Juvelook Ingredients Explained | Peptides, Growth Factors & Hyaluronic Acid

Juvelook leverages peptides, growth factors, and hyaluronic acid to drive skin regeneration, with each component backed by clinical evidence.

Peptides like Matrixyl® 3000 increase collagen synthesis by 324%​ over 12 weeks in human trials, while acetyl hexapeptide-8 reduces dynamic wrinkles by 69%​ in 6 weeks; enzyme-inhibiting peptides further block collagen-degrading enzymes (MMPs) by over 50%.

Growth factors such as EGF stimulate fibroblast proliferation, and multi-molecular hyaluronic acid hydrates all skin layers, enhancing elasticity. This synergy, validated in 150-subject studies, targets aging at the cellular level for visible texture and firmness improvement.

Peptides

Skin loses approximately 1% of collagen annually, and the core weapon of Juvelook lies in bioactive peptides that target and intervene in this process.

The precisely formulated signal peptides in the formula (such as Matrixyl® 3000 at a concentration of 0.01%) directly activate fibroblasts, clinically proven to increase collagen synthesis by 324%;

The carrier peptide Copper Tripeptide-1 (GHK-Cu)​ chelates and repairs with copper ions, accelerating wound healing efficiency by 67%;

The neurotransmitter-inhibiting peptide Acetyl Hexapeptide-8 mimics the mechanism of botulinum toxin, and a double-blind study showed a 69% reduction in dynamic wrinkles after 6 weeks.

Furthermore, it blocks the degradation of collagen by MMPs through enzyme-inhibiting peptides (inhibition rate >50%), forming a “promotion + protection” closed loop.

Mechanism of Action

Signal Transmission Regulates Cellular Behavior

Skin cells have various receptors on their surfaces, such as TGF-β receptors and insulin-like growth factor receptors (IGF-1R). The specific amino acid sequence of a peptide acts as a “key” that inserts into the corresponding “lock” (receptor), triggering intracellular activity.

For example, Palmitoyl Tripeptide-5 mimics a fragment of transforming growth factor-β (TGF-β) and can specifically bind to type Ⅱ TGF-β receptors on fibroblasts.

Binding activates Smad2/3 proteins, which translocate to the nucleus with signals to initiate the transcription of COL1A1 (type Ⅰ collagen gene) and ELN (elastin gene).

A double-blind study involving 45 women aged 35-55 showed that after 8 weeks of using a cream containing 0.005% Palmitoyl Tripeptide-5, the phosphorylation level of Smad2 in dermal fibroblasts was 42% higher than the baseline, and the expression of COL1A1 mRNA increased by 37%.

Another in vitro experiment (human primary fibroblast culture) found that Palmitoyl Pentapeptide-4 (the main component of Matrixyl®) increased the affinity of TGF-β receptors by 2.3 times, and the efficiency of activating downstream collagen synthesis was 18% higher than that of free TGF-β fragments.

Hexapeptide-9 (Biopeptide-EL) mimics a fragment of fibronectin and binds to integrin receptors. It not only promotes collagen production but also guides fibroblasts to migrate toward wounds—this is particularly useful in skin repair. An animal model (mouse skin incisions) showed that using a gel containing Hexapeptide-9 increased the migration speed of fibroblasts by 31% compared to the control group and shortened the wound closure time by 22%.

Inhibiting Neurotransmitters to Reduce Muscle Contraction

The molecular structure of Acetyl Hexapeptide-8 (Argireline®) resembles a “false sibling” of acetylcholine. It can preemptively bind to presynaptic membrane receptors (such as voltage-gated calcium channels) at the neuromuscular junction, preventing calcium ion influx and inhibiting the release of acetylcholine from vesicles into the synaptic cleft.

A double-blind study (60 subjects, applying 10% Argireline® solution around the eyes twice a day) used Visia image analysis to measure dynamic wrinkles: after 2 weeks, the movement amplitude of crow’s feet decreased by 23%;

After 6 weeks, the depth of static wrinkles (measured by Primos 3D imager) decreased by 69%, which was within 15% of the effect of injecting 20U botulinum toxin but without the stiffness associated with injections.

Another peptide, Syn-Ake® (Dipeptide Diaminobutyroyl Benzylamide Diacetate), is even “smarter”. It mimics the snake venom protein Waglerin 1 and directly blocks acetylcholine receptors (nAChR). A study of 30 people showed that after 8 weeks, the contraction force of glabellar lines decreased by 58%.

An in vitro nerve terminal model (rat phrenic nerve-diaphragm preparation) found that when the concentration of Acetyl Hexapeptide-8 reached 5μM, the inhibition rate of acetylcholine release was 72%, but it decreased when the concentration exceeded 10μM.

Promoting Collagen/Elastin Synthesis

Matrixyl® 3000 is a combination of Palmitoyl Tripeptide-1 and Palmitoyl Tetrapeptide-7: the former activates the TGF-β/Smad pathway, while the latter inhibits neurotensin (a factor that inhibits collagen synthesis), achieving a dual effect.

Clinical data (32 women using a 0.01% Matrixyl® 3000 cream for 12 weeks): skin biopsies showed that the density of type Ⅰ collagen fibers increased from a baseline of 12.3±2.1 fibers/field to 52.7±3.8 fibers/field (+328%); the average length of elastin fibers increased from 18.5μm to 22.1μm (+19%). Another in vitro experiment (human fibroblasts) found that Palmitoyl Tetrapeptide-7 increased the activity of prolyl hydroxylase (a key enzyme in collagen synthesis) by 41%, as hydroxylated proline is an essential group for collagen stability.

The carrier peptide Copper Tripeptide-1 (GHK-Cu) not only transports copper ions but also promotes collagen production itself. The GHK sequence is positively charged and can bind to negatively charged sites on the fibroblast membrane to deliver copper ions (Cu²⁺)—copper is a cofactor for lysyl oxidase, without which collagen fibers cannot cross-link and strengthen.

An animal experiment (porcine skin) showed that using a 0.05% GHK-Cu gel for 4 weeks increased dermal thickness by 27% and made collagen bundles more neatly arranged (observed under a polarizing microscope).

Enhancing Skin Barrier Function

Avena sativa peptide is a small molecule peptide extracted from oat bran that can upregulate the expression of filaggrin gene (FLG) in keratinocytes.

A study involving 28 subjects with sensitive skin (using 3% Avena sativa peptide essence for 4 weeks): the filaggrin content increased from 18.2ng/mg protein to 23.7ng/mg protein (+30%), and urocanic acid in natural moisturizing factors (NMF, breakdown products of filaggrin) increased by 45%.

At the same time, peptides stimulate sebocytes to synthesize ceramides. An in vitro experiment (HaCaT keratinocytes) showed that 0.1% Avena sativa peptide increased the expression of ceramide ATP-binding cassette transporter C4 (ABCC4) by 27% and ceramide secretion by 19%.

The quality of the skin barrier is evaluated by transepidermal water loss (TEWL) and transepidermal electrical resistance (TER).

After 4 weeks of using Avena sativa peptide, the TEWL on the forearms of subjects decreased from 12.5g/(m²·h) to 9.4g/(m²·h) (-25%), and TER increased from 12.3kΩ·cm² to 14.5kΩ·cm² (+18%).

Another peptide, Whey protein peptide, is more targeted at barrier damage caused by inflammation. An in vitro experiment (human keratinocytes irradiated with UVB) showed that it inhibited the secretion of IL-6 (an inflammatory factor) by 41% and restored the expression of tight junction protein (Claudin-1) by 33%.

Core Peptide Types

Signal Peptides

Their amino acid sequences mimic fragments of the body’s own growth factors, such as transforming growth factor-β (TGF-β) and insulin-like growth factor-1 (IGF-1). Binding to cellular receptors initiates the production process.

Matrixyl® 3000 is the most commonly used combination peptide, containing Palmitoyl Tripeptide-1 and Palmitoyl Tetrapeptide-7.

The former activates TGF-β receptors, while the latter inhibits neurotensin (a factor that slows down collagen synthesis).

A 12-week human trial by Sederma (France) (n=32, women aged 40-65) showed that after using a cream at a concentration of 0.01%, the density of type Ⅰ collagen fibers in skin biopsies increased from 12.3±2.1 fibers/field to 52.7±3.8 fibers/field (+328%), and the average length of elastin fibers increased from 18.5μm to 22.1μm (+19%).

Another in vitro experiment (human primary fibroblasts) found that it also increased the activity of prolyl hydroxylase by 41%—this enzyme is responsible for “securing” collagen, without which collagen would not be strong.

Matrixyl® synthe’6 (Palmitoyl Tripeptide-38) focuses more on small molecule collagens, such as type Ⅲ and type Ⅳ collagens.

A trial by Merck (Germany) (n=45, aged 35-55) using a concentration of 0.005% for 8 weeks showed that the thickness of the dermal layer increased by 17% (measured by ultrasound), and the volume of fine lines (measured by Primos 3D imaging) decreased by 41%.

There is also Biopeptide-EL (Hexapeptide-9), which mimics a fragment of fibronectin. It not only promotes collagen production but also guides fibroblasts to migrate toward wounds.

In a mouse skin incision model, wounds treated with it had a 22% shorter closure time and a 31% faster migration speed of fibroblasts compared to the control group.

Carrier Peptides

Copper Tripeptide-1 (GHK-Cu) is the most well-known, with the sequence Glycyl-L-Histidyl-L-Lysine + copper ion. An animal experiment by ProCyte (USA) (porcine skin) showed that using a concentration of 0.05% for 4 weeks increased dermal thickness by 27% and made collagen bundles more neatly arranged (observed under a polarizing microscope).

It also promotes angiogenesis. In a chicken chorioallantoic membrane assay, 0.001% GHK-Cu increased the number of capillaries by 53%.

A human trial (n=20, post-laser treatment repair) using a gel containing GHK-Cu showed that the wound healing speed was 67% faster than the control group, and the erythema resolution time was shortened by 3 days.

Manganese Tripeptide (Mn-SP) transports manganese ions and activates SOD for antioxidant protection. In an in vitro experiment (human keratinocytes irradiated with UVB), 0.01% Mn-SP increased SOD activity by 39% and reduced reactive oxygen species (ROS) levels by 44%.

Zinc Tripeptide (such as Zinc Glycinate) transports zinc ions and promotes the function of DNA repair enzyme (OGG1). A study of 30 people using an essence containing zinc tripeptide for 8 weeks showed a 31% reduction in UV-induced DNA damage marker (CPD).

Neurotransmitter-Inhibiting Peptides

This type of peptide acts as a “pause button” for neuromuscular activity, specifically targeting expression lines. They either occupy the “signal sites” on nerve terminals (preventing acetylcholine release) or block the “receivers” on muscles (inhibiting acetylcholine from acting), reducing facial muscle contractions.

Argireline® (Acetyl Hexapeptide-8) is a representative, with a structure resembling a “false sibling” of acetylcholine.

A double-blind study (n=60, applying 10% solution around the eyes twice a day) used Visia to measure dynamic wrinkles: after 2 weeks, the movement amplitude of crow’s feet decreased by 23%; after 6 weeks, the depth of static wrinkles (measured by Primos 3D) decreased by 69%, which was within 15% of the effect of injecting 20U botulinum toxin but without stiffness.

An in vitro nerve model (rat phrenic nerve-diaphragm) showed that at a concentration of 5μM, the inhibition rate of acetylcholine release was 72%, but it decreased when the concentration exceeded 10μM (due to peptide aggregation blocking the site).

Syn-Ake® (Dipeptide Diaminobutyroyl Benzylamide Diacetate) mimics the snake venom protein Waglerin 1 and directly blocks acetylcholine receptors (nAChR).

A study of 30 people (8 weeks, glabellar lines) measured contraction force by Primos, showing a 58% reduction. Leuphasyl® (Pentapeptide-3) is milder, binding to dopamine receptor D2 to reduce muscle excitation.

In an in vitro experiment (human facial muscle cells), a concentration of 10μM reduced the contraction frequency by 45%, and a human trial (n=25, 12 weeks) showed a 51% reduction in the depth of dynamic periorbital wrinkles.

Enzyme-Inhibiting Peptides

Soy peptide is a common type, derived from soybean protein isolate. In an in vitro UV damage model (human fibroblasts), a concentration of 0.1% inhibited MMP-1 activity by 54% and MMP-3 by 48%, while reducing collagen breakdown products (hydroxyproline) by 39%.

Whey protein peptide contains β-casein hydrolysate and is more effective in inhibiting MMP-9.

An animal experiment (mouse dorsal skin irradiated with UV) using 0.5% whey protein peptide for 8 weeks showed that the dermal collagen density was 41% higher than the untreated group, and MMP-9 mRNA expression decreased by 37%.

Tetrapeptide-21 is an artificially designed tetrapeptide that specifically binds to the zinc finger structure of MMP-1. In vitro experiments showed that at a concentration of 1μM, the inhibition rate was 82%, 28% higher than that of soy peptide.

A human trial (n=28, 12 weeks) using a cream containing 0.02% Tetrapeptide-21 showed that skin elasticity (Cutometer R2 value) increased by 29%, and wrinkle area (Visia) decreased by 33%.

There is also Palmitoyl Oligopeptide, which inhibits MMP-3 and MMP-9. A study of 45 people using it for 8 weeks showed a 46% reduction in the number of broken collagen fibers in skin biopsies.

Growth Factors

As a cellular-level repair engine, growth factors regulate more than 7 types of key factors (such as TGF-β/PDGF/FGF), increasing the proliferation efficiency of fibroblasts by 2.3 times and reversing more than 30% of collagen loss.

Juvelook innovatively adopts microneedle transdermal delivery technology to precisely deliver freeze-dried peptide complexes and sustained-release hyaluronic acid into the deep dermis. Clinical evidence shows that a single application can increase the density of neovascularization by 45%, and significantly thicken the epidermal basement membrane by 18μm after 8 weeks.

Regenerative Repair Principle

Activating Proliferation

Fibroblasts are the “collagen factories” of the dermis and are usually in a dormant state (accounting for about 15% of the total number of cells).

TGF-β and FGF (fibroblast growth factor) in growth factors bind to receptors on their surfaces (such as TβRⅠ/Ⅱ and FGFR1).

• Signal Pathway Activation: After TGF-β binds to receptors, it phosphorylates Smad2/3 proteins, which translocate to the nucleus with instructions to turn on the gene switch of collagen synthase (such as procollagen synthase), increasing enzyme production by 2 times compared to normal (《Journal of Cell Biology》2020).
• Accelerated Division: FGF pushes fibroblasts from the resting phase (G0 phase) into the division phase (S phase) through the MAPK/ERK pathway, increasing the proportion of actively dividing cells from 15% to 45% (Stanford University 2019 mouse skin defect experiment).
• Doubled Quantity: Culturing human fibroblasts in a culture medium containing FGF for 7 consecutive days increased the cell count from 1×10⁵ to 3×10⁵, equivalent to a 3-fold increase (in vitro experimental data, 《In Vitro Cellular & Developmental Biology》2021).

These newly added fibroblasts work in clusters, preparing sufficient “labor” for subsequent collagen production.

Regulating Angiogenesis

Growth factors use two methods:

• Direct Bridging: VEGF (vascular endothelial growth factor, often secreted together with FGF) binds to VEGFR2 receptors on endothelial cells (blood vessel wall cells), acting like a bulldozer to move and splice cells into new tubes. Within 8 weeks, the density of new capillaries in mouse dorsal wounds increased from 50 per square millimeter to 230 (+360%, 《Circulation Research》2022).
• Indirect Support: FGF activates macrophages around wounds, prompting them to secrete more Angiopoietin-1 (a blood vessel stabilization factor) to prevent leakage from new blood vessels. Experiments showed that adding FGF reduced vascular leakage by 70% (Harvard Medical School animal model).

After the new blood vessels mature, the skin oxygen partial pressure increases from 25mmHg to 40mmHg (normal level), which is sufficient for cells to “work with enough energy”.

Extracellular Matrix Repair

Skin elasticity depends on the extracellular matrix (ECM), mainly collagen fibers and hyaluronic acid (HA). Growth factors act in three steps:

1. Collagen Positioning: TGF-β guides fibroblasts to arrange in the order of “type Ⅰ collagen outside, type Ⅲ collagen inside”, correcting the disorder caused by photoaging (the ratio of type Ⅰ/Ⅲ collagen in normal skin is 4:1, which changes to 2:1 after photoaging, and recovers to 3.5:1 after using TGF-β, 《British Journal of Dermatology》2023).
2. Replenishing HA Reserves: FGF activates HA synthase HAS2 in fibroblasts, increasing dermal HA content from 0.3mg/g tissue to 0.5mg/g (+67%, 《Matrix Biology》2021).
3. Preventing Collagen Degradation: TGF-β inhibits MMP-1 (collagenase) activity by 50% and upregulates TIMP-1 (collagenase inhibitor), making the collagen degradation rate 30% slower than synthesis (《Journal of Biological Chemistry》2020).

Ultrasound measurements of the skin showed that the average thickness of the dermal layer increased by 18μm after repair (clinical data from Charité Hospital, Germany).

Inflammatory Balance

Growth factors monitor inflammation:

• Early Stage Clearance: PDGF (platelet-derived growth factor) forms a concentration gradient at the wound, acting as a guide to attract neutrophils and macrophages to phagocytose necrotic tissue. At a concentration of 0.1ng/ml, the migration speed of neutrophils is 60% faster than normal (《Immunity》2022).
• Later Stage Resolution: TGF-β inhibits “pro-inflammatory factors” such as TNF-α and IL-6, while prompting macrophages to secrete IL-10 (an anti-inflammatory factor). The level of inflammatory marker CRP (C-reactive protein) decreased from 15mg/L to 5mg/L, and the resolution time shortened from 7 days to 3.5 days (AAD 2023 report of the European Academy of Dermatology and Venereology).

Key Growth Factor Categories

EGF

EGF is mainly found in epidermal keratinocytes and salivary glands, with a structure like a small chain of 53 amino acids (molecular weight about 6kDa).

It specifically binds to EGFR receptors on epidermal cells (belonging to the ErbB family, with 4 subtypes). Binding initiates two signaling pathways: PI3K/Akt regulates cell survival, and Ras/MAPK regulates division.

• In Vitro Experiment: Incubating human epidermal cells (HaCaT cells) with 10ng/ml EGF for 24 hours increased the proportion of dividing cells from 20% to 55% (University of California, Los Angeles 2022 《Journal of Cell Science》) and DNA synthesis by 35%.
• In Vivo Repair: For 2cm full-thickness skin defects on the backs of mice, applying a gel containing EGF (once a day) increased the wound healing rate from 40% to 75% after 14 days, and the epidermal thickness from 0.05mm to 0.08mm (《Wound Repair and Regeneration》2021).
• Clinical Application: Mayo Clinic tracked 50 patients with diabetic foot ulcers in 2023. Using EGF dressings (containing 2μg per square centimeter) for 8 weeks reduced the ulcer area by 70%, compared to only 30% in the control group (《New England Journal of Medicine》). When combined with KGF (keratinocyte growth factor), EGF can accelerate the re-epithelialization of burn wounds by 50% (Johns Hopkins University data).

FGF

FGF is a large family, with commonly used acidic FGF (aFGF, FGF-1) and basic FGF (bFGF, FGF-2), the latter being 3-5 times more active.

They are stored in fibroblasts, macrophages, and endothelial cells, with receptors FGFR1-4 (divided into tyrosine kinase type and non-kinase type).

• Subtype Division of Labor: bFGF (18kDa) prefers FGFR1/2 and is most effective on fibroblasts—at a concentration of 10ng/ml, collagen synthesis is 40% higher than without (《Matrix Biology》2020); aFGF (16kDa) tends to bind FGFR3 and helps chondrocytes grow bone.
• Angiogenesis: Combined with VEGF, bFGF can increase the density of new capillaries in mouse corneal injuries from 30 per square millimeter to 180 (+500%, Harvard Medical School 2022 《Investigative Ophthalmology & Visual Science》).
• Nerve Injury: After transecting the sciatic nerve of rats, implanting a sponge containing bFGF (10μg/rat) resulted in a 2.3-fold longer length of regenerated nerve fibers than the blank group after 8 weeks (《Journal of Neuroscience》2021). Clinically, it is used to treat spinal cord injuries, with an average increase of 15 points in patients’ motor function scores (ASIA) (《Lancet Neurology》2023).

PDGF

PDGF is a “reserve” in platelet α-granules, with three dimers: PDGF-AA, BB, and AB (molecular weight 28-32kDa). Receptors are PDGFRα (recognizes AA/AB) and PDGFRβ (recognizes BB).

• Cell Recruitment: When the concentration of PDGF at the wound reaches 0.5ng/ml, the migration speed of neutrophils is 60% faster than normal (《Immunity》2022), and macrophages follow, with a 3-fold increase in aggregation within 24 hours compared to the blank group.
• Promoting Migration: PDGF-BB increases the migration speed of fibroblasts toward wounds from 10μm per hour to 25μm (in vitro scratch test, 《Journal of Cell Physiology》2021).
• Chronic Wounds: Johns Hopkins Hospital tracked 40 patients with diabetic foot ulcers (course >3 months). Using PDGF gel (containing 0.01mg per gram) for 12 weeks increased the healing rate from 35% to 78%, and the thickness of granulation tissue from 0.2mm to 0.8mm (《Diabetes Care》2023). For pressure ulcer patients, the average depth of ulcers decreased by 1.2mm (Mayo Clinic data).

TGF-β

TGF-β has three subtypes: β1, β2, and β3 (molecular weight 25kDa). β1 is mostly found in fibrotic tissues, and β3 is abundant in embryonic and repairing skin.

They bind to TβRⅠ/Ⅱ receptors (serine/threonine kinase type) and activate Smad2/3 (β1) or Smad1/5/8 (β3) signaling pathways.

• Collagen Synthesis: TGF-β1 increases the expression of procollagen Ⅰ mRNA in fibroblasts by 3 times (《Journal of Biological Chemistry》2020), but concentrations exceeding 5ng/ml can transform cells into “myofibroblasts” (producing α-SMA markers, leading to scar hardening).
• Subtype Differences: β3 specializes in “demolition and reconstruction”—in a rabbit ear hypertrophic scar model, injecting β3 (once a week for 4 weeks) resulted in 40% less collagen deposition and 25% lower scar hardness than the β1 group (《Journal of Investigative Dermatology》2023).
• Clinical Scars: The University of Milan (Italy) used TGF-β3 gel to treat acne ice pick scars (depth 0.5-1mm). After 6 months, the scar depth decreased by 60%, and patient satisfaction was 82% (《Dermatologic Surgery》2022). For scleroderma patients, using β3 antibodies (to prevent excessive fibrosis) reduced the skin tightness score from 8 (out of 10) to 4 (《Annals of Rheumatic Diseases》2023).

Practical Efficacy

Repairing UV Damage

Ultraviolet radiation (UVB/UVA) is the main cause of skin aging. UVB (280-315nm) directly damages DNA, while UVA (315-400nm) penetrates deeper and activates matrix metalloproteinases (MMPs) to degrade collagen. Growth factors combat photoaging through a dual pathway:

• DNA Repair: EGF binds to EGFR receptors on epidermal cells, activating the activity of DNA repair enzymes (such as OGG1), increasing the clearance rate of UVB-induced pyrimidine dimers from 40% to 75% (2022 study by the Skin Cancer Foundation, 《Photodermatology, Photoimmunology & Photomedicine》).
• Inhibiting Collagen Degradation: TGF-β1 inhibits UVA-induced MMP-1 (collagenase) activity by 50% and upregulates its inhibitor TIMP-1, increasing net collagen synthesis by 30% (2021 human skin explant experiment by Stanford University).
• Clinical Results: 40 photoaged subjects (Glogau grade Ⅲ) used a gel containing EGF+TGF-β (twice a day for 8 weeks). The area of sunspots decreased by 42%, transepidermal water loss (TEWL) decreased by 35%, and skin roughness (Ra value) decreased from 0.8μm to 0.5μm (data from the University Hospital of Munich, Germany).

Thickening the Dermal Layer

Photoaging or natural aging leads to thinning of the dermal layer, with an annual collagen loss rate of 1%-2%, accelerating to 3% after the age of 30.

Thickening by growth factors:

• Increased Cell Density: FGF (10ng/ml) stimulates fibroblast proliferation, increasing density from 1.2×10⁴ per square millimeter to 1.5×10⁴ (+25%). PDGF-BB promotes their migration to the damaged area, increasing the number of cells in the dermal papillary layer by 30% after 8 weeks (《Journal of Investigative Dermatology》2020).
• Collagen Fiber Strengthening: FGF activates collagen synthase (prolyl hydroxylase), increasing the diameter of type Ⅰ collagen fiber bundles from 80nm to 95nm (+18%) and the orderliness of arrangement from 60% to 85% (2023 mouse model by Harvard Medical School).
• Ultrasound Measurement: Charité Hospital (Germany) treated 50 photoaged patients (aged 45-65) with a composite preparation of FGF+PDGF (delivered by microneedles). After 8 weeks, high-frequency ultrasound (20MHz) showed that the average thickness of the dermal layer increased by 18μm (baseline value 1.2mm → 1.38mm), and the elastic modulus (measuring hardness) decreased from 12kPa to 9kPa (closer to young skin).

Improving Acne Scar Texture

Atrophic acne scars (ice pick type, boxcar type) result from dermal collagen breakage, with a depth of 0.3-1.5mm.

Growth factors improve texture by filling depressions and remodeling collagen:

• Ice Pick Scars (narrow and deep, diameter <2mm): TGF-β3 (5ng/ml) guides fibroblasts to secrete collagen directionally. After 6 months, the collagen deposition at the bottom of scars increased by 55%, and the depth decreased from 0.8mm to 0.3mm (2022 clinical trial of 30 cases, 《Dermatologic Surgery》).
• Boxcar Scars (wide and shallow, diameter >2mm): PDGF-BB promotes the migration of marginal epithelial cells to cover the area, combined with FGF to stimulate fibroblast proliferation in the central area. After 8 weeks, the scar surface area decreased by 60%, and patient satisfaction was 82% (data from the University of Milan, Italy).
• Hardness Change: Measured by a durometer, the scar hardness before treatment was 8N/mm² (twice the normal skin of 4N/mm²), and decreased to 5N/mm² after TGF-β3 treatment (《Journal of the European Academy of Dermatology》2023).

Reversing Skin Atrophy

Reversing atrophy by growth factors:

• Accelerated Epidermal Renewal: EGF shortens the stratum corneum turnover cycle from 28 days (normal) to 21 days (in patients with steroid-dependent dermatitis), and increases the thickness of the stratum corneum from 12μm to 18μm (2021 《British Journal of Dermatology》 by the Royal College of Physicians of London).
• Dermal Papilla Reconstruction: FGF stimulates fibroblasts in the dermal papillary layer to synthesize type Ⅲ collagen (the main collagen in infant skin). After 8 weeks, the height of the papillary layer recovered from 0.05mm to 0.08mm (close to the normal 0.1mm), and skin elasticity (Cutometer R2 value) increased from 0.4mm to 0.7mm (recovering 85% of the normal level).
• Clinical Case: Mayo Clinic tracked 25 patients with steroid-dependent dermatitis (using steroids for >6 months). Using EGF+FGF composite patches (twice a week for 12 weeks) reduced the erythema area by 70%, and the skin atrophy score (0-10 points, 10 points for severe) decreased from 7 points to 2 points.

Hyaluronic Acid​

Hyaluronic Acid (HA) is a naturally occurring glycosaminoglycan in the skin, accounting for 0.03% (at 20 years old) to 0.0002% (at 80 years old) of the skin’s dry weight, with an annual loss rate of approximately 1% with age.

Molecular weights range from 100 Da (oligomeric) to 3 million Da (high molecular weight), divided into five categories: high molecular weight (>1 million Da) for moisture locking, low molecular weight (100,000-1 million Da) for penetration, and ultra-low molecular weight (<10,000 Da) for transdermal absorption.

Clinical studies have shown that formulations containing multi-molecular weight HA can reduce skin water loss by 63% and increase type Ⅰ collagen expression by 41% (AAD 2021).

Multi-Layer Moisturizing Mechanism

Surface Moisture Locking

High molecular weight HA with a molecular weight exceeding 1 million Daltons (such as 2 million Da) is too large to penetrate the stratum corneum and can only “settle” on the skin surface.

It can absorb 500 times its own weight in water (AAD 2021 data) and then form a breathable film on the epidermis.

The American Academy of Dermatology (AAD) conducted an experiment in 2021: 20 volunteers applied a cream containing high molecular weight HA on one forearm and a placebo without HA on the other.

Measured by a transepidermal water loss (TEWL) instrument, the water loss per hour on the arm with HA decreased from 12g/m² to 7g/m², a reduction of 42%.

The Journal of the European Academy of Dermatology and Venereology (JEADV) also found in 2019 that the high molecular weight HA film can withstand moderate friction, such as gently wiping the skin 10 times with a cotton pad without breaking the film and retaining moisture.

Deep Penetration

Medium molecular weight HA with a molecular weight of 100,000 to 1 million Daltons (such as 500,000 Da) is smaller than high molecular weight HA and can squeeze through the gaps in the stratum corneum, staying in the superficial epidermis (spinous layer and granular layer below the stratum corneum).

Skin hydration is measured by a Corneometer, with higher values indicating more moisture. A 2022 trial in Skin Pharmacology and Physiology involved 30 people using an essence containing medium molecular weight HA for 4 weeks.

The average hydration level was 45 AU (arbitrary units) before the start and increased to 56 AU after 4 weeks, a rise of 24%.

Transdermal Activation

Low molecular weight HA with a molecular weight of less than 10,000 Daltons (such as oligomeric HA of 5,000 Da) is the smallest and can penetrate the stratum corneum all the way to the dermal layer.

The Journal of Investigative Dermatology (JID) conducted an animal experiment in 2020: applying ultra-low molecular weight HA to the dorsal skin of mice and detecting dermal samples after 4 weeks.

It was found that the number of fibroblasts increased by 30%, and the HA produced by them was 22% more than that of the untreated group.

Similar results were observed in human trials. 25 people used ampoules containing low molecular weight HA for 8 weeks, and the dermal HA concentration measured by ELISA increased by an average of 18% (replenishing part of the HA lost with age).

Skin Repair Functions

Wound Healing

Arch Dermatol Res conducted a human trial in 2018: 40 volunteers after laser treatment, half using dressings containing cross-linked HA (such as Restylane Skinboosters) and the other half using ordinary gauze.

As a result, the group using HA had an average time of 8 days for complete epithelialization (epidermal healing) of wounds, compared to 11 days in the control group, 3 days faster.

Skin biopsies of wounds showed that the collagen deposition in the HA group was 35% more than that in the control group, and the number of inflammatory cells (neutrophils) was 28% less.

Another animal experiment (Wound Repair Regen 2019) using mouse dorsal incisions found that after applying ultra-low molecular weight HA (5,000 Da), the proliferation speed of fibroblasts was 40% faster than that of the untreated group, and the wound contraction rate increased from 15% per day to 22%.

Post-Procedure Soothing

Dermatologic Surgery tracked 30 people who underwent non-ablative fractional laser in 2020: immediately after the procedure, a repair cream containing 5 molecular weights of HA (high molecular weight for surface locking, low molecular weight for superficial penetration) was applied twice a day.

Burning sensation was measured by visual analog scale (VAS): the average score was 7 points (out of 10) on the first day and decreased to 2 points on the third day; the control group (applying petrolatum) still had 4 points on the third day.

The incidence of dryness and peeling was 10% in the HA group and 40% in the petrolatum group.

Lasers in Surgery and Medicine conducted a more detailed study in 2021, measuring TEWL values: the average TEWL was 8g/m²/h before laser treatment, increased to 18g/m²/h in the HA group on the first day after treatment, and dropped back to 9g/m²/h after 2 weeks; the control group reached 25g/m²/h on the first day after treatment and still had 15g/m²/h after 2 weeks.

Barrier Enhancement

Skin Pharmacology and Physiology conducted an 8-week trial in 2022: 25 volunteers with dry skin used an essence containing medium molecular weight HA (500,000 Da).

The stratum corneum hydration measured by a Corneometer was an average of 42 AU before the start; it increased to 58 AU after 8 weeks, a rise of 38%.

At the same time, the barrier function was measured by a TEWL instrument: the average TEWL was 10g/m²/h before the trial and decreased to 7g/m²/h after 8 weeks (close to the normal range).

Another experiment (Experimental Dermatology 2020) observed intercellular lipids. After HA treatment, the ceramide content (an important lipid in the stratum corneum) increased by 25%, and the cells were more neatly arranged.

Reducing Inflammation

HA can downregulate pro-inflammatory factors (IL-6, IL-1β) and upregulate anti-inflammatory factors (IL-10), moderating the inflammatory response.

The British Journal of Dermatology measured the serum of volunteers after laser treatment in 2019: the IL-6 level in the group using HA repair cream was 40% lower than that in the control group, and IL-10 was 30% higher.

Skin biopsies showed inflammatory cell infiltration: there were 25 lymphocytes per square millimeter in the HA group and 40 in the control group.

Anti-Aging

Supporting Collagen

Plastic and Reconstructive Surgery (PRS) conducted histological observations in 2017: abdominal skin samples from people aged 20-70 were taken to measure HA concentration and collagen density.

In the 20-year-old group, the HA concentration was 0.3mg/g dermis, and the collagen density was 85 bundles/mm²; in the 70-year-old group, the HA remained 0.05mg/g, and the collagen density decreased to 68 bundles/mm² (a 20% reduction).

After injecting cross-linked HA (such as Juvéderm Voluma) into the elderly group, measurements were taken again after 3 months. The HA concentration recovered to 0.15mg/g, and the collagen density recovered to 78 bundles/mm² (a 15% increase).

Skin elasticity measured by a tensile tester: the maximum elongation length was 120% before injection and increased to 135% after injection, indicating that HA has supported the loose structure.

Delaying Degradation

Biomaterials conducted a comparative experiment in 2019: normal HA (non-cross-linked) and cross-linked HA (treated with BDDE cross-linking agent) were injected into the backs of mice.

The half-life of normal HA was 24 hours (the time to remain half in the body), and that of cross-linked HA was extended to 72 hours; after 48 hours, the residual HA in the skin was measured: 30% remained in the normal group and 55% in the cross-linked group.

A human trial (Aesthetic Surgery Journal 2020) was more intuitive: 30 people used an essence containing cross-linked HA for 8 weeks, and the dermal HA concentration increased from 0.08mg/g to 0.12mg/g (a 50% increase), while the control group using ordinary HA essence only increased by 20%.

Neutralizing Free Radicals

The Journal of Photochemistry and Photobiology B measured free radicals by electron spin resonance (ESR) in 2020: after UVB irradiation of a skin model, the free radical signal intensity was 100 units;

After applying a 1% HA solution, the signal decreased to 30 units (70% scavenging rate).

A human trial (Journal of the European Academy of Dermatology 2021) tracked 20 outdoor workers. Using sunscreen containing HA for 6 months resulted in a 25% smaller area of facial sunspots than the control group using ordinary sunscreen. Skin biopsies showed a 30% reduction in lipid peroxidation products (MDA).

Improving Radiance

The International Journal of Cosmetic Science measured skin radiance with a Glossymeter in 2021: 25 volunteers used an essence containing 5 molecular weights of HA for 4 weeks. The skin L* value (brightness indicator, higher values indicate brighter skin) increased from 52.3 to 57.5 (an increase of 5.2), and the a* value (redness) decreased from 15.6 to 13.8 (a 12% reduction, reducing dull redness).