Model catalog
Start with the biological or translational question. Explore curated starting configurations for 43 models, change scientist-facing inputs, and compare how model readouts respond.
Ask a question, choose a biological starting point, then inspect the response.
Each workspace leads with the model’s intended use, intervention or biological context, key readouts, controls, and interpretation limits.
Featured starting points
These models show distinct ways simulation can reduce uncertainty before committing to additional experiments.
Dose and response
Nivolumab exposure and tumor-size dynamics
Start with an exposure–response workflow that turns a dosing question into an interpretable tumor-size trajectory.
Biomarker dynamics
Rituximab exposure and CD19-positive B-cell dynamics
Explore a compact PK/PD and target-mediated model with a clinically legible CD19-positive B-cell readout.
ADC development
HER2 ADC population PK
Use a population-PK and model-based meta-analysis starting point for comparing HER2-directed antibody–drug conjugates.
Translational bridging
Pediatric bevacizumab minimal PBPK
Inspect an adult-to-pediatric minimal-PBPK bridge with curated exposure comparisons and transparent scope limits.
Mechanism exploration
T-cell-engager cytokine-release network
Explore a QSP starting point for understanding the connected cytokine response to T-cell-activating therapies.
Complete catalog
43 models
An exposure-response model connecting nivolumab steady-state exposure to competing tumor shrinkage and progression processes and their resulting tumor-size trajectory.
A coupled PK/PD model linking circulating rituximab to CD19-positive B-cell depletion, cell-dependent drug loss, and gradual B-cell repopulation.
A two-compartment population PK model for HER2-directed antibody–drug conjugates, representing central and peripheral disposition, concentration, and cumulative exposure across dose levels.
A minimal PBPK model connecting body-weight-scaled bevacizumab clearance and compartment volumes to central and peripheral antibody exposure.
A cytokine-network QSP model coupling drug exposure to resting, activated, cytotoxic, and exhausted T cells and to IL-6, IL-10, IL-1beta, IFN-gamma, and TNF-alpha dynamics.
A reduced QSP model linking AAV biodistribution and nuclear persistence to transgene expression, antibody production in plasma, brain interstitial fluid, and CSF, and reversible TargetX binding.
A reduced AUTOTAC PK/PD model linking ATC161 exposure to concentration-dependent degradation and recovery of alpha-synuclein aggregates.
A two-compartment population PK model representing pediatric atezolizumab exposure with body weight, albumin, tumor burden, and anti-drug-antibody effects on disposition.
A two-compartment population PK model representing atezolizumab concentration and exposure with body weight, albumin, sex, and anti-therapeutic-antibody covariates.
A two-compartment population PK model representing atezolizumab disposition, clinical covariate effects, time-varying clearance, concentration, and interval exposure.
A QSS-TMDD model representing intravenous or subcutaneous befovacimab disposition, TFPI turnover, free antibody, and antibody–TFPI complex dynamics.
A population QSS-TMDD model coupling bevacizumab disposition to VEGF165 turnover, free antibody, target-bound complex, and total circulating VEGF165.
A two-compartment population PK model representing cemiplimab exposure, covariate-dependent disposition, and gradual time variation in clearance.
A reduced subcutaneous PK model representing certolizumab pegol absorption from a depot, systemic elimination, blood concentration, and cumulative exposure.
A reduced plasma PK model representing first-order elimination, concentration, half-life, and cumulative exposure of a positively charged trastuzumab-vc-MMAE ADC.
A TMDD PK/PD model coupling intravenous crenezumab disposition to free and antibody-bound amyloid-beta 1-40 and 1-42 turnover.
A PK/PD model coupling dabigatran systemic and bypass-circuit disposition to effect-site concentration and idarucizumab exposure during cardiopulmonary bypass.
A PK/PD exposure-response model linking intravenous dazukibart disposition and IFN-beta binding to delayed changes in cutaneous, muscle, functional, and global disease assessments.
A coupled subcutaneous PK and indirect-response model linking dupilumab exposure to EASI and IGA response dynamics while accounting for patient and disease covariates.
A two-compartment population PK model representing eculizumab or SB12 disposition, body-weight effects, disease-specific central volume, concentration, and cumulative exposure.
A two-compartment PK model representing eculizumab central and peripheral disposition and cumulative exposure in generalized myasthenia gravis.
A reduced pharmacodynamic turnover model representing the time course of PASI response toward an efalizumab-associated steady state.
A reduced ADC–payload disposition model linking enfortumab vedotin concentration to formation and elimination of the released MMAE payload and their cumulative exposures.
A subcutaneous population PK model representing envafolimab absorption, systemic concentration, renal-function covariates, and time-varying clearance.
A subcutaneous quasi-steady-state TMDD model coupling erenumab disposition to CGRP-receptor abundance, unbound antibody, drug-target complex, and cumulative exposure.
A PK/PD model coupling dabigatran central, peripheral, and effect-site disposition to idarucizumab-associated reversal of the anticoagulation response in sheep.
A two-compartment population PK model for inotuzumab ozogamicin with linear and time-dependent clearance and clinically relevant body-size and disease covariates.
Mechanistic rat QSP coupling whole-body AAV biodistribution, intracellular transduction, transgene-derived anti-TargetX mAb, FcRn-aware protein PBPK, TargetX binding, and detailed brain/CSF transport across 725 explicit scalar states.
A coupled subcutaneous or intravenous PK/PD model linking mepolizumab absorption and distribution to concentration-dependent suppression and turnover of circulating eosinophils.
A reduced dose–exposure model for the CD37-directed ADC naratuximab emtansine, representing plasma decline and cumulative exposure across dose levels.
A reduced QSP model connecting nivolumab exposure and PD-1 checkpoint inhibition to effector and regulatory T-cell dynamics, tumor-cell burden, and tumor regression.
A two-compartment population PK model coupling panitumumab distribution to parallel linear and saturable Michaelis–Menten elimination.
A reduced pediatric PBPK model connecting body-size-dependent antibody disposition to central and peripheral exposure and optional target binding.
A two-compartment population PK model linking pembrolizumab dosing, body-size effects on disposition, central and peripheral antibody amounts, concentration, and cumulative exposure.
A two-compartment population PK model connecting pertuzumab dosing and lean-body-weight and albumin covariates to concentration and cumulative exposure during neoadjuvant therapy.
A mechanistic pharmacodynamic model connecting PROTAC concentration, target and E3-ligase binding, catalytic degradation, protein turnover, and the high-concentration hook effect.
A reduced PK/PD model linking ravulizumab exposure to concentration-dependent suppression and recovery of free complement C5.
A subcutaneous PK/PD model linking secukinumab absorption and distribution to IL-17A pathway inhibition, delayed PASI response, and tolerance dynamics.
A reduced tumor-growth model representing the balance between untreated tumor expansion and SKB264-associated tumor-cell killing.
A two-compartment PK/PD model coupling sutimlimab linear and nonlinear disposition to concentration-dependent recovery and turnover of hemoglobin.
A two-compartment population PK model with intramuscular absorption for the long-acting antibody combination tixagevimab–cilgavimab and covariate-dependent bioavailability and disposition.
A two-compartment population PK model representing vedolizumab central and peripheral disposition, prior anti-TNF effects on clearance, concentration, and cumulative exposure.
A translational PK/PD model coupling zenocutuzumab distribution and nonlinear clearance to concentration-dependent tumor-cell death and net tumor-volume dynamics.
