Pharmacokinetic and pharmacodynamic modelling for renal function dependent urinary glucose excretion effect of ipragliflozin, a selective sodium-glucose cotransporter 2 inhibitor, both in healthy subjects and patients with type 2 diabetes mellitus

Br J Clin Pharmacol. 2019 Aug;85(8):1808-1819. doi: 10.1111/bcp.13972. Epub 2019 Jun 20.

Abstract

Aims: To provide a model-based prediction of individual urinary glucose excretion (UGE) effect of ipragliflozin, we constructed a pharmacokinetic/pharmacodynamic (PK/PD) model and a population PK model using pooled data of clinical studies.

Methods: A PK/PD model for the change from baseline in UGE for 24 hours (ΔUGE24h ) with area under the concentration-time curve from time of dosing to 24 h after administration (AUC24h ) of ipragliflozin was described by a maximum effect model. A population PK model was also constructed using rich PK sampling data obtained from 2 clinical pharmacology studies and sparse data from 4 late-phase studies by the NONMEM $PRIOR subroutine. Finally, we simulated how the PK/PD of ipragliflozin changes in response to dose regime as well as patients' renal function using the developed model.

Results: The estimated individual maximum effect were dependent on fasting plasma glucose and renal function, except in patients who had significant UGE before treatment. The PK of ipragliflozin in type 2 diabetes mellitus (T2DM) patients was accurately described by a 2-compartment model with first order absorption. The population mean oral clearance was 9.47 L/h and was increased in patients with higher glomerular filtration rates and body surface area. Simulation suggested that medians (95% prediction intervals) of AUC24h and ΔUGE24h were 5417 (3229-8775) ng·h/mL and 85 (51-145) g, respectively. The simulation also suggested a 1.17-fold increase in AUC24h of ipragliflozin and a 0.76-fold in ΔUGE24h in T2DM patients with moderate renal impairment compared to those with normal renal function.

Conclusions: The developed models described the clinical data well, and the simulation suggested mechanism-based weaker antidiabetic effect in T2DM patients with renal impairment.

Keywords: Suglat; ipragliflozin; pharmacodynamics; pharmacokinetics; sodium-glucose cotransporter 2 inhibitor; type 2 diabetes mellitus.

Publication types

  • Clinical Trial, Phase I
  • Clinical Trial, Phase II
  • Clinical Trial, Phase III
  • Multicenter Study
  • Randomized Controlled Trial
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Administration, Oral
  • Aged
  • Area Under Curve
  • Blood Glucose / analysis
  • Blood Glucose / metabolism*
  • Diabetes Mellitus, Type 2 / blood
  • Diabetes Mellitus, Type 2 / drug therapy*
  • Diabetes Mellitus, Type 2 / metabolism
  • Dose-Response Relationship, Drug
  • Female
  • Glomerular Filtration Rate / physiology
  • Glucosides / pharmacology*
  • Glucosides / therapeutic use
  • Healthy Volunteers
  • Humans
  • Kidney / metabolism
  • Kidney / physiopathology
  • Male
  • Middle Aged
  • Models, Biological*
  • Renal Elimination / drug effects*
  • Sodium-Glucose Transporter 2 Inhibitors / pharmacology*
  • Sodium-Glucose Transporter 2 Inhibitors / therapeutic use
  • Thiophenes / pharmacology*
  • Thiophenes / therapeutic use

Substances

  • Blood Glucose
  • Glucosides
  • Sodium-Glucose Transporter 2 Inhibitors
  • Thiophenes
  • ipragliflozin