Speaker
Description
Anti-VEGF therapy has recently been approved by the FDA to prevent the progression of retinopathy of prematurity (ROP; a leading cause of childhood blindness) and preserve vision in preterm newborns. Following injection, it is known that these drugs leave the eye and enter the systemic circulation; however, from there, the distribution of these drugs to the developing organs is unknown. Whilst uptake of these growth-suppressing drugs into the developing organs is denied by the financially interested parties, emerging evidence from animal studies shows that anti-VEGF agents enter the brain, lungs, and heart, and restrict the growth of these organs. Clinicians currently have no quantitative way to predict these risks or adjust treatment accordingly, let alone make an informed decision on whether anti-VEGF therapy is the best treatment option.
In this talk, I will present a data-driven organ-level pharmacokinetic/pharmacodynamic model of intravitreal aflibercept therapy in growing preterm newborns with ROP to predict the drug load experienced by key developing organs. I use a Bayesian approach to validate the model against clinical data and predict a physiologically plausible parameter space in preterm newborns. We then use this model to predict guild dosing, timing and monitoring.
