Vesicle Controlled Salicylic Acid
Vesicle Controlled Salicylic Acid
Encapsulated sustained-release salicylic acid raw material; vesicle carrier achieves targeted delivery and controlled release. While retaining the efficacy of salicylic acid, it greatly reduces skin irritation; suitable for formulations for oily, acne-prone sensitive skin
Product overview
Vesicle-Controlled Salicylic Acid adopts vesicle controlled-release technology for precise release. It delivers efficient skincare performance with minimal irritation. Vesicle controlled-release forms stable, ordered and functional microspherical vesicle structures through intermolecular non-covalent interactions including hydrogen bonding, electrostatic forces and hydrophobic effects. The vesicle technology enables targeted delivery of active substances and sustained release, lowering adverse responses to protect skin and reduce irritation. Vesicle-Controlled Salicylic Acid provides a customized "clear & radiant transformation" formula and creates a new skincare standard for oily, sensitive and acne-prone skin
Composition Information
| Component Type | INCI | CAS | EC |
|---|---|---|---|
| Components | SALICYLIC ACID | 69-72-7 | 200-712-3 |
| Components | OLEIC/LINOLEIC/LINOLENIC POLYGLYCERIDES | ||
| Components | STEARAMIDOPROPYL DIMETHYLAMINE | 7651-02-7 | 231-609-1 |
| Components | PHOSPHATIDYLCHOLINE | 8002-43-5 | 232-307-2 |
Mechanism of Action
1. Controlled-release transdermal pathway: After nanovesicles contact stratum corneum, they interact with lipid structure of keratinocytes and widen intercellular gaps. The vesicle carrier transports salicylic acid into epidermis, and active ingredient is gradually released to reduce local irritation risk.
2. Soothing pathway: Downregulate expression of inflammatory factors IL‑1β, IL‑6, TNF‑α and OSM, relieve skin inflammatory response and alleviate redness caused by blemishes.
3. Skin microbiome balancing pathway: Inhibit proliferation of *Cutibacterium acnes* and *Malassezia*, reduce harmful microorganisms in hair follicles and improve inflammatory skin bumps.
4. Keratin regulating pathway: Gently turnover dead keratinocytes, unclog pores and relieve pore blockage.
5. Sebum regulation pathway: Long-term application reduces sebum secretion rate of sebaceous glands and improves oiliness of skin and scalp.
6. Soothing & repairing pathway: Ease skin discomfort; when applied on scalp, it improves scalp flaking and discomfort.
Experimental Data
1. Scalp sebum test: After 4 weeks of using anti-dandruff hair conditioner containing 2% Vesicle Smart-Controlled Salicylic Acid, scalp sebum secretion rate decreases by 31.54%.
2. In-vitro inflammatory cytokine test: Compared with the control group stimulated by heat-inactivated Cutibacterium acnes, IL‑1β is reduced by approx. 61.1%, IL‑6 by approx. 68%, TNF‑α by approx. 66.7% and OSM by approx. 75%.
Product specifications
| INCI Name: | SALICYLIC ACID, OLEIC/LINOLEIC/LINOLENIC POLYGLYCERIDES, STEARAMIDOPROPYL DIMETHYLAMINE, PHOSPHATIDYLCHOLINE |
|---|---|
| Source: | Intelligent vesicle encapsulation technology is adopted to construct stable and ordered microspherical vesicle structures. Salicylic acid is encapsulated within the nanovesicle system. |
| Recommended dosage: | 0.5%~5% |
Key benefits
1. Vesicular sustained and controlled release system; nanostructured vesicles achieve targeted transdermal delivery and slowly release salicylic acid to reduce irritation caused by instantaneous high concentration and enhance mildness.
2. Integrated multi-skincare benefits: anti-inflammation, bacteriostasis and keratolytic action, together with soothing and oil-control effects. Applicable for formulas targeting acne-prone skin and scalp care.
3. Unique transdermal mechanism: vesicles act on the stratum corneum, loosen corneocytes, alter phospholipid polarity of keratinocyte cell membranes and increase membrane fluidity to facilitate active ingredient penetration into skin.
4. Supported by human usage trial data; 4-week application markedly reduces scalp sebum secretion and effectively downregulates expression of multiple inflammatory factors.
