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Neovascular glaucoma (NVG), previously known as hemorrhagic glaucoma, congestive glaucoma, thrombotic glaucoma, and rubeotic glaucoma, is a severe form of secondary glaucoma characterized by the proliferation of fibrous vascular tissue in the anterior chamber angle. Our company is well-equipped to address your drug and therapy development requirements in Neovascular Glaucoma therapy.
Neovascular glaucoma (NVG) is a severe form of secondary glaucoma characterized by the proliferation of abnormal new blood vessels on the iris and the anterior chamber angle, leading to increased intraocular pressure. Recent literature estimates that NVG accounts for approximately 3.9% of all glaucoma cases. The condition is most commonly associated with ischemic retinal diseases, such as diabetic retinopathy and central retinal vein occlusion.
The pathogenesis of neovascular glaucoma (NVG) involves retinal ischemia, which triggers the production of angiogenic factors like vascular endothelial growth factor (VEGF). These factors lead to the formation of abnormal blood vessels in the iris and iridocorneal angle, creating a fibrovascular membrane that obstructs the aqueous humor outflow, thus increasing intraocular pressure. This process can transition NVG from an open-angle to a closed-angle form as the disease progresses, making early diagnosis and intervention crucial .
Biomarkers of neovascular glaucoma have been identified through various studies, particularly those analyzing aqueous humor and vitreous fluid for inflammatory and ischemia-related markers. Key biomarkers include:
Small molecule drugs aim to inhibit key pathways involved in the pathogenesis of NVG, particularly the vascular endothelial growth factor (VEGF) pathway, which is crucial for the abnormal blood vessel growth. Netarsudil, a Rho kinase inhibitor, has shown promise in reducing IOP by enhancing aqueous humor outflow and reducing fibrosis in the trabecular meshwork.
Gene therapies aim to correct or modify genetic defects that contribute to NVG. Techniques such as RNA interference (RNAi) can be used to silence the VEGF gene, reducing the production of VEGF and subsequent neovascularization. Studies using small interfering RNA (siRNA) to target VEGF mRNA have shown promise in preclinical models.
Cell therapies involve the use of stem cells or other cell types to repair or replace damaged tissues in the eye. Mesenchymal stem cells (MSCs) have been investigated for their potential to reduce inflammation, promote tissue repair, and secrete anti-angiogenic factors.
Monoclonal antibodies are engineered to target specific proteins involved in disease pathways. Bevacizumab (Avastin) has been widely used off-label for NVG. It binds to VEGF, preventing it from activating its receptors on endothelial cells, thereby inhibiting neovascularization and reducing IOP.
Our company adopts a partnership-driven approach. We collaborate closely with clients to craft tailored, innovative Neovascular Glaucoma therapy strategies and ensure robust support throughout the process.
We have established expertise in developing and utilizing relevant animal models that closely mimic the disease characteristics and response to therapy. These models enable us to evaluate the safety and efficacy of potential therapies.
Non-Genetically Engineering Models | ||
We provide diverse model choices customized to meet specific research needs related to Neovascular Glaucoma. These models allow researchers to simulate and study the complex biological processes associated with Neovascular Glaucoma. | ||
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Genetically Engineered Models | ||
Our expertise in genetic engineering techniques allows us to generate accurate and reliable models that recapitulate the genetic alterations observed in human Neovascular Glaucoma. | ||
Optional Models |
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Optional Species | Mice, Rats, Non-human primates, Others |
In addition to these models, our comprehensive services encompass other models that target specific signaling pathways and molecular targets.
If our services align with your goals, please contact us for more details.
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