DELIVERY SYSTEMS 65 astonishing 515.74 µg/cm2 . Despite this massive


high-payload delivery, an MTT cytotoxicity assay confirmed that the cell viability of the EpiTRI tissue remained perfectly intact (>100%), proving exceptional cellular tolerance and safety.


In vivo CRS validation of 24-hour targeted delivery to the DEJ (~ 120 µm depth) To visualize the real-time dynamic behaviour of this reservoir in vivo, a clinical study utilizing high- resolution confocal Raman spectroscopy (LabRAM Soleil) was conducted. A 2% diascorbyl azelate waterless serum was


applied to the forearm of human subject, and the specific characteristic Raman peaks of the intact molecule, its mono-cleaved intermediate, ascorbic acid, and azelaic acid were mapped continuously over 24 hours (Figure 2). The spatial distribution heatmaps provided


direct evidence of the targeted delivery mechanism.


Zero to two hours (penetration, reservoir initiation & early cleavage) Upon application, diascorbyl azelate successfully permeates into the stratum corneum, where it accumulates and forms a localized reservoir, effectively avoiding burst release. Concurrently, Raman signals indicate the


initiation of in situ cleavage, generating early traces of ascorbic acid and azelaic acid within the upper epidermal layers.


Four hours (viable epidermis entry & early bioavailability) Diascorbyl azelate penetrates the viable epidermis, enabling the early-stage release of active compounds within metabolically active skin layers. Progressive Raman spectral changes confirm continued in situ activation of ascorbic acid and azelaic acid, increasing their bioavailability in the skin.


Six to ten hours (reservoir formation & sustained in situ release) Diascorbyl azelate establishes a transient epidermal reservoir, supporting continuous and controlled in situ cleavage. This results in sustained and spatially distributed generation


Collagen gene expression on fibroblasts


400 350 300 250 200 150 100 50 0


stimulation 100 100 100 170 203 ** 70% Relative penetration %


12% 12% 10% 8% 6% 4% 2% 0%


0 2 4 6 8


Time (hr.) 10


12 NeoC101™ ■


Azelaic Acid (released) ■ Vitamin C (released) ■


24 Figure 3: Time-course relative penetration profiles of diascrobyl azelate and its released actives


Maximum penetration depth (µm) 0 hr


0


20 40 60 80 100 120


2 hr 4 hr 6 hr 8 hr 10 hr


NeoC101™ ■ Azelaic Acid (released) ■ Vitamin C (released) ■


12 hr 24 hr


Stratum Corneum Layer (0-20µm)


Viable Epidermis Layer (20-80µm)


DEJ Region (80-120µm)


Dermis (120-3000µm)


Figure 4: Maximum skin penetration depth (µm) of diascorbyl azelate and its released actives over 24 hours


of ascorbic acid and azelaic acid across the epidermis, maintaining prolonged exposure while avoiding burst release.


12 hours (deep penetration & enhanced accessibility) Ascorbic acid is detected at depths approaching ~120 µm, corresponding to the Dermal–Epidermal Junction (DEJ). Given that sodium-dependent


COL1A1 ■ COL7A1 ■ COL1A1 ■ stimulation stimulation 103% 385 * 285%


120 80 60 40 20 0


Control 1 ppm NeoC101™


Figure 5: Effect of diascorbyl azelate on collagen type 1, 4, 7 gene expression in human dermal fibroblasts


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vitamin C transporters (SVCT1/2) are expressed throughout the epidermis, this depth-dependent distribution suggests enhanced accessibility of bioavailable ascorbic acid across multiple skin layers, rather than localized uptake at a single site.


24 hours (full-epidermis coverage & synchronized DEJ convergence) By 24 hours, both intact diascorbyl azelate and its


DPPH radical scavenging activity (%) NeoC101™ ■ Vitamin C ■


*** 91


27 ± 2.1 µM


*** 50


49 ± 3.1 µM 15 4 7 1 10 Concentration (µM)


Figure 6: DPPH radical scavenging profiles and EC50 values of diascorbyl azelate and ascorbic acid


July 2026 PERSONAL CARE MAGAZINE 100 1000 24


*** ** 93 77


*** 91


*** 92


% of Control


Maximum penetration depth (µm) VEGF secreted (% of control)


DPPH scavenging activity (%)


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