Dry eye disease (DED) is a chronic, inflammation-driven disorder of the ocular surface. Clinically relevant in vivo models that capture tear film instability, epithelial damage, and ocular surface immune responses are essential for robust preclinical evaluation of new approaches in dry eye research. Ace Therapeutics develops customized animal models of DED to support preclinical efficacy studies, including disease characterization and therapeutic response assessment for innovative ophthalmic candidates.
DED is a multifactorial disorder of the ocular surface characterized by loss of tear film homeostasis driven by tear deficiency or excessive evaporation. Tear film instability and hyperosmolarity stress the lacrimal functional unit and meibomian glands, triggering innate and adaptive immune responses, cytokine release, goblet cell loss, and epithelial damage. These events sustain a chronic inflammatory vicious cycle that underlies both aqueous-deficient and evaporative DED and provides a mechanistic framework for experimental induction methods in preclinical in vivo DED models.
Fig. 1. Mechanisms of various experimental methods for induction of dry eye disease. (Rahman MM, et al., 2021)
Appropriate animal models of DED are critical tools for elucidating disease mechanisms and evaluating novel dry eye therapeutic candidates. No single animal model captures all key features of DED. Instead, diverse models are used to recapitulate specific aspects of tear film instability, aqueous deficiency, meibomian gland dysfunction (MGD), and chronic ocular-surface inflammation. Ace Therapeutics offers multiple animal models of DED, including scopolamine-induced models, benzalkonium chloride (BAC)–induced models, concanavalin A–induced models, and MGD-related models, providing flexible in vivo systems that can be aligned with the mechanistic focus and objectives of your preclinical dry eye studies.
For DED studies in animal models, key evaluations focus on changes in tear film, ocular surface integrity, and inflammation. At Ace Therapeutics, these commonly used endpoints can be incorporated into your preclinical dry eye projects as needed.
Schirmer test or phenol red thread test to quantify basal tear secretion and identify aqueous deficiency.
Tear breakup time (TBUT) to assess tear film instability and evaporative components of DED.
Fluorescein staining of the cornea and conjunctiva, scored with standardized grading scales to evaluate epithelial damage.
Selected cytokines and MMP-9 in tears or ocular tissues are quantified to evaluate ocular surface inflammation.
Building on the animal models of DED and evaluations described above, our scientific team can work with you to develop a fit-for-purpose DED model strategy aligned with your scientific objectives and stage of development. This includes discussing species selection, defining the most relevant disease mechanisms, and outlining practical study setups and readouts to support preclinical evaluation of drug candidate for dry eye disease in mechanism-relevant animal models.
Whether you are exploring new targets in DED, optimizing lead candidates, or expanding an existing preclinical program, Ace Therapeutics can provide mechanism-relevant animal models and ophthalmic evaluations to support your work. Our scientific team is available to discuss study concepts and model options tailored to your needs. Contact us to start a conversation about how we can support your next DED study!
References