Corneal toxicity of Xalatan is most probably caused by BAC. Monoprost delays corneal healing, which is not well understood. The Monoprost effects could be caused by its additive, macrogolglycerolhydroxystearate 40. This excipient is a known skin irritant, and its concentration is relatively elevated in Monoprost, 50 mg/mL, compared with its active ingredient, latanoprost (0.05 mg/mL).

Vismed Multi® application resulted in rapid corneal healing. Whether the toxicity seen for Optive® in one cornea is a valid result should be examined further. Cationorm® showed considerable corneal toxicity that could be caused by its additive, cetalkonium chloride. Otherwise, the electrostatic properties of Cationorm® led to a drug film on the area of epithelial loss that could hinder epithelial cell migration and adhesion in order to heal the lesion.

Purpose This study examined the impact of anti‐glaucoma medications and their additives on the corneal healing process and corneal toxicity. Methods BAK‐free PG analogues (Lumigan UD, Monoprost, Taflotan Sine), soft preserved Travatan BAK free, as well as polyquaternium‐1 (0.001%) and Macrogolglycerolhydroxystearate 40 (5%) were tested regarding corneal irritability and effect on corneal healing against HYLO COMOD (1 mg/mL sodium hyaluronate) as positive and 0.02% benzalkonium chloride (BAK) as negative control. Formulas were applied over three days, six times daily on rabbit corneas cultured on an artificial anterior chamber the Ex Vivo Eye Irritation Test (EVEIT) system. Initially, four corneal abrasions (2.5–4.5 mm2) were induced. All defects were monitored by fluorescein stains and photographs. Results For BAK, the corneal erosion size increased from 14.16 mm² to 88.89 mm². A delay of corneal healing is evident for Monoprost (14.84 mm² to 9.45 mm²) and Macrogolglycerolhydroxystearate 40 (11.58 mm² to 1.56 mm²) in comparison to a complete healing for HYLO COMOD, Lumigan, Taflotan Sine, Travatan and polyquaternium‐1®. For both Monoprost and macrogolglycerolhydroxystearate 40, a bright opaque halo around the remaining erosion area could be noticed. Histology revealed severe alterations of the superficia stroma. Cornea tested without erosions show no corneal toxicity of macrogol 4000. Conclusion Macrogolglycerolhydroxystearate 40, an additive found in Monoprost® shows corneal toxicity solely in case of corneal erosions. This excipient is a known skin irritant. Therefore, the use of Monoprost® in patients with epithelial defects should be questioned. Commercial interest

Purpose Evaluation of the impact of lubricant eye drops on the corneal healing process and corneal toxicity. Methods Optive and Cationorm were tested regarding corneal irritability and effect on corneal healing against Vismed and 0.01% benzalkonium chloride (BAK) as negative and positive control. Formulas were applied hourly over 3 days on rabbit corneas cultured on artificial anterior chambers (Ex‐Vivo Eye Irritation Test (EVEIT) system). Five corneae were used for each substance except for BAK (n=1). Initially, four corneal abrasions (2 ‐ 5.4 mm²) were induced. All defects were monitored by fluorescein stains and photographes. Results Optive and Vismed showed a complete corneal healing on day 2. In one cornea (Optive) erosion reoccurred on day 3. Erosion sizes of Cationorm treated corneae increased significantly from 12.20 mm² to a subtotal erosion of 51.89 mm² on day 3. Histology revealed epithelial loss and severe alterations of the superficial stroma for Cationorm. Glucose and lactate concentrations were about unchanged after application of Optive and Vismed. In contrast, Cationorm and BAK treated cornea showed a significant increase in lactate concentrations. Conclusion Vismed application led to a rapid corneal healing. Whether the toxicity seen for Optive in one cornea is a valid result should be examined in a long term application study. Cationorm shows considerable corneal toxicity that could be caused by its additive, cetalkonium chloride. Otherwise, Cationorms electrostatic properties lead to a drug film on the area of epithelial loss that could hinders epithelial cell migration and adhesion to heal the lesion. Commercial interest