Melanin is the pigment synthesized by melanocytes within melanosomes, then transferred to keratinocytes. It protects against UV… but it is also responsible for spots, PIH (Post-Inflammatory Hyperpigmentation), and uneven skin tone.

Tyrosinase is the key and rate-limiting enzyme of this pathway: it catalyzes the oxidation of tyrosine to DOPA and then DOPAquinone, obligatory entry steps of melanogenesis. Without tyrosinase overactivation, there is no melanin overproduction.

These results are accompanied by a decrease in biomarkers involved in inflammatory stress (IL-1α, IL-6), a reduction in oxidative stress (ROS), and better regulation of microbiological stress. Thus, the patented 1-LGVTY® technology acts on two levels:

1. It calms the inflammatory and oxidative signals that drive melanocytes to overproduce melanin.
2. It slows melanogenesis by reducing tyrosinase activity and melanin production.

Collagen, particularly type I collagen, is the major mechanical framework of the dermis: it represents ~80–85% of skin collagens and provides firmness, density, and resistance to deformation. Other key structural collagens include:

This protection of the collagen network results from a consistent mechanistic triptych:

Reduction of inflammation (↓ IL-1α, ↓ IL-6)

These cytokines normally activate:

• MMP-1, MMP-3, and MMP-9 → collagen fragmentation enzymes
• Inhibition of TGF-β1 → brake on neosynthesis. By reducing them, 1-LGVTY stops the catabolic spiral.

Reduction of oxidative stress (↓ ROS)

ROS are the direct trigger:

• of degradation of existing fibers,
• of activation of MMPs,
• of alteration of the extracellular matrix. The ability of 1-LGVTY® to reduce ROS in all skin compartments explains the observed structural preservation.

Restoration of fibroblast homeostasis

By lowering inflammatory and oxidative stress, fibroblasts are released from their "survival mode", which promotes:

• better expression of collagen I,
• normalization of collagen III and V synthesis,
• stabilization of collagen IV and the basement membrane (less micro-inflammation, better cohesion).

In our skin explant model subjected to combined UV + pollution stress, tissues treated with the patented 1-LGVTY® technology show a 98% stimulation of the CD44 receptor:

By preserving hyaluronic acid from fragmentation, maintaining optimal interactions with CD44, and controlling pro-inflammatory and oxidative environments, 1-LGVTY® restores a hydrated and functional extracellular matrix.

Hyaluronic acid (HA) directly interacts with:

• fibroblasts, through its main receptor CD44, which allows their binding to hyaluronic acid;
• collagen fibers, which HA partly organizes via its CD44-mediated anchorage to fibroblasts;
• elastin fibers, whose structuring HA supports in connection with CD44-dependent fibroblast activity;
• proteoglycans, with which HA forms matrix complexes, stabilized by HA–CD44 interactions.

These interactions are made possible by the CD44 receptor, a central player in hyaluronic acid signaling and anchoring, essential for skin stimulation, migration, and remodeling.

With aging, its synthesis decreases, its enzymatic degradation increases (via hyaluronidases), and its molecular quality fragments, leading to:

1. loss of deep hydration,
2. reduced cell cohesion,
3. decreased fibroblast activity,
4. dermal sagging.