Rapid and effective skin barrier repair in atopic dermatitis with a novel emollient plus combining biomimetic lipids and actives to restore the hydrolipidic film, the stratum corneum and tight junctions

Atopic dermatitis (AD) affects millions worldwide and markedly impairs quality of life. AD is characterized by genetically determined and inflammation-driven skin barrier dysfunction. Barrier impairment increases transepidermal water loss (TEWL), xerosis, pruritus and scratching, and facilitates the penetration of allergens, pathogens and irritants, thereby promoting type 2 inflammation.

Beyond the long-described ceramide deficiency in AD, recent lipidomic profiling of atopic skin has shown reduced levels of additional lipids originating from both sebum and the stratum corneum¹. In addition, tight junctions in the stratum granulosum are impaired in AD, facilitating allergen and irritant penetration; with reduced claudin-1 expression being inversely correlated with type 2 inflammation².

We therefore assessed two combinations of ingredients designed to reinforce barrier function, as well as a novel emollient balm for AD (AD balm) incorporating these actives.

1. Cavallo A, et al. Exp Dermatol. 2024 Mar;33(3):e15066.
2. De Benedetto A, et al. J Allergy Clin Immunol. 2011 Mar;127(3):773-86.e1-7.

Active ingredients were assessed in atopic-like models. First, a lipid blend reflecting lipids reduced in AD (fatty acids C12:0, C14:0, C16:0, C18:0, C18:1, C18:2, C20:1, C22:1; fatty alcohol FOHC22:0; wax esters C40:2, C42:2; squalane; ceramides N18P18 and A18P18; and phytosphingosine) was evaluated for stratum corneum strengthening via: i) filaggrin and loricrin synthesis in IL-4/IL-5/IL-13/IL-22/IL-31-treated normal human skin explants (immunostaining); and ii) long-chain ceramide synthesis in stripped human skin explants (LC-MS). Second, a duo of biomimetic ingredients (an amino acid and glycosphingolipids) was evaluated for tight junction reinforcement via claudin-1 synthesis in IL-1β/IL-33/histamine-treated human primary keratinocytes.

Clinical performance of the AD balm was evaluated in adults with moderate AD (SCORAD 25–50) in a comparative, double-blind study. Participants applied either AD balm (AD balm group, n=20) or a glycerin-containing cream (GC group; n=23) to face and body 1–2 times daily for 37 days; hygiene was standardized using a shower oil. Barrier function was assessed at day 8 (D8) and day 37 (D37) by measuring TEWL on non-lesional areas (forearm or leg). Tolerance was assessed by both patients and dermatologists.

On skin explants, the biomimetic lipid blend significantly increased filaggrin (+22%), loricrin (+180%), and NP and NS long-chain ceramides (both +51%). On 2D-keratinocytes, the duo of biomimetic actives synergistically increased claudin-1 (+250%) versus atopic-like controls.

Clinically, TEWL decreased significantly in the AD balm group from D8 (−29%, p<0.001) and further to D37 (−38%, p<0.001). In the GC group, TEWL only decreased significantly on D37 (−9%, p<0.05). At both time points, barrier improvement was significantly greater with AD balm than with GC (p<0.05). AD balm was very well tolerated, including on lesional areas when used alongside topical corticosteroids.

Replenishing with lipids reduced in AD and biologically supporting both the stratum corneum and tight junctions in the stratum granulosum, this novel emollient balm robustly improved skin barrier function in adults with moderate AD from 8 days of use. These effects may help improve hydration and provide sustained protection against penetration of flare triggers such as allergens and irritants.