Anti-Photoaging Potential of Artemia Extract: UV-Induced Damage Cascades, HSP70-Related Stress Protection, and GP4G Metabolic Insights
Anti-Photoaging Potential of Artemia Extract: UV-Induced Damage Cascades, HSP70-Related Stress Protection, and GP4G Metabolic Insights
1 Source and Bioactive Basis of Artemia Extract
1.1 Raw Material Source
The cosmetic ingredient name for Artemia-derived extract is generally Artemia Extract, a biological extract obtained from brine shrimp. Artemia, also known as brine shrimp or sea monkeys, are small crustaceans capable of surviving environmental stresses such as high salinity, desiccation, and temperature fluctuations. The European Commission’s CosIng cosmetic ingredient database describes Artemia Extract as a brine shrimp extract derived from Artemia salina and classifies its function as skin conditioning.
The research interest in Artemia Extract for skincare primarily stems from the exceptional survival capacity of Artemia embryos. Under unfavorable environmental conditions, Artemia embryos can enter a dormant, low-metabolic state and rapidly resume development when conditions improve. This process involves energy conservation, metabolic reactivation, protein protection, and cellular stress resistance, which have certain mechanistic parallels with the repair requirements of skin exposed to ultraviolet radiation, heat, and oxidative stress.
1.2 Key Bioactive Insights
Artemia Extract is not a single compound. Different Artemia extracts may contain nucleotides, peptides, proteins, and other water-soluble components. Their specific composition is influenced by factors such as the Artemia species, the condition of the raw material, the extraction process, and quality standards. Differences among raw material suppliers, extraction methods, and quality specifications can therefore affect the bioactive composition of the extract.
Two principal bioactive lines of investigation are frequently discussed in skincare research and commercial raw material documentation:
Bioactive Insight | Full Name or Definition | Relevance to Skincare |
HSP70-related stress response | Heat Shock Protein 70, an endogenous molecular chaperone protein | Participates in protein folding and quality control; early studies suggest that certain Artemia extracts may modulate cellular HSP70 expression |
GP4G | P1,P4-diguanosine 5′-tetraphosphate | Associated with nucleotide storage and metabolic conversion during Artemia embryonic development; its effects following topical application in humans require further validation |
2 Core Mechanisms of UV-Induced Photoaging
2.1 UV-Induced Damage Cascade
Long-term exposure of the skin to UV radiation may lead to reduced elasticity, fine lines, roughness, dullness, and sagging. One of the principal causes is UV-induced damage to the dermal extracellular matrix, particularly increased degradation of collagen fibers.
A representative pathway of UV-induced photoaging can be summarized as follows:
UVA / UVB → increased ROS → activation of MAPK signaling pathways → involvement of JNK / p38 / ERK branches in stress signaling → activation of the AP-1 transcription factor → increased MMP expression → degradation of type I and type III collagen → reduced dermal structural support, leading to wrinkles, sagging, and roughness
Both UVA, or ultraviolet A, and UVB, or ultraviolet B, can increase levels of ROS, or reactive oxygen species, in the skin. Excessive ROS can activate MAPK, or mitogen-activated protein kinase, signaling pathways and may involve branches such as JNK, or c-Jun N-terminal kinase, p38, and ERK, or extracellular signal-regulated kinase. The specific responses vary depending on the UV wavelength, irradiation dose, and cellular model.
MAPK signaling can subsequently activate AP-1, or activator protein 1. AP-1 can upregulate MMPs, or matrix metalloproteinases, thereby increasing the degradation of collagen and other extracellular matrix proteins.
2.2 Collagen Degradation and Changes in Skin Appearance
The dermis relies primarily on type I and type III collagen to maintain structural support. Following repeated UV exposure, MMP-1 can cleave collagen fibers, while MMP-3 and MMP-9 continue to participate in extracellular matrix degradation. Repeated cleavage disrupts the organization of collagen fibers and gradually weakens the dermal structure, resulting in fine lines, wrinkles, and reduced elasticity at the skin surface.
A key feature of UV-induced photoaging is the progressive amplification of damage signals. Artemia Extract is not intended to block UV radiation directly. Instead, after UV stress has occurred, it may help reduce the risk of further damage amplification by supporting HSP70-related proteostasis and GP4G-associated energy metabolism. Its proposed core mechanism can be summarized as follows.
Core mechanism underlying the anti-photoaging repair potential of Artemia Extract: Artemia Extract may participate in post-UV cellular repair through HSP70-related stress protection and GP4G-associated support of energy metabolism. Its primary role is to support proteostasis, cellular morphological stability, and the recovery of repair-related metabolism, while indirectly attenuating the UV-induced ROS–MAPK–AP-1–MMP damage-amplification cascade.
3 HSP70 and Proteostasis Protection
3.1 HSP70 and Molecular Chaperones
HSP70, or Heat Shock Protein 70, is an important class of molecular chaperone proteins. Molecular chaperones assist proteins in achieving correct folding, maintaining structural integrity, undergoing intracellular transport and repair, and being directed toward degradation when necessary. They therefore constitute an essential system for maintaining cellular proteostasis.
The basic functional process of HSP70 can be summarized as follows:
Recognition of unfolded or damaged proteins → binding to abnormal protein structures → ATP-dependent regulation of protein folding → assistance with protein refolding → clearance of proteins that cannot be repaired
ATP, or adenosine triphosphate, is one of the principal energy molecules in cells. The HSP70 chaperone cycle requires ATP, meaning that protein repair capacity is closely associated with the cellular energy state. The HSP70 family plays a central role in protein folding, macromolecular complex assembly, transmembrane transport, and protein quality control.
3.2 HSP70 and the Repair of UV-Induced Damage
UVB can induce epidermal cell apoptosis, inflammatory responses, and DNA, or deoxyribonucleic acid, damage. In cultured keratinocytes and HSP70-transgenic mouse models, HSP70 overexpression has been shown to reduce indicators of UVB-induced epidermal apoptosis, inflammation, and DNA damage. These studies demonstrate the protective activity of HSP70 itself.
In the context of anti-photoaging, the functions of HSP70 are concentrated at three levels:
Protein level: reducing protein misfolding and abnormal aggregation
Cellular level: lowering the risk of apoptosis and morphological abnormalities
Tissue level: helping maintain the stability of epidermal and dermal cells
Ultraviolet radiation, heat, and oxidative stress increase the risk of protein denaturation. By maintaining proteostasis, HSP70 may reduce the likelihood that cells will progress from transient stress to persistent damage. One reason Artemia Extract has attracted research interest is the evidence linking it to HSP70-related stress-protective responses.
4 Artemia Extract and HSP70-Related Protection
4.1 Cellular Stress Resistance
A publicly accessible 2001 conference abstract published in the Journal of Investigative Dermatology reported that Artemia Extract induced HSP70 in human cells in vitro and enhanced cellular tolerance to UVB stress. Such findings suggest that Artemia Extract may improve cellular stress resistance through HSP70-related responses.
The proposed pathway can be expressed as follows:
UV / heat / oxidative stress → increased risk of protein denaturation, mitochondrial stress, and DNA damage → enhanced HSP70-related stress protection → improved repair and clearance of abnormally folded proteins → improved cellular morphology and metabolic stability
Common forms of damage observed in skin cells after UV exposure include cellular shrinkage, reduced adhesion, cytoskeletal disruption, decreased mitochondrial activity, increased release of inflammatory mediators, and elevated rates of apoptosis. When HSP70-related protection is enhanced, cells may be better able to maintain normal morphology and basal metabolic organization.
4.2 Relationship to the MAPK/JNK Damage Cascade
Within the UV-induced photoaging pathway, ROS act as upstream stress signals, MAPK/JNK signaling functions as an amplification stage, and AP-1 and MMPs serve as downstream effectors of collagen degradation. Artemia Extract may reduce the likelihood of continued amplification of post-UV cellular stress by supporting HSP70-related protein protection and cellular homeostasis.
Currently available public evidence is insufficient to support the definitive conclusion that Artemia Extract directly inhibits JNK, p38, ERK, or AP-1. Based on the existing evidence, the proposed mechanistic pathway may be summarized as follows:
Reduction of cellular stress burden or improvement of stress tolerance → support for proteostasis → possible reduction in inflammation, apoptosis, and morphological abnormalities → reduced likelihood of further amplification of UV-induced damage
5 GP4G and the Rationale for Energy- and Nucleotide-Related Repair Support
5.1 Molecular Information on GP4G
The full name of GP4G is P1,P4-diguanosine 5′-tetraphosphate, also referred to as diguanosine tetraphosphate. Its molecular formula is:
C20H28N10O21P4
GP4G belongs to the dinucleoside polyphosphate family and consists of two guanosine molecules connected by a tetraphosphate chain. Its simplified structure is shown below:
Guanosine — P — P — P — P — Guanosine
5.2 GP4G and Nucleotide Metabolism During Artemia Embryonic Development
During dormancy, Artemia embryos must reduce metabolic consumption while preserving the energetic conditions required for the resumption of development. Classical biochemical studies have shown that Artemia cysts and newly hatched nauplii contain relatively high levels of guanine derivatives. As larval development proceeds, adenine compounds increase while guanine compounds decrease accordingly. Based on these observations, researchers proposed that GP4G may serve as a direct precursor for ATP formation during Artemia development.
Following UV-induced damage, skin cells must maintain adequate cellular energy and nucleotide homeostasis to support DNA repair, protein folding, cytoskeletal restoration, barrier renewal, and protein synthesis. The relevance of GP4G to skincare is therefore not that it simply “provides cells with energy directly,” but that it offers a plausible biochemical basis for the potential of Artemia Extract to support repair-related metabolism in stressed cells.
Energy-dependent repair processes in the skin after UV exposure include:
DNA damage recognition and repair
Protein refolding
The HSP70 molecular chaperone cycle
Restoration of mitochondrial function
Repair of cell membranes and the cytoskeleton
Skin barrier renewal
Collagen synthesis and extracellular matrix maintenance
5.3 Scope of GP4G Activity in Topical Human Skincare
The role of GP4G in the energy metabolism of Artemia embryos is supported by classical biochemical research. In topical human skincare, it may be regarded as a repair-supporting factor associated with energy metabolism. The current evidence can be summarized as follows:
Item | Strength of Evidence |
GP4G is a dinucleoside tetraphosphate | Established |
GP4G occurs in Artemia-related biological systems and is associated with nucleotide metabolism | Established |
GP4G is associated with Artemia embryonic dormancy, reactivation, and developmental metabolism | Relatively well supported |
Topical GP4G supports post-stress repair metabolism in skin cells | Supported by preclinical studies and related research materials, but human topical evidence remains limited |
Topically applied GP4G is extensively converted into ATP/GTP in human skin | Insufficient publicly available evidence |
Topical GP4G alone reverses photoaging | Insufficient publicly available evidence |
A study published in Scientific Reports in 2025 separately incorporated Artemia franciscana extract, a partially purified protein fraction containing Artemin and Hsp40, and GP4G into hyaluronic acid–phospholipid vesicles. The study evaluated cytocompatibility in L-929 mouse fibroblasts and examined histological changes using H&E staining and Masson’s trichrome staining after 14 consecutive days of treatment on the dorsal skin of male CD-1 mice.
The results showed that the relevant formulations did not exhibit obvious cytotoxicity and were associated with changes in dermal thickness and collagen staining. However, the study did not use a UV-irradiation or photoaging model and was not a human trial. It can therefore serve only as early preclinical evidence for the use of these ingredients and delivery systems in general skin anti-aging applications. It does not directly demonstrate repair of UV-induced damage or anti-photoaging efficacy in humans.
6 Potential Sites of Action of Artemia Extract in Post-UV Repair
6.1 Maintenance of Proteostasis
Ultraviolet radiation and heat stress can cause protein denaturation, misfolding, and aggregation. Research linking Artemia Extract to HSP70-related protective responses suggests that it may be suitable for supporting the maintenance of cellular proteostasis.
The proposed pathway is as follows:
UV / heat stress → increased protein denaturation and folding errors → enhanced HSP70-related protection → improved repair and clearance of damaged proteins → reduced risk of abnormal cellular morphology and apoptosis
6.2 Support for Energy Metabolism
Repair processes are highly energy-dependent. DNA repair, protein folding, cytoskeletal restoration, barrier renewal, and collagen synthesis require energy-related nucleotides such as ATP and GTP. The structure of GP4G and its metabolic role in Artemia embryos make it an important line of investigation related to energy recovery in Artemia Extract.
The proposed pathway can be expressed as follows:
UV stress → possible impairment of mitochondrial function and cellular energy status → increased demand for cellular energy and nucleotide homeostasis during repair → GP4G-related nucleotide metabolism provides a mechanistic basis → possible support for repair-related metabolism, although confirmation through human topical studies is still required
6.3 Control of Oxidative Stress and Inflammatory Amplification
Post-UV inflammatory amplification is associated with pathways such as NF-κB, or nuclear factor kappa-light-chain-enhancer of activated B cells. Studies of HSP70 indicate that increased expression may be associated with reduced UVB-induced inflammation, including decreases in inflammatory responses and DNA damage.
The potential role of Artemia Extract at this stage can be summarized as follows:
Excessive ROS → increased inflammatory and apoptotic signaling → possible enhancement of HSP70-related stress protection → reduced likelihood of further amplification of cellular damage → improved conditions for post-UV repair
7 Raw Material Safety and Basis for Use
7.1 Safety Assessment
The CosIng database includes the INCI name, source description, and skin-conditioning function of Artemia Extract. This listing is an ingredient information record and does not constitute approval under European Union regulations, a dedicated safety assessment of the ingredient by the Scientific Committee on Consumer Safety, or regulatory recognition of its anti-photoaging efficacy.
The safety of the finished product must still be evaluated on the basis of the specific formulation, raw material purity, impurities, use concentration, and conditions of exposure.
7.2 Use Concentration and Safety Evaluation
Publicly available commercial raw material information indicates that Ashland’s GP4G SP™ biofunctional is recommended for use at 1%–2%, with clinical testing reportedly conducted at a 2% use level. This range may serve as a formulation reference for GP4G-containing Artemia-derived ingredients.
It should be emphasized that Artemia Extract is not a single standardized ingredient. Differences in extraction processes, active-component content, and impurity control mean that the 1%–2% range cannot be regarded as a universally applicable safe-use level for all Artemia extracts.
For leave-on skincare products, safety should be evaluated in the context of the complete formulation. Products intended for the eye area, sensitive skin, or compromised skin barriers require particular attention to irritation, sensitization, and human tolerability.
7.3 Photostability and the Limits of Photoprotection
Artemia Extract is not a UV filter and cannot replace sunscreen agents. Its potential value in anti-photoaging products lies primarily in supporting cellular stress recovery after UV exposure rather than reducing the amount of UV radiation that enters the skin.
As a water-phase, biologically derived active ingredient, Artemia Extract may be affected by light exposure, temperature, pH, metal ions, preservative systems, and packaging conditions. Formulation development should therefore include careful evaluation of active-component stability, changes in color and odor, microbiological safety, and the tolerability of the finished product.
8 Research Reagents and Experimental Tools Related to the Anti-Photoaging Mechanisms of Artemia Extract
Table 1. Research on UV Exposure, Photoprotection, and Upstream Photoaging Prevention
Category | CAS No. | Aladdin Cat. No. | Product Name | Specification or Purity | Product Features and Applications |
Inorganic physical UV-screening material | 13463-67-7 | T431947 | Titanium(IV) oxide | Guaranteed reagent grade, ≥99% | Used in research on UV-screening materials, irradiation exposure controls, and evaluation of photoprotective systems |
Inorganic physical UV-screening material | 1314-13-2 | Zinc oxide | Reagent grade, high purity, ≥99.9% metals basis, powder, <5 μm | Used in UV screening, inorganic protective systems, and research on frontline protection against cutaneous light exposure | |
Organic UVA absorber | 70356-09-1 | 1-(4-tert-Butylphenyl)-3-(4-methoxyphenyl)-1,3-propanedione | ≥98% | Used in UVA-absorbing systems, photostability evaluation, and exposure-control studies related to photoaging | |
Organic UVB absorber | 88122-99-0 | Ethylhexyl Triazone | ≥98% | Used in UVB-absorbing systems, evaluation of protective efficiency, and research on photoprotective formulations | |
Broad-spectrum UV absorber | 187393-00-6 | Bis-Ethylhexyloxyphenol Methoxyphenyl Triazine | ≥98% | Used in broad-spectrum UV-protection systems, photostability studies, and evaluation of frontline anti-photoaging protection | |
Photostabilizing auxiliary UV absorber | 6197-30-4 | 2-Ethylhexyl 2-cyano-3,3-diphenylacrylate | ≥97% | Used for UV absorption, photostability enhancement, sunscreen systems, and photoaging-protection research |
Table 2. Reactive Oxygen Species Models, Free-Radical Detection, and Antioxidant Evaluation
Category | CAS No. | Aladdin Cat. No. | Product Name | Specification or Purity | Product Features and Applications |
Oxidative-stress model inducer | 7722-84-1 | Hydrogen peroxide solution | Suitable for microbiology, 3% | Used to establish cellular oxidative-stress models and ROS-induced damage models, and to evaluate antioxidant protection | |
Intracellular ROS detection probe | 4091-99-0 | 2′,7′-Dichlorodihydrofluorescein diacetate (DCFH-DA) | ≥97% | Used for fluorescent detection of intracellular ROS, monitoring of post-UV oxidative stress, and antioxidant intervention experiments | |
Free-radical-scavenging evaluation reagent | 1898-66-4 | 2,2-Diphenyl-1-picrylhydrazyl radical (DPPH, containing 10%–20% benzene) | ≥97% (HPLC) | Used to evaluate free-radical-scavenging capacity, screen antioxidant activity, and conduct antioxidant experiments related to photoaging | |
Total antioxidant-capacity evaluation reagent | 30931-67-0 | 2,2′-Azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) diammonium salt [AzBTS-(NH₄)₂] | ≥98% | Used for antioxidant-capacity evaluation, free-radical-scavenging assays, and comparison of the antioxidant performance of active ingredients | |
Reference standard for antioxidant evaluation | 53188-07-1 | Quinone dimethacrylate | ≥98%, white | Used for comparing antioxidant capacity, as a reference in free-radical-scavenging assays, and for calibration of oxidative-stress evaluation systems |
Table 3. Antioxidants, Redox-Active Compounds, and Cellular Stress-Protective Actives
Category | CAS No. | Aladdin Cat. No. | Product Name | Specification or Purity | Product Features and Applications |
Water-soluble antioxidant | 50-81-7 | L-Ascorbic acid | Anhydrous grade, Moligand™, ACS, ≥99% | Used in ROS scavenging, collagen protection, and intervention studies on post-UV oxidative damage | |
Stable ascorbic acid derivative | 86404-04-8 | 3-O-Ethyl-L-ascorbic acid | Moligand™, ≥98% (HPLC) (T) | Used in antioxidant-activity studies, skin-tone-related research, and intervention against post-UV oxidative stress | |
Stable ascorbic acid derivative | 129499-78-1 | 2-O-α-D-Glucopyranosyl-L-ascorbic acid | ≥98% (HPLC) | Used in stable antioxidant systems, photoaging intervention, and evaluation of activities related to oxidative stress | |
Lipid-soluble antioxidant derivative | 7695-91-2 | DL-α-Tocopheryl acetate | PharmPure™, European Pharmacopoeia (Ph. Eur.) | Used in lipid-phase antioxidation, protection of skin-barrier lipids, and research on photo-oxidative damage | |
Lipid-soluble antioxidant | 59-02-9 | D-α-Tocopherol | Moligand™, ≥97% (GC) | Used in membrane-lipid antioxidation, free-radical scavenging, and studies of UV-induced lipid peroxidation | |
Intracellular reducing-system molecule | 70-18-8 | Glutathione, reduced form | PharmPure™, European Pharmacopoeia (Ph. Eur.) | Used in redox-balance studies, cellular antioxidant defense, and ROS-scavenging experiments | |
Thiol-donor antioxidant | 616-91-1 | N-Acetyl-L-cysteine (NAC) | PharmPure™, USP, Moligand™, European Pharmacopoeia (Ph. Eur.), ≥98.5% | Used in cellular oxidative-stress intervention, glutathione-related pathway research, and as a positive control in ROS models | |
Phenolic-acid antioxidant | 1135-24-6 | Ferulic acid | Moligand™, ≥99% | Used in free-radical scavenging, auxiliary photoprotection, anti-photoaging formulations, and mechanistic research | |
Cytoprotective antioxidant | 497-30-3 | L-(+)-Ergothioneine | Moligand™, ≥98% | Used in protection against cellular oxidative stress, mitochondrial protection, and research on recovery from environmental stress | |
Carotenoid antioxidant | 472-61-7 | Astaxanthin | ≥98% (HPLC), mixture of cis and trans isomers | Used in studies of photo-oxidative damage, lipid peroxidation, and UV-related antioxidant activity | |
Lipoic-acid redox molecule | 1077-28-7 | DL-α-Lipoic acid | ≥99% | Used in redox regulation, mitochondrial metabolism, and cellular antioxidant-protection experiments | |
Mitochondrial lipid-phase antioxidant molecule | 303-98-0 | Coenzyme Q10 | ≥98% | Used in mitochondrial energy metabolism, lipid-phase antioxidation, and research on cellular energy status after UV exposure | |
Protein-stabilizing and anti-desiccation protectant | 99-20-7 | D-Trehalose, anhydrous | ≥99% | Used in protein stabilization, protection against desiccation stress, cellular stress-resistance studies, and maintenance of cellular homeostasis | |
Cellular osmoprotective active | 96702-03-3 | Ectoine | ≥99% | Used in cellular osmoprotection, recovery from heat stress, and protection against UV and environmental stress |
Table 4. GP4G-Related Nucleotides, Energy Molecules, and Repair-Metabolism Research
Category | CAS No. | Aladdin Cat. No. | Product Name | Specification or Purity | Product Features and Applications |
Guanosine nucleoside structural unit | 118-00-3 | Guanosine | PharmPure™, USP, endotoxin <500 EU/g; microbial limit ≤100 cfu/g | Used in studies of structural relationships with diguanosine tetraphosphate, guanosine nucleotide metabolism, and cellular repair metabolism | |
Adenosine nucleoside structural unit | 58-61-7 | Adenosine | PharmPure™, USP, endotoxin <1,000 EU/g; microbial limit ≤100 cfu/g | Used in studies of adenosine nucleotide metabolism, cellular energy regulation, and repair metabolism | |
Adenylate metabolic intermediate | 61-19-8 | 5′-Adenylic acid (5′-AMP) | Moligand™, ≥98% (HPLC) | Used in research on the adenylate cycle, energy-metabolism intermediates, and evaluation of cellular repair metabolism | |
Adenosine triphosphate energy molecule | 987-65-5 | Adenosine 5′-triphosphate disodium salt (ATP) | ≥98% | Used in studies of cellular energy metabolism, heat-shock-protein chaperone cycles, and energy requirements for post-UV repair | |
Guanosine triphosphate energy molecule | 56001-37-7 | Guanosine 5′-triphosphate disodium salt | ≥98% | Used in guanosine nucleotide metabolism, research related to diguanosine tetraphosphate, and cellular repair-metabolism experiments |
Table 5. Research on Collagen, the Extracellular Matrix, and MMP Pathways
Category | CAS No. | Aladdin Cat. No. | Product Name | Specification or Purity | Product Features and Applications |
Type III collagen model material | 9007-34-5 | Recombinant humanized type III collagen | Animal-origin-free, carrier-free, recombinant, ≥90% by SDS-PAGE, expressed in Nicotiana benthamiana | Used in studies of dermal collagen structure, extracellular-matrix models, collagen protection, and photoaging repair | |
Amino acid associated with collagen synthesis | 147-85-3 | L-Proline | UltraBio™, ≥99.5% | Used in studies of collagen-synthesis substrates, extracellular-matrix formation, and nutritional support for skin repair | |
Marker amino acid for collagen metabolism | 51-35-4 | L-Hydroxyproline | Moligand™, ≥99% | Used for collagen-content evaluation, detection of collagen degradation, and research on dermal-matrix metabolism | |
Extracellular-matrix hydration molecule | 9004-61-9 | Hyaluronic acid | Moligand™, derived from rooster comb | Used in extracellular-matrix hydration, moisturizing and repair studies, and skin-tissue support models | |
Salt form of an extracellular-matrix hydration molecule | 9067-32-7 | Sodium hyaluronate | European Pharmacopoeia (Ph. Eur.) | Used in studies of the skin hydration environment, barrier repair, hyaluronic acid–lipid vesicles, and extracellular-matrix support | |
Matrix metalloproteinase inhibitor | 142880-36-2 | GM6001, broad-spectrum MMP inhibitor | Moligand™, ≥98% | Used in studies of MMP-mediated collagen-degradation pathways, enzyme-inhibition controls, and mechanisms of UV-induced photoaging | |
Reference compound for retinoic-acid-pathway research | 302-79-4 | Retinoic acid | Moligand™, ≥98% | Used as a reference in photoaging studies and in research on collagen-metabolism regulation, cellular differentiation, and skin renewal |
Table 6. Soothing and Anti-Inflammatory Agents, Barrier Lipids, and Skin-Homeostasis Repair
Category | CAS No. | Aladdin Cat. No. | Product Name | Specification or Purity | Product Features and Applications |
Nicotinamide-based barrier and metabolic active | 98-92-0 | Nicotinamide | For cell culture, suitable for insect-cell culture, ≥99.5% (HPLC) | Used in studies of nicotinamide adenine dinucleotide-related metabolism, barrier-lipid synthesis, and inflammatory responses | |
Barrier-lipid component | 57-88-5 | Cholesterol | For cell culture, ≥99% (GC) | Used in stratum-corneum lipid models, stabilization of cell-membrane structure, and skin-barrier repair research | |
Centella asiatica triterpenic acid | 464-92-6 | Asiatic acid | Moligand™, ≥98% | Used in studies of inflammatory-response regulation, collagen maintenance, and post-UV skin repair | |
Centella asiatica glycoside-derived repair active | 34540-22-2 | Madecassoside | Moligand™, ≥98% | Used in soothing and repair studies, barrier recovery, and intervention against post-UV skin damage | |
Centella asiatica triterpenic acid | 18449-41-7 | Madecassic acid | Moligand™, ≥98% | Used in studies of inflammatory regulation, collagen-related pathways, and skin-tissue repair | |
Licorice-derived triterpenic acid | 471-53-4 | β-Glycyrrhetinic acid | Moligand™, ≥97% | Used in studies of inflammatory-response regulation, irritation relief, and post-UV skin soothing | |
Panthenol-based barrier-repair active | 81-13-0 | D-Panthenol | ≥98% | Used in skin moisturization, barrier recovery, irritation relief, and after-sun repair studies | |
Skin-conditioning and soothing active | 97-59-6 | Allantoin | ≥98% | Used in skin conditioning, irritation relief, barrier care, and post-UV soothing studies | |
Hydrolipid-film emollient | 111-01-3 | Squalane | ≥98% | Used in hydrolipid-film simulation, barrier-lipid supplementation, skin emollience, and barrier-stability research | |
Polysaccharide-based soothing and repair active | 9041-22-9 | β-D-Glucan from barley | ≥95% | Used in studies of cutaneous immune regulation, barrier repair, environmental-stress care, and soothing activity | |
Ceramide barrier lipid | 100403-19-8 | Ceramide mixture | ≥95% | Used in stratum-corneum lipid supplementation, transepidermal water-loss research, and barrier-repair models | |
Sesquiterpene alcohol soothing active | 515-69-5 | (±)-α-Bisabolol | ≥90% | Used in irritation relief, inflammatory-response regulation, sensitive-skin care, and after-sun soothing studies | |
Glycyrrhizinate soothing active | 68797-35-3 | Dipotassium glycyrrhizate hydrate | ≥75% (HPLC) | Used in inflammatory-mediator regulation, irritation relief, and post-UV soothing and repair studies |
Note: The products listed above are primarily intended for scientific research, analytical testing, cellular models, or mechanistic validation. Reagent-grade, pharmacopoeial-grade, or cell-culture-grade status is not equivalent to cosmetic-grade status and does not indicate that a product may be used directly in humans or cosmetic formulations. Specific applications should be determined according to the relevant product page, Safety Data Sheet (SDS), Certificate of Analysis (COA), and applicable regulations.
References
[1] European Commission. CosIng Database. ARTEMIA EXTRACT. Ref No. 31993; CAS No. 225234-40-2. Accessed July 10, 2026.
[2] Scientific Committee on Consumer Safety. The SCCS Notes of Guidance for the Testing of Cosmetic Ingredients and Their Safety Evaluation, 12th Revision. SCCS/1647/22, Corrigendum 2. 2023.
[3] Ashland. gp4g sp™ biofunctional. INCI: Water (and) Artemia Extract; recommended use level 1%–2%; clinically tested at 2%. Supplier technical information. Accessed July 10, 2026.
[4] Fisher GJ, Datta SC, Talwar HS, Wang ZQ, Varani J, Kang S, Voorhees JJ. Molecular basis of sun-induced premature skin ageing and retinoid antagonism. Nature. 1996;379(6563):335–339. doi:10.1038/379335a0.
[5] Matsuda M, Hoshino T, Yamashita Y, et al. Prevention of UVB radiation-induced epidermal damage by expression of heat shock protein 70. Journal of Biological Chemistry. 2010;285(8):5848–5858. doi:10.1074/jbc.M109.063453.
[6] Clegg JS, Warner AH, Finamore FJ. Evidence for the function of P1,P4-diguanosine 5′-tetraphosphate in the development of Artemia salina. Journal of Biological Chemistry. 1967;242(8):1938–1943. doi:10.1016/S0021-9258(18)96091-6.
[7] Mirtaleb MS, Khodabandeh Shahraky M, Deezagi A, Shafiee D. Investigation of the anti-aging effects of active components of Artemia franciscana loaded in hyalurosome. Scientific Reports. 2025;15:1293. doi:10.1038/s41598-024-83731-7.
[8] Domloge N, Cucumel K, Dal Farra C, Bauza E. Stress-free Hsp70 induction by artemia extract modulates p53 and p21 expression and enhances human cells protection from UVB. Journal of Investigative Dermatology. 2001;117(2):497. Meeting abstract.
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