Retinal neovascularization contributes significantly to vision loss, most commonly in age-related macular degeneration (AMD) and proliferative diabetic retinopathy (DR). These diseases are the leading cause of irreversible blindness and visual impairment in the world, striking most people age 60 or older. LIMR technology specifically addresses wet AMD and DR caused by abnormal leaky blood vessels that overgrow the macula, the part of the retina critical for central focused vision. Current treatments fail many patients, often later during treatment, thus defining a key medicinal gap.
Demographics of aging and obesity are increasing the incidence of AMD and DR in developed countries. Currently, 11 million Americans suffer from AMD. According to the nonprofit organization BrightFocus Foundation, that number is expected to double by 2050. More dramatically, AMD cases worldwide are expected to grow from 196 million in 2020 to 288 million by 2040.
DR develops in many Type 1 and Type 2 diabetes patients as a leading cause of blindness in adults. The number of vision-threatening cases of DR worldwide is predicted to increase from 37.3 million in 2010 to 56.3 million by 2030.
Additional retinopathies relevant to the technology include macular edema, diabetic macular edema, myopic choroidal neovascularization, and retinopathy of prematurity, all of lesser incidence than AMD or DR but representing significant clinical markets.
As the main standard of care, anti-VEGF biologics delivered by intraocular injection are effective in ablating angiogenesis driving these retinopathies. However, they are ineffective in about 30% of patients due to drug resistance (intrinsic or acquired).
Further, they are not selective for the disease state, as they also ablate normal revascularization that is desired after ablation of the pathogenic neovascularization. Thus, ophthalmologists await new agents such as LIMR's anti-RhoB technology that addresses resistance to anti-VEGF modalities and improves upon it by targeting only pathogenic neovascularization, while sparing normal retinal revascularization.
Potential new treatment for wet macular degeneration, diabetic retinopathy and other retinopathies (macular edema, diabetic macular edema, myopic choroidal neovascularization, and retinopathy of prematurity),
Stage of development
Preclinical proof of concept for uses of anti-RhoB antibodies to effectively treat wet macular degeneration has been published or submitted for publication.
- Anti-RhoB antibodies: U.S. Patent No. 9,879,092, issued Jan 30, 2018.
- Anti-RhoB uses: U.S. Patent Application No. 20,170,190,789, published July 6, 2017.
- Rhob peptide uses: WO Patent Application No. 2,018,213,331, published Nov 22, 2018.
Seeking licensee for commercialization or collaboration to complete preclinical studies.
- Adini I, Rabinovitz I, Sun JF, Prendergast GC and Benjamin LE (2003). RhoB controls Akt trafficking and stage-specific survival of endothelial cells during vascular development. Genes Dev 17:2721.
- Sabatel C, Malvaux L, Bovy N, Deroanne C, Lambert V, Gonzalez ML, Colige A, Rakic JM, Noel A, Martial JA and Struman I (2011). MicroRNA-21 exhibits antiangiogenic function by targeting RhoB expression in endothelial cells. PLoS ONE 6:e16979.
- Howe GA and Addison CL (2012). RhoB controls endothelial cell morphogenesis in part via negative regulation of RhoA. Vasc Cell 4:1.
- Almonte-Baldonado R, Bravo-Nuevo A, Gerald D, Benjamin LE, Prendergast GC and Laury- Kleintop LD (2018). RhoB antibody alters retinal vascularization in models of murine retinopathy. J Cell Biochem 294:4477.
Institutional contact: George C. Prendergast, PhD, LIMR President and CEO, 484.476.8475, [email protected]
L2C Partners contact: Merle Gilmore, 610.662.0940, [email protected]