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Palmitoyl tetrapeptide-7 injection (N-Palmitoylrigin) is a widely used synthetic lipopeptide active ingredient in skincare, with the core sequence Palmitoyl-Glycine-Glutamine-Proline-Arginine (Pal-GQPR). It has a molecular weight of approximately 694.91 g/mol and a CAS Registry Number of 221227-05-0. Derived from the amino acid fragment at positions 224–227 of the heavy chain of human immunoglobulin IgG, this peptide undergoes palmitoylation acylation modification to drastically boost lipophilicity. It can efficiently penetrate the stratum corneum barrier and reach the dermis to act on fibroblasts and keratinocytes.
As a classic anti-aging signaling peptide, its core advantage lies in targeted intervention against skin inflammaging. Unlike single collagen-stimulating ingredients, it delivers dual anti-aging efficacy through an integrated mechanism: mitigating inflammation to preserve the extracellular matrix (ECM) and exerting antioxidant effects to repair skin cells.
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Palmitoyl tetrapeptide-7 COA
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| Certificate of Analysis | ||
| Compound name | Palmitoyl Tetrapeptide-7 | |
| Grade | Pharmaceutical grade | |
| CAS No. | 221227-05-0 | |
| Quantity | 65g | |
| 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% | 0.24% |
| Loss on drying | ≤1.0% | 0.13% |
| 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% | 99.90% |
| Single impurity | <0.8% | 0.44% |
| Total microbial count | ≤750cfu/g | 400 |
| E. Coli | ≤2MPN/g | N.D. |
| Salmonella | N.D. | N.D. |
| Ethanol (by GC) | ≤5000ppm | 560ppm |
| Storage | Store in a sealed, dark, and dry place below 2-8°C | |
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| Chemical Formula | C34H62N8O7 |
| Exact Mass | 694.47 |
| Molecular Weight | 694.92 |
| m/z | 694.47 (100.0%), 695.48 (36.8%), 696.48 (6.6%), 695.47 (3.0%), 696.48 (1.4%), 696.47 (1.1%) |
| Elemental Analysis | C, 58.77; H, 8.99; N, 16.13; O, 16.12 |
Mechanisms of Extracellular Matrix (ECM) Remodeling
Regulate Inflammatory Pathways to Inhibit ECM Degradation
The skin extracellular matrix (ECM) is a three-dimensional meshwork composed of collagen, elastin, glycosaminoglycans, laminins and other components, serving as the core structural framework that sustains skin firmness, elasticity and plumpness. Imbalanced ECM metabolism-where degradation outpaces synthesis-is the primary pathological driver of skin sagging, wrinkle formation and rough texture. During skin aging, stressors including ultraviolet irradiation, environmental pollutants and cellular metabolic disorders trigger low-grade chronic skin inflammation, termed inflammaging.
This persistently activates inflammatory signaling cascades and triggers massive secretion of pro-inflammatory cytokines such as Interleukin-6 (IL-6) and Interleukin-8 (IL-8), completely disrupting the dynamic equilibrium of the ECM. The core regulatory mechanism of palmitoyl tetrapeptide-7 injection is to selectively block inflammation-mediated ECM degradation pathways, thereby delaying matrix loss at the source.
This ingredient specifically targets dermal fibroblasts and epidermal keratinocytes to precisely downregulate gene expression and secretion levels of pro-inflammatory factors IL-6 and IL-8, delivering both basal and stress-induced anti-inflammatory benefits.
Under normal physiological skin conditions, it lowers baseline cellular inflammation and reduces chronic, sustained ECM depletion. Its inhibitory effect is markedly amplified under external stress such as UV exposure and particulate pollution. Laboratory data demonstrates that it reduces UV-induced IL-6 secretion in skin cells by 86%, effectively halting explosive amplification of inflammatory cascades. Compared with broad-spectrum anti-inflammatory agents, N-palmitoylrigin exhibits high target specificity: it only suppresses abnormal aging-associated inflammatory signals without interfering with the skin's normal immune defense functions, thus avoiding adverse outcomes linked to immunosuppression including cutaneous hypersensitivity and impaired barrier function.
Excessive secretion of inflammatory cytokines is the primary trigger for the activation of matrix metalloproteinases (MMPs). The MMP enzyme family specifically breaks down Type I and Type IV collagen as well as elastin, acting as key mediators of ECM breakdown. By drastically lowering concentrations of pro-inflammatory factors such as IL-6, N-palmitoylrigin indirectly suppresses aberrant activation and overexpression of MMPs, effectively halting proteolytic hydrolysis of collagen and elastin and preserving the structural integrity of native skin ECM.
Meanwhile, it downregulates inflammation-triggered matrix degradation signals, reduces accumulation of ECM debris and prevents secondary inflammation caused by persistent cellular stimulation from degradation fragments. This establishes a virtuous cycle of anti-inflammation, matrix protection and microenvironment stabilization, fundamentally arresting cutaneous structural collapse and aging.
Activate Matrix Synthesis Pathways to Repair ECM Meshwork
Beyond its ECM-protective properties, N-palmitoylrigin mimics the function of endogenous human matrix signaling peptides to actively activate matrix synthetic machinery in skin cells, boost production of core ECM components and facilitate repair and remodeling of damaged matrix. Endogenous matrix peptides in human skin transmit repair signals upon minor ECM damage and induce fibroblasts to synthesize new matrix proteins. However, this native signaling pathway undergoes substantial attenuation with advancing age, diminishing the skin's intrinsic ECM repair capacity.
As an artificially optimized matrix-mimicking peptide, N-palmitoylrigin accurately substitutes natural signaling peptides to stimulate fibroblast proliferation and differentiation and reactivate the skin's self-repair program.
In vitro cellular assays confirm that this ingredient significantly upregulates expression of Type I collagen, Type IV collagen and Laminin V in fibroblasts. Among these, Type IV collagen synthesis rises by 327% and glycosaminoglycan synthesis increases by 287%, which effectively reinforces basement membrane architecture and elevates dermal matrix density. Type I collagen, the major structural protein of the dermis, determines skin firmness and supportive capacity.
Type IV collagen and laminins constitute the core basement membrane components that stabilize epidermal-dermal adhesion, ameliorating sagging skin, fine lines and enlarged pores. Additionally, it promotes ordered synthesis and cross-linking of elastin, repairs fractured elastic fiber networks and restores skin resilience to resolve age-related laxity and ptosis.
Within the Matrixyl 3000 composite system, palmitoyl tetrapeptide-7 injection exhibits perfect synergistic efficacy with Palmitoyl Tripeptide-1 to dramatically optimize ECM remodeling outcomes.
Palmitoyl Tripeptide-1 primarily directly stimulates de novo matrix synthesis, while N-palmitoylrigin eliminates inflammatory interference and blocks matrix degradation. Their combination delivers bidirectional regulation that simultaneously boosts synthesis and suppresses breakdown, maintaining a sustained ECM synthesis rate exceeding degradation and gradually repairing aged, impaired cutaneous meshwork. Compared with single-peptide ingredients, this composite formulation multiplies matrix remodeling efficacy, effectively addressing deep aging concerns including static wrinkles, dermal thinning and dehydrated, gaunt skin to achieve fundamental restoration of skin structure.
Optimize Cellular Microenvironment to Sustain ECM Dynamic Homeostasis
Healthy ECM homeostasis relies not only on balanced matrix protein synthesis and degradation but also on the skin's cellular microenvironment and metabolic status. Aged skin frequently suffers from metabolic dysregulation, buildup of inflammatory waste products and aberrant keratinocyte differentiation, which continuously destabilize ECM architecture and prevent long-lasting repair efficacy. N-Palmitoylrigin modulates cellular physiology across multiple dimensions to refine the skin microenvironment and provide stable support for ECM remodeling.
On one hand, it enhances phagocytic and metabolic activity of skin cells to accelerate clearance of ECM degradation fragments, oxidative waste and inflammatory metabolites, reducing dermal accumulation of harmful substances that would otherwise perpetuate inflammatory reactions and abnormal matrix breakdown, and ensuring unobstructed ECM metabolic circulation.
On the other hand, it modulates epidermal differentiation, downregulates expression of aging-related microRNA-145, augments basal stem cell activity in the skin and stabilizes epidermal barrier structure.
An intact epidermal barrier limits penetration of external irritants and reduces dermal inflammatory stress, shielding dermal ECM repair and maintenance from the skin surface and forming a layered anti-aging system that stabilizes the epidermal barrier and repairs dermal matrix. Furthermore, it regulates cutaneous water and nutrient metabolism, elevates the water-retention capacity of glycosaminoglycans to plump dermal interstitial tissue, rendering newly synthesized ECM fuller and more stable, preventing secondary sagging and collapse of repaired matrix and sustaining youthful skin structure long-term.
Research and development of N-palmitoylrigin dates back to the 1980s.
In 1981, scientists first isolated the GQPR tetrapeptide fragment from the heavy chain of human immunoglobulin IgG, verified its immunomodulatory and phagocytosis-stimulating bioactivity, and defined its fundamental biological functions, laying the core foundation for subsequent applied development.
In 2000, Franceschi et al. proposed the core inflammaging theory, establishing chronic low-grade inflammation as a central driver of skin aging. This provided theoretical backing for the development of targeted anti-inflammatory anti-aging peptides and accelerated translational research into skincare applications of the GQPR peptide.
Sederma, a renowned French raw material manufacturer now part of the Croda Group, optimized the structure of native GQPR based on the above research. Palmitoylation acylation modification was implemented to enhance skin penetration and bioavailability, yielding N-palmitoylrigin, which was assigned the commercial name Rigin.
The ingredient was initially named Palmitoyl Tetrapeptide-3 before being renamed palmitoyl tetrapeptide-7 injection in compliance with international cosmetic ingredient nomenclature standards.
In 2004, Sederma formulated it with Palmitoyl Tripeptide-1 to launch the iconic anti-aging complex Matrixyl 3000. Following validation of its anti-aging efficacy via multiple in vitro trials and human clinical studies, the ingredient entered large-scale global skincare applications and established itself as a benchmark anti-inflammatory anti-aging peptide raw material.
References
- PeptideInsight. Palmitoyl Tetrapeptide-7 (Pal-GQPR, Rigin)[EB/OL]. 2026.
- PeptideJournal. Palmitoyl Tetrapeptide-7: Anti-Aging Research[EB/OL]. 2025.
- Kopeptide Biotech. Research on Efficacy and Mechanism of Palmitoyl Tetrapeptide-7 Raw Material[EB/OL]. 2026.
- Sederma SAS. Clinical Research Report on Matrixyl 3000 Ingredient Efficacy[R]. 2004.
- Franceschi C. Inflammaging Theory and Skin Aging Mechanism[J]. International Journal of Cosmetic Science, 2000.
FAQ
What does it do for skin?
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It has collagen-boosting properties that target wrinkles and fine lines. It also helps restore the skin's firmness and elasticity by supporting the skin's structural components, leading to a firmer and more youthful appearance. Further, this peptide is known for its anti-inflammatory and hydrating benefits.
What skin problems can it improve?
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It targets multiple typical aging and sub-health skin problems. For aging skin, it improves fine dry lines, shallow static wrinkles, loose skin, and decreased elasticity by repairing ECM structure. For photodamaged skin, it relieves UV-induced redness, dullness, and rough texture, and delays photoaging progression. For sensitive and inflamed skin, it reduces chronic low-grade inflammation, calms skin redness, and stabilizes the skin barrier. In addition, it improves uneven skin tone caused by inflammation and oxidation, making the skin smoother, brighter, and more resilient.
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