![\"\"](\"http:\/\/www.puriactives.com\/en\/wp-content\/uploads\/2026\/10\/s20_00-300x169.png\")
<\/p>\nPuriActives\u00ae TocoPhos™Sodium Tocopheryl Phosphate<\/p>\n
PRODUCT & BRAND<\/p>\n
<\/p>\n
PuriPharm Co., Ltd.<\/b><\/p>\n
Vitamin E, reimagined for skin and scalp.<\/b><\/p>\n
INCI: SODIUM TOCOPHERYL PHOSPHATE<\/b><\/p>\n
A phosphorylated vitamin E active with aqueous compatibility and biological activation in skin, supported by peer-reviewed studies on oxidative-stress protection and moisturization.<\/p>\n
INGREDIENT OPPORTUNITY<\/p>\n
DESIGNED FOR AQUEOUS COMPATIBILITY<\/b><\/p>\n
A 6-O-phosphate group masks the oxidation-sensitive phenolic hydroxyl, with sodium counterions converting an oily antioxidant into a water-dispersible powder for serums, essences and gels. Kato et al. 2011; Zingg 2018.<\/p>\n
ACTIVATION AT THE SITE OF ACTION<\/b><\/p>\n
After uptake, cellular phosphatases hydrolyze the phosphate to release active \u03b1-tocopherol within cells. Hydrolysis was not observed in the culture medium itself. Nishio et al. 2011; Saleh et al. 2021.<\/p>\n
DUAL STRESS PROTECTION<\/b><\/p>\n
In human keratinocytes, the sodium salt suppressed UVB-induced reactive nitrogen species (RNS) and reduced prostaglandin E2 (PGE2) responses to UVB, IL-1\u03b2 and peroxide challenges. Nakama et al. 2009; Kato et al. 2011.<\/p>\n
MOISTURE AND BARRIER SUPPORT<\/b><\/p>\n
Topical treatment increased stratum corneum ceramides through serine palmitoyltransferase (SPT) and keratinocyte-differentiation pathways, improving moisture retention in hairless mouse skin. Kato & Takahashi 2012.<\/p>\n
Phosphorylated vitamin E connects skin-defense research, moisturization mechanisms and contemporary formulation opportunities.<\/p>\n
FORMULATION CHALLENGES<\/p>\n
THE CLASSIC MOLECULE AND ITS FORMULATION CHALLENGES<\/b><\/p>\n
OXIDATION SENSITIVITY<\/b><\/p>\n
The phenolic hydroxyl is \u03b1-tocopherol\u2019s antioxidant site and a key site of oxidation. Oxidation can deplete its activity.<\/p>\n
AN OIL IN AN AQUEOUS WORLD<\/b><\/p>\n
A viscous, hydrophobic liquid requires solubilization or emulsification for aqueous serums, essences and scalp formats.<\/p>\n
ESTERS SOLVE ONLY PART OF THE PROBLEM<\/b><\/p>\n
Tocopheryl acetate is stable but remains oily and depends on skin esterases. It produced much less tocopherol than the phosphate salt after 24 hours in a reconstructed human skin model. Kato et al. 2011, Figure 2A.<\/p>\n
WHAT PHOSPHATE CHEMISTRY CHANGES<\/b><\/p>\n
PROTECTED PHENOLIC HYDROXYL<\/b><\/p>\n
The 6-O-phosphate masks the oxidizable hydroxyl until enzymatic hydrolysis. Kato et al. 2011.<\/p>\n
A WATER-COMPATIBLE SALT<\/b><\/p>\n
Sodium counterions yield a powder suitable for incorporation into the aqueous phase.<\/p>\n
ACTIVATION AFTER UPTAKE<\/b><\/p>\n
Cellular phosphatases release \u03b1-tocopherol after uptake, rather than in the culture medium. Nishio et al. 2011.<\/p>\n
This chemistry supports development of water-based serums, essences, gels and leave-on scalp products.<\/p>\n
MOLECULAR IDENTITY<\/p>\n
VITAMIN E FAMILY STRUCTURES<\/b><\/p>\n
![\"\"](\"http:\/\/www.puriactives.com\/en\/wp-content\/uploads\/2026\/10\/s04_04-1-300x118.png\")
<\/p>\n
Adapted from Kato et al. 2011, Figure 1. Compound 1 is disodium tocopheryl phosphate, the TocoPhos™ active, shown with \u03b1-tocopherol and tocopheryl acetate.<\/p>\n
IONIZATION OF THE PHOSPHATE GROUP<\/b><\/p>\n
![\"\"](\"http:\/\/www.puriactives.com\/en\/wp-content\/uploads\/2026\/10\/s04_07-300x61.png\")
<\/p>\n
Adapted from Saleh et al. 2020, Figure 1. The phosphate undergoes two ionization steps, with pKa values of approximately 1.8 and 6.7. A predominantly dianionic state is described near pH 7.4.<\/p>\n
CHROMANOL HEAD: ANTIOXIDANT CORE<\/b><\/p>\n
The 6-position phenolic hydroxyl captures radicals in vitamin E; phosphorylation protects this site.<\/p>\n
6-O-PHOSPHATE: AN IONIZABLE HANDLE<\/b><\/p>\n
Ionization depends on pH. Near pH 7.4, the predominantly dianionic form supports water affinity while the phosphate protects the phenolic hydroxyl until hydrolysis.<\/p>\n
SODIUM SALT: THE INCI-DEFINED FORM<\/b><\/p>\n
Supplied as Sodium Tocopheryl Phosphate, a water-dispersible powder. The free acid has formula C29H51O5P, PubChem CID 94493.<\/p>\n
PHYTYL TAIL: LIPID ANCHOR<\/b><\/p>\n
After hydrolysis, the hydrophobic tail anchors released \u03b1-tocopherol in membranes, where it intercepts lipid peroxyl radicals.<\/p>\n
Near pH 7.4, this anionic amphiphile self-associates into approximately 9 nm aggregates, with a critical aggregation concentration (CAC) of approximately 4.2 mM. At pH 9 it is monomeric, providing a formulation variable. Saleh et al. 2020.<\/p>\n
VITAMIN E OPTIONS<\/p>\n
Conventional forms and formulation comparison<\/b><\/p>\n
![\"\"](\"http:\/\/www.puriactives.com\/en\/wp-content\/uploads\/2026\/10\/table_5_en_part1-300x118.png\")
<\/p>\n
Corresponding phosphate-salt properties<\/b><\/p>\n
![\"\"](\"http:\/\/www.puriactives.com\/en\/wp-content\/uploads\/2026\/10\/table_5_en_part2-300x114.png\")
<\/p>\n
*Reconstructed human skin model: tocopherol accumulation after topical treatment, Kato et al. 2011, Figure 2A. General chemistry: Zingg 2018. Photostability of the phosphorylated form: Saleh et al. 2021.<\/p>\n
Different systems call for different tools. The phosphate salt provides a route for aqueous and scalp-oriented formats.<\/p>\n
UPTAKE \u00b7 BIOCONVERSION \u00b7 ANTIOXIDANT ACTION<\/p>\n
ACTIVATION PATHWAY<\/b><\/p>\n
1 APPLICATION: an aqueous formulation deposits sodium tocopheryl phosphate at the skin surface.<\/b><\/p>\n
2 UPTAKE: keratinocytes internalize the phosphorylated active.<\/b><\/p>\n
3 BIOCONVERSION: cellular phosphatases hydrolyze the phosphate, releasing \u03b1-tocopherol.<\/b><\/p>\n
4 ANTIOXIDANT ACTION: \u03b1-tocopherol associates with membranes and intercepts lipid peroxyl radicals.<\/b><\/p>\n
\u2022 Deuterium tracing showed hydrolysis of \u03b1-TP to \u03b1-tocopherol in cells and mice, but not in culture medium, with lower plasma and liver lipid peroxidation. Nishio et al. 2011.<\/p>\n
\u2022 In reconstructed human skin, tocopherol accumulation was approximately 190 nmol\/g tissue at 24 hours with the phosphate salt; acetate remained near baseline. Kato et al. 2011, Figure 2A.<\/p>\n
EVIDENCE: INTRACELLULAR BIOCONVERSION<\/b><\/p>\n
![\"\"](\"http:\/\/www.puriactives.com\/en\/wp-content\/uploads\/2026\/10\/s06_21-300x139.png\")
<\/p>\n
HaCaT keratinocytes were incubated with 133 \u00b5g\/mL \u03b1-TP. Intracellular \u03b1-TP increased, and \u03b1-tocopherol (\u03b1-T) appeared in cell lysates at 2\u201324 hours, supporting uptake and enzymatic hydrolysis. Adapted from Saleh et al. 2021, Figure 8.<\/p>\n
Saleh et al. Scientific Reports. 2021. doi:10.1038\/s41598-021-01299-y<\/p>\n
STRESS BIOLOGY<\/p>\n
![\"\"](\"http:\/\/www.puriactives.com\/en\/wp-content\/uploads\/2026\/10\/03cb4c92-7d96-4c47-b726-df82b939c23c-300x274.png\")
<\/p>\n
PUBLISHED EVIDENCE<\/b><\/p>\n
UVB AND RNS IN HUMAN KERATINOCYTES<\/p>\n
Real-time fluorescence imaging showed UVB-triggered RNS generation involving neuronal nitric oxide synthase (nNOS). Sodium dl-\u03b1-tocopheryl phosphate suppressed this response. Nakama et al. 2009.<\/p>\n
SOOTHING-RELATED SIGNALS<\/p>\n
In UVB-exposed NHEK, the sodium salt reduced Cox-2 mRNA by 33\u201351% at 0.5 \u00b5M, inhibited p38 MAPK phosphorylation and lowered PGE2. Kato et al. 2011.<\/p>\n
MODEL CONTEXT MATTERS<\/p>\n
Intact \u03b1-TP is a weak radical scavenger in cell-free DPPH \/ ORAC assays. Cellular protection follows bioconversion to \u03b1-tocopherol, making the experimental model essential to interpretation. Saleh et al. 2021, Figure 7.<\/p>\n
KEY TERMS<\/p>\n
ROS: reactive oxygen species. RNS: reactive nitrogen species. nNOS: neuronal nitric oxide synthase. PGE2: prostaglandin E2. NHEK: normal human epidermal keratinocytes.<\/p>\n
EVIDENCE FOCUS: UV STRESS<\/p>\n
![\"\"](\"http:\/\/www.puriactives.com\/en\/wp-content\/uploads\/2026\/10\/s08_03-300x175.png\")
<\/p>\n
HaCaT keratinocytes were pretreated for 24 hours before UVA1 exposure. Viability was measured by Alamar Blue 24 hours later. Mean \u00b1 SD; *p < 0.05 and **p < 0.01 versus irradiated control. From Saleh et al. 2021, Figure 5.<\/p>\n
Saleh et al. Scientific Reports. 2021. doi:10.1038\/s41598-021-01299-y<\/p>\n
VIABILITY AFTER 226 J\/cm\u00b2 UVA1<\/b><\/p>\n
88% versus 70% cell viability<\/b><\/p>\n
80 \u00b5M \u03b1-TP pretreatment versus irradiated control. \u03b1-Tocopherol at the same concentration provided no significant protection in this model.<\/p>\n
INTRACELLULAR ROS AFTER 57 J\/cm\u00b2<\/b><\/p>\n
24.1% lower ROS versus control<\/b><\/p>\n
100 \u00b5M \u03b1-TP; H2DCFDA measurement within 2 hours after irradiation. \u03b1-Tocopherol reduced ROS by 23.9%.<\/p>\n
Protection coincided with phosphatase-mediated conversion to \u03b1-tocopherol. Intact \u03b1-TP was weak in cell-free assays but protective in cells. The phosphorylated form also had a higher LD50 in this model: 1676 versus 1070 \u00b5M.<\/p>\n
Additional UVB evidence: suppression of UVB-induced RNS in human keratinocytes. Nakama et al. 2009. J SCCJ 43(1):19. doi:10.5107\/sccj.43.19.<\/p>\n
MOISTURIZATION MECHANISM<\/p>\n
Ceramides are part of the lipid mortar of the stratum corneum. In keratinocytes, sodium tocopheryl phosphate acts on upstream processes involved in their synthesis.<\/p>\n
![\"\"](\"http:\/\/www.puriactives.com\/en\/wp-content\/uploads\/2026\/10\/mechanism_9_en-1-300x32.png\")
<\/p>\n
In NHEK, the sodium salt increased intracellular ceramides to approximately 1.8-fold at 50 \u00b5M (*), SPTLC2 expression to approximately 2.2-fold (**), differentiation markers and intracellular Ca\u00b2\u207a. Kato & Takahashi 2012.<\/p>\n
WHY THIS MATTERS TO FORMULATORS<\/b><\/p>\n
\u2022 Support for endogenous ceramide synthesis complements formulations that directly supply ceramides.<\/p>\n
\u2022 Differentiation markers such as TG1, involucrin and loricrin inform barrier-care positioning.<\/p>\n
\u2022 Supporting literature reports vitamin E upregulation of transglutaminase-1 and PPAR\u03b3 in human keratinocytes. De Pascale et al. 2006.<\/p>\n
Kato & Takahashi. Bioorg Med Chem. 2012;20(12):3837\u20133842. PMID 22579618. The schematic synthesizes the study pathway. Fold changes are approximate readings from the original figures. SPT: serine palmitoyltransferase. TG1: transglutaminase-1. CK10: cytokeratin 10. PPAR\u03b3: peroxisome proliferator-activated receptor \u03b3.<\/p>\n
EVIDENCE FOCUS: MOISTURIZATION<\/p>\n
IN VITRO: HUMAN KERATINOCYTES, NHEK<\/b><\/p>\n
\u25b2 Intracellular ceramides: approximately 1.8-fold versus control at 50 \u00b5M (*).<\/p>\n
\u25b2 SPT genes: SPTLC2 mRNA approximately 2.2-fold (**); SPTLC1 also increased (*).<\/p>\n
\u25b2 Differentiation markers TGM1, KRT10, IVL and LOR: approximately 2.2\u20133.3-fold (*\/**).<\/p>\n
\u25b2 Intracellular Ca\u00b2\u207a: significantly higher at 50\u201375 \u00b5M (*), consistent with differentiation signaling.<\/p>\n
![\"\"](\"http:\/\/www.puriactives.com\/en\/wp-content\/uploads\/2026\/10\/s10_06-1-300x243.jpg\")
<\/p>\n
Original figure, panel 4A: intracellular NHEK ceramides increase with dose at 0 \/ 10 \/ 50 \u00b5M, measured as \u00b5g\/mg protein.<\/p>\n
IN VIVO: HAIRLESS MICE, TOPICAL 1% \/ 2% FOR 4 WEEKS<\/b><\/p>\n
\u25b2 Stratum corneum ceramides: approximately 4.8\u20135.0 \u00b5g\/cm\u00b2 in the 1% (*) and 2% (**) groups, versus approximately 3 \u00b5g\/cm\u00b2 in untreated and placebo groups.<\/p>\n
\u25b2 Hygroscopicity at 30 seconds: higher with both 1% (*) and 2% (**) versus untreated \/ placebo.<\/p>\n
\u25b2 Moisture retention at 60 seconds: significantly higher with both concentrations (*).<\/p>\n
These findings link improved stratum corneum hydration with endogenous lipid processes.<\/p>\n
![\"\"](\"http:\/\/www.puriactives.com\/en\/wp-content\/uploads\/2026\/10\/s10_12-300x223.jpg\")
<\/p>\n
Original figure, panel 2B: stratum corneum hygroscopicity at 30 seconds and moisture retention at 60 seconds; untreated \/ placebo \/ 1% \/ 2%.<\/p>\n
Kato & Takahashi. Bioorg Med Chem. 2012;20(12):3837\u20133842. doi:10.1016\/j.bmc.2012.04.029. PMID 22579618. Panels 2B and 4A are excerpts from the paper. Fold changes are approximate readings from original axes; * \/ ** reproduce the authors\u2019 significance notation.<\/p>\n
EVIDENCE FOCUS: SKIN COMFORT<\/p>\n
![\"\"](\"http:\/\/www.puriactives.com\/en\/wp-content\/uploads\/2026\/10\/s11_03-275x300.png\")
<\/p>\n
NHEK were pretreated with the sodium salt at 0.1\u20132 \u00b5M for 24 hours before UVB, IL-1\u03b2, tBHP or H2O2 challenge. PGE2 was measured in culture medium. Kato et al. 2011, Figure 3.<\/p>\n
Kato et al. Bioorg Med Chem. 2011;19(21):6348\u20136355. doi:10.1016\/j.bmc.2011.08.067<\/p>\n
PGE2 REDUCTION VERSUS STIMULATED CONTROL<\/p>\n
UVB: 44 \/ 65 \/ 69% at 0.1 \/ 0.5 \/ 2 \u00b5M.<\/p>\n
tBHP: 74 \/ 87 \/ 90%; IL-1\u03b2: 41 \/ 58 \/ 57%.<\/p>\n
H2O2: approximately 50%; UVB alone increased PGE2 approximately fivefold.<\/p>\n
The acetate was weaker, and \u03b1-tocopherol had little effect at these concentrations.<\/p>\n
CELL DEATH UNDER OXIDATIVE STRESS<\/b><\/p>\n
![\"\"](\"http:\/\/www.puriactives.com\/en\/wp-content\/uploads\/2026\/10\/chart_11_en-300x170.png\")
<\/p>\n
Redrawn from US20090104258A1, Example 1. Keratinocytes, 1 mM H2O2 for 24 hours; flow cytometry. The y-axis is the percentage of apoptotic cells.<\/p>\n
Example 2 of the same patent publication: \u03b1-TP at 1 \u00b5g\/mL increased large stem-cell-derived colonies by 104% in a clonogenic assay under oxidative stress.<\/p>\n
DELIVERY SCIENCE<\/p>\n
\u03b1-TP FLUX ACROSS A SYNTHETIC MEMBRANE<\/b><\/p>\n
![\"\"](\"http:\/\/www.puriactives.com\/en\/wp-content\/uploads\/2026\/10\/chart_12_en-300x173.png\")
<\/p>\n
Redrawn from Saleh et al. 2023: steady-state flux of 2% \u03b1-TP from four vehicles across a synthetic membrane.<\/p>\n
In human skin, the emulsion outperformed the gel-like system:<\/p>\n
3\u00d7 viable-layer deposition at 3 hours and 5\u00d7 at 24 hours.<\/p>\n
Human-skin flux: 328.6 versus 175.2 \u00b5g\/cm\u00b2\/h. Cell-free DPPH activity of the delivered dose was higher: 73% versus 46%.<\/p>\n
SKIN DEPOSITION: pH 7.4 VERSUS \u03b1-TOCOPHEROL<\/b><\/p>\n
![\"\"](\"http:\/\/www.puriactives.com\/en\/wp-content\/uploads\/2026\/10\/s12_08-300x212.png\")
<\/p>\n
Porcine skin, 3 hours, infinite dose: \u03b1-TP at pH 7.4 reached approximately 506 \u00b1 296 \u00b5g in the stratum corneum and 170 \u00b1 29 \u00b5g in the epidermis. From Saleh et al. 2020, Figure 5. The source slide also describes approximately 8-fold \/ 4-fold differences; the comparison basis requires checking against the original paper.<\/p>\n
At pH 7.4, \u03b1-TP forms approximately 9 nm aggregates that fuse with stratum corneum lipids in cryo-electron microscopy. At pH 9, monomer deposition is lower. Formulation pH therefore affects aggregation and skin interactions.<\/p>\n
Saleh et al. Int J Pharm. 2023. doi:10.1016\/j.ijpharm.2023.122781. PMID 36849039. Saleh et al. Int J Pharm. 2020. doi:10.1016\/j.ijpharm.2020.120000.<\/p>\n
SKINCARE APPLICATION PORTFOLIO<\/p>\n
Formats and rationale<\/b><\/p>\n
![\"\"](\"http:\/\/www.puriactives.com\/en\/wp-content\/uploads\/2026\/10\/table_13_en_part1-300x123.png\")
<\/p>\n
Corresponding evidence anchors<\/b><\/p>\n
![\"\"](\"http:\/\/www.puriactives.com\/en\/wp-content\/uploads\/2026\/10\/table_13_en_part2-300x109.png\")
<\/p>\n
SCALPIFICATION<\/p>\n
The scalp shares keratinocytes, a ceramide barrier and UV \/ pollution exposure with facial skin, together with dense follicles and sebum.<\/p>\n
SHARED STRESS BIOLOGY<\/p>\n
UV reaches the scalp surface. ROS \/ RNS responses documented in keratinocytes inform this application rationale. Nakama 2009; Saleh 2021.<\/p>\n
SHARED HYDRATION MACHINERY<\/p>\n
The ceramide barrier also matters to scalp dryness and tightness. Kato & Takahashi 2012.<\/p>\n
SHARED COMFORT-RELATED SIGNALS<\/p>\n
PGE2-related stress pathways provide a basis for conceptual extension to scalp comfort. Kato et al. 2011.<\/p>\n
The scalp is a development extension for TocoPhos™. PuriPharm technical and application teams support joint scalp-formulation projects.<\/p>\n
![\"\"](\"http:\/\/www.puriactives.com\/en\/wp-content\/uploads\/2026\/10\/mechanism_14_en-300x273.png\")
<\/p>\n
SCALP PROTECTION AND COMFORT<\/p>\n
FOLLICULAR-ENVIRONMENT PROTECTION<\/b><\/p>\n
The scalp surface is UV-exposed skin. Keratinocyte findings on UVA1 survival and UVB-triggered RNS provide a rationale for leave-on antioxidant scalp care. Nakama et al. 2009; Saleh et al. 2021.<\/p>\n
HYDRATION BALANCE AND BARRIER SUPPORT<\/b><\/p>\n
SPT-related ceramide synthesis and improved stratum corneum moisture retention inform concepts for dry, tight-feeling scalps. Kato & Takahashi 2012.<\/p>\n
COMFORT FOR STRESSED SCALPS<\/b><\/p>\n
PGE2 \/ Cox-2 \/ p38 modulation and reduced stress-induced keratinocyte death provide a rationale for comfort-oriented products. Kato et al. 2011; US20090104258A1, Example 1.<\/p>\n
All three are development opportunities extrapolated from published epidermal evidence. Work with PuriPharm Co., Ltd. to translate them into scalp-care products.<\/p>\n
HAIRCARE FORMATS<\/p>\n
![\"\"](\"http:\/\/www.puriactives.com\/en\/wp-content\/uploads\/2026\/10\/table_16_en-1-300x198.png\")
<\/p>\n
PRACTICAL FORMULATION<\/p>\n
![\"\"](\"http:\/\/www.puriactives.com\/en\/wp-content\/uploads\/2026\/10\/table_17_en-300x178.png\")
<\/p>\n
SOLUBILITY VERSUS pH<\/b><\/p>\n
![\"\"](\"http:\/\/www.puriactives.com\/en\/wp-content\/uploads\/2026\/10\/s17_05-300x196.png\")
<\/p>\n
Adapted from Saleh et al. 2020, Figure 1. \u03b1-TP solubility rises with pH alongside changes in aggregation.<\/p>\n
Contact PuriPharm technical and application teams for grade-specific use levels, processing-temperature limits, shelf life and full technical documentation.<\/p>\n
Saleh et al. Int J Pharm. 2020. doi:10.1016\/j.ijpharm.2020.120000. Saleh et al. Int J Pharm. 2023. doi:10.1016\/j.ijpharm.2023.122781.<\/p>\n
SKINCARE CONCEPT GALLERY<\/p>\n
FORMULATION CONCEPT<\/b><\/p>\n
DAILY DEFENSE ANTIOXIDANT SERUM<\/b><\/p>\n
Aqueous gel serum \u00b7 Daily leave-on use<\/b><\/p>\n
Suggested ingredients: Niacinamide \u00b7 Panthenol \u00b7 Glycerin<\/b><\/p>\n
Aqueous delivery of a biologically activated antioxidant: keratinocyte uptake and conversion to \u03b1-tocopherol provide a rationale for ROS \/ RNS stress care.<\/p>\n
Evidence: Nishio 2011; Saleh 2021; Nakama 2009.<\/p>\n
FORMULATION CONCEPT<\/b><\/p>\n
CERAMIDE-SUPPORTING MOISTURIZER<\/b><\/p>\n
Oil-in-water cream \u00b7 Daily moisturization<\/b><\/p>\n
Suggested ingredients: Ceramide NP \u00b7 Glycerin \u00b7 Squalane<\/b><\/p>\n
Two complementary routes: direct ceramide supplementation and support for endogenous SPT-related synthesis.<\/p>\n
Evidence: Kato & Takahashi 2012.<\/p>\n
FORMULATION CONCEPT<\/b><\/p>\n
AFTER-SUN CARE LOTION<\/b><\/p>\n
Light emulsion \u00b7 After-sun comfort<\/b><\/p>\n
Suggested ingredients: Sodium Ascorbyl Phosphate \u00b7 Bisabolol \u00b7 Betaine<\/p>\n
A reported combination with magnesium ascorbyl phosphate inhibited PGE2 more than either ingredient alone. This informs a vitamin C phosphate combination concept; the proposed sodium derivative is not the identical tested combination.<\/p>\n
Evidence: Kato 2011, Figure 6; Nakama 2009.<\/p>\n
These concepts have published mechanistic evidence anchors. Contact PuriPharm Co., Ltd. for formulation collaboration.<\/p>\n
SCALP AND HAIRCARE CONCEPT GALLERY<\/p>\n
FORMULATION CONCEPT<\/b><\/p>\n
ANTIOXIDANT SCALP SERUM<\/b><\/p>\n
Aqueous leave-on serum \u00b7 Daily use<\/b><\/p>\n
Suggested ingredients: Niacinamide \u00b7 Panthenol \u00b7 Glycerin<\/b><\/p>\n
A scalp-surface serum with biologically activated antioxidant positioning, derived from epidermal UV-stress evidence.<\/p>\n
Evidence: Nakama 2009; Saleh 2021.<\/p>\n
FORMULATION CONCEPT<\/b><\/p>\n
LIGHT SCALP COMFORT EMULSION<\/b><\/p>\n
Fluid emulsion \u00b7 Leave-on comfort<\/b><\/p>\n
Suggested ingredients: Bisabolol \u00b7 Betaine \u00b7 Glycerin<\/b><\/p>\n
Emulsion vehicles provided greater viable-skin deposition in the cited comparison. PGE2 modulation informs a scalp-comfort concept.<\/p>\n
Evidence: Saleh 2023; Kato 2011.<\/p>\n
FORMULATION CONCEPT<\/b><\/p>\n
MOISTURIZING SCALP MASK<\/b><\/p>\n
Cream mask \u00b7 Weekly intensive care<\/b><\/p>\n
Suggested ingredients: Ceramide NP \u00b7 Butyrospermum Parkii (Shea) Butter<\/p>\n
Longer contact is consistent with a ceramide-synthesis rationale for dry, tight-feeling scalps.<\/p>\n
Evidence: Kato & Takahashi 2012.<\/p>\n
Develop a coordinated scalp-care range, from serums to masks, with PuriPharm Co., Ltd.<\/p>\n
FOUR KEY POINTS<\/p>\n
<\/p>\n
PROTECTED AND BIOLOGICALLY AVAILABLE<\/b><\/p>\n
Phosphate chemistry protects the antioxidant site, with cellular phosphatases releasing \u03b1-tocopherol after uptake.<\/p>\n
EVIDENCE FROM RELEVANT MODELS<\/b><\/p>\n
Human keratinocytes, reconstructed skin, in vivo barrier models and human skin delivery studies provide traceable evidence.<\/p>\n
FORMULATION DEVELOPMENT SUPPORT<\/b><\/p>\n
Aqueous-phase use, published vehicle and pH data, and preservative-testing evidence from an emulsion prototype.<\/p>\n
ONE ACTIVE, TWO CARE AREAS<\/b><\/p>\n
Skin defense and moisturization, alongside scalp-care concepts extrapolated from the same evidence base.<\/p>\n
Vitamin E, reimagined for formulation development.<\/p>\n
Work with us on your next skincare or scalp-care concept.<\/p>\n
PuriPharm Co., Ltd. \u00b7 Technical and Application Team<\/p>\n
SCIENTIFIC REFERENCES<\/p>\n
1. Nakama M. et al. Inhibitory effect of sodium dl-\u03b1-tocopheryl-6-O-phosphate on UVB-induced reactive nitrogen species in human keratinocytes. J Soc Cosmet Chem Jpn 43(1):19\u201325, 2009. doi:10.5107\/sccj.43.19<\/p>\n
2. Kato E., Sasaki Y., Takahashi N. Sodium dl-\u03b1-tocopheryl-6-O-phosphate inhibits PGE2 production in keratinocytes induced by UVB, IL-1\u03b2 and peroxidants. Bioorg Med Chem 19(21):6348\u20136355, 2011. doi:10.1016\/j.bmc.2011.08.067. PMID 21945458.<\/p>\n
3. Kato E., Takahashi N. Improvement by sodium dl-\u03b1-tocopheryl-6-O-phosphate treatment of moisture-retaining ability in stratum corneum through increased ceramide levels. Bioorg Med Chem 20(12):3837\u20133842, 2012. doi:10.1016\/j.bmc.2012.04.029. PMID 22579618.<\/p>\n
4. Nishio K. et al. \u03b1-Tocopheryl phosphate is hydrolyzed to \u03b1-tocopherol in cells and in vivo. Free Radic Biol Med 50(12):1794\u20131800, 2011. PMID 21443945.<\/p>\n
5. Saleh M. et al. Tocopheryl phosphate in keratinocyte UV-stress models. Scientific Reports 11:22400, 2021. doi:10.1038\/s41598-021-01299-y<\/p>\n
6. Gianello R. et al. \u03b1-Tocopheryl phosphate: chemistry and biological activity. Free Radic Biol Med 39(7):970\u2013976, 2005. PMID 16140216.<\/p>\n
7. Nakayama S. et al. Protective effect of \u03b1-tocopheryl phosphate against UVB-induced damage in cultured mouse skin. J Invest Dermatol 121:406\u2013411, 2003.<\/p>\n
8. De Pascale M.C. et al. Vitamin E upregulates transglutaminase-1 and PPAR\u03b3 in human keratinocytes. Arch Biochem Biophys 447:97\u2013106, 2006.<\/p>\n
9. Zingg J.-M. Vitamin E: regulatory role beyond antioxidant activity. Adv Food Nutr Res 83:311\u2013363, 2018.<\/p>\n
10. Ghayour-Mobarhan M. et al. Tocopheryl phosphate: a review of biological properties. J Diet Suppl, 2014. doi:10.3109\/19390211.2014.952859<\/p>\n
11. Ogru E. et al. Vitamin E phosphate: an endogenous form of vitamin E. Free Radic Res, 2003.<\/p>\n
FORMULATION AND PATENT REFERENCES<\/p>\n
12. Saleh M. et al. Ionization, pH-dependent solubility, self-association and skin deposition of \u03b1-tocopheryl phosphate. Int J Pharm 594:120000, 2020. doi:10.1016\/j.ijpharm.2020.120000<\/p>\n
13. Saleh M. et al. Vehicle-dependent delivery of \u03b1-tocopheryl phosphate to viable skin. Int J Pharm 636:122781, 2023. PMID 36849039 \u00b7 doi:10.1016\/j.ijpharm.2023.122781<\/p>\n
14. Patent publication US20090104258A1 (published 2009), cited by publication number and examples: Example 1 (oxidative-stress-induced keratinocyte apoptosis, flow cytometry) and Example 2 (clonogenic assay; large stem-cell-derived colonies +104%).<\/p>\n
15. Gavin A. et al. Tocopheryl phosphate mixture (TPM) as a skin-delivery enhancer for co-formulated actives. Drug Deliv Transl Res, 2016. doi:10.1007\/s13346-016-0331-x<\/p>\n
16. Mozafari M. et al. Tocopheryl phosphate-based delivery systems (review). Int J Transl Res.<\/p>\n","protected":false},"excerpt":{"rendered":"
PuriActives\u00ae TocoPhos™Sodium Tocopheryl Phosphat […]<\/p>\n","protected":false},"author":2,"featured_media":0,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":[],"categories":[25],"tags":[],"_links":{"self":[{"href":"http:\/\/www.puriactives.com\/en\/index.php?rest_route=\/wp\/v2\/posts\/2495"}],"collection":[{"href":"http:\/\/www.puriactives.com\/en\/index.php?rest_route=\/wp\/v2\/posts"}],"about":[{"href":"http:\/\/www.puriactives.com\/en\/index.php?rest_route=\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"http:\/\/www.puriactives.com\/en\/index.php?rest_route=\/wp\/v2\/users\/2"}],"replies":[{"embeddable":true,"href":"http:\/\/www.puriactives.com\/en\/index.php?rest_route=%2Fwp%2Fv2%2Fcomments&post=2495"}],"version-history":[{"count":1,"href":"http:\/\/www.puriactives.com\/en\/index.php?rest_route=\/wp\/v2\/posts\/2495\/revisions"}],"predecessor-version":[{"id":2539,"href":"http:\/\/www.puriactives.com\/en\/index.php?rest_route=\/wp\/v2\/posts\/2495\/revisions\/2539"}],"wp:attachment":[{"href":"http:\/\/www.puriactives.com\/en\/index.php?rest_route=%2Fwp%2Fv2%2Fmedia&parent=2495"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"http:\/\/www.puriactives.com\/en\/index.php?rest_route=%2Fwp%2Fv2%2Fcategories&post=2495"},{"taxonomy":"post_tag","embeddable":true,"href":"http:\/\/www.puriactives.com\/en\/index.php?rest_route=%2Fwp%2Fv2%2Ftags&post=2495"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}