INTRODUCTION
Melasma is a common, acquired disorder of skin hyperpigmentation that characteristically presents with symmetric brown macules and patches on the cheeks, forehead, and chin. The highest prevalence is seen in middle-aged females with Fitzpatrick skin types (FST) III-VI, although all racial/ethnic groups can be affected.1-3
The pathogenesis of melasma is multifactorial, with sun exposure, hormonal influences, thyroid disease, and family history, among other factors, leading to alterations in gene expression and molecular signaling within the skin.2-6 This ultimately results in increased melanogenesis, and in some cases melanocytosis, at sites of greater sun exposure and the development of characteristic hyperpigmentation of the skin due to excessive epidermal and dermal melanin deposition.7,8
Successful treatment of melasma often necessitates a multi-modality approach that combines one or more topical agent(s), sun avoidance, and broad-spectrum photoprotection. Procedural treatments including chemical peels and laser/light therapy and treatment with oral tranexamic acid can be considered in refractory cases.9 Hydroquinone (HQ) and Triple Combination Cream containing a retinoid, topical corticosteroid, and HQ (eg, tretinoin 0.05%, fluocinolone acetonide 0.01%, HQ 4%) are currently the gold standard therapies for melasma due to their proven efficacy.9,10 However, their use long-term is limited by potential side effects including exogenous ochronosis (HQ), skin atrophy (corticosteroids), telangiectasias (corticosteroids), irritation and allergic contact dermatitis (HQ, retinoids). Given the chronicity of melasma and its tendency to recur upon cessation of treatment, HQ-free topical therapies are needed for optimal control of the disease.
A HQ-free, retinol-free cosmetic topical brightener (CTB) containing tranexamic acid, phenylethyl resorcinol, niacinamide, and tetrapeptide-30 has been shown to target various melanogenesis pathways, resulting in a more even skin tone and reduced appearance of facial hyperpigmentation in several clinical studies.11-13 In vitro studies of this skin lightening agent using a human tissue model have demonstrated downregulation of micropathalmia transcription factor (MITF), a key regulator of melanocyte activation and melanin production, as well as downstream melanin-synthesizing genes tyrosinase (TYR), tyrosinase-related protein 1 (TYRP1) and DOPAchrome tautomerase (DCT).11 Overall, application of 2 μL of CTB to normal human-derived epidermal keratinocytes and melanocytes was associated with an average melanin
The pathogenesis of melasma is multifactorial, with sun exposure, hormonal influences, thyroid disease, and family history, among other factors, leading to alterations in gene expression and molecular signaling within the skin.2-6 This ultimately results in increased melanogenesis, and in some cases melanocytosis, at sites of greater sun exposure and the development of characteristic hyperpigmentation of the skin due to excessive epidermal and dermal melanin deposition.7,8
Successful treatment of melasma often necessitates a multi-modality approach that combines one or more topical agent(s), sun avoidance, and broad-spectrum photoprotection. Procedural treatments including chemical peels and laser/light therapy and treatment with oral tranexamic acid can be considered in refractory cases.9 Hydroquinone (HQ) and Triple Combination Cream containing a retinoid, topical corticosteroid, and HQ (eg, tretinoin 0.05%, fluocinolone acetonide 0.01%, HQ 4%) are currently the gold standard therapies for melasma due to their proven efficacy.9,10 However, their use long-term is limited by potential side effects including exogenous ochronosis (HQ), skin atrophy (corticosteroids), telangiectasias (corticosteroids), irritation and allergic contact dermatitis (HQ, retinoids). Given the chronicity of melasma and its tendency to recur upon cessation of treatment, HQ-free topical therapies are needed for optimal control of the disease.
A HQ-free, retinol-free cosmetic topical brightener (CTB) containing tranexamic acid, phenylethyl resorcinol, niacinamide, and tetrapeptide-30 has been shown to target various melanogenesis pathways, resulting in a more even skin tone and reduced appearance of facial hyperpigmentation in several clinical studies.11-13 In vitro studies of this skin lightening agent using a human tissue model have demonstrated downregulation of micropathalmia transcription factor (MITF), a key regulator of melanocyte activation and melanin production, as well as downstream melanin-synthesizing genes tyrosinase (TYR), tyrosinase-related protein 1 (TYRP1) and DOPAchrome tautomerase (DCT).11 Overall, application of 2 μL of CTB to normal human-derived epidermal keratinocytes and melanocytes was associated with an average melanin
