Key Takeaways
- Neuvasq presented new preclinical data at ARVO showing that targeting the Wnt co-receptors Gpr124 and Lrp6 may help repair and maintain the blood-retina barrier in retinal vascular diseases such as DME and wet AMD
- The company’s lead bispecific antibody candidate, NVQ401, demonstrated potent Wnt pathway activation and reversed vascular leakage
- NVQ501 combined β-catenin activation with anti-VEGF activity, delivering enhanced efficacy in preclinical studies
Neuvasq Biotechnologies announced new preclinical data supporting its novel therapeutic approach targeting the Wnt co-receptors Gpr124 and Lrp6. The findings were presented during an oral session at the Association for Research in Vision and Ophthalmology (ARVO) 2026 annual meeting in Denver, Colorado.
The presentation, titled “Novel multispecific Gpr124-targeting antibodies correct vascular pathology in preclinical retinopathy models,” showcased data demonstrating the potential of Neuvasq’s engineered antibody platforms to restore and maintain the integrity of the blood-retina barrier (BRB), a critical component in retinal vascular diseases including diabetic macular edema (DME) and wet age-related macular degeneration (AMD).
According to the company, selective activation of the Wnt/β-catenin signaling pathway through Gpr124 and Lrp6 was associated with reversal of vascular pathology across several preclinical disease models.
“The data presented at ARVO 2026 demonstrate that these novel therapeutic molecules targeting Gpr124/Lrp6 have the potential to improve the integrity and function of the blood-retina barrier,” said Ralph Laufer, PhD, Chief Scientific Officer of Neuvasq. “Selective activation of the Wnt/β-catenin pathway through these targets was associated with reversal of vascular pathology in preclinical disease models, supporting their potential to provide a new therapeutic approach combining very high potency with the possibility for long-lasting therapeutic effects.”
Neuvasq highlighted results from NVQ401, its lead bispecific antibody candidate, which was shown to potently activate Wnt receptor signaling in in vitro retinal models. The company said the molecule’s potency may support quarterly dosing intervals.
Preclinical studies demonstrated that NVQ401 reversed VEGF-induced vascular permeability in human retinal cells and produced robust efficacy across three retinopathy models. In the oxygen-induced retinopathy (OIR) model, NVQ401 reduced both neovascularization and avascular areas, suggesting potential benefits in controlling vascular leakage, suppressing abnormal blood vessel growth, and promoting normal retinal vascularization.
Building on these findings, Neuvasq also unveiled data for NVQ501, a trispecific antibody engineered to combine β-catenin activation with anti-VEGF functionality — two clinically validated mechanisms in retinal disease treatment.
In preclinical evaluations, NVQ501 potently activated β-catenin signaling in human retinal endothelial cells and fully inhibited VEGF-induced PLVAP expression, a key driver of retinal vascular damage. In the OIR model, NVQ501 demonstrated enhanced efficacy over NVQ401 in reducing neovascularization and, unlike the parent anti-VEGF therapy, achieved statistically significant reductions in avascular areas, according to Neuvasq.
Neuvasq believes the combination of β-catenin activation and VEGF neutralization could represent a next-generation therapeutic strategy for retinal vascular diseases and potentially establish a new standard of care.
The company also announced that NVQ501 is advancing toward chemistry, manufacturing and controls (CMC) and IND-enabling studies, with an anticipated timeline of approximately 15 months to submit an investigational new drug (IND) application.
