ArticleClinical pharmacokinetics2026
Population Pharmacokinetic Modeling of Encorafenib in Healthy Participants and Patients with BRAF V600-Mutant Solid Tumors: A Semi-mechanistic Autoinduction Model.
Article in Clinical pharmacokinetics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
objectiveEncorafenib is a potent and selective adenosine triphosphate-competitive BRAF V600-mutant kinase inhibitor. Encorafenib is approved for multiple indications in combination with binimetinib or cetuximab. This analysis aimed to develop a global population pharmacokinetics (popPK) model characterizing encorafenib disposition across tumor types.
methodsThe popPK analysis was based on nine phase 1 to 3 studies in participants with melanoma, colorectal cancer (CRC), non-small cell lung cancer, or other solid tumors, and healthy participants. A total of 1310 participants who received encorafenib as monotherapy or in combination were included. Nonlinear mixed effects modeling was performed using NONMEM v7.5.0. A semi-mechanistic enzyme turnover model was assessed to quantify the autoinduction effect. Stepwise covariate modeling using Perl-speaks-NONMEM (version 5.3.0) evaluated a broad range of covariates.
resultsA two-compartment model with first-order absorption and concentration-dependent autoinduction successfully characterized the concentration-time profile of encorafenib. Encorafenib apparent clearance (CL/F) was estimated to be 12.2 L/h after the first dose in a typical adult and increased by 186% to 35 L/h at steady state. This model indicates that maximum autoinduction is expected within 14 days of daily dosing (autoinduction half-life 64 h). Age and tumor type (melanoma, metastatic CRC, other [healthy, lung tumors, other solid tumors]) on CL/F and body weight on volume of distribution were significant covariates; these effects were not determined to be clinically significant.
conclusionsThis model successfully described the PK of encorafenib over time and across tumor types. No dose modifications are suggested on the basis of intrinsic or extrinsic factors evaluated.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.