LCKLSL

the 5 μg/ml concentration exhibited the strongest inhibitory effect with only 1.8% RNV area (Figure 1A, C, and D).

the 2.5 μg/ml group showed 5.8% RNV area (Figure 1A, C, and D).

the 1.25 μg/ml group demonstrated 6.28% RNV area (Figure 1A, C, and D).

Maximal HUVEC metabolic activity was observed under 24-h hypoxic induction, with subsequent dose-response analysis identifying 10 μM LCKLSL as the optimal concentration for significant anti-proliferative effects (Figure 4A and B).

TUNEL assays revealed comparable apoptotic rates between LCKLSL-treated and control group (p>0.05) (Figure 4C and D), confirming the non-cytotoxic profile of LCKLSL within the experimental dose range.

wound healing assays demonstrated that LCKLSL significantly suppressed hypoxia-induced endothelial cell migration capacity (Figure 5)

tube formation assays showed significant suppression of capillary-like network complexity (Figure 6)

transwell invasion assays showed reduction in cellular invasiveness (Figure 6)

10 μM LCKLSL treatment significantly suppressed surface tPA binding in HRMECs under stimulation of hypoxia (1% O2) and VEGF (20 ng/ml) (Figure 9B)

Quantitative analysis demonstrated equivalent retinal thickness measurements between treatment and control groups (p>0.05) (Figure 2C).

ERG recordings... revealed transient reductions in a-wave and b-wave amplitudes on day 3 post-intervention. However, these functional changes showed no statistical significance (p>0.05) (Figure 2D, E, and F).

ERG recordings... revealed transient reductions in a-wave and b-wave amplitudes on day 3 post-intervention. However, these functional changes showed no statistical significance (p>0.05) (Figure 2D, E, and F).

Systemic safety assessment confirmed... no significant abnormalities in body weight in LCKLSL peptide-administered mice (Figure 3).