This natural sinergystic combination is a powerful anti-inflammatory, soothing and barrier enhancer product ideal for the care of atopic skins. Its regular use has demonstrated to reduce the frequency and intensity of the sprouts in more than 20 volunteers affected by atopic dermatitis and ezcema during the dermatological tests.

Mechanism of action
The active core consists on a combination of four plant extracts developed with our proprietary platforms SimDerma and INCOS. SCB-001 acts on key cellular and molecular targets associated to the atopic skin. First, preventing the activation of NF-κB in dermal cells and inhibiting T cell activation (Fig. 1). Second, activating PPARα receptor in keratinocytes (Fig. 2), which promotes the corneal envelope construction.  Third, antagonizing the TRPV1 receptor (Fig 3), blocking the itchiness and stinging. Last, protecting against oxidative stress as measured by Nrf2 inhibition in response to oxidative stress (Fig. 4). Moreover, hyaluronic acid provides an add-on benefit due to its hygroscopic properties reducing the transepidermal water loss and improving barrier function.

Figure Explanation
1 Figure 1. Anti-inflammatory effects of SCB-001 A) Triggering of T-cell response after stimulation of CD3/CD28 receptors (pink charts), in non-stimulated control cells (grey chart) and in CD3/CD28 stimulated cells in presence of SCB-001 at a dilution rate of 1/20 (green chart) measured by flow cytometry. B) Dose-dependent inhibition of TNFα-induced NF-κB activation by SCB-001.
Both, the decrease in T-cell and NF-κB activation, demonstrate the powerful anti-inflammatory activity of SCB-001.
2 Figure 2. Protective effect of SCB-001 against barrier disruption. A) Transepidermal electrical resistance in HaCaT cells after 24h cultured in absence or presence of 10 mM Caprilic acid (barrier disruptor) and several concentrations of SCB-001. B) SCB-001 activates the PPARα receptor in NIH-3T3 fibroblasts transfected with Gal4-DBD-PPARα/Gal4-Luc plasmids.
3 Figure 3. Soothing effect of SCB-001 is mediated by antagonizing the TRPV-1 channel expressed in sensory neurons. TRPV-1–expressing cells were loaded with Fura-2 and preincubated with SCB-001  1/10 (blue line), 1/20 (green line) or Capzasepine as a positive control of TRPV-1 antagonism cells (black line). Then the cells were subjected to capsaicin treatment and the calcium recorded during 100s. SCB-001 significantly inhibited TRPV-1 activation mediated by capsaicin.
4 Figure 4. Nrf2 inhibition in HaCaT-ARE-Luc cells. The cells were preincubated with increasing concentrations of SCB-001 or with N-Acetyl-L-Cysteine (antioxidant positive control) for 15 min and then treated with the prooxidant tert-butylhydroquinone (TBHQ), that activates the Nrf2 pathway, during 12 h. SCB-001 at 1/20 clearly showed inhibitoy activity thus reflecting its potent antioxidant activity.