Effect of a Tranexamic Acid, Kojic Acid, and Niacinamide Containing Serum on Facial Dyschromia: A Clinical Evaluation

May 2019 | Volume 18 | Issue 5 | Original Article | 454 | Copyright © May 2019

Seemal Desai MD,a,b Eloisa Ayres MD,c Hana Bak MD,d,e Megan Manco MS,f Stephen Lynch PhD,g Susana Raab MS,g Ana Du BS,g DesTenee Green BS,g Cezary Skobowiat PhD,g Janet Wangari-Talbot PhD,g Qian Zheng MD PhDg

aUniversity of Texas Southwestern Medical Center, Dallas, TX bInnovative Dermatology, Plano, TX cEZSkin Dermatologia, Niterói, Rio de Janeiro, Brazil dCheongdam-Hana Dermatology, Seoul, Korea eYonsei University Wonju College of Medicine, Wonju, Korea fSkinceuticals, New York, NY gL’Oréal Research and Innovation, Clark, NJ

Figure 2This in vitro study demonstrated that PGE2 stimulation is a reliable method for melanogenesis studies in normal human epidermal melanocytes. In this model, TXA dose dependently inhibited melanogenesis. The observation that TXA alone had no significant effect on melanogenesis also indicates that the mechanism of action of TXA involves blocking PGE2-induced melanin production in melanocytes.


It has been well established that TXA delivered orally or by injection is an effective approach in the treatment of melasma.However, only a limited number of studies have assessed the effectiveness of topical TXA on facial dyschromia. The objective of this study was to demonstrate the clinical efficacy of a novel topical facial serum containing 1% kojic acid, 5% niacinamide, and 3% TXA in improving key markers of discoloration. Kojicacid is a well-known skin-lightening agent that acts through inhibiting the rate limiting enzyme tyrosinase.10,11 It has been suggested that niacinamide suppresses melanin transfer from melanocytes to keratinocytes.13 Finally, we have established that TXA controls pigmentation by inhibiting the release of inflammatory mediators, specifically prostaglandins, which are involved in melanogenesis. Therefore, the combination of these three ingredients with distinct modes of action in an optimized hydroglycolic serum, synergistically target multiple biological pathways associated with the development of discoloration.After 12 weeks of topical product application, an average 81% reduction in PIH was reported while melasma and hyperpigmentationimproved by 60%. Marked improvements in skin tone and skin homogeneity were also observed, by 54% and 59%, respectively. The significant decrease in melanin index scores on melasma and PIH lesional skin compared to perilesional normal skin provides further evidence of product efficacy. In terms of perceived effectiveness, as measured by self-assessment questionnaires, questionnaires,subjects rated the topical serum highly favorable for both efficacy and aesthetics. Overall satisfaction with the serum was over 90% at all time points, which is promising considering the lack of satisfaction with non-prescription topical discoloration treatments.The role of PGE2 in the signaling pathways involved in growth, differentiation, and apoptosis of melanocytes has been well-established. 23 PGE2 is also released abundantly by keratinocytes following exposure to UV radiation (UVR).23,24 Keratinocyte-derived PGE2 stimulates the formation of dendrites in melanocytes and activates melanocyte and tyrosinase activity. TXA inhibitsPG production, and thus reduces the melanocyte tyrosinase activity. 14 We demonstrated that 50-100 μM TXA suppressed themelanogenesis of PGE2-stimulated melanocytes in culture. This function of TXA is particularly relevant in the treatment of melasma,hyperpigmentation, and PIH.In conclusion, this study demonstrates that a novel topical facial serum containing 3% TXA, 1% kojic acid, and 5% niacinamide,is a safe and effective treatment for melasma, hyperpigmentation, and PIH. In addition, TXA’s mechanism of action has beenfurther clarified by an in vitro study showing the suppression of PGE2-induced inflammation in normal human epidermal melanocytes.


Dr. Desai, Dr. Ayres, and Dr. Bak have served as consultants to SkinCeuticals. Stephen Lynch, Susana Raab, Ana Du, DesTeneeGreen, Janet Wangari-Talbot, and Qian Zheng are employed by L'Oreal Research and Innovation. Cezary Skobowiat was employedby L'Oreal Research and Innovation at the time of this work. Megan Manco was employed by SkinCeuticals at the time of this work.


The authors would like to thank Kumar Pillai, PhD for his critical review and editorial assistance with this manuscript.


1. Victor FC1, Gelber J, Rao B, Melasma: a review. J Cutan Med Surg. 2004;8(2):97-1022. Grimes PE. Melasma: etiologic and therapeutic considerations. Arch Dermatol. 1995;131:1453-7.3. Miot LD, Miot HA, Silva MG, Marques ME. Physiopathology of melasma. An Bras Dermatol. 2009;84(6):623-35.4. Perper M, Eber AE, Fayne R, Verne SH, Magno RJ, Cervantes J, ALharbi M, ALOmair I, Alfuraih A, Nouri K. Tranexamic acid in the treatment of melasma: a review of the literature. Am J Clin Dermatol. 2017;18(3):373-381.5. Taraz M, Niknam S, Ehsani AH. Tranexamic acid in treatment of melasma: A comprehensive review of clinical studies. Dermatol Ther. 2017;30(3).6. Molinar VE, Taylor SC, Pandya AG. What's new in objective assessment and treatment of facial hyperpigmentation? Dermatol Clin. 2014;32(2):123-35.7. Sofen B, Prado G, Emer J., Melasma and postinflammatory hyperpigmentation: management update and expert opinion. Skin Therapy Lett. 2016;21(1):1-7.8. Ikino JK, Nunes DH, Silva VP, Frode TS, Sens MM. Melasma and assessment of the quality of life in Brazilian women. An Bras Dermatol. 2015;90(2):196– 200.