At Ace Therapeutics, we empower our clients' glaucoma research by providing genetic mouse models that enable them to gain critical insights into disease mechanisms and support their preclinical development of novel therapeutics.
Background on Genetic Mouse Models of Glaucoma
Glaucoma, a leading cause of irreversible blindness, is significantly influenced by genetic factors. Key genes like MYOC and Optn play crucial roles in its pathogenesis. MYOC mutations are associated with elevated intraocular pressure (IOP) and optic nerve damage. Optn mutations disrupt autophagy, leading to retinal ganglion cell (RGC) death. Genetic mouse models of glaucoma are crucial for understanding these genetic factors, as they offer a controllable platform for manipulating specific genes, observing phenotypic changes, and developing novel therapeutics.
Fig. 1 Pathways possibly implicated in POAG revealed by linkage and association studies. (Iglesias A I, et al., 2015)
Get to Know Our Genetic Models of Glaucoma
Ace Therapeutics provides a variety of genetic mouse models of glaucoma, helping researchers investigate the genetic basis of glaucoma and facilitate the development of innovative therapeutics.
Genetic Mouse Models of Ocular Hypertension
Our ocular hypertension mouse models offer an ideal platform for researchers to explore the genetic factors underlying elevated IOP and the consequent optic nerve damage associated with glaucoma. With our diverse genetic mouse models of ocular hypertension, researchers can choose the appropriate model to meet their specific research objectives.
- Custom DBA/2 Mouse Glaucoma Models
- Custom Transgenic MYOC Mouse Models of Glaucoma
- Custom Pitx2 Mutant Mouse Models of Glaucoma
- Custom Foxc1 Mutant Mouse Models of Glaucoma
- Custom Foxc2 Mutant Mouse Models of Glaucoma
- Custom Lmx1b Mutant Mouse Models of Glaucoma
- Custom Pax6 Mutant Mouse Models of Glaucoma
- Custom Prss56 Mutant Mouse Models of Glaucoma
- Custom Sh2pxd2b Mutant Mouse Models of Glaucoma
Genetic Mouse Models of Normal Tension Glaucoma (NTG)
Our mouse models of NTG are specifically designed to help researchers explore the genetic factors associated with this distinct type of glaucoma. Unlike ocular hypertension models, the NTG models are designed to simulate optic nerve damage and vision loss that may occur despite normal IOP. They provide a valuable platform for evaluating novel therapeutic approaches to protect RGCs and prevent vision loss.
- Custom Optn Mutant Mouse Models of Glaucoma
- Custom Slc1a3 Mutant Mouse Models of Glaucoma
- Custom EAAC1 KO Mouse Models of Glaucoma
- Custom Transgenic TBK1 Mouse Models of Glaucoma
Integrated Preclinical Services for Glaucoma Drug Development
Leverage our genetic mouse models of glaucoma as part of a comprehensive preclinical solution that includes study design and in vivo efficacy evaluation. Discover how our integrated preclinical services can support the development of your therapeutics.
- Glaucoma Basic Research Services
- Glaucoma Drug Discovery Services
- Preclinical Glaucoma Drug Development Services
Why Choose Ace Therapeutics
With years of experience in the development of genetic mouse models of glaucoma, Ace Therapeutics maintains a team of scientists with expertise in ophthalmic genetics and model development. Choosing us as your partner in glaucoma research offers several key advantages:
- Custom glaucoma model development
- Comprehensive preclinical services
- High-quality and reliable data
Whether you are exploring the genetic underpinnings of glaucoma or evaluating innovative therapeutics, Ace Therapeutics offers tailored solutions designed to facilitate your discoveries. Ready to enhance your glaucoma research with our specialized support? Contact us now to discuss how our genetic mouse models can be the cornerstone of your glaucoma research.
References
- Iglesias A I, et al. Genes, pathways, and animal models in primary open-angle glaucoma. Eye (Lond), 2015, 29(10): 1285-1298.
- Wang H W, et al. Research progress on human genes involved in the pathogenesis of glaucoma (Review). Mol Med Rep, 2018, 18(1): 656-674.