Vildagliptin 50mg tablets
Requires a prescription from a doctor or prescriber
Vildagliptin (LAF237) is an orally active antihyperglycemic agent that selectively inhibits the dipeptidyl peptidase-4 (DPP-4) enzyme.
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MHRA alerts for Vildagliptin
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.
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Suspected adverse reactions reported for Vildagliptin
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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 Vildagliptin
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EudraVigilance data is published by the European Medicines Agency (EMA). A suspected adverse reaction is not necessarily caused by the medicine.
12 branded products available
MHRA licensed products
View all licensed products for Vildagliptin on the MHRA register
Galvus 50mg tablets
Galvus 50mg tablets
Vildagliptin 50mg tablets
Vildagliptin 50mg tablets
Vildagliptin 50mg tablets
Vildagliptin 50mg tablets
Vildagliptin 50mg tablets
Vildagliptin 50mg tablets
Vildagliptin 50mg 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)
100 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
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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
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NHS UK identifiers
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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: 10 · Randomised trials: 17 · 2005–2025
Showing the 50 most relevant studies, sorted by most relevant.
David R. Matthews, Päivi M. Paldánius, Pieter Proot, et al.
The Lancet, 2019
- Vildagliptin
- Diabetes Mellitus, Type 2
- Glycated Hemoglobin
Anja Schweizer, S. Dejager, James E. Foley, et al.
Diabetes Obesity and Metabolism, 2010
- Vildagliptin
- Adamantane
- Cerebrovascular Disorders
Changyu Pan, Wenying Yang, Jacqueline Barona, et al.
Diabetic Medicine, 2008
- Vildagliptin
- Adamantane
- Blood Glucose
Gordon T. McInnes, Marc Evans, Stefano Del Prato, et al.
Diabetes Obesity and Metabolism, 2015
- Vildagliptin
- Adamantane
- Cardiovascular Diseases
Juliane Colombo Carrer de Macedo, D. Guadagnini, H. Assalin, et al.
Scientific Reports, 2025
- Diabetes Mellitus, Type 2
- Neuroprotective Agents
- Dipeptidyl-Peptidase IV Inhibitors
Dipeptidyl peptidase 4 (DPP-4) inhibitors (DPP-4i) are widely used to treat Type 2 diabetes (T2D) and are known for their cardiovascular and renal safety profiles. Systematic reviews have also shown that DPP-4i are associated with reduced dementia risk via unknown mechanisms. To examine vildagliptin (DPP-4i) effects on the intestinal microbiota in T2D patients, plasma metabolomics were conducted and inflammatory profiles collected to investigate correlations with potential neuroprotective effects. We examined 29 patients with T2D (not well controlled with metformin) before, and at 30 and 60 days after vildagliptin was introduced, and investigated intestinal microbiota, plasma metabolomic, and inflammatory profiles. In patients after 2 months, vildagliptin induced mild microbiota changes, represented by significant increases in Bariatricus and Butyricimonas genera and the Marinifilaceae family (short-chain fatty acids producers), reduced insulin, HOMA-IR, MCP1, and interferon (IFN)-γ levels, and elevated interleukin (IL)-4 and IL-10 levels, all of which represented an anti-inflammatory profile. Metabolomics results showed that leucine, 2-oxoisocaproate (branched-chain amino acid metabolite), and inosine were significantly reduced after vildagliptin was introduced. Additionally, choline, dimethylamine, and betaine levels were significantly higher, which may contribute to explain DPP-4i protective effects against dementia, as these metabolites are neuroprotective. In our T2D patient cohort (not well controlled with metformin), vildagliptin, in addition to improved glucose control and improved insulin resistance, modulated the intestinal microbiota, anti-inflammatory cytokine profiles, and metabolomics, and when combined, may contribute to explain DPP-4i’s neuroprotective effects.
Abstract licence: CC BY-NC-ND
Valentina Lukashevich, Anja Schweizer, Q. Shao, et al.
Diabetes Obesity and Metabolism, 2011
- Vildagliptin
- Adamantane
- Diabetes Mellitus, Type 2
Selvaraj V
2025
de Macedo JCC, Guadagnini D, Assalin HB, et al.
2025
Eleni Bekiari, Chrysoula Rizava, Eleni Athanasiadou, et al.
Endocrine, 2015
- Vildagliptin
- Adamantane
- Blood Glucose
A. Schweizer, S. Dejager, Emanuele Bosi
Diabetes Obesity and Metabolism, 2009
- Vildagliptin
- Adamantane
- Blood Glucose
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
Not available
Mechanism
Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GI…
Food interactions
1 warning
Human targets
1 target
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
1.7 hours
Half-life
Protein binding
9.3%
[L32803]
Volume of distribution
71 L
[L32803]
…
Metabolism
69%
Elimination
85%
Clearance
13 L/h
[L32803]
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Oral vildagliptin was approved by the European Medicines Agency in 2008 for the treatment of type II diabetes mellitus in adults as monotherapy or in combination with [metformin], a sulfonylurea, or a thiazolidinedione in patients with inadequate glycemic control following monotherapy. It is marketed as Galvus.[L32803] Vildagliptin is also available as Eucreas, a fixed-dose formulation with metformin for adults in who do not adequately glycemic control from monotherapy.[L32813] Vildagliptin is currently under investigation in the US.
[L32803]
It is also indicated as dual therapy in combination with metformin, a sulphonylurea, or a thiazolidinedione in adults patients with insufficient glycemic control despite maximal tolerated dose of monotherapy.
[L32803]
Vildagliptin is also marketed in a combination product with [metformin] for the treatment of adults with type II diabetes mellitus who inadequately respond to either monotherapy of vildagliptin or metformin. This fixed-dose formulation can be used in combination with a sulphonylurea or insulin (i.e., triple therapy) as an adjunct to diet and exercise in adults who do not achieve adequate glycemic control with monotherapy or dual therapy.
[L32813]
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 651 interactions
[L32808]
There is limited information regarding overdose with vildagliptin. In one study, patients experienced muscle pain, mild and transient paresthesia, fever, edema, and a transient increase in lipase levels at a dose of 400 mg. At 600 mg, one subject experienced edema of the feet and hands and increases in creatine phosphokinase (CPK), aspartate aminotransferase (AST), C-reactive protein (CRP) and myoglobin levels.
Supportive management is recommended in case of an overdose. There is no known antidote, and vildagliptin and its major metabolite cannot be removed via hemodialysis.
[L32803]
Vildagliptin exerts its blood glucose-lowering effects by selectively inhibiting dipeptidyl peptidase-4 (DPP-4), an enzyme that rapidly truncates and inactivates GLP-1 and GIP upon their release from the intestinal cells. DPP-4 cleaves oligopeptides after the second amino acid from the N-terminal end. Inhibition of DPP-4 substantially prolongs the half-life of GLP-1 and GIP, increasing the levels of active circulating incretin hormones.[A232523] The duration of DPP-4 inhibition by vildagliptin is dose-dependent.[A232533] Vildagliptin reduces fasting and prandial glucose and HbA1c. It enhances the glucose sensitivity of alpha- and beta-cells and augments glucose-dependent insulin secretion. Fasting and postprandial glucose levels are decreased, and postprandial lipid and lipoprotein metabolism are also improved.[A232488][A232528]
In clinical trials, treatment with vildagliptin 50-100 mg daily in patients with type 2 diabetes significantly improved markers of beta-cells, proinsulin to insulin ratio, and measures of beta-cell responsiveness from the frequently-sampled meal tolerance test. [L32803] Vildagliptin has improves glycated hemoglobin (HbA1c) and fasting plasma glucose (FPG) levels.[A232488]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[L32803]
Plasma concentrations of vildagliptin increase in an approximately dose-proportional manner.
[A232488]
Food delays Tmax to 2.5 hours and decreases Cmax by 19%, but has no effects on the overall exposure to the drug (AUC). Absolute bioavailability of vildagliptin is 85%.
[L32803]
[L32803]
[L32803]
[L32803]
[L32803]
Vildagliptin is metabolized to pharmacologically inactive cyano (57%) and amide (4%) hydrolysis products in the kidney.
[A232488]
LAY 151 (M20.7) is a major inactive metabolite and a carboxylic acid that is formed via hydrolysis of the cyano moiety: it accounts for 57% of the dose.
[L32803]
Other circulating metabolites reported are an N-glucuronide (M20.2), an N-amide hydrolysis product (M15.3), two oxidation products, M21.6 and M20.9.
[L32818]
[L32803]
[L32803]
Proteins and enzymes this drug interacts with in the body
PMID:10900005 PMID:10951221 PMID:11772392 PMID:17287217
Acts as a positive regulator of T-cell coactivation, by binding at least ADA, CAV1, IGF2R, and PTPRC .
PMID:10900005 PMID:10951221 PMID:11772392 PMID:14691230
Its binding to CAV1 and CARD11 induces T-cell proliferation and NF-kappa-B activation in a T-cell receptor/CD3-dependent manner .
PMID:17287217
Its interaction with ADA also regulates lymphocyte-epithelial cell adhesion .
PMID:11772392
In association with FAP is involved in the pericellular proteolysis of the extracellular matrix (ECM), the migration and invasion of endothelial cells into the ECM .
PMID:10593948 PMID:16651416
May be involved in the promotion of lymphatic endothelial cells adhesion, migration and tube formation .
PMID:18708048
When overexpressed, enhanced cell proliferation, a process inhibited by GPC3 .
PMID:17549790
Also acts as a serine exopeptidase with a dipeptidyl peptidase activity that regulates various physiological processes by cleaving peptides in the circulation, including many chemokines, mitogenic growth factors, neuropeptides and peptide hormones such as brain natriuretic peptide 32 .
PMID:10570924 PMID:16254193
Removes N-terminal dipeptides sequentially from polypeptides having unsubstituted N-termini provided that the penultimate residue is proline PMID:10593948
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 A10BH02
ATC A10BD08
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)
Vildagliptin
Additional database identifiers
ChemSpider
5293734
BindingDB
11695
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3009
GenAtlas
DPP4
GeneCards
DPP4
GenBank Gene Database
U13735
GenBank Protein Database
535388
Guide to Pharmacology
1612
UniProt Accession
DPP4_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