Science behind ALVIZON™

• A clinical study of GA patients, published in the BMJ (Hong. T. et al, Open Ophthalmology, 2022) concludes that intravitreal ALVIZON™:
  • Is clinically safe and well tolerated.
  • Does not increase IOP.
  • Improves visual acuity (LLVA) in several patients.
  • Results in no spread of the GA lesion vs historical controls.
• GA lesions involve accumulation of macrophages under the RPE, indicating chronic inflammation.
• Genome-based evidence indicates that Dry-AMD involves complement factor C3 dysregulation and cell-mediated immunity within the retina.
• Laboratory studies from human donor eyes with dry AMD, show that complement factor C3 is synthesised by macrophages within the retina, in response to chemokine signalling by other retinal cells.
• In a mouse model of Dry-AMD, accumulation of macrophages, and therefore C3, is prevented by intraocular administration of ALVIZON™.
• Treatment with ALVIZON™ in the mouse model of GA improves photoreceptor function, measured using the electroretinogram (ERG).
• The mode of action of ALVIZON™ appears to be the result of several therapeutic effects including:
  • Switching off the signals within the retina that promote macrophage activation and C3 expression.
  • Restoring homeostasis and normal cell function in residual cells, including rod photoreceptors.
  • ALVIZON™ acts through nuclear receptors that are not expressed at the cell surface.
  • Being fat soluble ALVIZON™ can pass through the cell membrane and cytoplasm and engage with nuclear receptors.