DPP-4 Inhibitors

Written by Megan Boucher

Last updated 31st December 2025
6 Revisions

DPP-4 inhibitors are oral antidiabetic agents used in the treatment of type 2 diabetes. They share the suffix “-gliptin”, examples include sitagliptin, saxagliptin, vildagliptin, linagliptin, and alogliptin.

This article outlines their mechanism of action, key pharmacokinetic parameters, cautions and contraindications, side effects, and clinically significant drug interactions.

Mechanism Of Action

DPP-4 inhibitors increase the amount of incretin hormones available. The enzyme dipeptidyl peptidase 4 (DPP-4) rapidly hydrolyzes gastrointestinal incretin hormones, rendering them inactive.

Incretin hormones include glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). 

They are released throughout the day, increasing at mealtimes, and have several functions:

  • Stimulate the production and secretion of insulin in response to eating (glucose-dependent insulin secretion)
  • GLP-1 enhances the sensitivity of alpha cells to glucose, resulting in more glucose-appropriate glucagon secretion
  • Slow digestion and decrease appetite

Thus, DPP-4 inhibitors indirectly enhance insulin release, suppress glucagon secretion, and improve glycaemic control.

Fig 1: mechanism of action of DPP-4 inhibitors

 

Key Pharmacokinetic Parameters

The table below describes the key pharmacokinetic parameters for DPP-4 inhibitors:

Drug  Clearance  Half-life Time to peak (Tmax) Metabolism by CYP enzymes 
Sitagliptin  Primarily renal  12.4 hours 1-4 hours CYP3A4 (main), CYP2C8
Saxagliptin Renal and hepatic  Saxagliptin: 2.5 hours 

Major metabolite: 3.1 hours

2-4 hours CYP3A4/5

Major metabolite is also a DPP4 inhibitor but 50% potency 

Linagliptin Faeces (80%), urine (5%) >100 hours (saturable tight binding of linagliptin to DPP-4) 1.5 hours Weak CYP3A4 substrate
Alogliptin Urine (76%), faeces (13%) 21 hours 1-2 hours Negligible
Vildagliptin Urine (85%), faeces (15%) 3 hours  1.7 hours Negligible 

Cautions and contraindications

Cautions and contraindications for the use of DPP-4 inhibitors are listed below:

Cautions  Contraindications 
Saxagliptin: Severe renal impairment/

moderate hepatic impairment/ Moderate-severe heart failure/elderly

Viladagliptin: end stage renal impairment on haemodialysis 

History of pancreatitis 

Ketoacidosis 

Type 1 diabetes

Hepatic impairment (saxagliptin/alogliptin/vildagliptin)

Heart failure (vildagliptin/alogliptin)

Adverse effects

Fig 2: Adverse effects of DPP-4 inhibitors

 

Other adverse effects include:

  • Increased risk of infection with saxagliptin, alogliptin and vildagliptin 
  • Hypersensitivity reactions (including anaphylaxis, angioedema, stevens-johnson syndrome) 
  • Sitagliptin: interstitial lung disease, impaired renal function, thrombocytopenia, and acute renal failure.
  • Saxagliptin: erectile dysfunction, dyslipidaemia, and hypertriglyceridaemia.
  • Linagliptin: cough, increased amylase and lipase levels.
  • Vildagliptin: peripheral oedema and nasopharyngitis 

Interactions

Clinically significant drug interactions are described as follows:

Interacting Drug/Class Effect
Beta-blockers May mask symptoms of hypoglycaemia (e.g., tremor).
ACE inhibitors Increased risk of angioedema (especially with vildagliptin).
Digoxin Sitagliptin increases plasma levels — monitor for toxicity.
Rifampicin May reduce plasma concentrations of linagliptin and saxagliptin.
Ketoconazole (and strong CYP3A4 inhibitors) May increase sitagliptin* and saxagliptin levels, especially in renal impairment.

*Sitagliptin is metabolised primarily by CYP3A4, in severe renal impairment metabolism plays a more significant role in sitagliptin elimination, therefore potent CYP3A4 inhibitors (ketoconazole, itraconazole, ritonavir, clarithromycin) may increase sitagliptin plasma levels in severe renal impairment 

The blood glucose-lowering effects of DPP-4 inhibitors may also be enhanced or inhibited by other substances: 

Fig 3: drugs that affect the glucose lowering effects of DPP-4 inhibitors

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