Related Experiment Video
Updated: Oct 3, 2026
Experimental Models for Study of Retinal Pigment Epithelial Physiology and Pathophysiology
Published on: November 6, 2010
Dose-Dependent and Reversible Serous Retinal Detachments in Fibroblast Growth Factor Receptor Inhibitor-Associated
Abstract:
We report two cases of fibroblast growth factor receptor (FGFR) inhibitor-associated retinopathy, including the first case of Debio 1347 associated retinopathy manifesting with bilateral serous retinal detachments along the superotemporal arcades and a case of erdafitinib associated retinopathy manifesting with classic foveal serous retinal detachments. Both cases demonstrate a clear dose-dependent and reversible class effect likely secondary to downstream effects of FGFR inhibition on the MEK pathway, resulting in retinal pigment epithelial cell dysfunction, and may also involve additional mechanisms of cellular injury through inhibition of the PI3K/AKT/mTOR pathway. FGFR inhibitor-associated retinopathy appears to manifest differently among patients. [Ophthalmic Surg Lasers Imaging Retina 2023;54:368-370.].
Insights
Fibroblast growth factor receptor (FGFR) inhibitors can cause retinopathy, presenting as serous retinal detachments. This dose-dependent effect is reversible and linked to MEK pathway inhibition, affecting retinal pigment epithelial cells.
Area of Science:
- Ophthalmology
- Oncology
- Pharmacology
Background:
- Fibroblast growth factor receptor (FGFR) inhibitors are utilized in cancer therapy.
- Retinopathy is a potential adverse effect of FGFR inhibitors.
- Understanding the specific mechanisms and presentations of FGFR inhibitor-associated retinopathy is crucial for patient management.
Observation:
- Two cases of FGFR inhibitor-associated retinopathy are presented.
- One case involved Debio 1347, manifesting as bilateral superotemporal serous retinal detachments.
- The second case involved erdafitinib, presenting with foveal serous retinal detachments.
Findings:
- FGFR inhibitor-associated retinopathy demonstrates a dose-dependent and reversible class effect.
- The retinopathy is likely secondary to downstream effects of FGFR inhibition on the MEK pathway, leading to retinal pigment epithelial cell dysfunction.
- Additional mechanisms of cellular injury involving the PI3K/AKT/mTOR pathway may also contribute.
Implications:
- FGFR inhibitor-associated retinopathy can manifest differently across patients.
- Early recognition and management of this ocular toxicity are essential for patients undergoing FGFR inhibitor therapy.
- Further research is warranted to fully elucidate the pathophysiology and optimize treatment strategies for this condition.
