Dry eye disease is a multifactorial disease of the tear film and ocular surface that produces symptoms of chronic ocular discomfort.1 An estimated 25 million people in western Europe have dry eye disease and the prevalence is increasing as the general population
is ageing.2
Over the past decade, significant progress has been made into understanding the basic pathophysiology observed in dry eye
disease. An emerging body of research has provided insights into the chronic inflammatory nature of dry eye and revealed potential
clues for the design of novel treatments.3,4
Currently, only cyclosporine emulsion (0.05%) is approved in the US for dry eye; no pharmaceutical dry eye treatments are
approved in Europe. Cyclosporine is approved for increasing tear production after 24 weeks of treatment and not approved for
relief of symptoms.
There remains an unmet medical need for a secondgeneration pharmaceutical treatment with faster onset of activity with the
ability to improve both signs and symptoms of dry eye disease.
Inhibition of T-cell activation and trafficking to sites of inflammation
Activated CD4+ lymphocytes (Tcells) appear to play a central role in ocular surface inflammation associated with dry eye.3,4 Lifitegrast (SAR 1118) is an investigational small molecule aimed at inhibiting activation and mobility of T-cells.5 Normally these immune response cells are activated as part of the host defence process but under conditions of continuous
exposure to stress factors (e.g., autoantigens, environmental insults, mechanical and osmotic stresses), can lead to a state
of perpetual lymphocyte activation and migration. The unchecked cycle of Tcell migration, proliferation and cytokine release
on the ocular surface leads to changes in the quality of the tear film that results in subsequent epitheliopathy and symptomatic
discomfort for patients.
