Leuphasyl, aka Pentapeptide-18, has been suggested by researchers to be able to penetrate skin cells and induce a decrease in wrinkle depth and development along the skin surface. Research suggests that Leuphasyl may potentially inhibit impulse signals at the neuromuscular synapse. Due to this, muscle and contractile force may reduce drastically.^[3]

Leuphasyl is the synthetic equivalent of enkephalins, which are endorphin peptides that regulate nociception. The peptide may also affect mood/behavior, movement, neuroendocrine functions, and pain perception.^[2]

The peptide has been suggested to block electrical impulses at the neuromuscular junction, the synaptic space between a motor nerve terminal end and a muscle. Consequently, Leuphasyl may reduce muscular contraction, reducing instances of wrinkle development on the skin structure. Leupahsyl has been reported in research findings to potentially mitigate wrinkle development by 28% to 34.7% in animal models.^[1] More specifically, the scientists suggest that “Our results emphasize that only for Leuplasyl 2% there are important ameliorations. The size of the wrinkles trajectory was smaller with the following average: 34.7% for frontal region…; 28.4% for periorbital zone.”

Leuphasyl (Pentapeptide-18) appears to attach enkephalin receptors to nerve cells, releasing acetylcholine into the synaptic gap. Leuphasyl may induce Ach release by modulating synaptic vesicle fusion directly. Following the release of Ach, Leuphasyl may bind to Ach receptors and induce muscle cramps, at which point Pentapeptide-18 enters the picture to inhibit the reaction. It is unclear if or how Pentapeptide-18 accomplishes this, but it has been suggested to function to reduce the prevalence of wrinkles around corrugator supercilii muscle and the preorbital zone while interfering with neuromuscular signaling.

An experiment by Dr. Howard Maibach, a Professor of Dermatology at the University of California, suggested that after 28 days of exposure to the peptide, 5% of Leuphasyl singularly reduced 11% of wrinkles. In addition, 5% Leuphasyl combined with 5% Argireline reduced wrinkles by approximately 25% on average, rounding up to a 45% average.

The mean wrinkle reductions for Leuphasyl, Argireline, and their combination were 11.64%, 16.26%, and 24.62%, respectively.^[5] The scientists report that “This study suggested a synergistic effect between Leuphasyl and Argireline.” In this context, Leuphasyl may act to prevent the formation of wrinkles, while the attached molecules—GHK-cu and Argireline—may help reduce the lines that form.

 

Disclaimer: The products mentioned are not intended for human or animal consumption. Research chemicals are intended solely for laboratory experimentation and/or in-vitro testing.  Bodily introduction of any sort is strictly prohibited by law.  All purchases are limited to licensed researchers and/or qualified professionals. All information shared in this article is for educational purposes only.

 

References

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1. Montiel, A. V. F., Puche, J. C. & Montiel, A. P. Cosmetic or dermopharmaceutical composition comprising enkephalin-derived peptides for reducing and/or eliminating facial wrinkles. (2015).
2. Puig, A., Garcia-Anton, J., Perez, R. & Mangues, M. Eyeseryl and Leuphasyl: Synthetic Peptides as Advanced Cosmetic Actives. Available at: cosmeticsciencetechnology.com/companies/articles/821.pdf.
3. Dragomirescu, A. O., Andoni, M., Ionescu, D. & Andrei, F. The Efficiency and Safety of Leuphasyl—A Botox-Like Peptide. Cosmetics 1, 75–81 (2014).
4. Wilson, A. J., Chin, B. C., Hsu, V. M., Mirzabeigi, M. N. & Percec, I. Digital Image Correlation: A Novel Dynamic Three-Dimensional Imaging Technique for Precise Quantification of the Dynamic Rhytid and Botulinum Toxin Type A Efficacy. Plast. Reconstr. Surg. 135, 869e–876e (2015).
5. Gorouhi, F., and H. I. Maibach. “Role of peptides in preventing or treating aged skin.” International journal of cosmetic science 31, no. 5 (2009): 327-345.

Vilon peptide is classified as a potential immunomodulatory bioregulator. Vilon research has indicated that the peptide may modulate the vascular system and improve hemostasis.

 

Vilon Peptide and Cancer:

One of Villon’s potential functions is the reduction of cancer cell proliferation and metastasis. However, Vilon research findings suggest that the peptide may potentially reduce cancer incidence and prevent cancer progression.^[1,2] Researchers note that “Vilon stimulated apoptosis both in young and old rats, but the inhibitory effect of cyclophosphan was abolished in the presence of vilon in culture media.” 

 

Vilon Peptide and Cell Aging

Vilon peptide is considered to be a potential “anti-aging” peptide for its hypothesized action in mitigating the cycle of cell aging and death (apostasis).^[3] The anti-aging function of the Vilon peptide may be bourne from its perceived impact on the gastrointestinal tract (GI tract). Here, the peptide has been suggested to enhance enzyme activity. Vilon also has been suggested to increase barrier function, thereby decreasing the development of leaky gut, improving disease resistance, and bettering the overall GI tract function. The peptide also has been suggested to increase the absorption of glucose and glycine in the small intestine.^[5] The researchers note that “Vilon stimulated active glucose accumulation in the serous sac of the medial small intestine.”

 

Vilon Peptide and the Immune System

Vilon peptide may be a modulator of chromatin structure. The peptide may induce an unrolling of chromatin, activate synthetic processes by reactivating ribosomal genes in the unrolled chromatin, release repressed genes, and does not appear to induce the decondensation of pericentromeric chromatin structure. The overall action of these functions may scale down to the reactivation of genes in the DNA that are silent.

Chromatin is considered to exist in two states: wound (heterochromatin) and unwound (euchromatin).^[6] The apparatus that converts genes into proteins and functional components of the cell appears unable to access the heterochromatin state. Genes in these DNA regions may be unavailable for protein production in general.

Chromatin appears to modulate the genes available for transcription, and it is a way that different cells or the same cells can have varying functions over a period. Chromatin condensation is one of the considered factors in cell aging and senescence and loss of tissue function. The potential of the peptide to reactivate these cells by heterochromatin unraveling may possibly restore immune function.^[7] The result is concluded from suggested findings in lymphocytes—white blood cells of the immune system like the killer cells, T cells, and B cells that produce antibodies and coordinate immune response to pathogens such as cancer.

Vilon peptide appears to activate interleukin-2 signaling in splenocytes coupled with Vilon activity in lymphocytes. There is protection against microbial infections, and natural protection against autoimmune reactions, due to the activation of splenocytes and lymphocytes.

Vilon may play a role in the thymus, where it may increase CD5 T-cell proliferation. CD5 T-cells and cytotoxic CD8 T-cells are considered to be a marker of mature T-helper cells. CD8 T-cells are anti-microbial cells, and CD5 T-cells regulate the immune system and prevent autoimmune reactions. In a nutshell, the Vilon peptide appears to potentially rejuvenate immune functions by reactivating genes that are silent by chromatin changes. It may not reactivate genes that are naturally silent in the affected cells. Vilon may possibly enhance the immune system while it prevents autoimmune reactions.

 

Vilon and the Heart and Kidney

Scientists believe that Vilon peptide may act in a way that is beneficial within the vascular system. However, this is not well studied and does not have enough results to support the hypotheses created in this area. Nonetheless, the Vilon peptide has been suggested to modulate the expression of 36 and more different genes in the heart. When researchers combined exposure with Epithalon, the number was updated to include a possible total of 144 genes.

In the kidney, Vilon peptide may reduce transforming growth factor-beta-1 concentration and the micro vessel permeability. Research models of diabetes exhibited optimized coagulation on the exposure to Vilon. The peptide appeared to increase natural anticoagulant antithrombin III levels and Protein C while enhancing fibrinolysis.

 

Disclaimer: The products mentioned are not intended for human or animal consumption. Research chemicals are intended solely for laboratory experimentation and/or in-vitro testing.  Bodily introduction of any sort is strictly prohibited by law.  All purchases are limited to licensed researchers and/or qualified professionals. All information shared in this article is for educational purposes only.

 

References

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1. Khavinson VKh, Anisimov VN. A synthetic dipeptide vilon peptide (L-Lys-L-Glu) inhibits growth of spontaneous tumors and increases life span of mice. Dokl Biol Sci. 2000;372:261-263.
2. Barykina OP, Iuzhakov VV, Chalisova NI, Kvetnoĭ IM, Konovalov SS. Sochetannoe vliianie vilona i tsiklofosfana na transplanty opukholeĭ i éksplantaty limfoidnoĭ tkani mysheĭ i krys raznogo vozrasta [Combined effect of vilon and cyclophosphane on tumor transplants and lymphoid tissue explants in mice and rats of various age]. Adv Gerontol. 2003;12:128-131.
3. Khavinson VK, Anisimov VN, Zavarzina NY, et al. Effect of vilon on biological age and lifespan in mice. Bull Exp Biol Med. 2000;130(7):687-690. doi:10.1007/BF02682106.
4. Anisimov VN, Loktionov AS, Khavinson VK, Morozov VG. Effect of low-molecular-weight factors of thymus and pineal gland on life span and spontaneous tumour development in female mice of different age. Mech Ageing Dev. 1989;49(3):245-257. doi:10.1016/0047-6374(89)90075-4.
5. Khavinson VKh, Egorova VV, Timofeeva NM, Malinin VV, Gordova LA, Gromova LV. Effect of Vilon and Epithalon on glucose and glycine absorption in various regions of small intestine in aged rats. Bull Exp Biol Med. 2002;133(5):494-496. doi:10.1023/a:1019878224754.
6. Lezhava T, Khavison V, Monaselidze J, et al. Bioregulator Vilon-induced reactivation of chromatin in cultured lymphocytes from old people. Biogerontology. 2004;5(2):73-79. doi:10.1023/B:BGEN.0000025070.90330.7f.
7. Lezhava T, Monaselidze J, Kadotani T, Dvalishvili N, Buadze T. Anti-aging peptide bioregulators induce reactivation of chromatin. Georgian Med News. 2006;(133):111-115.
8. Anisimov SV, Bokheler KR, Khavinson VKh, Anisimov VN. Studies of the effects of Vilon and Epithalon on gene expression in mouse heart using DNA-microarray technology. Bull Exp Biol Med. 2002;133(3):293-299. doi:10.1023/a:1015859322630.

Vialox, also termed Pentapeptide-3V, is a peptide developed to induce partial muscle paralysis, potentially resulting in a decreased prevalence of wrinkles and creases forming along skin structures.^[1]

Pentapeptide-3V may prevent muscle contraction by exhibiting a curare-like effect at the neuromuscular junction, disallowing the nervous system signals from reaching the muscles.

Pentapeptide-3V is of primary interest because of its influential ability to communicate between muscles and nerves.

Pentapeptide-3V may affect the signal transmission between nerves and muscles. In normal conditions, signals are transmitted following the release of acetylcholine from its axon by nerves. Contraction occurs following the conduction of acetylcholine across the neuromuscular junction to bind to a receptor on the muscle. Pentapeptide-3V appears to halt contraction by binding to the AChR.^[3] By doing this, it may block acetylcholine from binding. This may result in a reduced amount of acetylcholine binding and reduced strength and number of muscle contractions.

Acetylcholine appears to bind to a muscle receptor, limiting sodium ion release at the neuromuscular junction. Depolarization occurs, resulting in electrical pulses that cause wrinkles and muscle contraction. By binding to AChR, Pentapeptide-3V may potentially inhibit this process. When Pentapeptide-3V binds to AChR, it may inhibit acetylcholine binding.

Pentapeptide-3V appears to only affect peripheral AChRs and may not potentially affect central neuronal receptors, unlike the other nicotinic acetylcholine receptor antagonists. This suggests that Pentapeptide-3V only acts on the neuromuscular junction.

The overall result of Pentapeptide-3V activity is suggested to be a reduction in acetylcholine binding following the reduction in the frequency and intensity of muscular contractions.^[4]

Pentapeptide-3V may potentially reduce average skin roughness by 11% and relief by 8%. Because relief is proportional to wrinkle size, Vialox can reduce wrinkles by an average of 8%. These are in approximately 60% and 47% of the animal subjects examined. According to Reddy et al. “this product is effective in smoothing … wrinkles and provides an immediate tightening effect to the skin.”^[5]

Pentapeptide-3V, a protein composed of lysine, threonine, and serine, is considered an abundant protein in skin collagen. It appears to act directly on the dermis to stimulate collagen production. Ancillary compounds examined in studies, such as Vitamin A, according to research conducted by specialists in the Department of Dermatology, suggest that Pentapeptide-3V may potentially increase collagen growth, improving skin compaction. Pentapeptide-3V may stimulate collagen production in the skin, reversing aging and minimizing wrinkles. Vialox may also improve the production of melanin to act in mitigatory fashion against UV radiation.

 

Disclaimer: The products mentioned are not intended for human or animal consumption. Research chemicals are intended solely for laboratory experimentation and/or in-vitro testing.  Bodily introduction of any sort is strictly prohibited by law.  All purchases are limited to licensed researchers and/or qualified professionals. All information shared in this article is for educational purposes only.

 

References

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1. Servent, D. et al. Only Snake Curaremimetic Toxins with a Fifth Disulfide Bond Have High Affinity for the Neuronal α7 Nicotinic Receptor. J. Biol. Chem. 272, 24279–24286 (1997) DOI: 10.1074/jbc.272.39.24279
2. Zhmak, M. N., Utkin, Y. N., Andreeva, T. V., Kudryavtsev, D. S., Kryukova, E. V., Tsetlin, V. I., … & Shelukhina, I. V. E. (2017). U.S. Patent No. 9,550,808. Washington, DC: U.S. Patent and Trademark Office.
3. Gupta, V. K. Biotechnology of Bioactive Compounds: Sources and Applications. (John Wiley & Sons, 2015)
4. Reddy, B. Y., Jow, T., & Hantash, B. M. (2012). Bioactive oligopeptides in dermatology: Part II. Experimental dermatology, 21(8), 569-575.

Syn-Coll, also known as Palmitoyl Tripeptide-5 or Tripeptide-5, is a peptide that researchers suggest may act to increase the production of Type I and Type III collagen while possibly also inhibiting its degradation. Palmitoyl Tripeptide-5 is suggested to act by activating transforming growth factor-𝛃.^[1] Collagen type I is present in the bones, muscles, and skin. Type III collagen, on the other hand, is present in the skin, vascular system, and lungs. By increasing Type I and Type III collagen, Syn-Coll may potentially promote tissue repair processes as well as contributing to structural support for the extracellular matrix of the skin.

Fibroblasts are considered to be among the most commonly occurring cells in the skin. The main function of these cells appears to be the production collagen proteins. The number of active fibroblasts and levels of collagen declines naturally, potentially leading to increasing instances of creasing across the skin surface. Palmitoyl Tripeptide-5 appears to function similarly to Thrombospodin-1 to stimulate transforming growth factor-induced collagen degradation.

 

Functions of Palmitoyl Tripeptide-5

TSP-1 is a naturally occurring peptide that appears to increase TGF-𝛃 activities. Palmitoyl Tripeptide-5 appears to exhibit the same characteristics as TSP-1, increasing Type I and III collagen levels in the dermal (skin) fibroblasts.^[2] The researchers noted that “Investigator assessments of both periocular and perioral wrinkles showed statistically significant improvements over Baseline within minutes of initial application; these positive findings continued to improve through Months 1 and 3.” Experimental results suggest that Syn-Coll increases Type I and III collagen levels by 2-3 folds above the normal levels.^[3]

TSP-1 is considered to be an extracellular matrix (ECM) protein. It appears to cohabit with collagen and elastin in the skin. A specific part of TSP-1 is harvested for use in Palmitoyl Tripeptide-5 production. This part stimulates latent TGF-𝛃. Just like TSP-1, Syn-Coll may function to enhance tissue repair. It appears active in the post-natal development of skin structures.^[4]

Palmitoyl Tripeptide-5 may also potentially deactivate matrix metalloproteinases I and III (MMP1 and MMP3). Matrix metalloproteinases are enzymes that act to degrade collagen. These enzymes may be beneficial, as they recycle collagen following cell aging, but they have been suggested to hike in conditions such as inflammation to abnormal levels.

By inhibiting MMP1 and MMP3 activity, Palmitoyl Tripeptide-5 may potentially help to prevent collagen breakdown. These hypotheses suggest that Syn-Coll may promote Type I and Type III collagen formation and inhibit collagen breakdown by the abovementioned enzymes.

In terms of wrinkle reduction, Syn-Coll has been suggested to be approximately 3.5x more effective than a placebo. According to scientists, Palmitoyl Tripeptide-5 is 60% more effective than Palmitoyl Pentapeptide.^[5]  Palmitoyl Tripeptide-5 has been suggested to alter the effects of photo-aging damage. Syn-Coll may also rarefy pores, potentially diminishing inconsistencies in skin texture and increasing skin elasticity and firmness. Palmitoyl Tripeptide-5 is considered to be cold-processible.

 

Disclaimer: The products mentioned are not intended for human or animal consumption. Research chemicals are intended solely for laboratory experimentation and/or in-vitro testing.  Bodily introduction of any sort is strictly prohibited by law.  All purchases are limited to licensed researchers and/or qualified professionals. All information shared in this article is for educational purposes only.

 

References

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1. Thorsen, M., Yde, B., Pedersen, U., Clauden, K. & Lawesson, S.-O. Studies on amino acids and peptides-V. Tetrahedron 39, 3429–3435 (1983).https://doi.org/10.1016/S0040-4020(01)91596-0
2. Trookman, N. S., Rizer, R. L., Ford, R., Ho, E. & Gotz, V. Immediate and Long-term Clinical Benefits of a Treatment for Facial Lines and Wrinkles. J. Clin. Aesthetic Dermatol. 2, 38–43 (2009).
3. Varga, J., Rosenbloom, J. & Jimenez, S. A. Transforming growth factor beta (TGF beta) causes a persistent increase in steady-state amounts of type I and type III collagen and fibronectin mRNAs in normal human dermal fibroblasts. Biochem. J. 247, 597–604 (1987).
4. Murphy-Ullrich, J. E. & Poczatek, M. Activation of latent TGF-beta by thrombospondin-1: mechanisms and physiology. Cytokine Growth Factor Rev. 11, 59–69 (2000).
5. Bucay, V. W. & Day, D. Adjunctive Skin Care of the Brow and Periorbital Region. Clin. Plast. Surg. 40, 225–236 (2013).

Pal AHK is a peptide also termed Palmitoyl Tripeptide-3. Experiments on Pal AHK suggest that the peptide can activate fibroblast production through its interaction with transforming growth factor-𝛽 (TGF-𝛽). Due to the peptide’s potential to enhance collagen production and reduce creasing across the skin structure, it has been widely researched.

 

Pal AHK Peptide Overview

Pal AHK peptide is associated with palmitoyl fatty acid molecules. This fatty acid feature appears to make AHK soluble in fats. Due to this, the rate at which Pal AHK peptide may potentially penetrate the skin increases and may increase its absorption by cells. Pal AHK present in the skin may activate the production of TGF-𝛽.

The activation of fibroblast production in the skin by Palmitoyl Tripeptide-3 may potentially increase the extracellular matrix (ECM) synthesis in the skin.^[2] The extracellular matrix (ECM) is a complex network of minerals and extracellular macromolecules. It is dominated by enzymes, elastin, glycoproteins, collagens, and hydroxyapatite, considered responsible for providing biochemical and structural support to the surrounding cells. By increasing the extracellular matrix (ECM) synthesis in the cell, Pal AHK peptide may possibly increase the production of ECM components, increasing cell-to-cell attachment and communication, cell growth, and cell movement.^[3]

Experiments suggest that Pal AHK peptide may possibly modulate the synthesis of vascular endothelial growth factor (VEGF). Vascular endothelial growth factor (VEGF) is a signaling molecule activated in the production of new blood vessels.^[4] The scientists also explain that “Vascular endothelial growth factor (VEGF) is an endothelial cell mitogen and permeability factor that is potently angiogenic.” By enhancing vascular endothelial growth factors, Pal AHK may possibly boost the production of new blood vessels in the skin. Increased vascular endothelial growth factor (VEGF) by Palmitoyl Tripeptide-3 may allow for increased blood supply to the skin.

The vascular endothelial growth factor (VEGF) may prevent disease conditions such as macular degeneration, diabetes, and even cancer, though research in this area is ongoing. The vascular endothelial growth factor (VEGF) is an angiogenic factor suggested to influence angiogenesis by paving the way for endothelial cell proliferation, migration, and permeability. By increasing the production of VEGF, Pal AHK peptide may possibly enhance the prevention of cancer, macular degeneration, and diabetes while potentially preventing the onset of possible cardiac and cardiac-related diseases.

The production of new blood vessels may improve wound healing by depositing the injury site with collagen. This is considered to be due to the vascular endothelial growth factor (VEGF). Therefore, increasing VEGF by Palmitoyl Tripeptide-3 may increase the wound healing process. It is vital to note that in a laboratory setting, the vascular endothelial growth factor (VEGF) may exhibit mitogenic, chemotactic, and permeability action. These may be impactful in the regeneration and repair of non-healing wounds following diabetes and artery occlusive diseases.

Palmitoyl Tripeptide-3 may potentially increase VEGF production and contribute to modest visual improvement—averaging about two lines of vision. When Palmitoyl is added to AHK, it may potentially increase the penetrating rate of Pal AHK peptide in the cell membrane. Thus, increasing collagen production.

Pal AHK peptide has been suggested to minimize muscle contractions, therefore, decreasing and inhibiting the onset of wrinkling along the skin surface.

Oxidative stress (free-radical attack) is a considered cause of reduced follicle growth and loss. The peptide may potentially decrease follicle loss and enhance growth by decreasing oxidative stress. Due to the reduction of oxidative stress by Palmitoyl Tripeptide-3, dihydrotestosterone formation in follicles may increase.^[5] The scientists note that “Animal studies indicate that palmitoyl tripeptide-3/5 may increase collagen synthesis… Studies [suggest] that palmitoyl tripeptide-3/5 can prevent collagen breakdown by interfering with MMP1 and MMP3 collagen degradation.” The inhibition of oxidative stress by Pal AHK peptide may potentially be achieved by boosting superoxide dismutase production. As a result, it may mitigate the damaging action of oxidative stress.

 

Disclaimer: The products mentioned are not intended for human or animal consumption. Research chemicals are intended solely for laboratory experimentation and/or in-vitro testing.  Bodily introduction of any sort is strictly prohibited by law.  All purchases are limited to licensed researchers and/or qualified professionals. All information shared in this article is for educational purposes only.

 

References

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1. Åubkowska, B., Grobelna, B. & Maćkiewicz, Z. The use of synthetic polypeptides in cosmetics. Copernic. Lett. 1, 75 (2010).
2. Gorouhi, F. & Maibach, H. I. Role of peptides in preventing or treating aged skin. Int. J. Cosmet. Sci. 31, 327–345 (2009).
3. Lourith, N. & Kanlayavattanakul, M. Biopolymeric agents for skin wrinkle treatment. J. Cosmet. Laser Ther. 18, 301–310 (2016).
4. Nör JE, Christensen J, Mooney DJ, Polverini PJ. Vascular endothelial growth factor (VEGF)-mediated angiogenesis is associated with enhanced endothelial cell survival and induction of Bcl-2 expression. Am J Pathol. 1999;154(2):375-384. doi:10.1016/S0002-9440(10)65284-4.

Decapeptide-12 is considered to be an anti-tyrosinase peptide. The peptide has been suggested to inhibit the activities of tyrosinase, an enzyme that catalyzes the production of melanin and other pigments.^[1] According to research “tyrosinase activity and melanin production … is controlled primarily by a post-translational regulation of pre-existing enzyme and not by regulating tyrosinase gene activity.”

Tyrosinase may be present in plant and animal cells, where it appears to aid the catalyzation of melanin. The peptide has also been suggested to aid in dihydroxyphenylalanine catalysis. Decapeptide-12 may potentially foster the catalysis of the first two steps in the biochemical synthesis of melanin and is expressed by melanocytes. Notably, tyrosinase may be in melanosomes-synthesized in the melanocytes.

Type I oculocutaneous a lack of tyrosinase has been linked to albinism. In contrast, skin hyperpigmentation has been linked to melanin synthesis. It may also be caused by a mutation that causes tyrosinase to become overactive. Decapeptide-12, considered to be a tyrosinase inhibitor, is of interest to the researchers due to its potential to improve the function of the enzyme cascade of pigment production.

Decapeptide-12 appears to inhibit tyrosinase activities by reversibly binding to tyrosinase in several pigment-producing cells.^[2] The peptide may potentially prevent the oxidation of phenols by tyrosinase, the first step in melanin production. Tyrosinase is primarily found in melanosomes—unique parts within cells that produce pigments. Tyrosinase varies in structure according to species or even in closely related species.

Tyrosinase is also considered to aid the oxidation of phenolic compounds in fruits and vegetables to quinones (i.e., what turns potato black after it is sliced). This conversion may cause taste and odor alterations in the fruits and vegetables. This conversion may cause some kinds of proteins to be harder to digest and potentially decrease the nutritional value of the food. Decapeptide-12 has been researched in conjunction with the preservative potential that may be induced in fruits and vegetables when tyrosinase activity is inhibited.

Tyrosinase peptide inhibitors, possibly Decapeptide-12, are considered potential insecticides as they appear to inhibit tyrosinase’s activities in insects. Tyrosinase may act to heal wounds, parasite encapsulation, and develop an insect’s exoskeleton. Therefore, the inhibition of tyrosinase may hamper its activities in insects leading to an insect’s death.

Decapeptide-12 appears to potentially reduce skin pigmentation, according to research in animal models aimed at determining its action in research models of melasma (photodamage). According to studies, approximately 40% of the research models in the experiment developed a 100% decrement of pigmentation-hyperpigmentation. About 15% of the models of grade 3 photodamage exhibited an apparent turnaround and moved into grade 1 photodamage. Research models of severe photodamage (photodamage grade 4) were observed to have only minor repairs, lowering them to photodamage grade 3.^[3] The exposure to Decapeptide-12 peptide to nearly all research models of Melasma (photodamage) appeared to result in changes to skin tone.^[4]

According to research, Decapeptide-12 may be 17 times greater in impact than control hyperpigmentation procedures.^[5] Studies report that “This inhibition partially depended on whether L-dopa or L-tyrosine was the substrate, suggesting that tyrosinase may contain contains two distinct catalytic sites.” Including hydroquinone, with no evidence of melanocyte damage. Research studies in cultured melanocytes for more than 7 days suggested a 27% – 43% decrease in melanin content.

Decapeptide-12 appears to synergize with glycolic acid to remove the dead stratum corneum layers concentrated with hyperpigmented cells.  Decapeptide-12 may potentially protect skin cells from hyperpigmentation. This may be possible through preventing UV rays from reaching the skin’s sensitive layers and shielding the skin from any harmful interaction of UV rays with melanocytes, possibly preventing the spread of new damage.

 

Disclaimer: The products mentioned are not intended for human or animal consumption. Research chemicals are intended solely for laboratory experimentation and/or in-vitro testing.  Bodily introduction of any sort is strictly prohibited by law.  All purchases are limited to licensed researchers and/or qualified professionals. All information shared in this article is for educational purposes only.

 

References

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1. Iozumi, K., Hoganson, G. E., Pennella, R., Everett, M. A. & Fuller, B. B. Role of tyrosinase as the determinant of pigmentation in cultured human melanocytes. J. Invest. Dermatol. 100, 806–811 (1993).
2. Chen J, Bian J, Hantash BM, et al. Enhanced skin retention and permeation of a novel peptide via structural modification, chemical enhancement, and microneedles. Int J Pharm. 2021;606:120868. doi:10.1016/j.ijpharm.2021.120868
3. Kassim, A. T., Hussain, M. & Goldberg, D. J. Open-label evaluation of the skin-brightening efficacy of a skin-brightening system using decapeptide-12. J. Cosmet. Laser Ther. Off. Publ. Eur. Soc. Laser Dermatol. 14, 117–121 (2012).
4. Hantash, B. M. & Jimenez, F. A split-face, double-blind, randomized and placebo-controlled pilot evaluation of a novel oligopeptide for the treatment of recalcitrant melasma. J. Drugs Dermatol. JDD 8, 732–735 (2009).
5. Abu Ubeid, A., Zhao, L., Wang, Y. & Hantash, B. M. Short-sequence oligopeptides with inhibitory activity against mushroom and human tyrosinase. J. Invest. Dermatol. 129, 2242–2249 (2009)