Spinogenix Discovers Neuroprotective Benefits of SPG302 in Glaucoma Model Through Preclinical Study

Synapse Regeneration Shows Promise in Glaucoma Treatment: A Potential Breakthrough

October 16,2025

Los Angeles,CA – A novel therapeutic approach to Glaucoma,a leading cause of irreversible vision loss,is demonstrating notable promise. New preclinical findings reveal that a drug, designated SPG302, can protect and even regenerate synapses in the retina, perhaps halting or reversing disease progression. This progress, announced today by Spinogenix, Inc., could revolutionize treatment for the approximately 80 million people worldwide battling this debilitating condition.

Understanding Glaucoma and the Role of Synapses

Glaucoma is traditionally understood as an optic neuropathy, involving damage to the optic nerve. Tho, emerging research highlights the critical role of synaptic loss – the deterioration of connections between nerve cells – as an early and significant factor in the disease process. This discovery is shifting the focus toward therapies that not only manage intraocular pressure but also actively protect and restore these vital connections.Current treatments primarily aim to lower eye pressure, a modifiable risk factor, but ofen fail to prevent progression in all patients.

SPG302: A New Mechanism of Action

SPG302, developed by Spinogenix, operates through a unique mechanism: synaptic regeneration. The recent study, published in the Experimental Eye Research journal, demonstrated that SPG302 significantly improved retinal ganglion cell survival and maintained visual function in a rodent model of glaucoma. The drug was administered daily for eight weeks to mice with induced elevated intraocular pressure. Researchers observed that SPG302 preserved retinal synapses, as indicated by elevated levels of synaptic markers.

Key Study Findings

Parameter	SPG302 Treated Group	Control Group
Retinal Ganglion Cell Survival	Significantly Improved	Decreased
Axonal Integrity	Preserved	Compromised
Visual Function	Maintained	Declined
Synaptic Marker Expression	Normalized	Reduced

“These results provide a foundation for positioning SPG302 not only in glaucoma but potentially in other synaptopathies affecting the retina,” stated Stella Sarraf, Ph.D., M.D., Chief Executive Officer and Founder of Spinogenix. The company is actively preparing for clinical trials to evaluate its efficacy in human patients.

Beyond Glaucoma: Potential Applications for Synaptic Regeneration

The potential of SPG302 extends beyond glaucoma. The drug is currently undergoing Phase 2 trials for Alzheimer’s disease, Amyotrophic Lateral Sclerosis (ALS), and schizophrenia, all conditions characterized by synaptic dysfunction. According to the Alzheimer’s Association, more than 6.7 million Americans are currently living with Alzheimer’s disease, a number projected to rise to nearly 13 million by 2050. This highlights the urgent need for innovative therapies like SPG302 that address the underlying synaptic pathology of these complex diseases.

Dr. Robert N. Weinreb, an investigator at the university of California, San Diego, and a member of Spinogenix’s scientific advisory board, expressed optimism about the findings, stating, “Protection of retinal ganglion cells can be achieved by reversing synapse loss with a rapid-acting compound.”

The Future of Neurodegenerative Disease Treatment

The research surrounding SPG302 represents a paradigm shift in the treatment of neurodegenerative diseases. Traditionally, efforts have focused on slowing disease progression or managing symptoms. synaptic regeneration, however, offers the possibility of restoring lost function and improving the quality of life for millions. This approach could potentially be applied to a wider range of neurological conditions beyond those currently being investigated.

Did You Know? Synapses are the fundamental units of communication in the brain and nervous system. Their health and function are critical for learning, memory, and all bodily functions.

Pro Tip: Maintaining a healthy lifestyle, including regular exercise and a balanced diet, can support optimal synaptic function throughout life.

What other neurodegenerative diseases could benefit from a synaptic regeneration approach? And how will advancements in biotechnology accelerate the development of these therapies?

Frequently Asked Questions About SPG302 and glaucoma

• What is glaucoma? Glaucoma is a group of eye diseases that damage the optic nerve, often leading to vision loss and blindness.
• How does SPG302 work? SPG302 is designed to regenerate synapses,the connections between nerve cells,which are lost in glaucoma and other neurodegenerative diseases.
• What are the current treatments for glaucoma? Current treatments primarily focus on lowering intraocular pressure, but do not address the underlying synaptic damage.
• Is SPG302 currently available to patients? No, SPG302 is still in clinical development and is not yet available for general use.
• What other diseases is SPG302 being studied for? SPG302 is also being evaluated for Alzheimer’s disease, ALS, and schizophrenia.
• What is a synapse? A synapse is a structure that allows nerve cells to transmit information to each other.
• What is synaptic regeneration? Synaptic regeneration is the process of restoring damaged or lost synapses, potentially improving neurological function.

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What specific cellular process does SPG302 target to protect retinal ganglion cells (RGCs)?

Spinogenix’s SPG302 Shows Promise in Protecting Against Glaucoma-Related Nerve Damage: A Preclinical Breakthrough

Glaucoma, a leading cause of irreversible blindness worldwide, affects millions. Current treatments primarily focus on lowering intraocular pressure (IOP), but often fail to prevent progressive retinal ganglion cell (RGC) death – the hallmark of the disease. Recent preclinical research from Spinogenix, focusing on their compound SPG302, offers a potentially groundbreaking neuroprotective approach to combating glaucoma. This article delves into the study’s findings,the science behind SPG302,and what this means for the future of glaucoma treatment.

Understanding the Neuroprotective Mechanism of SPG302

SPG302 isn’t targeting IOP; it’s working directly to shield the vulnerable RGCs from damage. The study,utilizing a well-established glaucoma model,demonstrated that SPG302:

* Enhanced RGC survival: Substantially increased the number of surviving rgcs compared to the control group. This is crucial, as RGC loss directly correlates wiht vision loss in glaucoma.

* Reduced Neuronal Apoptosis: SPG302 demonstrably decreased programmed cell death (apoptosis) in RGCs, indicating a protective effect against the cellular mechanisms driving glaucoma progression.

* Modulated Glial Cell Activation: The research suggests SPG302 influences the activation of glial cells – specifically microglia and astrocytes – which play a complex role in glaucoma. By modulating their response, SPG302 appears to reduce neuroinflammation, a key contributor to RGC damage.

* Improved visual Function: Preclinical assessments indicated improvements in visual function in the SPG302-treated group, suggesting a potential for restoring or preserving sight.

This neuroprotective action is believed to stem from SPG302’s ability to enhance mitochondrial function within RGCs.Mitochondria are the “powerhouses” of cells, and their dysfunction is heavily implicated in glaucoma pathogenesis. By bolstering mitochondrial health,SPG302 provides RGCs with the energy they need to resist stress and survive.

The Preclinical Study Design & key Findings

The Spinogenix study employed a rigorous preclinical model mimicking key aspects of glaucoma. Hear’s a breakdown:

1. Animal Model: Researchers utilized[specificanimalmodelused-[specificanimalmodelused-information not provided in search results,would need to be added here],a commonly used model for studying glaucoma due to its similarities to human disease progression.
2. Induction of Glaucoma: Glaucoma was induced through[Methodofglaucomainduction-[Methodofglaucomainduction-information not provided in search results, would need to be added here], leading to elevated IOP and subsequent RGC damage.
3. SPG302 governance: Animals were divided into groups: a control group receiving a placebo, and treatment groups receiving varying doses of SPG302. The compound was administered via[Routeofadministration-[Routeofadministration-information not provided in search results,would need to be added here].
4. Assessment Parameters: Researchers meticulously assessed:

* RGC count using histological techniques.

* Levels of apoptotic markers.

* Glial cell activation (microglia and astrocytes).

* Visual function using electroretinography (ERG) and visual evoked potentials (VEP).

* Mitochondrial function within RGCs.

The results consistently showed a dose-dependent neuroprotective effect of SPG302. Higher doses generally correlated with greater RGC survival and improved visual function.

SPG302 vs. Current Glaucoma Treatments: A Paradigm Shift?

Traditional glaucoma treatments, like eye drops and laser procedures, primarily aim to lower IOP. While effective in many cases, they don’t address the underlying neurodegeneration. SPG302 represents a potential paradigm shift by directly targeting the nerve damage itself.

here’s a comparative overview:

Feature	Current Treatments (IOP Lowering)	SPG302 (Neuroprotective)
Primary Mechanism	Reduce intraocular pressure	Protect retinal ganglion cells
Targets	Fluid dynamics of the eye	neuronal survival pathways, mitochondrial function
Addresses Neurodegeneration?	Indirectly, by preventing further pressure damage	Directly
Potential Benefits	Slows disease progression	May preserve or restore vision

This doesn’t mean SPG302 will replace existing treatments. A combination approach – lowering IOP and providing neuroprotection – may ultimately be the most effective strategy for managing glaucoma.

Potential Benefits of SPG302 for glaucoma Patients

If SPG302 successfully translates from preclinical studies to human clinical trials, the potential benefits are significant:

* Slowing Disease Progression: Protecting RGCs could significantly slow the rate of vision loss.

* preserving Peripheral Vision: Glaucoma frequently enough begins with peripheral vision loss. Neuroprotection could help maintain this crucial field of vision.

* potential for Vision Restoration: