
- Anti-Obesity Agents
- Weight Loss
This systematic review and network meta-analysis evaluated the efficacy and safety of obesity management medications (OMMs) in terms of reducing body weight and impact on obesity-related complications. Here a Medline and Embase search was performed up to 31 January 2025 for randomized controlled trials comparing OMMs versus placebo/active comparators in adults. Primary endpoint was percentage of total body weight loss (TBWL%) at the end of the study. Secondary endpoints were TBWL% at 1, 2 and ≥3 years, lipid profile, blood pressure, hemoglobin A1c, fasting plasma glucose, mental health, serious adverse events, quality of life, cardiovascular morbidity and mortality, remission of obesity-related complications and all-cause mortality. Fifty-six clinical trials were identified-orlistat (22), semaglutide (14), liraglutide (11), tirzepatide (6), naltrexone/bupropion (5) and phentermine/topiramate (2)-enrolling 60,307 patients (32,598 OMM and 27,709 placebo). All OMMs showed a significantly greater TBWL% versus placebo (P < 0.0001), more than 10% for semaglutide and tirzepatide. Both tirzepatide and semaglutide showed normoglycemia restoration, remission of type 2 diabetes and reduction in hospitalization due to heart failure. Semaglutide was effective in reducing major adverse cardiovascular events and reducing pain in knee osteoarthritis. Tirzepatide was effective in remission of obstructive sleep apnea syndrome and metabolic dysfunction-associated steatohepatitis. These results support the need to individualize the selection of OMMs.
Abstract licence: CC BY-NC-ND
S. K. Graff, F. M. Mário, P. Ziegelmann, et al.
International Journal of Clinical Practice, 2016
Jay P Patel, Daksh Hardaswani, Jay P Patel, et al.
Cureus, 2025
Obesity, a multifaceted and chronic condition characterized by excessive fat accumulation, poses significant risks to overall health and is associated with various metabolic and cardiovascular complications. This literature review evaluates and compares the effectiveness of four pharmacological agents semaglutide, liraglutide, orlistat, phentermine, and emerging agents like setmelanotide, amycretin, retatrutide, cagrilintide, and cotadutide in managing weight loss among obese. A detailed analysis was conducted on their mechanisms of action, dosing regimens, efficacy in weight loss, safety profiles, and their impact on obesity-related comorbidities. Although all agents presented distinct benefits, side effects such as gastrointestinal discomfort with orlistat and GLP-1 receptor agonists, and potential dependency with phentermine, necessitate tailored treatment approaches. This review highlights the importance of integrating pharmacotherapy with lifestyle interventions to achieve sustainable weight management and identifies areas for future research to optimize therapeutic outcomes for individuals with obesity.
Abstract licence: CC BY
Zeinab Nikniaz, L. Nikniaz, M. Farhangi, et al.
BMC Endocrine Disorders, 2023
Takrori E, Peshin S, Singal S
2025
- Gastrointestinal Diseases
- Anti-Obesity Agents
- Obesity
Background: With rising obesity rates, pharmacological interventions are increasingly used in non-diabetic adults. While being effective in managing weight, these agents frequently cause gastrointestinal (GI) side effects, affecting adherence and long-term outcomes. Objective: To systematically evaluate the frequency, severity, and types of GI adverse effects (AEs) associated with anti-obesity medications in obese adults without diabetes. Methods: Following PRISMA 2020 guidelines, PubMed, Google Scholar, BMJ, and Web of Science were searched (last search July 2025). Eligible studies included randomized controlled trials, non-randomized trials, cohort studies, cross-sectional, and case-control studies. Only reports of GI AEs in non-diabetic adults were included. Risk of bias was assessed using Cochrane RoB 2 and Newcastle-Ottawa scales. Results: Out of 733 articles screened, 12 studies met predefined inclusion criteria, including one large cohort of 18,386 participants, along with randomized and observational trials of smaller size. The most frequently reported GI symptoms were nausea, vomiting, diarrhea, and constipation, predominantly with GLP-1 receptor agonists such as semaglutide and tirzepatide, especially during dose escalation. Orlistat commonly linked to steatorrhea and flatulence, while phentermine was associated with reduced GI motility. Newer agents, including retatrutide and orforglipron, also demonstrated notable GI side effect profiles. Natural products and investigational agents reported fewer adverse events but lacked long-term data and standardized reporting. Limitations: Evidence was limited by heterogeneity in study design and inconsistent reporting of GI outcomes. Conclusion: GI side effects are common across anti-obesity medications, particularly GLP-1 receptor agonists. Although generally mild to moderate, these symptoms can impact adherence and lead to treatment discontinuation. Tailored titration schedules, proactive patient counseling, and standardized adverse event reporting may improve tolerability. Further research is warranted to evaluate long-term GI outcomes and compare safety across emerging pharmacologic agents.
Abstract licence: CC BY
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
None known
Half-life
1-2 hours
Mechanism
Orlistat is a potent and selective inhibitor of various lipase enzymes responsible for the metabolism of fat.
Food interactions
1 warning
Human targets
4 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
360 mg
[L31993]…
Half-life
1-2 hours
[A229918][L11130]
Protein binding
99%
[L11130]
Volume of distribution
Metabolism
42%
[L31988]
In a radiolabeled orlistat mass balance study in obese patients, two metabolites were identified.…
Elimination
2%
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Orlistat is a lipase inhibitor used in the treatment of obesity that works by inhibiting fat-metabolizing enzymes. It was approved by the FDA for use in combination with a reduced-calorie diet in 1999.[L11130] This drug is a generally well-tolerated and effective weight-loss aid and is now available in both over-the-counter[L31963] and prescription preparations, depending on the dosage quantity.[L11130]
[L31963]
Orlistat in the 120 mg prescription formulation is also indicated to reduce the risk of weight regain following weight loss.
[L11130]
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 139 interactions
[L32078]
Single orlistat doses of 800 mg and multiple doses of up to 400 mg three times a day for 15 days have been administered to healthy weight and obese subjects without clinically significant adverse findings. In addition, doses of 240 mg three times a day have been given to obese patients for 6 months without a significant adverse effects. Post-marketing reports of overdoses cases indicate no adverse events or adverse events that are similar to those reported with the recommended dose.
If a significant overdose with orlistat occurs, the patient should be observed for at least 24 hours. Based on the results of clinical studies, systemic effects caused by orlistat are likely to be rapidly reversible.
[L32068]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[L31993]
After an oral dose with 360 mg of radiolabeled orlistat, plasma radioactivity achieved a peak at about 8 hours. Plasma concentrations of unchanged parent drug were close to the lower end of detection limits (<5 ng/mL). In plasma samples of patients taking orlistat, the detection of unchanged drug was sporadic and very low concentrations were detected (<10 ng/mL or 0.02 μM) with no evidence suggesting drug accumulation.
[L11130]
[A229918][L11130]
[L11130]
[L11130]
[L31988]
In a radiolabeled orlistat mass balance study in obese patients, two metabolites were identified. The first metabolite, M1, was the hydrolyzed β-lactone ring product of orlistat. The second metabolite, M3, was produced from M1’s cleavage of the N-formyl leucine side-chain.
Both metabolites accounted for about 42% of total plasma radioactivity. Both M1 and M3 are considered pharmacologically inactive.
[A229918][L11130]
[A229743][L32068]
Fecal elimination of orlistat is estimated between 95-97%.
[L11130]
Complete excretion by both routes occurs within in 3 to 5 days.
[L32068]
Proteins and enzymes this drug interacts with in the body
PMID:10358049 PMID:2243091
Shows a preferential hydrolysis at the sn-3 position of triacylglycerol PMID:2243091
PMID:15620723 PMID:27768894 PMID:27851727
Mediates many cannabinoid-induced effects, acting, among others, on food intake, memory loss, gastrointestinal motility, catalepsy, ambulatory activity, anxiety, chronic pain. Signaling typically involves reduction in cyclic AMP .
PMID:1718258 PMID:21895628 PMID:27768894
In the hypothalamus, may have a dual effect on mitochondrial respiration depending upon the agonist dose and possibly upon the cell type. Increases respiration at low doses, while decreases respiration at high doses.
At high doses, CNR1 signal transduction involves G-protein alpha-i protein activation and subsequent inhibition of mitochondrial soluble adenylate cyclase, decrease in cyclic AMP concentration, inhibition of protein kinase A (PKA)-dependent phosphorylation of specific subunits of the mitochondrial electron transport system, including NDUFS2. In the hypothalamus, inhibits leptin-induced reactive oxygen species (ROS) formation and mediates cannabinoid-induced increase in SREBF1 and FASN gene expression. In response to cannabinoids, drives the release of orexigenic beta-endorphin, but not that of melanocyte-stimulating hormone alpha/alpha-MSH, from hypothalamic POMC neurons, hence promoting food intake.
In the hippocampus, regulates cellular respiration and energy production in response to cannabinoids. Involved in cannabinoid-dependent depolarization-induced suppression of inhibition (DSI), a process in which depolarization of CA1 postsynaptic pyramidal neurons mobilizes eCBs, which retrogradely activate presynaptic CB1 receptors, transiently decreasing GABAergic inhibitory neurotransmission. Also reduces excitatory synaptic transmission (By similarity).
In superior cervical ganglions and cerebral vascular smooth muscle cells, inhibits voltage-gated Ca(2+) channels in a constitutive, as well as agonist-dependent manner .
PMID:17895407
In cerebral vascular smooth muscle cells, cannabinoid-induced inhibition of voltage-gated Ca(2+) channels leads to vasodilation and decreased vascular tone (By similarity). Induces leptin production in adipocytes and reduces LRP2-mediated leptin clearance in the kidney, hence participating in hyperleptinemia. In adipose tissue, CNR1 signaling leads to increased expression of SREBF1, ACACA and FASN genes (By similarity).
In the liver, activation by endocannabinoids leads to increased de novo lipogenesis and reduced fatty acid catabolism, associated with increased expression of SREBF1/SREBP-1, GCK, ACACA, ACACB and FASN genes. May also affect de novo cholesterol synthesis and HDL-cholesteryl ether uptake. Peripherally modulates energy metabolism (By similarity).
In high carbohydrate diet-induced obesity, may decrease the expression of mitochondrial dihydrolipoyl dehydrogenase/DLD in striated muscles, as well as that of selected glucose/ pyruvate metabolic enzymes, hence affecting energy expenditure through mitochondrial metabolism (By similarity). In response to cannabinoid anandamide, elicits a pro-inflammatory response in macrophages, which involves NLRP3 inflammasome activation and IL1B and IL18 secretion (By similarity). In macrophages infiltrating pancreatic islets, this process may participate in the progression of type-2 diabetes and associated loss of pancreatic beta-cells PMID:23955712
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that carry this drug through the body
PMID:19021548
Major calcium and magnesium transporter in plasma, binds approximately 45% of circulating calcium and magnesium in plasma (By similarity).
Potentially has more than two calcium-binding sites and might additionally bind calcium in a non-specific manner (By similarity). The shared binding site between zinc and calcium at residue Asp-273 suggests a crosstalk between zinc and calcium transport in the blood (By similarity). The rank order of affinity is zinc > calcium > magnesium (By similarity).
Binds to the bacterial siderophore enterobactin and inhibits enterobactin-mediated iron uptake of E.coli from ferric transferrin, and may thereby limit the utilization of iron and growth of enteric bacteria such as E.coli .
PMID:6234017
Does not prevent iron uptake by the bacterial siderophore aerobactin PMID:6234017
ATC A08AB01
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)
Orlistat
Additional database identifiers
Drugs Product Database (DPD)
11884
ChemSpider
2298564
BindingDB
24567
ZINC
ZINC000008214635
HUGO Gene Nomenclature Committee (HGNC)
HGNC:9155
GenAtlas
PNLIP
GeneCards
PNLIP
GenBank Gene Database
J05125
GenBank Protein Database
339597
Guide to Pharmacology
2590
UniProt Accession
LIPP_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:6622
GeneCards
LIPF
GenBank Gene Database
X05997
GenBank Protein Database
758063
UniProt Accession
LIPF_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2159
GenAtlas
CNR1
GeneCards
CNR1
GenBank Gene Database
X54937
GenBank Protein Database
29915
Guide to Pharmacology
56
UniProt Accession
CNR1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3594
GenAtlas
FASN
GeneCards
FASN
GenBank Gene Database
U26644
GenBank Protein Database
1049053
Guide to Pharmacology
2608
UniProt Accession
FAS_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:9035
GenAtlas
PLA2G4A
GeneCards
PLA2G4A
GenBank Gene Database
M72393
GenBank Protein Database
190007
Guide to Pharmacology
1424
UniProt Accession
PA24A_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3594
GenAtlas
FASN
GeneCards
FASN
GenBank Gene Database
U26644
GenBank Protein Database
1049053
Guide to Pharmacology
2608
UniProt Accession
FAS_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:399
GenAtlas
ALB
GeneCards
ALB
GenBank Gene Database
V00494
GenBank Protein Database
28590
UniProt Accession
ALBU_HUMAN
DrugBank citations
If you use DrugBank data in your research, please cite the following publications:
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Structured knowledge from the free knowledge base
ATC classifications (Wikidata)
Linked open data from Wikidata (Q424163), 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.