Key Findings
These findings support the ability of SMRTActiv™ to target key biological drivers of atopic dermatitis — extending beyond symptom-focused care.
Barrier Integrity
Regulating barrier-related lipid structure, genes, and proteins, including filaggrin (FLG), loricrin (LOR), involucrin (IVL), aquaporins (AQP3 and AQP9), and ceramide synthase (CERS3).
Also, supports expression of key cell–cell junction proteins essential for barrier cohesion.
↓ Reduced transepidermal water loss (TEWL)
Inflammation Modulation
↓ Reduced expression of pro-inflammatory mediators (IL-1β, TSLP, TRPA1, TRPV3)
↓ Decreased TNFα-induced cytokine release from human keratinocytes
↓ Repressed interferon-driven inflammatory gene networks (STAT1-57 module)
↓ Lower LDH secretion (biomarker of cellular stress)
Microbiome Rebalancing
↓ Reduced Staphylococcus aureus colonization
↑ Increased abundance of commensal skin flora (S. epidermidis, C. acnes)
Normalization of skin surface pH
Mechanistic Benchmarking
Preclinical markers demonstrate mechanistic alignment with prescription-grade topical therapies without immunosuppressive signaling
Interrupting the Itch– Inflammation Cycle in AD
Clinical Insights. Real Solutions.
Engage with our team to explore the science behind CuralysMD™ and how our platform redefines eczema care through clinically validated barrier-first dermatology.
