• New preclinical data show NUZ-001 increases activity of multiple protein clearance pathways in neuronal models
• Demonstrates enhanced activity of both autophagy and proteasomal systems, key processes involved in clearing aggregated proteins
• Supports a differentiated, multi-pathway approach targeting disrupted protein homeostasis in neurodegenerative disease

Neurizon Therapeutics Limited (ASX: NUZ & NUZOA; OTCQB: NUZTF), a clinical-stage biotech company dedicated to advancing innovative treatments for neurodegenerative diseases, announces new preclinical findings that further characterise the biological mechanism of action for its lead compound, NUZ-001. The data demonstrate that NUZ-001 and its sulfone metabolite increases activity of multiple protein clearance pathways in neuronal systems. These findings provide additional insight into how NUZ-001 may assist neurons in managing the accumulation of aggregated proteins - a key feature of neurodegenerative diseases such as Amyotrophic Lateral Sclerosis (ALS). The new findings show that NUZ-001 increases activity in two critical and complementary pathways involved in maintaining protein balance within neurons: autophagy and the Ubiquitin-proteasome system. Autophagy supports the bulk degradation of damaged or aggregated proteins, while the proteasome selectively removes smaller protein aggregates. Both pathways play an essential role in maintaining cellular homeostasis. Increasing activity across these systems may help improve the ability of neurons to process and clear aggregated proteins. This multi-pathway activity represents a differentiated approach compared to therapies that focus on a single pathway and may support a broader restoration of cellular protein balance. These findings further expand the understanding of the biological activity of NUZ-001 and its potential relevance in neurodegenerative disease. Impairment of protein clearance pathways is a recognised feature of diseases such as ALS, contributing to the accumulation of protein aggregates leading to neuronal damage. By increasing activity across both autophagy and proteasomal systems, NUZ-001 demonstrates a broader effect on pathways involved in protein homeostasis. This approach may support neuronal resilience and offers a differentiated profile compared to single-pathway strategies.

These results strengthen the scientific foundation of NUZ-001 and support its continued development as a potential therapy targeting underlying disease biology across ALS and related neurodegenerative disorders.