UCLB spinout could hold the key to treating an early trigger for diabetic blindness 

A pioneering discovery by UCL scientists, supported by UCLB, could transform the fight against diabetic blindness for millions worldwide.

The breakthrough, published today in Science Translational Medicine, identifies a key protein responsible for the earliest stages of diabetic retinopathy: a leading cause of vision loss among working-age adults.

The research, led by the UCL Institute of Ophthalmology and funded by Diabetes UK and Moorfields Eye Charity, reveals that the protein LRG1 triggers damage to the retina’s blood vessels soon after diabetes develops. This early-stage damage, previously undetected, sets the stage for long-term visual impairment.

UCLB’s involvement comes through its support of Senya Therapeutics, a spinout founded by Professors John Greenwood and Stephen Moss. Senya Therapeutics holds the global patent rights for LRG1 and is developing therapies targeting this protein. UCLB Associate Director Dr. Mark Fisher has served on Senya’s board since its inception.

“Senya Therapeutics is examining therapeutic uses for the targeting of the LRG1 protein, which is another example of the exciting developments UCLB has helped oversee that could lead to real-world impact across a broad variety of use cases,” said Dr. Fisher.

The role of LRG1 in neovascularisation in the retina was described by John and Stephen more than 10 years ago. Its role in wider disease has been confirmed by other researchers over recent years. Diabetic retinopathy is one of the diseases being addressed in a portfolio of developments at Senya Therapeutics.

Dr Giulia De Rossi, UCL lecturer and Diabetes UK RD Lawrence Fellow added: “Our discovery shows that diabetic eye disease starts earlier than we thought, and LRG1 is a key culprit in this early damage. Targeting this protein could give us a way to protect vision before serious damage occurs and prevent, rather than treat, blindness in millions of people living with diabetes.”

Current treatments for diabetic retinopathy only begin after symptoms appear, by which point irreversible damage may have occurred. Existing therapies, which target a different protein (VEGF), are effective for only about half of patients and rarely reverse established harm. The new research shows that LRG1 acts earlier than VEGF, making it a promising new therapeutic target.

The UCL team has already developed a drug that blocks LRG1 activity, which has shown success in pre-clinical studies and could soon enter human trials. This therapy could not only halt the onset of diabetic retinopathy but may also benefit patients in later stages of the disease.

Professor John Greenwood, Joint Senior Author and world expert in LRG1 biology, said: “This study delivers vital insight into the disease and shows that therapeutic targeting of LRG1 has real clinical potential. The discovery that LRG1 is an early initiating factor driving diabetic retinopathy is enormously exciting.”