“SwitchGene” Gene Therapy _ Oculus BioMed

THE OPPORTUNITY

OBM has partnered with world leading research institute – The Centre for Eye Research Australia (“CERA”) to develop “SwitchGene” eye gene therapies – an approach to treating eye diseases including its potential use in treating diabetic retinopathy (“DR”). 

“SwitchGene” is a novel approach to the treatment of ocular neovascularisation with the potential to eliminate the requirement for regular IVT injections and for controlling the level of VEGF activity on an individualised basis.  It also has potential for treating other VEGF-aberrant ocular diseases in addition to DR.

Current treatments for DR and DME include inhibitors of VEGF, steroids and laser therapy.  Despite these treatments, many patients remain refractory and have sub-optimal response to therapy with persistent fluid and impaired vision.

According to a cross-sectional study of a primary care database in the UK, the prevalence of DR in 2017 was 33.78%.   The study also found that there were upward trends in the prevalence of DR, most marked and accelerating in VTDR in type 1 DM but slowing in type 2 DM, and in the overall prevalence of DR.  A projection by the National Eye Institute (NEI) suggests that the number of people aged 40 and older with diabetic retinopathy in the US is projected to increase from 7.7 million in 2014 to approximately 11 million by 2030.   A global projection estimates that from 2020 to 2045, the number of DR patients worldwide will increase from 103.12 million to 160.5 million, with 44.82 million people experiencing vision problems.

Our Approach and Tech

The technology, referred to as “SwitchGene”, utilises a novel adeno-associated virus (“AAV”) construct to introduce into the eye a decoy receptor, [The Therapy], that binds intracellular vascular endothelial growth factor (“VEGF”).  [The Therapy] is administered as a fusion protein with a destabilizing domain resulting in its degradation unless switched on by administering a stabilizer.  Intravitreal injection of the AAV vector bound fusion protein and subsequent administration of the stabilizer compound has been shown to effect tuneable suppression of ischemia-induced retinal neovascularisation.