Palmitoyl tetrapeptide-3 (Tego pep) is a synthetic signal-functional polypeptide with the CAS number 1228558-05-1, molecular formula C₂₄H₄₄N₆O₉ and molecular weight of 560.65. Derived from the amino acid fragment at positions 341–344 of the heavy chain of human immunoglobulin G, it is modified via palmitoylation. It is widely adopted in efficacy skincare and biological anti-inflammatory research. Its core merit lies in targeted regulation of inflammation and immune balance, focusing on ameliorating cutaneous aging triggered by chronic low-grade inflammation. It suppresses inflammatory responses induced by external irritants such as ultraviolet rays and pollutants, alleviates the degradation of cutis matrix by pro-inflammatory factors, and moderately modulates the activity of cutaneous immune cells. Featuring triple effects of anti-inflammation, anti-aging and cutis repair alongside extremely high safety and zero irritation, it suits all cutaneous types, especially sensitive cutis, ranking among the core active ingredients for mild efficacy skincare.
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Palmitoyl Tetrapeptide-3 COA
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| Certificate of Analysis | ||
| Compound name | Palmitoyl Tetrapeptide-3 | |
| Grade | Pharmaceutical grade | |
| CAS No. | 1228558-05-1 | |
| Quantity | 30g | |
| Packaging standard | PE bag+Al foil bag | |
| Manufacturer | Shaanxi BLOOM TECH Co., Ltd | |
| Lot No. | 202601090056 | |
| MFG | Jan 9th 2026 | |
| EXP | Jan 8th 2029 | |
| Structure |
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| Item | Enterprise standard | Analysis result |
| Appearance | White or almost white powder | Conformed |
| Water content | ≤5.0% | 0.32% |
| Loss on drying | ≤1.0% | 0.28% |
| Heavy Metals | Pb≤0.5ppm | N.D. |
| As≤0.5ppm | N.D. | |
| Hg≤0.5ppm | N.D. | |
| Cd≤0.5ppm | N.D. | |
| Purity (HPLC) | ≥99.0% | 99.98% |
| Single impurity | <0.8% | 0.26% |
| Total microbial count | ≤750cfu/g | 450 |
| E. Coli | ≤2MPN/g | N.D. |
| Salmonella | N.D. | N.D. |
| Ethanol (by GC) | ≤5000ppm | 500ppm |
| Storage | Store in a sealed, dark, and dry place below 2-8°C | |
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Selective Inhibition Mechanism against MMP Family
Dynamic equilibrium of the dermal extracellular matrix is the core of maintaining firm, smooth and plump cutis. The matrix metalloproteinase (MMP) family acts as a key enzyme system governing cutaneous matrix degradation. The human cutis contains multiple MMP subtypes with striking disparities in substrate specificity, expression profiles and physiological functions. Among them, MMP-1, MMP-2 and MMP-9 are the primary subtypes responsible for cutaneous aging, collagen loss and cutaneous laxity. Unlike conventional broad-spectrum MMP inhibitors, palmitoyl tetrapeptide-3 features high subtype-selective inhibitory activity. It avoids indiscriminate suppression of all MMP subtypes that would disrupt normal skin matrix remodeling metabolism, and only targets and inhibits abnormally overexpressed aging-related MMP subtypes. It stabilizes dermal matrix homeostasis via synergistic multi-pathway effects, whose detailed inhibitory mechanisms are elaborated in three tiers as follows.
Targeted Inhibition of Inflammation-Mediated Aberrant Transcriptional Activation of MMPs
In both chronological cutaneous aging and UV-induced photoaging, inflammatory stress serves as the core trigger for excessive upregulation of MMPs. UVB irradiation and oxidative stress trigger inflammatory cascades in keratinocytes and dermal fibroblasts, which secrete abundant pro-inflammatory cytokines including IL-6 and TNF-α. These cytokines further activate two core intracellular transcriptional pathways, NF-κB and AP-1, driving excessive transcription of MMP-1, MMP-2 and MMP-9 genes. Consequently, collagen degradation outpaces collagen synthesis, ultimately inducing aging manifestations such as fine lines, laxity and epidermal thinning. Tego pep precisely blocks this inflammation-proteolysis cascade. Its peptide chain specifically binds to inflammatory receptors on fibroblasts, markedly downregulates the synthesis and release of pro-inflammatory cytokines like IL-6, and attenuates the activation of transcriptional pathways triggered by inflammatory signals at the source.
Numerous in vitro cellular experiments verify that this active peptide reduces IL-6 secretion by over 40% in UVB-stimulated dermal fibroblasts, thereby suppressing NF-κB nuclear translocation and AP-1 transcription factor activation to block gene transcription of aging-associated MMP subtypes. In contrast to non-selective MMP inhibitors, tego pep does not inhibit basal MMP expression required for normal cutaneous metabolism. It only counteracts abnormal transcription induced by inflammatory stress, which not only prevents collagen loss from excessive proteolysis but also preserves the physiological functions of MMPs in matrix remodeling and cellular metabolism, delivering precise inhibitory effects. Additionally, its palmitoyl lipid chain enhances cellular adhesion and extends its residence time in the dermis, continuously and stably restraining inflammation-mediated abnormal MMP activation to sustain long-term anti-inflammatory and anti-aging cutaneous status.
Differentiated Modulation of MMP Subtype Activities for Selective Suppression
Distinct differences in protein structure and catalytic activity across MMP subtypes constitute the structural basis and core functional mechanism underlying the selective inhibition by palmitoyl tetrapeptide-3. During cutaneous aging, MMP-1, an interstitial collagenase, specifically degrades type I and type III fibrillar collagens in the dermis, acting as the key enzyme responsible for damaged collagen frameworks and fine lines. As gelatinases, MMP-2 and MMP-9 primarily break down collagen degradation fragments and type IV basement membrane collagen, disrupting the cutaneous barrier and dermal junction structures and aggravating cutaneous laxity and dullness. Certain low-expressed MMP subtypes participate in physiological cutaneous wound repair and cell renewal; over-inhibition of these subtypes impairs the skin's self-repair capacity.
Tego pep enables differentiated regulation according to functional discrepancies among MMP subtypes, exerting prominent inhibitory effects on high-risk aging-related subtypes while producing negligible interference with physiological subtypes. At the enzymatic activity level, the peptide undergoes spatial molecular embedding to bind the catalytic active centers of MMP-1 and MMP-9, occupying substrate binding pockets and blocking the binding pathway between enzymes and collagen substrates to directly reduce catalytic activity. In vitro enzymatic activity assays demonstrate that its half-maximal inhibitory concentration (IC50) against MMP-1 and MMP-9 falls within the low molar range. It reduces MMP-1 activity by 25%–30% and MMP-9 activity by 20%–28% under inflammatory conditions, effectively arresting abnormal degradation of fibrillar collagens and basement membrane collagens.
Meanwhile, the peptide exhibits no significant inhibitory impact on MMP-3, MMP-7 and other subtypes involved in routine cutaneous metabolism, without interfering with fundamental dermal matrix remodeling and cellular turnover. Such selectivity stems from the high matching degree between its specific peptide sequence and the active centers of high-risk MMP subtypes: it only recognizes characteristic structures of aging-related subtypes and fails to bind physiological MMP variants. This achieves precise targeted inhibition at the molecular level and eliminates side effects of broad-spectrum inhibitors, including disrupted cutaneous metabolism and compromised repair capacity.
Upregulation of TIMP Expression to Establish an Endogenous MMP Homeostasis Regulatory System
Human cutis inherently contains the tissue inhibitor of metalloproteinase (TIMP) family, which endogenously binds and suppresses MMP activity. Under physiological conditions, MMPs and TIMPs maintain dynamic balance to stabilizecutis matrix metabolism. One core driver of cutaneous aging is diminished TIMP expression, which weakens endogenous MMP suppression and leads to abnormal MMP accumulation and excessive collagen breakdown. Tego pep remodels the endogenous MMP-TIMP balance by modulating TIMP gene expression, realizing long-term selective inhibition through an indirect pathway.
Studies confirm that tego pep significantly boosts gene transcription and protein synthesis of TIMP-1 and TIMP-2 in fibroblasts. TIMP-1 specifically binds MMP-1 and MMP-9, while TIMP-2 targets MMP-2 activity, perfectly matching the high-risk MMP subtypes subject to its selective inhibition. This regulatory mode differs from direct enzymatic activity blockade, representing physiological endogenous modulation that restores dysregulated metabolic mechanisms in aged cutis rather than merely inhibiting enzyme activity via exogenous intervention. Elevated endogenous TIMP expression enables the cutis to autonomously suppress abnormally activated aging-related MMP subtypes without impairing MMP functions essential for normal physiological metabolism, yielding persistent and stable matrix protection.
Chemical Properties
Its molecular structure comprises a hydrophobic palmitoyl moiety and a hydrophilic GQPR peptide chain, presenting typical amphipathic characteristics. It boasts stable physicochemical properties compatible with conventional production and storage conditions of skincare products.
At ambient temperature, it appears as white or off-white crystalline powder, odorless and non-irritating, with purity exceeding 99% and extremely low impurity content, suitable for topical cutaneous application.
It exhibits distinctive solubility: it is barely water-soluble with aqueous solubility below 0.1 mg/mL at room temperature, soluble in organic solvents such as DMF, and disperses well in oil-water composite systems. Uniform distribution can be achieved through formulation optimization, matching diverse skincare dosage forms including lotions, essences and creams.
The polypeptide possesses superior acid-base stability, retaining intact molecular structure and steady biological activity for long durations in neutral to weakly acidic environments with pH ranging from 5.0 to 7.0. This matches the weakly acidic physiological environment of human cutis, preventing structural degradation after topical application and sustaining persistent bioactivity.
References
- Schagen S K. Topical peptide treatments with effective anti-aging results[J]. Cosmetics, 2017, 4(2): 16.
- Mondon P, et al. Evaluation of dermal extracellular matrix and epidermal–dermal junction modifications using matrix‐assisted laser desorption/ionization mass spectrometric imaging[J]. Journal of cosmetic dermatology, 2015, 14(2): 152-160.
- Fengzhu Li, et al. Clinical evidence of the efficacy and safety of a new multi-peptide anti-aging topical eye serum[J]. J Cosmet Dermatol, 2023, 22(12):3340-3346.
- MolAid Chemistry. Handbook on Physicochemical Properties and Applications of Palmitoyl Tetrapeptide-3[EB/OL]. 2026.
- Sohu Popular Science. Research on Skin Physiological Regulatory Mechanisms of Palmitoyl Tetrapeptide-3[EB/OL]. 2025.
FAQ
What is palmitoyl Tripeptide 3?
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Palmitoyl Tripeptide-3, also known as Palmitoyl Tripeptide-3, is an advanced cosmetic ingredient that is frequently used in skincare products. This peptide, composed of three amino acids, has the ability to stimulate collagen production and improve skin elasticity.
What are the core advantages of the product compared with ordinary skincare peptides?
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Most common anti-aging peptides mainly focus on directly stimulating collagen synthesis to improve superficial wrinkles. Differently, the product targets the source of skin aging-inflammatory damage. It blocks the NF-κB inflammatory signaling pathway, regulates skin immune balance, and inhibits the degradation of collagen and elastin caused by chronic low-grade inflammation. It achieves triple effects of inflammation suppression, skin barrier stabilization and anti-aging, effectively improving inflammatory aging problems such as skin redness, sensitivity, dullness and sagging caused by ultraviolet radiation, pollution and stress.
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