Providing Novel Therapies that Work Better, Have Fewer Side Effects and are Easier to Use than Currently Available Treatments

Topical GAL-101 in dry AMD: A Potential Game Changer in Phase 2 Trial with Strong Partner

GAL-101 is Galimedix’s most advanced compound and is currently being evaluated in a Phase 2 clinical study, called eDREAM, for the treatment of geographic atrophy, an advanced form of dry age-related macular degeneration (AMD). Dry AMD is one of the leading causes of adult blindness.

Delivered topically as an eye drop, GAL-101 is designed to provide a patient-friendly treatment, targeting toxic Aβ in the retina. An oral formulation of GAL-101 has completed successfully clinical Phase 1 development.

GAL-101 has demonstrated compelling efficacy in relevant ophthalmic pre-clinical models: the eye drop formulation has been shown to effectively deliver GAL-101 to the retina, its intended site of action, and to protect neuronal retinal cells from toxic damage.

eDREAM (NCT06659549) is a Phase 2 clinical study evaluating GAL-101 eye drops in non-foveal geographic atrophy (GA), an ad­vanced form of age-related macular degeneration (AMD). AMD affects more than 200 million adults and involves degeneration of the retina, the light-sensitive tissue at the back of the eye. GA is an advanced form of AMD in which certain areas of the retina slowly lose photoreceptors, the cells that allow us to see. At first, the damage usually appears away from the center of vision. Over time, the damaged area grows and can reach the fovea, the part of the retina responsible for sharp, central vision. When this happens, everyday activities like reading, recognizing faces, or driving become severely impaired/limited.

Phase 2 eDREAM Trial Investigating the Potential of GAL-101 Eye Drops to Improve and Maintain Patients’ Vision Longer

With our Phase 2 eDREAM clinical study we want to find out whether GAL-101 eye drops can slow or stop the growth of these damaged areas, helping to preserve vision for as long as possible and prevent the disease from reaching the fovea. In addition, we will test whether treatment leads to early improvement in vision.

Up to 110 patients with GA will be enrolled in the study at clinical sites in the US, Armenia, France, Georgia, Germany, Ireland, Israel, and Italy.

Over a period of at least 12 months, patients will apply the eye drops daily and attend regular clinic visits to measure vision and retinal sensitivity to light, check whether the area affected by GA is growing and monitor overall eye health.

Learn More About the eDREAM Study
For more information on the eDREAM study, please contact Luciana Summo, Ph.D., info@galimedix.com or visit clinicaltrials.gov.

Toxic Amyloid Beta (Aβ) Leads to Vision Loss in Glaucoma

Glaucoma, a leading cause of irreversible blindness worldwide, is characterized by the progressive death of nerve cells that transfer visual information from the eye to the brain. While commonly linked simply to the effects of raised intraocular pressure (IOP), a growing amount of data suggest the disease shares common pathogenic mechanisms with other neurodegenerative conditions, such as Alzheimer’s disease, strongly associated with the formation of toxic Aβ oligomers. Multiple studies implicate Aβ in the development of the characteristic progressive retinal ganglion cell (RGC) apoptosis and consequential disconnection of the eye from the brain.

Many Patients do not Benefit from Current Treatment Options

Although drug, laser, and surgical incision treatments are available to address glaucoma, all current approaches work by lowering IOP. However,  many glaucoma patients do not have elevated IOP: The majority of Asian glaucoma patients and an estimated 20-30% of patients in the Western World experience so-called normal tension glaucoma (NTG). Particularly for these patients, today’s regimens result in very limited efficacy.
Additionally, even in a significant subset of glaucoma patients with elevated IOP and subsequent treatment, glaucoma-related vision loss continues, despite IOP lowering.

Topical GAL-101: Creating a New Treatment Paradigm to Fulfill Substantial Unmet Need

With over 90% neuroprotective efficacy shown in relevant glaucoma pre-clinical models, Galimedix’s Phase 2-ready compound GAL-101, holds great promise to be the first glaucoma therapy that directly addresses the disease via neuroprotection, providing an option for the many patients for whom treatments alleviating IOP are ineffective. Delivered as an eye drop, it is designed to be a convenient and safe treatment and thus ideally suited to slowing the progression of chronic diseases like glaucoma, in which long-term therapeutic efficacy is dependent on patient compliance over many years.

An oral capsule formulation of GAL-101 is also in development.

GAL-101 has demonstrated compelling efficacy in relevant ophthalmic pre-clinical models, protecting neuronal retinal cells from toxic damage, and an excellent safety and tolerability profile in Phase 1 testing.

Therapeutic Strategies Targeting Amyloid Beta (Aβ) Bring Breakthroughs in Fight against Alzheimer’s Disease (AD)

While the causes of AD are still not fully understood, one hallmark of the condition is the accumulation of protein deposits in the brain called Aβ plaques. After decades of failed drug development attempts, recent approvals based on statistically significant, clinically meaningful Phase 3 data with Aβ-targeting antibodies (aducanumab, lecanemab, donanemab) have marked a new era in treating this debilitating disease, validating the importance of toxic Aβ oligomers and protofibrils as a key target.

However, while progress has been made with the introduction of these Aβ-targeting antibodies, they also have notable safety issues and a challenging route of administration, resulting in a remaining medical need for more efficacious, safer, and easier-to-use treatments for the 55 million people worldwide living with AD.

Oral Small Molecule GAL-101 Designed to Overcome Limitations of Current Therapies

To avoid known pitfalls of today’s drugs, Galimedix is developing the small molecule GAL-101, belonging to a new pharmacological class of Aβ aggregation modulators that act upstream of most other Aβ-targeting agents.

In contrast to antibodies that eliminate toxic oligomers only after their formation, require parenteral administration and have poor access to the central nervous system (CNS), GAL-101 is specifically designed to address Aβ before it turns into toxic oligomers. In pre-clinical testing, GAL-101 has been shown to prevent and eliminate all forms of toxic Aβ species while leaving healthy Aβ forms intact. GAL-101 also has shown the potential for neuroprotection and for symptomatic alleviation in pre-clinical models of AD. Additionaly, orally available GAL-101 has shown no antibody-specific immunological side effects (e.g., ARIA), very low systemic toxicity, robust storage stability, and easy and inexpensive manufacturing.