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Best Peptides for Wound Healing & Tissue Repair

Whether you're recovering from surgery, managing a chronic wound, or dealing with a stubborn tendon injury, your body's repair machinery depends on a tightly orchestrated cascade of cellular events.

Whether you're recovering from surgery, managing a chronic wound, or dealing with a stubborn tendon injury, your body's repair machinery depends on a tightly orchestrated cascade of cellular events. Peptides -- short chains of amino acids that act as signaling molecules -- sit at the center of that cascade. They direct cell migration, trigger collagen production, build new blood vessels, and dial down the inflammation that slows healing.

This guide covers the peptides with the strongest research backing for wound healing and tissue repair, what the science actually says about each one, and how they compare.

Table of Contents

How Your Body Heals: A Quick Primer

Wound healing moves through four overlapping phases:

  1. Hemostasis (seconds to hours): Blood clotting stops the bleeding. Platelets aggregate and release growth factors.
  2. Inflammation (hours to days): Immune cells flood the wound site to clear debris and fight infection. Pro-inflammatory cytokines like TNF-alpha and IL-6 peak during this stage.
  3. Proliferation (days to weeks): Fibroblasts lay down collagen. New blood vessels form (angiogenesis). Keratinocytes migrate across the wound bed to rebuild the skin barrier.
  4. Remodeling (weeks to months): Collagen III is gradually replaced by stronger collagen I. The tissue reorganizes and gains tensile strength -- though repaired skin typically recovers only 80-85% of its original strength [1].

Every peptide in this guide targets one or more of these phases. Some accelerate collagen production. Others speed up cell migration or suppress the excessive inflammation that stalls healing. The most effective ones hit multiple phases at once.

What Makes Peptides Useful for Wound Healing?

Peptides have several properties that make them particularly well-suited for tissue repair:

  • Low molecular weight allows them to penetrate tissue more effectively than larger proteins
  • High specificity for cellular receptors means targeted action with fewer off-target effects
  • Multiple mechanisms of action -- many wound-healing peptides simultaneously promote angiogenesis, reduce inflammation, and stimulate collagen synthesis
  • Low toxicity profiles compared to small-molecule drugs, even at high concentrations
  • Endogenous origins -- several of these peptides are based on molecules your body already produces, meaning your cells have the receptors to respond to them

The challenge? Most peptides break down quickly in the body. Short half-lives, enzymatic degradation, and delivery difficulties are ongoing problems that researchers are working to solve with hydrogels, nanoparticles, and other advanced formulations.

The Top Peptides for Wound Healing & Tissue Repair

BPC-157: The Gastric Pentadecapeptide

BPC-157 (Body Protection Compound-157) is a 15-amino-acid peptide originally isolated from human gastric juice. It was first described in 1992, and since then, it has become one of the most heavily studied peptides in tissue repair research.

What the research shows:

BPC-157's wound healing effects have been tested across a wide range of injury types in animal models -- skin incisions, excisional wounds, deep burns, diabetic ulcers, alkali burns, and tendon transections [2].

In a foundational 1997 study, researchers tested BPC-157 in three rat models: skin incisional wounds, colon-colon anastomoses, and angiogenesis using sponge implantation. Across all three models, BPC-157-treated animals showed significantly better outcomes than controls. The effects held whether the peptide was given orally or applied locally [3].

For burn wounds specifically, a 2001 study found that BPC-157 given intraperitoneally to mice with 20% total body area burns decreased inflammatory cell infiltration, lowered water content in burned skin, and increased both breaking strength and elongation of the healing tissue [4].

BPC-157 also accelerates tendon repair. A 2003 study showed that the peptide fully improved recovery of transected rat Achilles tendons -- biomechanically (increased load of failure), functionally, microscopically (more organized fibroblast and collagen formation), and macroscopically (smaller defect size) [5].

How it works:

BPC-157 activates the ERK1/2 signaling pathway, boosting cellular proliferation, migration, and vascular tube formation in a dose-dependent manner [6]. It upregulates VEGF expression in wounded tissues, promoting angiogenesis. It also interacts with the nitric oxide system through the Akt-eNOS axis, supporting vasodilation and vascular stability. The combined result is what researchers describe as an upgraded triad: collagen deposition, inflammatory cell recruitment, and blood vessel formation all appear earlier and progress faster [2].

Limitations:

Despite promising animal data, human clinical evidence for BPC-157 in wound healing is exceedingly sparse. The FDA classified BPC-157 as a Category 2 bulk drug substance in 2023, and WADA has banned its use in professional sports. All published studies report positive effects, which raises concern about publication bias [7].

TB-500 (Thymosin Beta-4): The Cell Migration Specialist

TB-500 is a synthetic 43-amino-acid peptide based on thymosin beta-4 (TB4), one of the most abundant intracellular proteins in mammalian cells. TB4 is found in high concentrations in wound fluid and platelets -- the body's first responders to tissue damage.

What the research shows:

The landmark study on TB4 and wound healing, published in The Journal of Investigative Dermatology, tested the peptide in a rat full-thickness wound model. Topical or intraperitoneal TB4 increased re-epithelialization by 42% at day 4 and by 61% at day 7 compared to saline controls. Treated wounds also contracted 11% more than controls by day 7, with increased collagen deposition and angiogenesis [8].

A 2003 mouse study confirmed that TB4 in solution or gel form promoted accelerated wound healing in healthy, diabetic, and aged mice. A seven-amino-acid synthetic peptide based on the actin-binding region of TB4 produced repair results in aged animals comparable to the full molecule [9].

TB4 has also reached human clinical trials. Phase II trials showed improved wound healing in patients with pressure ulcers, stasis ulcers, and epidermolysis bullosa. The peptide was well tolerated with favorable safety profiles [9].

How it works:

The active segment within TB-500 (amino acids 17-23: LKKTETQ) promotes actin polymerization, which controls cell shape and movement. By sequestering G-actin and maintaining the pool of monomeric actin available for rapid filament assembly, TB-500 enables keratinocytes, fibroblasts, and endothelial cells to migrate more efficiently into wound sites [10].

Different segments of the peptide handle different jobs. The first four amino acids regulate anti-inflammatory and anti-fibrotic responses. Amino acids 1-15 contribute anti-apoptotic properties. The peptide also upregulates matrix metalloproteinase production, which breaks down the basement membrane to allow cell movement [10].

Limitations:

Like BPC-157, TB-500 is classified as a Category 2 bulk drug substance by the FDA (2023). While the Phase II trial data is encouraging, larger confirmatory trials have not been completed. Most of the mechanistic evidence comes from preclinical work.

GHK-Cu: The Copper Peptide Gene Regulator

GHK-Cu (glycyl-L-histidyl-L-lysine copper complex) is a naturally occurring tripeptide found in human plasma. It was first isolated in 1973 by Loren Pickart, who discovered that it caused old human liver tissue to synthesize proteins at rates typical of younger tissue.

What the research shows:

GHK-Cu's influence on wound healing is well-documented across animal models. In rabbit experimental wounds, GHK alone or combined with helium-neon laser improved wound contraction, granulation tissue formation, antioxidant enzyme activity, and blood vessel growth [11].

Collagen dressing incorporating GHK accelerated healing in both healthy and diabetic rats. The treated group showed higher glutathione and ascorbic acid levels, better epithelialization, and a dramatic 9-fold increase in collagen synthesis in healthy rats [11].

Clinical studies on diabetic ulcers and Mohs surgical wounds found that GHK-Cu significantly improved re-epithelialization and overall wound healing [11]. Following laser resurfacing and microneedling, clinical use shows reduced downtime and minimal scarring.

How it works:

GHK-Cu is perhaps the most genetically active peptide on this list. It modulates the expression of over 4,000 human genes, many of them related to tissue repair, inflammation control, and antioxidant defense [12]. It stimulates collagen synthesis, glycosaminoglycan production, and decorin expression. It attracts immune and endothelial cells to injury sites and modulates both metalloproteinases and their inhibitors -- balancing tissue breakdown and rebuilding [11].

Plasma levels of GHK decline significantly with age: from about 200 ng/mL at age 20 to 80 ng/mL by age 60, which coincides with the well-known decrease in regenerative capacity as we get older [11].

Limitations:

GHK-Cu has a plasma half-life under 30 minutes and is rapidly cleared after dermal injection, with about 95% excreted quickly. Its high hydrophilicity limits skin absorption. These pharmacokinetic challenges have spurred development of hydrogel, nanoparticle, and slow-release formulations to extend its therapeutic window [13].

LL-37: The Antimicrobial Wound Healer

LL-37 is the only cathelicidin antimicrobial peptide produced by humans. This 37-amino-acid peptide, named for its two N-terminal leucine residues, is expressed by white blood cells and epithelial cells throughout the body.

What the research shows:

A key study in the Journal of Investigative Dermatology revealed that LL-37 levels surge in wounded skin, peaking at 48 hours post-injury and declining to baseline once the wound closes. The critical finding: in chronic ulcers that fail to heal, LL-37 levels are low and immunoreactivity is absent from the ulcer edge epithelium [14]. This suggests LL-37 is not just present during healing -- it may be required for it.

In vivo wound healing experiments using dexamethasone-treated mice showed that topical application of both synthetic and recombinant LL-37 increased vascularization and re-epithelialization [15]. In ob/ob mice (a model for diabetic wound healing), adenoviral delivery of LL-37 to excisional wounds significantly improved both re-epithelialization and granulation tissue formation [15].

LL-37 also has potent antimicrobial and anti-biofilm properties. It can eradicate preformed biofilms in vitro, which is particularly relevant for chronic wounds colonized by drug-resistant bacteria [16].

How it works:

LL-37 activates keratinocyte migration through changes in actin dynamics and focal adhesion complex signaling (including FAK and paxillin phosphorylation). It induces Snail and Slug transcription factors, activates matrix metalloproteinases, and triggers the MAPK and PI3K/Akt pathways [15]. It also suppresses keratinocyte apoptosis by upregulating COX-2, helping cells survive the harsh wound environment [17].

Limitations:

Clinical application is hindered by low proteolytic stability (the peptide breaks down easily), potential cytotoxicity at high concentrations, and high production costs. Modified LL-37 analogs are in development to address these challenges [18].

KPV: The Anti-Inflammatory Tripeptide

KPV (Lysine-Proline-Valine) is derived from the C-terminal end of alpha-melanocyte-stimulating hormone (alpha-MSH). Despite being just three amino acids long, KPV packs a disproportionate anti-inflammatory punch.

What the research shows:

A landmark study published in Gastroenterology demonstrated that nanomolar concentrations of KPV inhibit NF-kB and MAP kinase inflammatory signaling pathways and reduce pro-inflammatory cytokine secretion. Oral KPV administration reduced the severity of DSS- and TNBS-induced colitis in mice [19].

In human bronchial epithelial cells, KPV translocates to the nucleus and competitively blocks the interaction between importin-alpha-3 and the p65RelA subunit of NF-kB. This directly prevents the inflammatory transcription factor from doing its job [20].

A 2025 study in keratinocytes showed KPV effectively inhibits the ERK/p38 MAPK/NF-kB axis and caspase-1 activation, reducing both inflammation and apoptotic cell death [21].

How it works:

KPV enters cells through the PepT1 transporter (the same transporter that absorbs dietary peptides in your gut). Once inside, it suppresses NF-kB nuclear translocation and stabilizes IkB-alpha, the protein that keeps NF-kB locked in the cytoplasm. The result is a selective reduction in pro-inflammatory cytokines (IL-1-beta, IL-6, IL-12, TNF-alpha, IFN-gamma) without broadly suppressing immune function -- IL-10, an anti-inflammatory cytokine, remains unchanged [19].

Limitations:

KPV is primarily studied as an anti-inflammatory rather than a direct wound healer. Its contribution to tissue repair comes through resolving the inflammation that stalls healing rather than directly stimulating collagen production or cell migration. Long-term safety data in humans is not available.

Collagen Peptides: The Structural Foundation

Collagen peptides (hydrolyzed collagen) are not a single peptide but a family of low-molecular-weight fragments derived from collagen protein. They provide the amino acid building blocks -- particularly glycine, proline, and hydroxyproline -- that your body uses to build new connective tissue.

What the research shows:

A retrospective study of 5,335 surgical cases found that hydrolyzed collagen applied to surgical wounds reduced surgical site infection rates and promoted healing of acute wounds compared to untreated controls [22].

In vitro and animal studies show collagen peptides accelerate wound closure through TGF-beta/Smad and PI3K/Akt/mTOR signaling pathways, boosting fibroblast proliferation and collagen synthesis [23]. Researchers estimate collagen peptides improve wound healing efficiency by 10-30% across different wound types [23].

For oral supplementation, blood levels of hydroxyproline peak about 2 hours after ingestion at concentrations sufficient to promote wound closure in laboratory models [24]. This suggests orally consumed collagen peptides may reach therapeutic concentrations in the skin.

Limitations:

While topical collagen dressings are widely used in clinical wound care, the evidence for oral collagen supplements in wound healing is weaker. High-quality randomized controlled trials are limited, and the field is still in relatively early clinical development [22].

Peptide Comparison Table

PeptidePrimary Wound Healing MechanismBest Research Evidence ForRoute StudiedHuman Clinical DataKey Limitation
BPC-157Angiogenesis, collagen synthesis, ERK1/2 activationTendon, ligament, skin wounds, burnsOral, IP, topicalVery limitedNo FDA approval; publication bias concerns
TB-500Actin regulation, cell migration, re-epithelializationSkin wounds (including diabetic/aged), pressure ulcersTopical, IP, SCPhase II trials (dermal)Category 2 FDA classification
GHK-CuGene regulation (4,000+ genes), collagen turnoverSkin repair, diabetic ulcers, post-procedure healingTopical, SC, systemicClinical wound studiesVery short half-life (~30 min)
LL-37Antimicrobial, anti-biofilm, keratinocyte migrationInfected wounds, chronic ulcers, diabetic woundsTopical, adenoviralLimited clinicalStability and cost challenges
KPVNF-kB inhibition, inflammation resolutionInflammatory wound conditions, gut healingOral, topicalNone (preclinical)Indirect wound healer
Collagen PeptidesStructural amino acids, TGF-beta/Smad signalingSurgical wounds, skin repairOral, topicalRetrospective surgical dataLimited RCTs for oral form

Combining Peptides for Wound Healing

Because these peptides work through different mechanisms, researchers and clinicians have explored combining them for potentially synergistic effects. For a deeper look at combination strategies, see our Peptide Stacking Guide.

Common pairings studied or discussed in the literature include:

  • BPC-157 + TB-500: BPC-157 drives angiogenesis and collagen production while TB-500 accelerates cell migration. Together, they address both the vascular and cellular components of repair. This is one of the most widely discussed combinations in regenerative medicine contexts.
  • GHK-Cu + Collagen Peptides: GHK-Cu activates the genetic machinery for tissue remodeling while collagen peptides supply the raw structural material. This pairing makes physiological sense for skin repair and post-procedure recovery.
  • LL-37 + BPC-157 or TB-500: For infected or contaminated wounds, LL-37 handles the antimicrobial challenge while BPC-157 or TB-500 drives the repair process.

It is worth noting that formal clinical trials on peptide combinations for wound healing are essentially nonexistent. The rationale for stacking is based on complementary mechanisms rather than direct combination studies.

Growth hormone secretagogues like CJC-1295 and Ipamorelin are sometimes discussed in wound healing contexts because growth hormone and IGF-1 support tissue repair. However, their effects on wound healing are indirect -- mediated through systemic hormonal changes rather than local tissue signaling.

What the Research Doesn't Tell You (Yet)

Honesty about the evidence gaps matters. Here is what you should know:

Most evidence is preclinical. BPC-157, TB-500, KPV, and LL-37 have strong animal data but limited or no large-scale human clinical trials for wound healing specifically. GHK-Cu has the most clinical data in dermatological settings, and collagen peptides have some retrospective surgical data.

Dosing is not standardized. Animal studies use widely varying doses and routes of administration. Translating these to human dosing remains largely guesswork outside of specific clinical trial protocols.

Regulatory status is complicated. The FDA classified both BPC-157 and TB-500 as Category 2 bulk drug substances in 2023, meaning they cannot be legally compounded by commercial pharmacies in the U.S. None of the peptides on this list (except collagen peptides as supplements) have FDA approval for wound healing.

Long-term safety data is thin. While short-term safety profiles appear favorable across these peptides, multi-year safety data from controlled human studies is lacking for most of them.

Delivery remains a challenge. Short half-lives, enzymatic degradation, and poor bioavailability continue to limit the practical utility of many therapeutic peptides. Researchers are actively developing hydrogels, nanofiber dressings, nanoparticle conjugates, and other delivery systems to address these problems.

Frequently Asked Questions

Which peptide is best for wound healing after surgery? GHK-Cu has the most clinical evidence for post-procedure skin healing, with studies showing reduced downtime after laser resurfacing and improved outcomes in Mohs surgical wounds. BPC-157 has strong preclinical evidence for various wound types but lacks robust human surgical data. Collagen peptide dressings are already used in standard clinical wound care. The best choice depends on the wound type, location, and your healthcare provider's assessment. See our guide on best peptides for joint health for recovery from orthopedic procedures.

Can peptides help with chronic wounds that won't heal? Chronic non-healing wounds are often stuck in a prolonged inflammatory phase. The research on LL-37 is particularly relevant here -- studies show that chronic ulcers have abnormally low levels of this peptide compared to normally healing wounds [14]. KPV's NF-kB inhibition could theoretically help resolve the inflammation keeping wounds in this stalled state. TB-500 showed positive results in Phase II trials for pressure ulcers and stasis ulcers. However, chronic wounds require medical evaluation to identify and address underlying causes (infection, vascular disease, diabetes) alongside any peptide therapy.

Are wound healing peptides safe? The peptides discussed in this guide generally show favorable safety profiles in the studies that have been conducted. BPC-157 has been used in ulcerative colitis and multiple sclerosis clinical trials with no reported toxicity [2]. TB-500 was well tolerated in Phase II dermal trials. GHK-Cu has established safety data for cosmetic use. However, long-term controlled safety studies in humans are lacking for most of these peptides, and regulatory agencies have expressed caution.

How do peptides compare to traditional wound care? Peptides are not replacements for standard wound care (cleaning, debridement, moisture management, infection control, pressure offloading). They are potential adjuncts -- additions to proper wound management that may accelerate healing. No peptide will compensate for a wound that is not properly cleaned, dressed, and monitored.

Do oral collagen supplements actually help wounds heal? There is some evidence that orally consumed collagen peptides reach the bloodstream at concentrations relevant to wound healing within about 2 hours of ingestion [24]. A retrospective surgical study also found benefits from topical hydrolyzed collagen [22]. However, rigorous randomized controlled trials specifically testing oral collagen for wound healing outcomes are limited. The amino acids in collagen supplements (glycine, proline, hydroxyproline) are used throughout the body, not exclusively directed to wound sites.

What about peptides for tendon and ligament repair? BPC-157 has the strongest preclinical evidence for connective tissue repair, with studies showing improved outcomes in transected Achilles tendons [5] and tendon explant models [25]. TB-500 also shows promise for musculoskeletal repair. For a focused look at this topic, see our guide on best peptides for tendon and ligament repair.

The Bottom Line

The science of peptide-based wound healing is genuinely promising. BPC-157 and TB-500 demonstrate broad tissue repair effects across dozens of animal studies. GHK-Cu brings a unique genetic reprogramming approach backed by clinical wound data. LL-37 fills the niche of antimicrobial wound defense. KPV targets the inflammatory bottleneck that stalls chronic wounds. Collagen peptides provide the structural raw materials.

But promising preclinical data is not the same as proven clinical therapy. Most of these peptides need larger, well-designed human trials before we can make definitive claims about efficacy or establish standardized treatment protocols. The regulatory situation is complex, particularly following the FDA's 2023 classifications.

If you are considering peptides for wound healing, the conversation should happen with a healthcare provider who can evaluate your specific situation, the available evidence, and the regulatory realities. Peptides are tools -- potentially powerful ones -- but they work best as part of a thorough approach to wound management, not as standalone miracles.

For related reading, explore our guides on best peptides for inflammation, best peptides for muscle growth and recovery, and best peptides for anti-aging and longevity.

References

  1. Collagen in Wound Healing. International Journal of Molecular Sciences. 2021. PMC8151502. https://pmc.ncbi.nlm.nih.gov/articles/PMC8151502/

  2. Sikiric P, et al. Stable Gastric Pentadecapeptide BPC 157 and Wound Healing. Current Pharmaceutical Design. 2021. PMC8275860. https://pmc.ncbi.nlm.nih.gov/articles/PMC8275860/

  3. Seiwerth S, et al. BPC 157's effect on healing. Journal of Physiology (Paris). 1997;91(3-5):173-8. PMID: 9403790. https://pubmed.ncbi.nlm.nih.gov/9403790/

  4. Mikus D, et al. Pentadecapeptide BPC 157 cream improves burn-wound healing and attenuates burn-gastric lesions in mice. Burns. 2001;27(8):817-27. PMID: 11718984. https://pubmed.ncbi.nlm.nih.gov/11718984/

  5. Staresinic M, et al. Gastric pentadecapeptide BPC 157 accelerates healing of transected rat Achilles tendon and in vitro stimulates tendocytes growth. Journal of Orthopaedic Research. 2003;21(6):976-83. PMID: 14554208. https://pubmed.ncbi.nlm.nih.gov/14554208/

  6. Hsieh MJ, et al. Body protective compound-157 enhances alkali-burn wound healing in vivo and promotes proliferation, migration, and angiogenesis in vitro. Wound Repair and Regeneration. 2015. PMC4425239. https://pmc.ncbi.nlm.nih.gov/articles/PMC4425239/

  7. Buchanan B, et al. Regeneration or Risk? A Narrative Review of BPC-157 for Musculoskeletal Healing. Current Reviews in Musculoskeletal Medicine. 2025. PMC12446177. https://pmc.ncbi.nlm.nih.gov/articles/PMC12446177/

  8. Malinda KM, et al. Thymosin beta4 accelerates wound healing. Journal of Investigative Dermatology. 1999;113(3):364-8. PMID: 10469335. https://pubmed.ncbi.nlm.nih.gov/10469335/

  9. Goldstein AL, et al. Utilizing Developmentally Essential Secreted Peptides Such as Thymosin Beta-4 to Remind the Adult Organs of Their Embryonic State -- New Directions in Anti-Aging Regenerative Therapies. Cells. 2021. PMC8228050. https://pmc.ncbi.nlm.nih.gov/articles/PMC8228050/

  10. Philp D, et al. Thymosin beta 4 and tissue repair. Annals of the New York Academy of Sciences. Various publications on TB4 mechanisms.

  11. Pickart L, Margolina A. GHK Peptide as a Natural Modulator of Multiple Cellular Pathways in Skin Regeneration. BioMed Research International. 2015. PMC4508379. https://pmc.ncbi.nlm.nih.gov/articles/PMC4508379/

  12. Pickart L, Margolina A. Regenerative and Protective Actions of the GHK-Cu Peptide in the Light of the New Gene Data. International Journal of Molecular Sciences. 2018. PMC6073405. https://pmc.ncbi.nlm.nih.gov/articles/PMC6073405/

  13. Singh A, et al. Exploring the Role of Tripeptides in Wound Healing and Skin Regeneration: A Comprehensive Review. International Journal of Medical Sciences. 2025;22:4175. https://www.medsci.org/v22p4175.htm

  14. Heilborn JD, et al. The Cathelicidin Anti-Microbial Peptide LL-37 is Involved in Re-Epithelialization of Human Skin Wounds and is Lacking in Chronic Ulcer Epithelium. Journal of Investigative Dermatology. 2003;120(3):379-89. https://www.jidonline.org/article/S0022-202X(15)30191-3/fulltext

  15. Ramos R, et al. Wound healing activity of the human antimicrobial peptide LL37. Peptides. 2011;32(7):1469-76. PMID: 21693141. https://pubmed.ncbi.nlm.nih.gov/21693141/

  16. Duplantier AJ, van Hoek ML. The Human Cathelicidin Antimicrobial Peptide LL-37 as a Potential Treatment for Polymicrobial Infected Wounds. Frontiers in Immunology. 2013. PMC3699762. https://pmc.ncbi.nlm.nih.gov/articles/PMC3699762/

  17. Barlow PG, et al. The human antimicrobial peptide LL-37 suppresses apoptosis in keratinocytes. Journal of Investigative Dermatology. 2008. PMID: 18923446. https://pubmed.ncbi.nlm.nih.gov/18923446/

  18. Antimicrobial Peptides of the Cathelicidin Family: Focus on LL-37 and Its Modifications. International Journal of Molecular Sciences. 2025;26(16):8103. https://www.mdpi.com/1422-0067/26/16/8103

  19. Dalmasso G, et al. PepT1-Mediated Tripeptide KPV Uptake Reduces Intestinal Inflammation. Gastroenterology. 2008;134(1):166-78. PMC2431115. https://pmc.ncbi.nlm.nih.gov/articles/PMC2431115/

  20. Bhatt HN, et al. Inhibition of cellular and systemic inflammation cues in human bronchial epithelial cells by melanocortin-related peptides: mechanism of KPV action and a role for MC3R agonists. Journal of Physiology, Pathophysiology and Pharmacology. 2012. PMC3403564. https://pmc.ncbi.nlm.nih.gov/articles/PMC3403564/

  21. Lysine-Proline-Valine peptide mitigates fine dust-induced keratinocyte apoptosis and inflammation. Biochemical Pharmacology. 2025. https://www.sciencedirect.com/science/article/abs/pii/S004081662500117X

  22. Collagen-Based Products in Wound, Skin, and Health Care. Bioengineering. 2025. PMC12359144. https://pmc.ncbi.nlm.nih.gov/articles/PMC12359144/

  23. Deciphering the Wound-Healing Potential of Collagen Peptides and the Molecular Mechanisms: A Review. Journal of Agricultural and Food Chemistry. 2024. https://pubs.acs.org/doi/10.1021/acs.jafc.4c02960

  24. Mayneris-Perxachs J, et al. Potentiating cutaneous wound healing in young and aged skin with nutraceutical collagen peptides. Clinical and Experimental Dermatology. 2021;46(1):109. https://academic.oup.com/ced/article/46/1/109/6598409

  25. Chang CH, et al. The promoting effect of pentadecapeptide BPC 157 on tendon healing involves tendon outgrowth, cell survival, and cell migration. Journal of Applied Physiology. 2011;110(3):774-80. PMID: 21030672. https://pubmed.ncbi.nlm.nih.gov/21030672/