立他司特治疗干眼的效果？

Author: Medicalhalo

Release time: 2025-10-19 11:44:20

Treat dry eyes

Lifitegrast is a lymphocyte function-associated antigen-1 antagonist used to reduce inflammation in dry eye disease (DED).

A study has been conducted, design: 12-week, phase III, randomized, double-blind, multi-center, placebo-controlled study. Participants: Adults ≥18 years of age, Schirmer tear test (without anesthesia) ≥1 and ≤10 mm, corneal fluorescein stain score ≥2.0 (0-4 scale), Eye Dryness Score (EDS) ≥40 (0-100 visual analogue scale [VAS]), and history of artificial tear use within 30 days of study entry.

Methods: After a 14-day placebo run-in, participants were randomly assigned in a 1:1 ratio to lifitgrast eye solution 5.0% or placebo twice daily for 84 days. Primary outcome measure: The primary efficacy endpoint was change from baseline to day 84 in patients with EDS. Key secondary efficacy endpoints were change from baseline to days 42 and 14 in patients with EDS. Other secondary efficacy endpoints include additional VAS items (burning/tingling, itching, foreign body sensation, eye discomfort, photophobia, pain), Ocular Discomfort Score (ODS), and safety/tolerability of lifitegrast versus placebo.

In the study, 711 participants were randomly assigned: placebo, 356; lifegrast, 355. On Day 84, subjects in the lifitegrast group had a significant improvement in EDS from baseline compared with the placebo group. Mean changes at day 42 in EDS patients also significantly favored longevity compared with baseline. There were no statistically significant differences in ODS between treatment groups at days 84, 42, and 14.

On day 42, the lifitegrat group had greater improvements in itching, foreign body sensation, and eye discomfort compared with the placebo group. Most treatment-emergent adverse events were mild to moderate in severity, and no serious ocular adverse events were reported.

Conclusions: In patients with DED, Lifitegrast significantly improved dry eye symptoms as measured by EDS compared with placebo, and topical application of Lifitegrast 5.0% eye solution rapidly reduced dry eye symptoms, reduced ocular surface staining, and had an acceptable long-term safety profile. Improvement in EDS was observed as early as day 14, and lifitgrast was well tolerated.

dry eye disease

Dry eye disease (DED) is a multifactorial ocular surface disease characterized by discomfort, reduced tear quality, and chronic inflammation that affects approximately 20 million patients in the United States alone. DED is associated with local inflammation of the ocular surface and periocular tissue, leading to the homing and activation of T cells, the release of cytokines and the development of hypertonic tears. This inflammatory environment can lead to symptoms of dry eyes and discomfort. Homing of T cells to the ocular surface is affected by binding of lymphocyte function-associated antigen-1 (LFA-1; CD11a/CD18; the cell surface adhesion protein αLβ2 and its cognate ligand intercellular adhesion molecule-1 (ICAM-1; CD54), which is expressed on inflamed ocular/periocular epithelium and vascular endothelium. The binding of LFA-1/ICAM-1 within the immune synapse activates T cells and releases cytokines.

Mechanism of action of Ritalast

lifitgrast is a novel T-cell integrin antagonist designed to mimic the binding epitope of ICAM-1. It acts as a molecular decoy, blocking the binding of LFA-1/ICAM-1 and inhibiting downstream inflammatory processes.

In vitro studies have shown that lifitegrast inhibits T cell adhesion to iCAM-1-expressing cells and inhibits the secretion of pro-inflammatory cytokines, including interferon gamma, tumor necrosis factor alpha, macrophage inflammatory protein 1α, interleukin (IL)-1α, IL-1β, IL-2, IL-4, and IL-6, which are factors known to be associated with DED.