Shire files dry eye drug in Europe

Shire has filed its lifitegrast dry eye drug in Europe, following approval in the US last year at the second time of asking.

Branded as Xiidra in the US, the drug would be the first and only treatment in a new class of drugs – lymphocyte function-associated antigen-1 (LFA-1) antagonists – to address the signs and symptoms of dry eye disease in adults in Europe.

In late 2015, the FDA had rejected lifitegrast, asking for more trial data and further product quality information.

In 2013, Shire paid $160 million plus undisclosed milestone payments to buy SARcode Bioscience along with lifitegrast – at the time the dry eye drug was the California biotech’s lead product.

That is looking like a good deal as the drug is a significant part of a Shire plan to generate $10 billion a year in product sales by 2020, and could push through the billion dollar sales boundary by then.

Although Shire is best known as a rare disease specialist, it is also trying to make inroads into ophthalmology.

On the horizon there is already competition from Novartis, which already has a strong presence in ophthalmology and in April took an option to develop a potential rival dry-eye drug from US-based Lubris.

Shire’s filing for lifitegrast is supported by the largest development program to date for an investigational-stage dry eye disease candidate, consisting of five clinical trials with more than 2,500 patients.

In these studies, the signs of dry eye disease were measured using corneal staining and the symptoms by using patient reported eye dryness score.

Lifitegrast binds to the integrin LFA-1, a cell surface protein found on leukocytes and blocks the interaction of LFA-1 with intercellular adhesion molecule-1 (ICAM-1).

ICAM-1 plays a prominent role in ocular surface inflammation and may be over-expressed in corneal and conjunctival tissues in dry eye disease.

LFA-1/ICAM-1 interaction can contribute to the formation of an immunological synapse resulting in T-cell activation and migration to target tissues.

Lifitegrast may inhibit recruitment of previously activated T cells, activation of newly recruited T cells and the release of pro-inflammatory cytokines, interrupting the cycle of inflammation.