Solutions
Online Inquiry

Glaucoma

There has been an increasing prevalence of glaucoma, which without treatment, ultimately leads to blindness. Glaucoma is the most common condition which leads to a progressive degeneration of the optic nerve while exhibiting a narrowing of vision. At Protheragen, we focus on advancing the field of glaucoma therapeutics research and development through comprehensive services and innovative solutions.

Overview of Glaucoma

Formed by a myriad of factors, glaucoma has different forms, each having distinct pathological features and presentations. The most common is Primary open-angle glaucoma (POAG), which has a normal chamber angle, but low outflow of aqueous humor resulting in elevated IOP. In comparison, primary angle-closure glaucoma (PACG) is due to a physically obstructed angle which causes elevated IOP and acute symptoms. Other forms include secondary glaucoma such as exfoliation syndrome (XFS) and pigmentary glaucoma which involve the accumulation of fibrillar material GFS followed by the dispersion of iris pigment.

Schematic overview of pathogenic mechanisms leading to the sight-threatening endpoints of DR.Fig.1 Schematic diagram of the ocular anterior segment in open-angle and closed-angle glaucoma. (Wiggs J. L., et al., 2017)

MYOC, OPTN, and TBK1 are genes that were found to be associated with early onset, and ABCA1, AFAP1, and GMDS are for adult-onset glaucoma. These genes will be a turning point when it comes to developing targeted therapies and drugs.

Diagnostics Development for Glaucoma

Especially in young-onset glaucoma, genetic testing is gaining prominence in glaucoma diagnosis. The MYOC, OPTN, and TBK1 genes, which can be detected by targeted genetic sequencing, are known to harbor mutations linked with the more advanced types of glaucoma. Molecular diagnostics, such as biomarkers in the aqueous humor or blood, are additionally being investigated for their usefulness in diagnosing glaucoma at an early stage and in predicting the progression of the disease.

Therapeutics Development for Glaucoma

Pharmacological Therapies

Reducing IOP is the primary goal for treating glaucoma, and pharmacological means remain the first step in therapeutics. Prostaglandin analogues like latanoprost and bimatoprost are useful in increasing aqueous humor outflow, lowering IOP. Beta-blockers and alpha2-adrenergic agonists decrease the volume of aqueous humor produced while carbonic anhydrase inhibitors prevent secretion. More effective therapeutics consist of several medications to lower IOP even further.

Gene Therapies

Molecular chaperones such as sodium 4-phenylbutyrate have proved effective in reducing ER stress as well as decreasing intraocular pressure in MYOC mutant animal models. Furthermore, attention is focused on the therapeutic of glaucoma with neuroprotective mechanisms aimed at reducing oxidative stress and protecting mitochondria, with certain antihypoxic as well as mitochondriotropic substances offering hope.

Our Services

A variety of associated services in relation to glaucoma diagnostics and therapeutics are offered at Protheragen. Our advanced facilities, along with our specialists, are capable of performing all aspects of the research, starting from the basic to the preclinical phases.

Diagnostics Development

  • Karyotype Analysis Service
  • Omics Analysis Service
  • Biomarker Development Service
  • Artificial Intelligence Service
  • Customized Diagnostics Development

Therapeutic Development

  • Small Molecule Drug
  • Cell Therapy
  • Gene Therapy
  • Therapeutic Antibody
  • Therapeutic Peptide
  • Therapeutic Protein
  • Customized Therapy Development

Preclinical Research

  • Pharmacodynamics Study Services
  • Pharmacokinetics Study Services
  • Drug Safety Evaluation Services
  • Customized Research Services

Animal Models of Glaucoma

Protheragen excels in the development of customized animal models for glaucoma research. Our team of experts can create models that replicate specific aspects of human glaucoma, including elevated IOP, optic nerve degeneration, and visual field loss.

Primary Open Angle Glaucoma (POAG) Models

  • Spontaneous inheritance
  • Transgenic, Myoc mutation
  • Transgenic, wdr36 mutation

Primary Angle Closure Glaucoma (PACG) Models

  • Transgenic, Vav2/Vav3 knockout
  • Episcleral vein injection of saline, obstruction of outflow

Primary Congenital Glaucoma (PCG) Models

  • Spontaneous inheritance  
  • Transgenic, Cyp1b1 and Tyr mutations

Normal Tension Glaucoma (NTG) Models

  • Transgenic, Glast or Eaac1 mutation

Autoimmune Glaucoma Models

  • Immunization against HSP27 and HSP60, RGC loss

Pigmentary Glaucoma Models

  • DBA/2J strain, Gpnmb, and Tyrp1 mutation

If you are interested in our services, please feel free to contact us.

References

  • Wiggs, Janey L., and Louis R. Pasquale. "Genetics of glaucoma." Human molecular genetics 26.R1 (2017): R21-R27.
  • Schuster, Alexander K., et al. "The diagnosis and treatment of glaucoma." Deutsches Ärzteblatt International 117.13 (2020): 225.