We Age Because Our Cells Age
The principle of our solution is quite straightforward: Stop and even reverse cellular aging.
For age-related ophthalmologic disorders, visual loss occurs mainly for two reasons:
●Our cells age and start to lose their functions.
●The number of cells decreases as we age.
Cell culture (in vitro) and animal (in vivo) studies revealed that our patented treatment approach enabled us to prevent and slow down cellular aging of ocular structures, which can lead to healthier and functioning tissues for longer years which may ensure to maintain of the quality of vision.
This approach can start a new era in the prevention and treatment of age-related ophthalmologic disorders.
Telomere Science Behind TelomEye
Every cell in our body has chromosomes. At the end of each chromosome, there are tiny particles called telomeres. Telomeres protect important DNA information and get shorter as we age. This is accepted as one of the 9 major hallmarks of aging.
But there is a safe way in the DNA to keep them longer and even grow them again. Lengthening or maintaining telomeres (TMP) means cellular rejuvenation. Stem and reproductive cells use this method against aging to stay younger and functional as long as a human lives.
We use a safe and new treatment approach in a unique ophthalmic formulation to overcome and repair this DNA damage to prevent and delay age-related ophthalmic diseases.
What We Have Done Till Now
We tested our unique treatment protocol on human cell cultures for safety and efficacy protocols and dosage designation of the formulation.
We designed animal studies for six months and used the treatment in different concentrations against placebo and control groups. The ophthalmologic examinations during the six-month experiment have shown that aging in tested rabbits’ ocular structures has slowed down.
After completing six months trial, all the eyes were enucleated for histopathological examination, which showed that the implications of aging of the tissues were subtle in particular treatment dosage groups.
Finally, the tissues were sent for DNA analysis for telomere length. The treatment groups’ telomere lengths were statistically significantly longer than the control and placebo groups.
Those were all quite solid supports for protecting the ocular structures against aging. These results inspired us to conduct further clinical trials on humans to show safety, efficacy and proof of our concept. We are expecting to have our final results by 2025-26.