EYE AREA CARE 117
disruption, while demonstrating efficacy across seven interconnected soft tissues and translating these effects into clinically visible improvements. Based on this rationale, a novel AI-designed
peptide was developed to attenuate PAR-1 activation and interrupt the Amplifying Release Cycle at its origin. By targeting a key upstream regulator of endothelial permeability and inflammation, this strategy aims to reduce microenvironmental flooding and its downstream consequences across multiple periocular soft tissues. Such an approach may provide a more comprehensive route to eye contour rejuvenation than conventional strategies focused on individual visible signs of ageing.
Results and methodology Artificial intelligence-assisted discovery was used as a tool to accelerate the identification of peptide sequences with potential interaction against biological targets involved in endothelial barrier function. Molecular modelling, receptor conformation analysis and virtual peptide screening enabled the selection of multiple candidate peptide sequences designed to modulate PAR-1 activity. These candidates were subsequently refined
through scientific expertise in cosmetic peptide discovery, prioritizing sequences with the best balance between biological activity, development feasibility and safety profile. The final candidate was then validated through functional cellular assays in endothelial cells to confirm its ability to modulate PAR-1 activation while ensuring optimal efficacy and safety. These studies demonstrated that the AI-designed peptide attenuated PAR-1 activation, as measured by calcium mobilization (data not shown). This antagonist-like activity provides a mechanistic rationale for the downstream effects subsequently observed in endothelial barrier models, supporting the reduction of vascular and lymphatic permeability and the broader biological effects later observed across multiple periocular soft tissues.
Biological activity across seven soft tissues The vascular network contributes to nutrient
A
160 140 120 100 80 60 40 20 0
Control ****
Figure 1. Mechanism of action of PAR-1 activation, endothelial permeability and Amplifying Release Cycle in the periocular microenvironment. PAR-1 activation increases vascular and lymphatic permeability, promoting leakage of haemoglobin, waste matter, cytokines, fluids and lipids into the eye contour microenvironment. This self-amplifying leakage–inflammation–tissue damage loop may progressively affect interconnected soft tissues, including the epidermis, dermis, adipose tissue, muscles and ligament-support structures
delivery, oxygenation and tissue homeostasis. During ageing, increased vascular permeability can facilitate the leakage of fluids, inflammatory mediators and haemoglobin-derived compounds into surrounding tissues, contributing to vascular dark circles and local microenvironment disruption. In a human vascular endothelial model, the AI- designed peptide significantly reduced endothelial permeability by approximately 52.7% compared with untreated control conditions (Figure 2). The lymphatic system complements vascular
function by clearing interstitial fluids, waste products and inflammatory mediators. Impaired lymphatic clearance is associated with fluid retention, edema and under-eye puffiness. In human dermal lymphatic endothelial cells, treatment reduced lymphatic permeability by approximately 19.9% (Figure 2), supporting improved fluid homeostasis and tissue drainage capacity.
B -52.7% ****
160 140 120 100 80 60 40 20 0
100ng/mL Interleukin-1β
0.2 mg/mL Caffeine
10 µg/mL Eyeseryl All-In peptide
Control * Together, these findings suggest that the
peptide acts at a key upstream level of the periocular microenvironment. By supporting endothelial cohesion and reducing both vascular and lymphatic permeability, it may help limit microenvironmental flooding and its downstream consequences, including inflammation, pigmentation changes, extracellular matrix degradation and tissue swelling.
Restoring the skin compartment: epidermis and dermis The eyelid epidermis contributes to barrier integrity, hydration and resistance to external stressors. In a 3D aged pigmented eyelid skin model built from eyelid-derived cells, the test peptide produced a dose-dependent increase in ceramide content. At 10 µg/mL, ceramide level increased to 764.8% of untreated control values (Figure 3), indicating strong reinforcement of the
*
-19.8%
100ng/mL Interleukin-1β
10 µg/mL Eyeseryl All-In peptide
Figure 2: Efficacy of the AI-designed peptide in reducing endothelial permeability in human vascular endothelial cells (A) and human lymphatic endothelial cells (B). Control corresponds to untreated cells. Statistical significance was determined using Student’s t-test (*p < 0.05; ****p < 0.0001)
www.personalcaremagazine.com October 2026 PERSONAL CARE MAGAZINE
Vascular permeability (%)
Vascular permeability (%)
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