Search the PBPK Model Repository

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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Found 155 Matches

Brand Name(s) include: Malarone

Disease: Malaria

Drug Class: Antimalarials

Date Updated: March 2021

The model at-a-glance

  Absorption Model

  • First-Order

  Volume of Distribution

  • Full PBPK (Method 2)

Note: A Kp scalar (0.04) was used in the model

  Route of Elimination

  • No metabolism; a biliary CLint was input based on clinical data

  Perpetrator DDI

  • None

  Validation

  • Two clinical studies describing single and multiple dose exposure of atovaquone were used to verify the PBPK model. 100% of studies were within 1.5-fold.

  Limitations

  • There are some data to suggest atovaquone is an inhibitor of BCRP.  This is currently not included within the model.

  Updates in V19

  • Updated in vitro­ data
    • LogP: 5.8 -> 8.4
    • Caco-2 Papp 164 > 300 x 10-6 cm/s
    • Propranolol Papp 101 x 10-6 cm/s
  • Optimized ka and tlag
  • Converted from minimal PBPK model to full PBPK model

 

Carboxyprimaquine

Disease: Malaria

Drug Class: Antimalarials

Date Updated: March 2022

Related Files:  Primaquine (parent)

The model at-a-glance

  Absorption Model

N/A

  Volume of Distribution

Full PBPK (Method 2)

  Route of Elimination

  • Formed from primaquine by MAO. This is entered as ‘user-UGT’ as a surrogate within the simulator
  • Pathway of elimination is not defined; elimination is assigned as IV clearance that was manually optimized to fit the clinical data

  Perpetrator DDI

  • None

  Validation

  • Six clinical studies describing single and multiple dose exposure of carboxyprimaquine were used to verify the PBPK model.  The AUC for all verification studies were within 1.5-fold of the observed values.

  Limitations

  • Clinical data for carboxyprimaquine is highly variable

  Updates in V19

  • Converted from minimal PBPK model to full PBPK model

 

Darolutamide_RES_V21R1_Simcyp_20230615

The RES-Darolutamide_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. Darolutamide shows dose proportional PK between 100 to 700 mg BID. It is a BSCII compound, where the metabolite is a potent BCRP-inhibitor too. Darolutamide is possibly a weak CYP3A inducer in the clinic. The back-conversion of Keto-darolutamide to Darolutamide is efficiently catalyzed via cytosolic AKR1C3 (in vitro). This back-conversion is also observed in incubations of feces under anaerobic conditions (in vitro). In the compound fit-for-purpose compound file, the back-conversion was fixed to recover the concentration time profile for the 600 mg BID as this was the dose for the reported Rosuvastatin DDI. Note that two workspaces need to be run to simulate the Darolutamide DDI and then the results have to be combined. This is due to having to switch the position of Darolutamide and rosuvastatin (limitations on functionality on inhibitory metabolite in the Simcyp Simulator currently).

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