Fig. 2 |. Intrinsic (pink) and extrinsic (blue) factors affecting the abundance and/or activity of drug transport proteins and mechanisms that may be involved, including specific regulatory pathways and/or inhibitory effects.

Changes represent protein levels unless noted as mRNA. The examples provided are based on a combination of preclinical and/or clinical data. For details on post-transcriptional and post-translational mechanisms involved in regulation of drug transport proteins, see section ‘Factors regulating transporter activity’ and a 2022 International Transporter Consortium publication7. Polymorphisms: Although some literature suggests that SLCO1B1*37 showed increased transport activity, a review of the literature suggests that the activity of this variant is similar to SLCO1B1*1 (wild type)229. ABC, ATP binding cassette; Asians, defined in ref. 15 as Chinese and Japanese subjects living in the US for at least 12 months; AUC, area under the plasma (serum) concentration-time profile; AUCliver, area under the liver concentration-time profile; BCRP, breast cancer resistance protein; C1h, plasma (serum) concentration at 1 hour; Cmax, maximum plasma concentration; CLrenal, renal clearance; CLsec, renal secretion clearance; Cmax, maximum plasma concentration; DDIs, drug–drug interactions; HCV, hepatitis C virus; MCT1, monocarboxylate transporter 1; MRP, multidrug resistance-associated protein; NASH, nonalcoholic steatohepatitis; NR, nuclear receptor; OAT, organic anion transporter; OATP, organic anion transporting polypeptide; OCT, organic cation transporter; OSTα/β, organic solute transporter alpha/beta; PEPT1, peptide transporter 1; P-gp, P-glycoprotein; SLC, solute carrier; Tmax, time required for maximal hepatic activity; T1/2max, time required for peak activity to decrease by 50%; TKIs, tyrosine kinase inhibitors; ↑, increase, or ↓, decrease, in the protein abundance and/or activity as detailed in the references provided in Supplementary Materials.