Peptides for Eczema & Dermatitis Research

Atopic dermatitis affects roughly 10% of adults and up to 20% of children worldwide. The standard treatment playbook -- topical steroids, calcineurin inhibitors, and newer biologics like dupilumab -- works for many people, but not everyone. Long-term steroid use thins skin. Biologics are expensive. And a significant number of patients still deal with persistent flares, skin infections, and the relentless itch that defines this disease.

That gap between what treatments exist and what patients actually need has pushed researchers toward peptides -- small protein fragments that can target inflammation, repair damaged skin barriers, and fight the bacterial infections that make eczema worse. Some of these peptides are in clinical trials. Others are backed by strong preclinical data. A few remain largely theoretical.

This guide breaks down the research on each one, what it does, and where the evidence actually stands.

Why Eczema Is Hard to Treat
How Peptides Fit Into the Picture
Peptides With the Strongest Eczema-Relevant Research
GLP-1 Agonists and Eczema: An Unexpected Connection
Peptide Comparison Table
The Brain Natriuretic Peptide (BNP) Discovery
What About Peptide Combinations?
Frequently Asked Questions
The Bottom Line
References

Why Eczema Is Hard to Treat

Eczema is not one problem. It is several problems happening simultaneously, which is exactly why single-target treatments often fall short.

Barrier dysfunction. Your skin's outer layer (stratum corneum) keeps moisture in and irritants out. In eczema, this barrier is compromised -- filaggrin gene mutations contribute in about 30% of patients, but barrier breakdown also occurs without them [1]. Water escapes (measured as transepidermal water loss, or TEWL), and allergens, bacteria, and irritants get in.

Immune dysregulation. Eczema is driven primarily by Type 2 (Th2) immune responses, with cytokines like IL-4, IL-13, and thymic stromal lymphopoietin (TSLP) dominating. Th17 and Th22 pathways also contribute, especially in chronic disease [2].

Microbial imbalance. More than 90% of eczema patients are colonized with Staphylococcus aureus, compared to about 5% of healthy individuals. S. aureus toxins trigger inflammation and damage the barrier further -- creating a vicious cycle [3].

Neurogenic itch. The itch of eczema actively drives the disease through the itch-scratch cycle. Neuropeptides and nerve growth factors perpetuate flares.

Effective treatment needs to address multiple problems simultaneously. That is where peptides become interesting.

How Peptides Fit Into the Picture

Peptides are short chains of amino acids -- typically between 2 and 50 amino acids long. Unlike large biologic drugs (antibodies like dupilumab that must be injected), many peptides are small enough to penetrate skin, survive in the gut, or act on very specific cellular targets.

For eczema, peptides offer potential advantages across three categories:

Anti-inflammatory peptides that reduce cytokine production and immune activation
Barrier-repair peptides that rebuild the skin's protective structure
Antimicrobial peptides that control S. aureus and other pathogens without contributing to antibiotic resistance

Some peptides hit more than one of these categories. Here is what the research says about each.

Peptides With the Strongest Eczema-Relevant Research

AMTX-100 (cSN50.1): The Gene-Silencing Peptide

What it is: AMTX-100 is a cell-penetrating peptide developed at Vanderbilt University. It works as a Nuclear Transport Checkpoint Inhibitor (NTCI) -- it blocks inflammatory transcription factors from entering the cell nucleus, effectively silencing 15 genes involved in eczema inflammation [4].

How it works: The peptide targets two nuclear transport proteins (importin alpha-5 and importin beta-1) that shuttle inflammatory signals into the nucleus. By blocking this transport, AMTX-100 suppresses expression of TSLP -- the cytokine now considered the "master switch" of atopic dermatitis [4].

Research status: This is the most clinically advanced peptide therapy specifically developed for eczema.

In preclinical models, topical AMTX-100 suppressed TSLP expression and reduced itching, inflammation, and skin lesions without apparent toxicity [4]
Phase 1 clinical trial results showed reduced pruritus (itch), decreased affected body surface area, and no significant adverse events [5]
A Phase 2b trial (randomized, double-blind, placebo-controlled) enrolled patients at 8-10 clinical sites across the United States [5]

Why it matters for eczema: Most existing treatments target one or two inflammatory pathways. AMTX-100 suppresses 15 inflammatory genes simultaneously, hitting the problem at its source rather than downstream. And because it is a topical cream, it avoids the systemic side effects of biologics.

Limitations: Full Phase 2b results have not yet been publicly published. Until larger controlled trials are complete, efficacy in the broader eczema population remains unconfirmed.

KPV: The Anti-Inflammatory Tripeptide

What it is: KPV is a tripeptide (Lysine-Proline-Valine) derived from the C-terminal end of alpha-melanocyte-stimulating hormone (alpha-MSH). It retains the anti-inflammatory activity of its parent molecule but without the pigmentation effects [6].

How it works: KPV inhibits NF-kB activation and reduces production of pro-inflammatory cytokines including TNF-alpha and IL-6. It also modulates the MAPK signaling pathway, reducing oxidative stress in skin cells [6, 7].

Research on eczema and dermatitis:

In animal models, KPV (and the related peptide K(D)PT) suppressed contact dermatitis reactions and induced hapten-specific tolerance when administered both intravenously and topically [6]
Alpha-MSH applied topically in a cream reduced nickel-induced contact eczema in humans -- one of the few direct human eczema studies for any peptide in this class [6]
KPV has antimicrobial activity against Staphylococcus aureus and Candida albicans, both directly implicated in eczema flares [8]
A 2025 study showed KPV protects keratinocytes from pollution-induced damage (PM10 exposure) by inhibiting ROS production and blocking MAPK/ERK activation [7]

Why it matters for eczema: KPV hits three problems at once: it reduces inflammation, fights relevant pathogens, and protects skin cells from environmental damage. It also does not thin skin like steroids or suppress systemic immunity.

Limitations: KPV is highly hydrophilic, which means it does not penetrate intact skin easily. Delivery methods like iontophoresis, microneedles, and nanoparticles are being developed to solve this problem [9]. Most evidence comes from cell and animal studies; large human trials specifically for eczema have not been conducted.

LL-37 and Defensins: Your Skin's Missing Antibiotics

What they are: LL-37 is the only human cathelicidin antimicrobial peptide. Human beta-defensins (HBD-1, HBD-2, HBD-3) are a family of antimicrobial peptides produced by keratinocytes. Together, they form the skin's first-line defense against infection.

The eczema connection: A landmark study published in the New England Journal of Medicine revealed that eczema patients have significantly lower levels of LL-37 and HBD-2 in their skin compared to patients with psoriasis. The difference was stark -- even though both conditions involve inflamed, barrier-disrupted skin, psoriasis patients rarely get skin infections while eczema patients are constantly battling S. aureus [3].

A 2023 study added an important detail: LL-37 is the only antimicrobial peptide consistently reduced in both lesional and non-lesional eczema skin. Other AMPs may actually increase at the protein level in active lesions, but LL-37 decreases -- suggesting it plays a unique and early role in the disease [10].

Why this matters:

The AMP deficiency explains why eczema patients get infections that psoriasis patients do not
LL-37 does more than kill bacteria -- it also regulates wound healing, angiogenesis, and cytokine production [11]
LL-37 may reduce itch by inducing expression of semaphorin 3A, a nerve-repulsive factor that is downregulated in eczema skin [11]
LL-37 and HBD-2 work synergistically -- together they kill S. aureus more effectively than either alone [3]

Therapeutic implications: Vitamin D supplementation can boost LL-37 production in skin. UV phototherapy, a proven eczema treatment, may work partly by increasing antimicrobial peptide expression. Direct application of synthetic AMPs or AMP-boosting compounds is an active area of research [12].

Limitations: Delivering antimicrobial peptides topically at therapeutic concentrations without causing irritation is challenging. AMPs can be degraded by skin proteases, and at high concentrations, some can cause cytotoxicity.

GHK-Cu: The Barrier Repair Peptide

What it is: GHK-Cu (glycyl-L-histidyl-L-lysine copper complex) is a naturally occurring tripeptide found in human plasma. It declines with age -- from about 200 ng/mL at age 20 to 80 ng/mL by age 60 [13].

How it works: GHK-Cu stimulates collagen synthesis, elastin production, and glycosaminoglycan formation. It increases production of barrier proteins and lipids, reduces transepidermal water loss (TEWL), and has direct anti-inflammatory effects -- specifically reducing TNF-alpha-induced IL-6 secretion in dermal fibroblasts [13, 14].

Relevance to eczema:

GHK-Cu supports production of the proteins and lipids that reinforce the skin barrier -- the exact structures compromised in eczema
It reduces TEWL, the hallmark measurement of barrier dysfunction in atopic dermatitis [14]
Researchers have proposed GHK-Cu as a topical alternative to corticosteroids for inflammatory skin conditions, based on its anti-inflammatory profile without skin-thinning effects [14]
GHK-Cu has antimicrobial properties that may help prevent secondary infections in damaged eczema skin

Limitations: Most GHK-Cu research focuses on anti-aging and wound healing, not eczema specifically. The peptide is hydrophilic and does not easily penetrate the stratum corneum -- liposomal formulations improve penetration [15]. People with active eczema should introduce copper peptides cautiously, as irritated skin may react differently than healthy skin.

For more on copper peptides in skincare, see our copper peptides guide and the broader best peptides for skin anti-aging overview.

BPC-157: The Gut-Skin Connection

What it is: BPC-157 is a 15-amino-acid peptide derived from human gastric juice. It was originally studied for gastrointestinal protection and wound healing, but its mechanisms have direct relevance to eczema through the gut-skin axis [16].

The gut-skin axis in eczema: Research consistently shows connections between gut health and atopic conditions. Many eczema patients have concurrent gut inflammation, food sensitivities, or altered gut microbiome composition. The gut microbiome influences systemic immune function, and disruptions can drive the Th2-dominant immune responses that characterize eczema [17].

How BPC-157 may be relevant:

In animal studies, BPC-157 accelerates wound closure, reduces inflammation, and improves the quality of healed tissue [16]
Its anti-inflammatory properties may help reduce the redness and swelling of eczema flares
By supporting gut lining integrity, BPC-157 may address upstream contributors to eczema rather than treating skin symptoms alone [16]
Unlike corticosteroids, BPC-157 does not cause skin thinning, stretch marks, or hormonal disruption

Limitations: No clinical trials have tested BPC-157 specifically for eczema. The gut-skin connection, while biologically plausible, has not been validated as a direct treatment pathway for atopic dermatitis. Most evidence is preclinical.

For more on BPC-157's gut-healing properties, see our guide on best peptides for gut health.

svL4: The Multivalent Peptide

What it is: svL4 is a tetravalent peptide (meaning it has four active binding sites) studied specifically for eczema resolution in animal models [18].

Research findings: In a study published in Biomedicines, eczema was induced on mouse skin using either lipopolysaccharide or a combination of staphylococcal enterotoxin B and house dust mite extract -- two of the most relevant real-world eczema triggers. Topical treatment with 1 micromolar svL4 produced striking results [18]:

Within 14 days, neutrophils (inflammatory white blood cells) were absent from treated skin
The epidermis returned to normal morphology
In contrast, topical dexamethasone (a potent steroid) was ineffective at restoring normal epidermal structure

The peptide contains glutamine residues that serve as cross-linking substrates for transglutaminase 2, an enzyme involved in skin barrier formation. This suggests svL4 may work partly by directly supporting barrier reconstruction [18].

Limitations: This is a single preclinical study. No human data exists. The finding that svL4 outperformed dexamethasone is provocative but needs replication and human testing.

GLP-1 Agonists and Eczema: An Unexpected Connection

Semaglutide and other GLP-1 receptor agonists were developed for diabetes and obesity, but emerging evidence suggests they may affect inflammatory skin diseases [19].

GLP-1 agonists reduce systemic inflammation markers (like hsCRP) independent of weight loss. They may also modulate gut microbiota and boost short-chain fatty acid (SCFA) production, which has anti-inflammatory effects on skin through the gut-skin axis [20]. A retrospective cohort study has examined GLP-1 agonist use and atopic dermatitis outcomes in obese patients [19].

Important nuances: Unlike psoriasis and hidradenitis suppurativa, eczema patients are not necessarily overweight, making the metabolic benefits of GLP-1 drugs less directly relevant. The data for eczema specifically is sparse [19]. GLP-1 agonists can also cause skin reactions in some patients, including eczematous eruptions and pruritus [21].

Peptide Comparison Table

Peptide	Primary Mechanism	Eczema Relevance	Research Stage	Route
AMTX-100	Suppresses 15 inflammatory genes via nuclear transport blockade	Directly developed for eczema; suppresses TSLP	Phase 2b clinical trial	Topical cream
KPV	NF-kB inhibition, cytokine suppression	Anti-inflammatory + antimicrobial against S. aureus	Preclinical; one human study (alpha-MSH cream)	Topical (delivery challenges)
LL-37	Antimicrobial, immunomodulatory	Deficient in eczema skin; explains infection susceptibility	Well-characterized in humans	Boosted via Vitamin D/UV
GHK-Cu	Barrier repair, collagen synthesis, anti-inflammatory	Reduces TEWL, supports barrier proteins	Extensive skincare research; limited eczema-specific data	Topical (liposomal preferred)
BPC-157	Tissue repair, gut healing, angiogenesis	Gut-skin axis; anti-inflammatory	Preclinical (extensive animal data)	Oral or subcutaneous
svL4	Transglutaminase cross-linking, barrier reconstruction	Outperformed steroids in mouse eczema model	Single preclinical study	Topical
Semaglutide	GLP-1 agonism, systemic inflammation reduction	Gut-skin axis modulation; relevant in obese patients	FDA-approved (not for eczema); retrospective skin data	Injection or oral

The Brain Natriuretic Peptide (BNP) Discovery

Not all peptide research for eczema is about treatment. Some is about understanding what drives the disease.

In 2023, researchers at North Carolina State University identified brain natriuretic peptide (BNP) as an active participant in eczema pathology. BNP is expressed in sensory neurons -- the same neurons that convey itch sensation from skin to brain via the spinal cord. Previous work had shown BNP helps transmit itch signals, but this research went further, demonstrating that BNP is directly involved in activating atopic dermatitis [22].

This discovery matters because it opens a completely new therapeutic target. If BNP signaling can be blocked, it might be possible to interrupt both the itch and the inflammatory cascade of eczema at their neurological source.

What About Peptide Combinations?

No single peptide addresses inflammation, barrier dysfunction, and microbial imbalance equally well. Some researchers are exploring multi-peptide approaches:

KPV + BPC-157: KPV handles inflammation and antimicrobial activity; BPC-157 supports tissue repair and gut health. See our peptide stacking guide.
GHK-Cu + antimicrobial peptides: Barrier repair plus infection control.
Anti-inflammatory peptide + vitamin D: Since vitamin D boosts natural LL-37 production, combining exogenous anti-inflammatory peptides with supplementation could address both immune and antimicrobial deficits.

These combinations are theoretical rather than clinically tested. For broader guidance, see our best peptides for inflammation and best peptides for wound healing guides.

Frequently Asked Questions

Are any peptides FDA-approved for eczema? No peptide therapy is currently FDA-approved specifically for eczema. AMTX-100 is the furthest along in clinical development, currently in a Phase 2b trial. Semaglutide and other GLP-1 agonists are FDA-approved for diabetes and obesity but not for dermatologic conditions.

Can I use copper peptide serums on eczema? GHK-Cu is widely available in skincare products. However, eczema-affected skin is compromised and may react unpredictably to new products. If you want to try copper peptide serums, patch-test on a small area of unaffected skin first and introduce them during a calm period, not during a flare. Talk to your dermatologist before adding new products to an eczema management routine.

How does vitamin D relate to peptide therapy for eczema? Vitamin D directly increases your skin's production of LL-37 and beta-defensins -- the antimicrobial peptides that eczema patients are deficient in. Several studies have shown that vitamin D supplementation can reduce eczema severity, likely through this AMP-boosting mechanism. It is one of the most accessible peptide-related interventions available [12].

Is BPC-157 proven to help eczema? No. BPC-157 has extensive preclinical data for wound healing and gut repair, but no clinical trials have tested it for eczema specifically. The rationale for its use in eczema is based on the gut-skin axis theory -- the idea that improving gut health can reduce systemic inflammation and improve skin conditions. This connection is biologically plausible but not clinically validated for eczema.

Why are eczema patients prone to skin infections? The landmark Ong et al. study in the New England Journal of Medicine showed that eczema patients produce significantly less LL-37 and HBD-2 -- the skin's natural antibiotic peptides -- compared to psoriasis patients. This deficiency, combined with a disrupted skin barrier, creates conditions where S. aureus and other pathogens thrive.

What is the most promising peptide for eczema right now? Based on clinical development stage, AMTX-100 (cSN50.1) is the leader -- it is the only peptide designed specifically for eczema that has reached Phase 2b clinical trials. Based on breadth of supportive evidence, KPV and LL-37-boosting strategies (via vitamin D) have the most robust preclinical backing.

The Bottom Line

Peptide research for eczema is moving on multiple fronts. AMTX-100 is the closest to becoming an actual treatment, with its ability to silence 15 inflammatory genes through a single topical application. KPV offers a multi-target approach combining anti-inflammatory, antimicrobial, and skin-protective properties. The discovery that eczema patients lack key antimicrobial peptides like LL-37 has changed how researchers think about the disease entirely.

But perspective matters here. Most of this research is preclinical. AMTX-100 is still in Phase 2b. KPV faces delivery challenges. GHK-Cu has not been tested specifically for eczema in controlled trials. The svL4 results are from a single mouse study.

What makes the peptide approach genuinely promising is that eczema is a multi-mechanism disease, and peptides can be designed or selected to match those mechanisms -- inflammation, barrier repair, infection control -- in ways that single-target drugs cannot. Whether that promise translates into approved treatments depends on the clinical trials that are now underway or being planned.

If you have eczema, work with your dermatologist. Do not replace proven treatments with experimental peptides. But do ask about vitamin D status (it directly affects your antimicrobial peptide levels), and keep an eye on the AMTX-100 trial results. The peptide pipeline for eczema is more active than it has ever been.

References

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Brunner PM, Guttman-Yassky E, Leung DY. The immunology of atopic dermatitis and its reversibility with broad-spectrum and targeted therapies. J Allergy Clin Immunol. 2017;139(4S):S65-S76. PubMed
Ong PY, Ohtake T, Brandt C, et al. Endogenous antimicrobial peptides and skin infections in atopic dermatitis. N Engl J Med. 2002;347(15):1151-1160. NEJM
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Amytrx Therapeutics. AMTX-100 Phase 1 Clinical Trial Data Presented at Revolutionizing Atopic Dermatitis Conference. June 2023. Press Release
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Lysine-Proline-Valine peptide mitigates fine dust-induced keratinocyte apoptosis and inflammation by regulating oxidative stress and modulating the MAPK/NF-kB pathway. Peptides. 2025. ScienceDirect
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Antimicrobial Peptide Loss, Except for LL-37, is not Characteristic of Atopic Dermatitis. J Invest Dermatol. 2023. PMC
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Role of Antimicrobial Peptides in Skin Barrier Repair in Individuals with Atopic Dermatitis. Int J Mol Sci. 2020;21(20):7607. MDPI
Seiwerth S, Rucman R, Turkovic B, et al. BPC 157 and wound healing. Front Pharmacol. 2021;12:627533. Frontiers
Salem I, Ramser A, Isham N, Ghannoum MA. The gut microbiome as a major regulator of the gut-skin axis. Front Microbiol. 2018;9:1459. PMC
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The Use of GLP-1 Agonists in the Management of Cutaneous Disease. J Clin Aesthet Dermatol. 2025. JCAD
The Gut-Skin Axis: Exploring the Role of SCFAs, Obesity, and GLP-1 Receptor Agonists in Atopic Dermatitis. J Integr Dermatol. 2025. JID
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