ArticleCommunications medicine2026
The 5-HT1A receptor antagonist WAY-100635 maleate promotes retinal ganglion cell differentiation and protects the retino-visual circuits.
Article in Communications medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundGrowing evidence implicates early metabolic dysfunctions in retinal ganglion cells (RGCs) as a contributor to both high- and normal-tension glaucoma, yet no approved therapy directly protects RGCs to preserve vision. We aimed at identifying a safe, druggable neuroprotective strategy that restores RGC metabolic homeostasis for glaucoma therapy.
methodsUsing a live-cell mitochondrial screen in human embryonic stem cell-derived retinal ganglion cells (H7; female donor), we identified the clinically tested 5-HT1A antagonist WAY-100635 (WAY) as a neuroprotective agent. Mechanisms are probed by pharmacologic competition with agonist 8-OH-DPAT, cAMP assays, and PGC-1α dependent mitochondrial-biogenesis tests. RGC metabolism and survival are assessed by Seahorse and apoptosis assays. In vivo efficacy is evaluated in acute optic-nerve crush (ONC) and microbead-induced ocular-hypertension glaucoma models using histology, brain MRI, visual-acuity, contrast sensitivity testing, and flash VEPs to quantify cortical responses in wild-type C57BL/6 J male mice. Statistics used two-tailed Student's t-tests or ANOVA, as appropriate.
resultsHere we show that WAY elicits a reversible cAMP surge that drives PGC-1α dependent mitochondrial biogenesis and reduces apoptosis in hRGCs. In glaucoma-associated OPTN
conclusionsA clinically tested 5-HT1A antagonist WAY restores RGC metabolic homeostasis and preserves visual-pathway function across acute and chronic injury models, without detected systemic toxicity, supporting development of a neuroprotective candidate for glaucoma and potentially for other mitochondrial optic neuropathies.
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