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

Tyrosinase is the key rate-limiting enzyme in this pathway: it catalyzes the oxidation of tyrosine into DOPA and then DOPAquinone, the mandatory entry steps of melanogenesis. Without over-activation of tyrosinase, there is no overproduction of melanin.

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 inhibits 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 ensures firmness, density and resistance to deformation. Other key structural collagens include:

This protection of the collagen network stems from a coherent 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 → a brake on neosynthesis. By reducing them, 1-LGVTY halts the catabolic runaway.

Reduction of oxidative stress (↓ ROS)

ROS are the direct trigger for:

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

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) interacts directly with:

• fibroblasts, through its primary receptor CD44, which enables their binding to hyaluronic acid;
• collagen fibers, which hyaluronic acid partly organizes through its CD44-mediated anchoring to fibroblasts;
• elastin fibers, whose structuring hyaluronic acid supports in connection with the CD44-dependent activity of fibroblasts;
• proteoglycans, with which hyaluronic acid forms matrix complexes, stabilized by HA–CD44 interactions.

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

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

1. a loss of deep hydration,
2. a decrease in cellular cohesion,
3. a reduction in fibroblast activity,
4. a sagging of the dermis.