Diabetic retinopathy damages the blood vessels in the retina and is the leading cause of vision loss in working-age adults. About one-third of people with diabetes develop some form of retinopathy. Current treatment includes laser therapy, anti-VEGF injections into the eye, and careful blood sugar control to slow progression.
What's actually going on in research
Trials are testing longer-acting anti-VEGF drugs to reduce injection frequency, combination therapies that address inflammation alongside leaky vessels, gene therapy approaches, and drugs delivered as eye implants. Research also focuses on identifying people at highest risk through AI analysis of retinal images and on early interventions before vision loss begins.
Longer-acting anti-VEGF drugs
New formulations aim to extend the time between eye injections from every month or two to three or four months. Several drugs in late-stage trials use different approaches to sustain drug levels in the eye.
Gene therapy
Trials are testing one-time gene therapy that would enable the eye to produce its own anti-VEGF protein. If successful, this could replace the need for repeated injections over years.
Sustained-release implants
Small drug-releasing devices placed in the eye aim to deliver medication continuously for months at a time. These could reduce the treatment burden for people requiring frequent anti-VEGF injections.
What to know before you search
Eligibility typically depends on retinopathy severity, whether the center of the retina is affected, visual acuity level, and previous treatments received.
What types of trials are currently open
- Anti-VEGF trials — Testing new drugs that block vascular endothelial growth factor, which drives abnormal blood vessel growth in the retina. These trials often compare injection frequency and vision outcomes.
- Combination therapy trials — Testing anti-VEGF drugs combined with steroids or other drugs that target inflammation and fluid buildup.
- Gene therapy trials — Testing one-time treatments that introduce genetic instructions for the eye to produce anti-VEGF protein on its own.
- Prevention trials — Testing whether early treatment in people with mild retinopathy can prevent progression to vision-threatening disease.
- Device and delivery trials — Testing implants, port systems, and new injection techniques to deliver drugs more effectively or reduce treatment burden.
Recently added Diabetic Retinopathy trials
To Investigate the Feasibility and Acceptability of Trained Non-medical Professionals Performing Laser Treatment for Proliferative Diabetic Retinopathy (PDR), and the Potential Impact on Service Capacity. Assess Feasibility of Conducting a Full Trial Comparing Trained ECPs With Ophthalmologists
To Investigate the Feasibility and Acceptability of Trained Non-medical Professionals Performing Laser Treatment for Proliferative Diabetic Retinopathy (PDR), and the Potential Impact on Service Capacity. To assess Feasibility of Conducting a Full Trial Comparing Trained ECPs With Ophthalmologists in performing laser treatment in line with the established protocols.
Oral N-Acetylcysteine on Diabetic Macular Edema
Diabetic retinopathy (DR) is one of the leading causes of preventable visual impairment among working-age adults, with diabetic macular edema (DME) representing one of its most important vision-threatening complications. Diabetic macular edema develops when diabetes-associated retinal vascular dysfunction leads to disruption of the blood-retinal barrier (BRB), allowing fluid and plasma components to accumulate within the retinal tissue and impair macular function. The development and persistence of DME involve a complex interplay between vascular, inflammatory, metabolic, and oxidative mechanisms. Hyperglycemia is a central driver of the molecular abnormalities underlying diabetic retinal injury. Chronic exposure to elevated glucose activates several interrelated pathways, including the polyol, advanced glycation end-products (AGEs), protein kinase C (PKC), and hexosamine pathways. These metabolic disturbances promote the generation of reactive oxygen species (ROS), inflammatory signaling, endothelial dysfunction, and progressive impairment of the retinal neurovascular unit. Together, these processes contribute to damage to endothelial cells, pericytes, Müller cells, and other retinal components, ultimately compromising the integrity of the BRB. Oxidative stress is therefore considered an important component of the pathophysiology of DR and DME. Excessive ROS production can directly damage cellular structures and can also amplify inflammatory and angiogenic signaling. This may increase the expression of several mediators implicated in retinal vascular dysfunction. The resulting vascular instability and increased permeability facilitate fluid extravasation into the retinal layers and contribute to the development and progression of DME. Malondialdehyde (MDA), a product of lipid peroxidation, is widely used as a marker of oxidative damage. Increased MDA concentrations have been reported in patients with diabetic retinopathy and have been associated with the presence or severity of retinal disease, supporting the involvement of oxidative stress in diabetic retinal injury. Assessment of MDA may therefore provide a useful systemic indicator of the oxidative component of the disease process. Angiopoietin-2 (Ang-2), an important regulator of vascular stability, has also been implicated in diabetic retinal vascular dysfunction. Increased Ang-2 can promote endothelial destabilization and enhance vascular permeability, particularly in the presence of inflammatory and VEGF-related signaling. Thus, oxidative stress and angiogenic dysregulation may represent interconnected components of the vascular injury that ultimately leads to BRB disruption and retinal fluid accumulation. Current management of DME relies predominantly on ophthalmic interventions, with corticosteroids and laser photocoagulation having roles in selected clinical settings. Although these approaches have substantially improved visual and anatomical outcomes, persistent or recurrent edema occurs in a proportion of patients, reflecting the multifactorial nature of DME and the involvement of various pathways. N-acetylcysteine (NAC) is a thiol-containing compound and a precursor of L-cysteine and reduced glutathione. In addition to its established mucolytic properties, NAC has antioxidant activity through direct scavenging of reactive oxygen species and, importantly, through restoration of intracellular glutathione availability. Its ability to modulate oxidative stress has led to extensive investigation of NAC in a variety of clinical conditions characterized by oxidative and inflammatory injury. Experimental evidence suggests that attenuation of oxidative stress with NAC may reduce diabetes-related retinal injury and suppress the expression of vascular and inflammatory mediators, including VEGF and intercellular adhesion molecule-1 (ICAM-1). However, the potential clinical relevance of oral NAC in patients with diabetic retinal disease remains insufficiently characterized.
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