Alogliptin 25mg tablets
Requires a prescription from a doctor or prescriber
Alogliptin is a selective, orally-bioavailable inhibitor of enzymatic activity of dipeptidyl peptidase-4 (DPP-4).
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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 Alogliptin
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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 Alogliptin
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Vipidia 25mg tablets
Alogliptin 25mg 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)
25 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.
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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
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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: 12 · Randomised trials: 14 · 2007–2026
Showing the 50 most relevant studies, sorted by most relevant.
F. Zannad, C. Cannon, W. Cushman, et al.
Lancet, 2015
Holdt-Caspersen NS, Dethlefsen C, Vestergaard P, et al.
2024
- Diabetes Mellitus, Type 2
- Benzhydryl Compounds
- Glucosides
The adherence to oral antidiabetic drugs (OADs) among people with type 2 diabetes (T2D) is suboptimal. However, new OADs have been marketed within the last 10 years. As these new drugs differ in mechanism of action, treatment complexity, and side effects, they may influence adherence. Thus, the aim of this study was to assess the adherence to newer second-line OADs, defined as drugs marketed in 2012-2022, among people with T2D. A systematic review was performed in CINAHL, Cochrane Trials, Embase, PubMed, PsycINFO, and Scopus. Articles were included if they were original research of adherence to newer second-line OADs and reported objective adherence quantification. The quality of the articles was assessed using JBI's critical appraisal tools. The overall findings were reported according to the preferred reporting items for systematic reviews and meta-analyses (PRISMA) guidelines and summarized in a narrative synthesis. All seven included articles were European retrospective cohort studies investigating alogliptin, canagliflozin, dapagliflozin, empagliflozin, and unspecified types of SGLT2i. Treatment discontinuation and medication possession ratio (MPR) were the most frequently reported adherence quantification measures. Within the first 12 months of treatment, 29%-44% of subjects on SGLT2i discontinued the treatment. In terms of MPR, 61.7%-94.9% of subjects on either alogliptin, canagliflozin, dapagliflozin, empagliflozin or an unspecified SGLT2i were adherent. The two investigated adherence quantification measures, treatment discontinuation and MPR, suggest that adherence to the newer second-line OADs may be better than that of older OADs. However, a study directly comparing older and newer OADs should be done to verify this.
Abstract licence: CC BY
Prakash V, Goel N
2025
Inhibitors of dipeptidyl peptidase-4 (DPP-4) enzyme are one of the commonly recommended hypoglycemic agents. Although efficient in controlling hyperglycemia, their cardiovascular (CV) safety has been debated for long-term use, particularly in relation to heart failure risk. This review analyzed the cardiovascular safety profile after the consumption of various DPP-4 inhibitors in hyperglycemic patients. The systematic review and meta-analysis was conducted by utilizing widespread empirical research and randomized control trials (RCTs), evaluating sitagliptin, saxagliptin, alogliptin, and linagliptin. Databases searched included PubMed, Embase, Cochrane CENTRAL, and Clinical Trials.gov through September 2025. Outcomes assessed were: HHF, i.e., hospitalization for heart failure, MACE, i.e., major adverse cardiovascular events (CV death, nonfatal myocardial infarction (MI), nonfatal cerebrovascular attack (CVA), all-cause mortality, and cardiovascular mortality. Random-effects metHFa-analyses were conducted, with heterogeneity assessed via I² statistics. Seven large RCTs (n > 70,000 participants) were included, along with supporting observational data. Pooled analysis demonstrated no significant increase in MACE intake of DPP-4 inhibitors when compared to placebo (hazard ratio (HR) 0.99, 95% confidence interval (CI) 0.93-1.05, heterogeneity (I²) = 5%). However, an increased probability of HHF was found (HR 1.14, 95% CI 1.02-1.27, I² = 28%), largely driven by saxagliptin (HR 1.27, 95% CI 1.07-1.51) and, to a lesser extent, alogliptin. While no significant heart failure (HF) risk was observed by the intake of drugs sitagliptin (HR 1.00, 95% CI 0.83-1.20) and linagliptin (HR 1.02, 95% CI 0.89-1.17), no differences were noted in all-cause or CV mortality across the class. DPP-4 inhibitors, as a group of drugs, are safe with respect to MACE, but saxagliptin and possibly alogliptin are linked with an increased risk of HHF. Sitagliptin and linagliptin appear neutral regarding HF risk. These findings highlight the importance of drug-specific evaluation when selecting a DPP-4 inhibitor for type-2 diabetic patients, particularly those having an elevated risk of heart failure.
Abstract licence: CC BY
M. Siddiqi, Rizwana Noor, Ayesha Younas, et al.
Hypertension, 2025
Ortiz-Seller A, Real JT, Morcillo E, et al.
2026
- Diabetic Retinopathy
- Diabetes Mellitus, Type 2
- Dipeptidyl-Peptidase IV Inhibitors
AimsTo update evidence on the relationship between dipeptidyl peptidase-4 (DPP-4) inhibitors and incident diabetic retinopathy (DR) in type 2 diabetes.MethodsWe searched Embase, PubMed, Web of Science, and ClinicalTrials.gov (to July 2025) for randomized controlled trials (RCTs) and pooled odds ratios (ORs) with 95 % credible intervals (CrIs) using a Bayesian network meta-analysis. Network meta-regression assessed estimated effect modification; a model-based network meta-analysis (MBNMAdose) evaluated dose-response. Evidence certainty was appraised with Confidence in Network Meta-Analysis (CINeMA).ResultsForty-three trials (74,546 participants; 779 DR events) were analyzed. No DPP-4 inhibitor significantly changed the DR risk versus placebo (ORs ranged from 0.31 [omarigliptin] to 2.31 [saxagliptin]; all CrIs crossed 1.0). Rankings suggested omarigliptin as most favorable, alogliptin/linagliptin/sitagliptin intermediate, and saxagliptin/teneligliptin least favorable. Baseline DR incidence moderated treatment effects; other prespecified covariates were not significant. MBNMAdose showed no dose-response relationship for DR.ConclusionsCurrent randomized evidence indicates class-level neutrality of DPP-4 inhibitors on DR incidence, with no dose-response signal. Choice among gliptins may therefore be guided primarily by glycemic efficacy, safety, and participant characteristics rather than retinal risk.
Abstract licence: CC BY-NC-ND
Langford, Oliver, Aronson, Jeffrey K, van Valkenhoef, Gert, et al.
2018
Ji-Yeon Park, Joonyub Lee, Yoon-Hee Choi, et al.
Diabetes & Metabolism Journal, 2024
- Diabetes Mellitus, Type 2
- Metformin
- Piperidines
J. G. Penaforte-Saboia, C. E. Couri, Natasha Vasconcelos Albuquerque, et al.
Diabetes, Metabolic Syndrome and Obesity, 2024
Ming-Tong Xu, Kan Sun, Wenjie Xu, et al.
BMC Medicine, 2023
Tomoe Abe, Yasutaka Takeda, Ichiro Sakuma, et al.
Metabolic Syndrome and Related Disorders, 2024
- Diabetes Mellitus, Type 2
- Metformin
- Piperidines
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
21 hours
Mechanism
Alogliptin inhibits dipeptidyl peptidase 4 (DPP-4), which normally degrades the…
Food interactions
1 warning
Human targets
1 target
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
800 mg
Half-life
21 hours
Protein binding
20%
Volume of distribution
12.5 mg
Metabolism
1%
The N-acetylated metabolite is inactive. Cytochrome enzymes that are involved with the metabolism of alogliptin are CYP2D6 and CYP3A4 but the extent to which this occurs is minimal. Approximately 10-20% of the dose is hepatically metabolized by cytochrome enzymes.
Elimination
76%
Clearance
9.6 L/h
Systemic clearance = 14.0 L/h.
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Known interactions with other medicines. Always consult a healthcare professional.
Showing 50 of 1467 interactions
How the body processes this drug — absorption, distribution, metabolism, and elimination
The absolute bioavailability of NESINA is approximately 100%. Food does not affect the absorption of alogliptin.
The N-acetylated metabolite is inactive. Cytochrome enzymes that are involved with the metabolism of alogliptin are CYP2D6 and CYP3A4 but the extent to which this occurs is minimal. Approximately 10-20% of the dose is hepatically metabolized by cytochrome enzymes.
Systemic clearance = 14.0 L/h.
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
Enzymes involved in drug metabolism — important for understanding drug interactions
ATC A10BD13
ATC A10BD09
ATC A10BH04
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)
Alogliptin
Additional database identifiers
Drugs Product Database (DPD)
22181
ChemSpider
9625485
BindingDB
16285
PDB
T22
ZINC
ZINC000014961096
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: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
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