The majority of diagnosed dry eye patients fail to get a satisfactory response with current treatments. Over 60% of patients using currently approved drug therapies in the U.S. discontinue their treatment within 12 months of initiation. In particular, local intolerabilities and lack of efficacy are considered to be key reasons for the high discontinuation rates.
In addition to dryness-related symptoms, impairment of visual function plays a significant role in the reduction of work productivity and patients’ health-related quality of life. Ocular surface damage leads to on visual symptoms that affect functions such as reading, looking at screen displays, driving and night vision.
Two major sub-categories of DED exist: aqueous tear-deficient and evaporative. Aqueous tear-deficient DED is marked by reduced tear volume while evaporative DED is caused by Meibomian gland dysfunction (MGD).
To understand DED, the underlaying causes and effects on the different physiological layers of the tear film and the ocular surface tissues have to be considered:
Tear film instability due to altered lipid layer
Tear film instability due to altered tear volume and composition
Meibomian gland dysfunction due to abnormal lipid secretion or obstruction
Mucin dysfunction due to damage
Epithelium dysfunction due to inflammation
Nerve dysfunction due to degeneration
Inflammation is the key underlying driver of the disease as chronic immunologic processes have a pivotal role in the pathology of dry eye.
an inflammatory response is a result from stress to the ocular surface, suggested as both, a cause and consequence of DED
leading to a vicious cycle of inflammatory response and ocular damage
Inflammation result from microtrauma, hyperosmotic stress, aging, environmental irritants, and systemic inflammatory conditions
If left untreated or undertreated, DED progressively damages the ocular surface and may lead to functional vision impairments
Evaporative dry eye disease mainly occurs due to Meibomian gland dysfunction leading to a deficient lipid layer and increased evaporation rates. Secrets from the Meibomian glands are the sole source of the natural tear lipid layer.
Dry eye disease is initially marked by signs e.g., reduction in tear production, mucus discharge, fast tear break-up time, corneal fluorescein staining, and patient reported symptoms e.g., burning, irritation, redness of increasing frequency. Corneal staining is considered the most critical and relevant objective clinical sign.
Despite multiple therapeutic options approved, there is a large unmet need for therapies that can rapidly and reliably repair corneal surface damage secondary to dry eye disease. Currently no drug therapy is available to treat specifically evaporative DED is caused by Meibomian gland dysfunction (MGD). Also, better comfort is a high unmet need.
The EyeSol® technology opens completely new and intriguing opportunities to overcome the limitations of water- or oil-based dry eye therapies.
Our products target key drivers of the disease and have constantly demonstrated significant improvement in sign and symptoms of dry eye in clinical trials.