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Matrix Approach Assessment of Cabotegravir Drug–Drug Interactions with OAT1/OAT3 Substrates and UGT1A1/UGT1A9 Inhibitors Using Physiologically-Based Pharmacokinetic Modeling

Title: Matrix Approach Assessment of Cabotegravir Drug–Drug Interactions with OAT1/OAT3 Substrates and UGT1A1/UGT1A9 Inhibitors Using Physiologically-Based Pharmacokinetic Modeling
Authors: Helen Tracey; Simon T. Bate; Susan Ford; Parul Patel; Jackie Bloomer; Aarti Patel; Kunal S. Taskar
Source: Pharmaceutics ; Volume 17 ; Issue 4 ; Pages: 531
Publisher Information: Multidisciplinary Digital Publishing Institute
Publication Year: 2025
Collection: MDPI Open Access Publishing
Subject Terms: PBPK modeling; cabotegravir; OAT1; OAT3; UGT1A1; UGT1A9; drug–drug interactions; HIV
Description: Background/Objective: Cabotegravir (CAB), available as an oral tablet and as a long-acting (LA) nanosuspension for intramuscular injection, is approved as a combination therapy for the treatment, and as a monotherapy for the prevention, of HIV-1 infection. People living with HIV may receive multiple concomitant medications, with the associated risk of drug–drug interactions (DDIs). CAB is an inhibitor of OAT1/OAT3 renal transporters and a substrate of the UDP-glucuronosyltransferase enzymes UGT1A1 and 1A9, in vitro. While the effect of induction of UGT1A1/UGT1A9 on CAB exposure had been investigated in the clinic, the effect of the risk of DDIs with CAB via inhibition of these enzymes, or as an inhibitor of OAT1/OAT3 transporters, had not been evaluated. Methods: A physiologically-based pharmacokinetic (PBPK) model was developed and verified for orally dosed CAB to investigate the DDI risks associated with CAB, using a matrix approach to extensively qualify the PBPK platform and the substrates and/or inhibitors of either OAT1/OAT3 or UGT1A1/UGT1A9. The effect of uncertainties in in vitro inhibition values for OAT1/OAT3 was assessed via sensitivity analysis. Results: A mean increase of less than 25% in systemic exposure for OAT1/OAT3 substrates was predicted, with the potential for an increase of up to 80% based on the sensitivity analysis. On co-dosing with UGT1A1/UGT1A9 inhibitors, the predicted mean increase in CAB exposure was within 11%. Conclusions: PBPK modelling indicated that clinically relevant DDIs are not anticipated with OAT1/3 substrates or UGT1A1/1A9 inhibitors and CAB. With maximal exposure of the LA formulation of CAB being lower than the oral, the results of these simulations can be extrapolated to LA injectable dosing.
Document Type: text
File Description: application/pdf
Language: English
Relation: Pharmacokinetics and Pharmacodynamics; https://dx.doi.org/10.3390/pharmaceutics17040531
DOI: 10.3390/pharmaceutics17040531
Availability: https://doi.org/10.3390/pharmaceutics17040531
Rights: https://creativecommons.org/licenses/by/4.0/
Accession Number: edsbas.458E2348
Database: BASE