Lifitegrast: A novel drug for treatment of dry eye disease

Abstract

Dry eye disease (DED) is an inflammatory disorder of ocular surfaces leading to severe disability, especially in the elderly age group. The mainstay of therapy includes artificial tears, punctual plugs, topical anti-inflammatory agents, and corticosteroids. In the past few years, only cyclosporine-A emulsions have been added to the existing therapy, but it is discontinued by most patients as it causes burning sensation in the eye. Hence, progress in new research for a better therapeutic option led to the discovery of lymphocyte function-associated antigen intercellular adhesion molecule 1 antagonist, lifitegrast. It hinders the T-cell activation, release of inflammatory mediators, and consequently inhibits the inflammatory pathways in DED. It was approved by the US Food and Drug Administration in July 2016 for the treatment of DED. This review highlights the development process and approval of lifitegrast.

<p>A Review of Topical Cyclosporine A Formulations—A Disease-Modifying Agent for Keratoconjunctivitis Sicca</p>

“…The central mechanism of KCS is a vicious cycle where inflammation-stimulated by desiccating or hyperosmolar stress-leads to ocular surface damage. 3,4 Hyperosmolarity can be caused by a number of factors, including lacrimal gland destruction due to Sjögren syndrome; age-related degeneration of the lacrimal gland, conjunctiva, and meibomian glands; damage to sensory nerves during refractive surgery; reduced tear production due to systemic medications; and meibomian gland disease. 3 Irrespective of the etiology of KCS, chronic inflammation-especially T-cell mediated immune response-and tear hyperosmolarity are common perpetuating factors.…”

“…3 Irrespective of the etiology of KCS, chronic inflammation-especially T-cell mediated immune response-and tear hyperosmolarity are common perpetuating factors. [3][4][5] At the onset of the inflammatory response, levels of mitogen-activated protein kinases (MAPKs) and nuclear factor κB increase on the ocular surface. 6,7 Activation of MAPK cascades triggers secretion of various inflammatory mediators, including interleukin-1β (IL-1β) and tumor necrosis factor α, which mediate activation of resident dendritic cells and T-cell recruitment to the ocular surface.…”

Neuropathic Corneal Pain

“…89 Further, a new class of anti-inflammatory agents has become available with Lifitegrast 5%, which was recently approved by the FDA for the treatment of signs and symptoms of dry eye disease. 90 Moreover, antibiotics such as topical and oral tetracycline and azithromycin have been used successfully for anti-inflammatory therapy. 91,92 Nevertheless, topical loteprednol is the author’s first-line choice as an anti-inflammatory agent.…”

Sjögren’s Syndrome as an Ocular Problem: Signs and Symptoms, Diagnosis, Treatment

“…Interaction between LFA-1 and ICAM-1 leads to T-lymphocyte adhesion to endothelial cells, migration to tissue, antigen presentation and recognition facilitating the formation of an immunological synapse. It releases inflammatory mediators, cytokines, chemokines, TNF-α, and IL-1 which are responsible for perpetuation and intensification DED inflammation [2,22,[75][76][77][78][79]. The clinical efficacy of lifitegrast in patients with DED has been reported: improvement in symptom scores and ocular staining score in patients using it for 12 weeks.…”

“…The clinical efficacy of lifitegrast in patients with DED has been reported: improvement in symptom scores and ocular staining score in patients using it for 12 weeks. No serious ocular adverse events occurred [22,[75][76][77][78][79]. However, there are no studies comparing lifitegrast and other anti-inflammatory agents, evaluating whether lifitegrast in combination therapy could work better in DED-those problems need further studies [79].…”