See how a mechanistic PBPK model enables prediction of ocular exposure and target occupancy to optimize anti-VEGF therapies.
Understanding drug exposure in ocular tissues is one of the biggest challenges in ophthalmology drug development. Direct measurement is often impractical or invasive, leaving critical questions about drug distribution, efficacy, and dosing unanswered.
In this poster, we show how a minimal PBPK model with detailed ocular physiology can bridge that gap, predicting drug exposure and target occupancy across compartments like vitreous humor, aqueous humor, and retina.
What you’ll learn
Download this poster to explore how PBPK modeling can:
- Predict drug exposure in inaccessible ocular compartments: Simulate PK across vitreous humor, aqueous humor, and retina without invasive sampling
- Estimate target occupancy to inform efficacy: Quantify VEGF binding and target engagement across tissues and dosing regimens
- Compare therapies and optimize dosing strategies: Evaluate differences between anti-VEGF antibodies and test alternative dosing intervals
- Translate preclinical data to humans: Scale validated rabbit models to human predictions for clinical relevance
Why it matters
In ophthalmology, dosing decisions are often constrained by limited visibility into where drugs go—and how long they act.
This work shows how a mechanistic PBPK approach can:
- Provide insight into the drivers of drug efficacy (binding affinity, half-life, dose)
- Enable comparison across therapies with different pharmacological profiles
- Support design of extended dosing regimens while maintaining efficacy
Instead of relying solely on clinical trial iteration, teams can use modeling to predict and optimize outcomes earlier.
Authors:
Aijaz Shaliban, Johannes Kast, Dan Li, Islam Younis, Georgi Kapitanov, Piet H. van der Graaf, Suruchi Bakshi
