Quickly find freely available drug and population models in our PBPK model repository.
The models provided have been collated from published examples which authors have shared in our Published Model Collection or developed as part of various global health projects in our Global Health Collection. This search facility searches both model collections simultaneously.
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Prepared: June 2023 The RES-Velpatasvir_V21 model has been developed primarily as inhibitor of hepatic OATP1B1 and OATP1B3, and intestinal BCRP using the New GI physiology in Simcyp V21 with altered GI tract population inputs that became default in V22. There are limited PK and DDI studies available for Velpatasvir and it is generally used in a fixed dose combination using 100 mg Velpatasvir. Thus, the Velpatasvir file is a Fit-for-purpose PBPK model for 50 mg to 100 mg QD. The Rosuvastatin DDI is a 100 mg QD study. Example workspaces for Velpatasvir PK and the DDI with Rosuvastatin are attached. The BCRP component of Rosuvastatin (V21 using the New GI physiology) was optimised using Eltrombopag and then verified with other BCRP-Inhibitors available on the members area or within the Simcyp Simulator, see attached ‘BCRP-Inhibitor V21’ document for details.
Simcyp developed fexofenadine compound file. Compound summary included. This was developed as a research file and its current status and limitations are outlined in summary document.
Brand Name(s) include: Basoquin, Camoquin, Flavoquin, Coarsucam
Disease: Malaria
Drug Class: Antimalarials
Date Updated: June 2021
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Absorption Model |
First-Order |
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Volume of Distribution |
Full PBPK (Method 2) |
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Route of Elimination |
CYP2C8 = 72%; Additional HLM = 28% |
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Perpetrator DDI |
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Validation |
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Limitations |
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Updates in V19 |
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A Pemigatinib PBPK article accepted by CPT PSP with leading author as Tao Ji The submitted workspace files for Pemigatinib is using minimal PBPK model with ADAM functions for Pemigatinib that incorporates CYP3A4-mediated metabolism derived from in vitro data, mass balance data, and clinical PK data, for the purpose of evaluation of clinical DDIs with strong CYP3A inhibitors and/or inducers.
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