ratings depict escalating improvement from week 2 to 16 in skin
dyspigmentation, including skin lightening, pigmentation, and
evenness. The ratings at week 2 showed statistically significant
improvements in skin pigmentation and tone. By weeks 8
through 16, panelists experienced significant improvement
in skin pigmentation. By week 16, panelists also reported
significant improvements in skin evenness. When viewed
in conjunction with the expert grading and colorimetry data,
subjects reported a positive perception of product performance.
DISCUSSION
The cell-targeted skin brightening test product’s multi-modal technologies included the following:
• Cell-targeted “Drone†Encapsulate: the encapsulate technology is chemically engineered with multiple Palmitoyl sh-Tripeptide-5 Norisoleucyl sh-Nonapeptide-1 surface ligand peptides that solely target the melanocyte MC1 receptors to suppress melanogenesis. Once bound to the MC1 receptors, the encapsulate enters the cell by endocytosis and is metabolized in the cytoplasm where the encapsulate then releases a secondary peptide, Palmitoyl sh-Octapeptide-24 Amide, that antagonistically inhibits tyrosinase gene expression inside the melanocyte cell to restrict the biochemical pathway of melanogenesis.4
• Tranexamic acid: UV radiation induces the synthesis of plasminogen activator within keratinocytes. Plasminogen activator increases plasmin activity in keratinocytes, which in turn releases Arachidonic acid. Free Arachidonic acid stimulates pigment-producing cells, resulting in increased pigment synthesis. Tranexamic acid acts as a plasmin inhibitor, depleting the keratinocyte pool of Arachidonic acid to prevent excess pigment production.5
• Niacinamide: downregulates melanin transfer from the melanocyte dendrites to the skin surface keratinocytes cells to mitigate visible pigmentary accumulation at the upper skin surface.6 Niacinamide also functions as an anti-inflammatory to prevent the onset of inflammatory induced new pigment formation.
• Diglucosyl Gallic Acid: inhibits the Microphthalmiaassociated transcription factor (MITF) transcription factor involved in the melanin synthesis pathway.7
The investigator noted significant improvement in skin brightening and reduction of existing pigmentation by week 2. By week 8, significant improvement in brightening of pigmentation and skin evenness were noted. By weeks 12 and 16, increasing levels of significant improvement in both brightening and evenness were noted among the study subjects. The instrumental colorimetry data indicated a trend of improvement in reducing visible pigmentation. Combined with the gradually improving subject self-assessments reporting reduced pigmentation, less unevenness of skin complexion, and lightening of skin pigmentation, this research demonstrates the possible value of a cell-targeted dyspigmentation treatment modality.
• Cell-targeted “Drone†Encapsulate: the encapsulate technology is chemically engineered with multiple Palmitoyl sh-Tripeptide-5 Norisoleucyl sh-Nonapeptide-1 surface ligand peptides that solely target the melanocyte MC1 receptors to suppress melanogenesis. Once bound to the MC1 receptors, the encapsulate enters the cell by endocytosis and is metabolized in the cytoplasm where the encapsulate then releases a secondary peptide, Palmitoyl sh-Octapeptide-24 Amide, that antagonistically inhibits tyrosinase gene expression inside the melanocyte cell to restrict the biochemical pathway of melanogenesis.4
• Tranexamic acid: UV radiation induces the synthesis of plasminogen activator within keratinocytes. Plasminogen activator increases plasmin activity in keratinocytes, which in turn releases Arachidonic acid. Free Arachidonic acid stimulates pigment-producing cells, resulting in increased pigment synthesis. Tranexamic acid acts as a plasmin inhibitor, depleting the keratinocyte pool of Arachidonic acid to prevent excess pigment production.5
• Niacinamide: downregulates melanin transfer from the melanocyte dendrites to the skin surface keratinocytes cells to mitigate visible pigmentary accumulation at the upper skin surface.6 Niacinamide also functions as an anti-inflammatory to prevent the onset of inflammatory induced new pigment formation.
• Diglucosyl Gallic Acid: inhibits the Microphthalmiaassociated transcription factor (MITF) transcription factor involved in the melanin synthesis pathway.7
The investigator noted significant improvement in skin brightening and reduction of existing pigmentation by week 2. By week 8, significant improvement in brightening of pigmentation and skin evenness were noted. By weeks 12 and 16, increasing levels of significant improvement in both brightening and evenness were noted among the study subjects. The instrumental colorimetry data indicated a trend of improvement in reducing visible pigmentation. Combined with the gradually improving subject self-assessments reporting reduced pigmentation, less unevenness of skin complexion, and lightening of skin pigmentation, this research demonstrates the possible value of a cell-targeted dyspigmentation treatment modality.
CONCLUSION
Based on expert grading and subject self-assessment, the study
technology resulted in highly significant skin dyspigmentation
improvement. When correlated with the perceptible colorimetry
ΔE differences, the study product demonstrated the ability
to provide a safe and effective modality for facial skin
dyspigmentation improvement.
DISCLOSURES
Zoe Diana Draelos, MD, received funding from ZO Skin Health
to conduct the research detailed in this manuscript. Frederick
Woodin is an employee of ZO Skin Health.
REFERENCES
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2. Vachiramon V. Pigmentary changes associated with skin aging. The Dermatologist. 2011;19(11):n.p.
3. Mokrzycki WS, Tatol M, Color difference ΔE – A survey. Machine Graphic & Vision. 2012; 08(10):1-28.
4. Infinitec Activos S.L., X50 PureWhite: The Cosmetic DroneTM for Whitening. 2017:1-33.
5. Tse T W, Hui E, Tranexamic acid: an important adjuvant in the treatment of melasma. J Cosmet Dermatol. 2013;12(1):57-66.
6. Hakozaki T, Minwalla L, Zhuang J, Chhoa M, Matsubara A, Miyamoto K, Greatens A, Hillebrand GG, Bissett DL, Boissy RE. The effect of niacinamide on reducing cutaneous pigmentation and suppression of melanosome transfer, Br J Dermatol. 2002;147(1):2-31.
7. Su TR, Lin JJ, Tsai CC, Huang TK, Yank ZH, Wu MO, Zheng YQ, Su CC, Wu YJ. Inhibition of melanogenesis by gallic acid: Possible involvement of the PI3K/ Akt, MEK/ERK and Wnt/β-catenin signaling pathways in B16F10 cells. Int J Mol Sc. 2013; 14(10):20443-20458.
2. Vachiramon V. Pigmentary changes associated with skin aging. The Dermatologist. 2011;19(11):n.p.
3. Mokrzycki WS, Tatol M, Color difference ΔE – A survey. Machine Graphic & Vision. 2012; 08(10):1-28.
4. Infinitec Activos S.L., X50 PureWhite: The Cosmetic DroneTM for Whitening. 2017:1-33.
5. Tse T W, Hui E, Tranexamic acid: an important adjuvant in the treatment of melasma. J Cosmet Dermatol. 2013;12(1):57-66.
6. Hakozaki T, Minwalla L, Zhuang J, Chhoa M, Matsubara A, Miyamoto K, Greatens A, Hillebrand GG, Bissett DL, Boissy RE. The effect of niacinamide on reducing cutaneous pigmentation and suppression of melanosome transfer, Br J Dermatol. 2002;147(1):2-31.
7. Su TR, Lin JJ, Tsai CC, Huang TK, Yank ZH, Wu MO, Zheng YQ, Su CC, Wu YJ. Inhibition of melanogenesis by gallic acid: Possible involvement of the PI3K/ Akt, MEK/ERK and Wnt/β-catenin signaling pathways in B16F10 cells. Int J Mol Sc. 2013; 14(10):20443-20458.
AUTHOR CORRESPONDENCE
Zoe Draelos MD zdraelos@northstate.net
