A single drop of latanoprost in beagle dogs results in significant miosis, anterior bowing of the peripheral iris, narrowing of the iridocorneal angle, and shallowing of the anterior chamber. Subsequent measurements show reductions in pupil diameter, anterior chamber angle (ACA), and angle opening distance (AOD) by 84%, 14%, and 16%, respectively^[2].

Benzalkonium chloride latanoprost (BAK-latanoprost) and 0.02% BAK significantly trigger apoptosis in the apical layers, correlating with a notable decrease in cell viability. Conversely, preservative-free latanoprost (PF-latanoprost) slightly reduces cell viability, with only a few apoptotic cells observed in the superficial layers, not reaching statistical significance when compared with PBS^[1].

At a concentration of 0.1 μM, latanoprost significantly enhances cell viability compared to the control. Similarly, 0.1 μM latanoprost noticeably promotes neurite outgrowth, comparable to the effects of ciliary neurotrophic factor (CNTF), and elevates the levels of p-Akt and p-mTOR expression. Latanoprost facilitates neurite extension via FP receptor-mediated modulation of the PI3K-Akt-mTOR signaling pathway^[3].

Latanoprost at concentrations of 0.03 or 0.3 μg/mL, along with bimatoprost, increases MMP-9 activity by 75% ± 27% and 75% ± 24%, respectively, in human CBSM cells^[4].