Efficacy and Tolerability of a Cosmetic Skin Care Product With Trans-4-t-butylcyclohexanol and Licochalcone A in Subjects With Sensitive Skin Prone to Redness and Rosacea

June 2017 | Volume 16 | Issue 6 | Original Article | 605 | Copyright © June 2017

Zorica Jovanovic PhD,a Nariman Angabini MD,b Sonja Ehlen MD,c Zrinka Bukvic Mokos MD,d Milica Subotic MD,e and Gitta Neufang PhDa

aMedical Management, Beiersdorf AG, Hamburg, Germany bHautärzte-Team Duisburg, Duisburg, Germany cHautarztpraxis im Vorderen Westen, Kassel, Germany dDepartment of Dermatology and Venerology, School of Medicine University of Zagreb, Zagreb, Croatia eDepartment of Dermatology and Venerology, Clinical Centre Vojvodina, Novi Sad, Serbia


BACKGROUND: Sensitive skin and rosacea are skin conditions, which may affect the quality of life of the patients considerably. In vitro and in vivo data indicated that the combination of trans-t-butylcyclohexanol and licochalcone A is an effective combination for alleviating the increased sensitivity of rosacea subtype I.

OBJECTIVE: Objective of this open dermocosmetic study was to investigate the efficacy and tolerability of a skin care product containing the anti-inflammatory licochalcone A and the TRPV1 antagonist trans-t-butylcyclohexanol in subjects with sensitive skin prone to redness and rosacea.

METHODS: 1221 subjects with sensitive skin and rosacea stage 0-II applied the test product twice daily for 4 weeks. Clinical assessment of sensitive skin and rosacea symptoms were performed at baseline and after 4 weeks. Additionally, at treatment end the test subjects filled a self-assessment questionnaire.

RESULTS: After 4 weeks of application, both, clinical and subjective assessment have shown improvement of all symptoms of sensitive skin and rosacea in a significant number of subjects (P less than 0.001). The test product was efficacious and very well tolerated also when used in conjunction with pharmacological treatments of the skin condition under scrutiny.

Conclusions: The study confirmed the good tolerability and efficacy of the skin care product in the management of sensitive skin prone to redness and rosacea when used alone or in combination with other therapies.

J Drugs Dermatol. 2017;16(6):605-611.


Sensitive skin, which affects over 50% of adults1-3 started to become subject of scientific interest during the second half of the last century.4 Its pathophysiology is not yet fully understood.5 It has been observed that not only physical (UV, heat, cold, and wind), but also chemical (cosmetics, soaps, water, and pollutants), and sometimes psychological (stress) or hormonal (menstrual cycle) factors can trigger the typical sensitive skin sensations of stinging, burning, pain, pruritus, and tingling.6 Therefore, following possibly interrelated potential pathomechanisms have been discussed so far for sensitive skin:Disrupted epidermal barrier function, leading to increased skin permeability for irritants, increased transepidermal water loss (TEWL) and decreased protection of nerve endings.5,7-9 Functional hyperreactivity of cutaneous nerves equipped with sensory neuroreceptors such as endothelin and transient receptor potential (TRP) channels. The fact that these receptors are located also on keratinocytes is supporting the hypothesis for their role in sensitive skin.10-12 TRP channels are possibly even more relevant being the only proteins that can be activated by the several kinds of triggers of sensitive skin.13,14 In the skin, TRPV1 is known to mediate sensation of pain, itch, warmth, and afferent functions to chemical stimuli.5 In keratinocytes stimulation of TRPV1 results in increased Ca2+-influx, which induces finally cell death and disruption of the epidermal barrier.5,15 Immune responses and progression of inflammation are possibly also involved in the pathophysiology of sensitive skin, with the TRPV1 playing a critical role also in this case.5 This is indicated by the fact that blocking of TRPV1 signalling in T cells reduces the secretion of proinflammatory cytokines such as interleukin 2 (IL-2), interferon gamma (IFN-γ) and tumour necrosis factor alpha (TNFα).16 Activation of TRPV1 leads to release of substance P, which on its