Science

Introduction

 

NIA10 with N-Acetyl Glucosamine contains a 10% concentration of niacinamide (one of the two major forms of vitamin B3).

 

Niacinamide is a biologically active form of niacin (vitamin B3). It is well tolerated by the skin in comparison to other common forms of this vitamin (e.g., nicotinic acid), which often induce uncomfortable skin flushing reactions.

 

Clinical evaluation of topical formulations containing niacinamide have shown several cosmetic benefits for skin, such as the reductions in hyperpigmentation, redness, and surface sebum.1

 

Mechanism

 

Hyperpigmentation is caused by melanogenesis, which is a complex process of melanin synthesis in melanosomes of melanocytes.

 

One of the interactions between keratinocytes and melanocytes regarding melanogenesis is the cytokine signaling pathway.

 

Studies reported that the UV-induced increase in interleukin-1α in the epidermis triggers the release of endothelin-1 from keratinocytes, stimulating melanin production in melanocytes.2

 

In addition to the cytokine signaling pathway, another important interaction between melanocytes and keratinocytes is the transfer of melanosomes from melanocytes to surrounding keratinocytes.

 

The modulation of protease-activated receptor 2 activation has been shown to affect melanosome transfer by interfering with keratinocyte phagocytosis, which changes pigment production and deposition.3-4 Data suggested that topical application of niacinamide downregulates melanogenesis and the number of melanosomes transferred.4 

 

Sebum is the thin film of lipids composed of triglycerides, diglycerides, fatty acids, wax esters, squalene, sterols, sterol esters, and phospholipids.5-6

 

It is secreted by the sebaceous glands, which are most numerous on the face, with a density of 400–800 glands/cm2 6-8

 

Possible functions of sebum include the regulation of transepidermal water loss; protection against sunburn; and delivery of antioxidants to the skin surface.9-10

 

However, excessive sebum on the face is responsible for both facial shine and the formation of comedonal and inflammatory acne lesions. Studies have shown that topical application of niacinamide decreases facial sebum production.11

 

It is theorized that niacinamide possibly changed the movement of sebum to the skin surface by altering the reservoir in the duct connecting the sebaceous gland to the skin surface at the follicular ostia.12

 

N-acetyl glucosamine (NAG) is a basic component of hyaluronic acid on the cell surface.13-15

 

Topical application of NAG stimulates the production of hyaluronic acid and subsequently hydrates and alleviates dry skin. It has also been reported to be effective in reducing the production of melanin in melanocytes via the inhibition of glycosylation, which is a required process in the conversion of inactive pro-tyrosinase to active tyrosinase.16-22

 

As a result, the combination of niacinamide and NAG could be more effective cosmetically. 

 

Formulator’s Notes

NIA10 with N-acetyl glucosamine contains a low concentration of salicylic acid, which helps breaking down follicular keratotic plugs and softening the top layer of skin cells whilst Zinc PCA in the product further reduces sebum secretion, hence limits bacterial proliferation. A combination of solvents is specifically used in the formulation to aid the penetration of the active ingredients deeper into the epidermis.

1. K., P., (2014). Cosmeceuticals and Cosmetic Practice. 1st ed. Wiley.
2. Imokawa G, Yada Y, Miyagishi M. Endothelin-1 as a new melanogen: coordinated expression of its gene and the tyrosinase gene in UVB-exposed human epidermis. J Invest Dermatol 1995; 105: 32–7.
3. Seiberg M, Paine C, Sharlow E et al. The protease-activated receptor-2 regulates pigmentation via keratinocyte–melanocyte interactions. Exp Cell Res 2000; 254: 25–32.
4. Seiberg M, Paine C, Sharlow E et al. Inhibition of melanosome transfer results in skin lightening. J Invest Dermatol 2000; 115: 162–7.
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6. Strauss JS, Pochi PE. Handbuch der Haut – unt Geschlechtskrankheiten; Normale und Pathologische Anatomie der Haut I. In: Gans O, Steigleder GK, editor. Berlin: Springer-Verlag; 1999. p. 184. 3.
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17. Imokawa G. Analysis of initial melanogenesis including tyrosinase transfer and melanosome differentiation through interrupted melanization by glutathione. J Invest Dermatol 1989; 93: 101–7.
18. Imokawa G, Mishima Y. Importance of glycoproteins in the initiation of melanogenesis: an electron microscopic study of B-16 melanoma cells after release from inhibition of glycosylation. J Invest Dermatol 1986; 87: 319–25.
19. Imokawa G, Mishima Y. Analysis of tyrosinases as asparagines-linked oligosaccharides by concanavalin A lectin chromatography: appearance of new segment of tyrosinases in melanoma cells following interrupted melanogenesis induced by glycosylation inhibitors. J Invest Dermatol 1985; 85: 165–8.
20. Imokawa G, Mishima Y. Functional analysis of tyrosinase isozymes of cultured malignant melanoma cells during the recovery period following interrupted melanogenesis induced by glycosylation inhibitors. J Invest Dermatol 1984; 83: 196–201.
21. Mishima Y, Imokawa G. Selective aberration and pigment loss in melanosomes of malignant melanoma cells in vitro by glycosylation inhibitors: premelanosomes as glycoprotein. J Invest Dermatol 1983; 81: 106–14.
22. Imokawa G, Mishima Y. Loss of melanogenic properties in tyrosinases induced by glycosylation inhibitors within malignant melanoma cells. Cancer Res 1982; 42: 1994– 2002.