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PEPTIDES 25


further, by 12% at three days and 22% at five days. Interestingly, other common skin actives


had different effects. RA showed little impact on collagen deposition, while HA increased total collagen by 10%—but only after five days, not at three—demonstrating how the bioactive peptide acts more consistently over time. Looking at Type I collagen specifically,


researchers found that higher doses of the bioactive peptide (1.0–2.0 mg/mL) increased the area of extracellular collagen per cell by 1.4–1.6 times, while lower doses had minimal effect. These findings suggest that the bioactive peptide not only promotes collagen secretion but also enhances the structural remodeling of the skin’s collagen network, setting it apart from traditional skin care compounds.


Bioactive peptide does not trigger fibrosis in skin cells While boosting collagen is key for healthy, youthful skin, it is important that this process does not inadvertently promote fibrosis — a condition where excessive collagen leads to stiff, scar-like tissue. Encouragingly, studies show that the bioactive peptide increases collagen without triggering fibrotic responses in dermal fibroblasts. Researchers measured levels of αSMA, a


protein and gene marker associated with fibrosis, after treatment with the bioactive peptide. Across all tested doses and up to 120 hours, neither αSMA protein nor mRNA levels were significantly affected compared to untreated cells (Figures 5 and 6). For comparison, RA and HA had mixed effects:


RA initially reduced αSMA protein 2.4-fold at 72 hours but caused a 2.8-fold increase at 120 hours, while HA showed minimal change. As expected, TGFβ, a well-known inducer of fibrosis, dramatically increased αSMA protein from 3.2- to 12.4-fold over the same time frame and elevated αSMA and TGFβ mRNA 7.0- and 3.1-fold, respectively.


These findings demonstrate that the bioactive


peptide can safely stimulate collagen production without activating fibrosis pathways, highlighting its potential as a gentle yet effective skin care ingredient.


The bioactive peptide does not trigger inflammation in skin cells Healthy skin relies on a delicate balance of


Untreated


2.0 1.5 1.0 0.5 0.0


24h - No VC In Media *** ** * *


5.0 4.0 3.0 2.0 1.0 0.0


27P peptide (mg/mL)


Topical Figure 3: Pro-Collagen1A1 Secretion in Mattek 3D Skin Equivalent Model Untreated 10 ng/mL TGFβ 50 ng/mL VC 72h - With 50 µg/mL VC In Media ** * *


27P peptide (mg/mL)


Topical Topical


0.5 ng/mL 27P peptide


VC+0.5 ng/mL 27P peptide


Figure 4: Intracellular Col1A1 in 2D Dermal Fibroblasts


extracellular matrix (ECM) production and inflammatory signaling. To ensure that boosting collagen doesn’t come at the cost of inflammation, researchers tested the effects of the bioactive peptide on inflammatory markers IL6 and IL8 in dermal fibroblasts. After 24 hours, treatment with 0.5 mg/mL


bioactive peptide had no effect on IL6 or IL8 mRNA, while a slightly higher dose (1.0 mg/mL) caused only modest increases (1.3-fold for IL6 and 1.8-fold for IL8). Importantly, these small changes did not translate into significant protein-level changes,


10 ng/mL TGFβ 0.25 ng/mL


either in short-term tests up to 24 hours or in longer-term studies in the presence of vitamin C (Figures 7 and 8). In fact, vitamin C alone slightly reduced IL6 mRNA and IL8 protein levels. For comparison, RA and TGFβ, both known to


induce inflammation, caused dramatic increases in IL6 and IL8. RA increased IL6 mRNA 9.7-fold and IL6 protein 9.0-fold at 24 hours, with effects lasting up to 120 hours. TGFβ induced even stronger IL6 responses (19.1-fold mRNA, 30-fold protein). IL8 was similarly elevated by RA but not by TGFβ or any treatment. Hyaluronic acid actually


2.0 ng/mL DNA ■ α-SMA ■


Figure 5: 72h aSMA Protein Expression in Dermal Fibroblasts www.personalcaremagazine.com January 2026 PERSONAL CARE MAGAZINE


Pro-C1 secretion Fold-Change


Untreated 27P peptide 50 µg/mL VC 2.0 10.0 10 ng/mL TGFβ


Untreated 2.0 10.0 10 ng/mL TGFβ


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