Mechanistic Insights Backed by Molecular Evidence

Preclinical studies on the SMRTActiv™ platform demonstrate a robust ability to impact key biological pathways associated with the skin and barrier dysfunction.

Mechanistic Insights Backed by Molecular Evidence

Preclinical studies on the SMRTActiv™ platform demonstrate a robust ability to impact key biological pathways associated with the skin and barrier dysfunction.

Key Findings:

  • Barrier Reinforcement:
  • ↑ Expression of FLG (filaggrin), IVL (involucrin), LOR (loricrin) LCE (late cornified envelope), AQP3 and AQP9
  • ↑ Ceramide synthase expression and tight junction proteins
  • ↓ Transepidermal water loss (TEWL)
  • Inflammatory Regulation:
  • ↓ Pro-inflammatory mediators: IL-1B, TSLP, TRPA1, TRPV3
  • ↓ TNFα-induced cytokine release from human keratinocytes
  • ↓ LDH secretion (a biomarker for cell damage and Dupilumab non-response)
  • Microbiome Balance:
  • ↓ Staphylococcus aureus colonization
  • ↑ S. epidermidis and Cutibacterium acnes abundance
  • Normalizes skin pH
  • Mechanistic Equivalence to Calcineurin Inhibitors:
  • Preclinical markers show comparable results to prescription-grade topical therapies — without immunosuppression

These insights validate the unique ability of SMRTActiv™ to treat the root causes of atopic dermatitis — not just its symptoms.

Interrupting the Itch–Inflammation Cycle in AD

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Preclinical Data

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