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What We
Solve For

What We Solve For

For people with chronic diseases of the retina and the optic nerve, we develop medicines that make healthy vision more accessible and manageable, promoting better compliance and visual outcomes.

Retinal Diseases

Retinal diseases like wet age-related macular degeneration, diabetic macular edema and diabetic retinopathy can lead to permanent vision loss. They all share the same mechanism of vision decline caused by excess vascular endothelial growth factor (VEGF). VEGF is a protein produced by cells that stimulates the formation of new abnormal blood vessels, a process called neovascularization, and induces vascular permeability, leading to leakage and swelling of the retina. Swelling of the retina leads to vision decline and death of the retinal cells, which can irreversibly cause blindness if not adequately treated.

Wet AMD
DR and DME
HEALTHY EYE
Wet AMD
HEALTHY EYE
Wet AMD
Wet age-related macular degeneration (wet AMD)
It is estimated that 11 million people in the US and 170 million people worldwide have age-related macular degeneration (AMD), a leading cause of vision loss in the elderly. The prevalence of the disease is approximately 85 to 90% nonexudative, or dry, AMD and 10 to 15% wet AMD. Wet AMD is caused by the growth of abnormal blood vessels under the central portion of the retina, or macula. Early intervention is essential to treat wet AMD; without treatment, vision rapidly declines. The above graphic illustrates the primary effects of wet AMD compared to a healthy eye.
HEALTHY EYE
DME
HEALTHY EYE
DME
Diabetic retinopathy (DR) and diabetic macular edema (DME)
DR, which includes DME, is the leading cause of acquired vision loss in the young and middle-age adult population. Of an estimated 463 million people with diabetes mellitus, or DM, worldwide, approximately one-third have signs of DR and of these, a further one-third of DR is vision-threatening DR, including DME. Approximately 30 million people in the United States have diabetes, 10 million of whom suffer from DR, including 1.5 million with DME. DME affects central vision and can lead to a decline in vision ranging from slight visual blurring to blindness, substantially affecting independence and quality of life. If left untreated, DME is the most common cause of vision loss in patients with DR. The above graphic illustrates the primary effects of DME compared to a healthy eye.
Unmet Needs For Patients With Retinal Diseases

Despite the significant benefits of existing therapeutic options, the need for frequent intravitreal injections is burdensome for both patients and retinal specialists.

The three greatest unmet needs from a retinal specialist perspective
Long-acting sustained drug delivery
Therapies that reduce treatment burden
New treatment mechanisms of action
Some of the challenges patients experience when on anti-VEGF therapy
Psychosocial burden of repeated intravitreal injections
Time burden of both treatment and monitoring visits
Expected visual acuity benefits not always met
“It takes me often up to 12 hours including travel time to visit my doctor and my spouse needs to accompany me, which represents a big burden for both of us.”
Anti-VEGF Patient

In clinical trials, intravitreal injections of anti-VEGF drugs resulted in significant gains in visual acuity for patients with retinal diseases. However, in settings outside of clinical trials, patients often receive less frequent injections than in clinical trial settings. Long-term observational studies in the United States, Europe and Japan have demonstrated that many patients with wet AMD lose visual acuity due to the challenges associated with receiving anti-VEGF injections at an optimal frequency.

The diagram below shows the declining visual acuity (VA) results over four years after the first anti-VEGF injection in patients with wet AMD in the United States.

Solving The Unmet Needs For Patients With Retinal Diseases

We believe that our proprietary technologies will allow us to develop therapeutics that may provide superior results to patients compared to existing ocular treatments, which present several critical limitations. We believe our product candidates present a number of competitive advantages over existing therapeutics:

Extended durability and sustained drug delivery to improve visual outcomes in clinical practice
Currently approved anti-VEGF therapies work effectively but have limited durability. In fact, most patients need to be injected every four to 12 weeks to experience positive visual outcomes. It has emerged that higher fluctuation in retinal thickness is associated with poorer visual outcomes. If approved, GB-102 would be an important intravitreal injection offering a six-month duration of action. Controlled and sustained drug delivery could limit the fluctuation in retina thickness associated with poorer visual outcomes. GB-102, with only two injections a year, could provide a better balance between patient quality of life and disease-monitoring requirements, and deliver, in a real-world setting, increased compliance and ultimately improved visual outcomes.

Differentiated mechanism of action
Our retina programs, GB-102 and GB-103, use sunitinib, a pan-VEGF inhibitor, which blocks all VEGF receptor types associated with angiogenesis, vascular permeability, cellular proliferation and fibrosis. GB-102 and GB-103 could potentially provide additional benefits over traditional anti-VEGF A inhibitors, as supported by an emerging body of evidence highlighting the mechanistic and clinical benefit of blocking the effect of VEGF-C and VEGF-D, in addition to VEGF-A. Moreover, sunitinib is a dual leucine zipper kinase, or DLK, inhibitor, which may result in a neuroprotective effect. Sunitinib’s broader mechanism of action has the potential to provide visual outcome benefits superior to the traditional anti-VEGF-A treatments.

Pan-VEGF Inhibitor

  • Blocks all VEGF receptors associated with angiogenesis, vascular permeability, cellular proliferation and fibrosis
  • Could provide benefits over traditional VEGF A inhibitors

Neuroprotectant

  • DLK pathway inhibitor
  • Blocking DLK promotes retinal ganglion cell survival
DLK: Dual Leucine Zipper Kinase​
Siu (2018) Zack (2011, 2012)

Versatile proprietary technologies
Our proprietary technologies can be tailored for different pharmacokinetic profiles. Our polymers can be tuned to provide varying drug elution profiles for a significant number of small molecules. Our proprietary technologies have the potential to deliver combination therapies by either co-delivering two therapeutic compounds or co-administering our product with another approved drug.

Designed for Safety

Our polymers are biodegradable and bioabsorbable. They are designed to hydrolyze over a determined period of time and leave no residue in the eye. In preclinical studies, our proprietary technologies have not been associated with inflammation typically observed with the intraocular administration of conventional PLGA microparticles.

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