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Peptides for Fibrosis & Scar Tissue Research

Fibrosis is your body's repair system stuck in overdrive. When tissue is injured, fibroblasts rush to the site, lay down collagen, and close the wound. Normally, this process shuts off once the job is done. In fibrosis, it does not.

Fibrosis is your body's repair system stuck in overdrive. When tissue is injured, fibroblasts rush to the site, lay down collagen, and close the wound. Normally, this process shuts off once the job is done. In fibrosis, it does not. Collagen keeps accumulating, the tissue stiffens, and organ function declines.

The numbers are stark. Fibrotic diseases — including liver cirrhosis, pulmonary fibrosis, kidney disease, heart failure, and pathological scarring — account for an estimated 35% of deaths worldwide [1]. And until recently, the drug options for reversing established fibrosis were limited to a handful of FDA-approved therapies with modest efficacy and significant side effects.

Peptides are changing that picture. Because they are small (2–50 amino acids), structurally diverse, and capable of targeting specific signaling pathways with high selectivity and low toxicity, peptides have become a major focus of antifibrotic drug development [2]. From BPC-157's collagen-remodeling properties to semaglutide's FDA-approved liver fibrosis indication, the research is moving fast.

Here is what the science supports — and where the gaps remain.

Table of Contents

How Fibrosis Works: The Core Problem

Normal wound healing follows a predictable sequence: inflammation, proliferation (new tissue formation), and remodeling (reorganization of the new tissue). In the remodeling phase, the body breaks down excess collagen and replaces it with properly organized tissue. The balance between collagen production and collagen degradation determines whether you get a thin scar or a thick, raised one — or whether an internal organ keeps working or slowly hardens.

Fibrosis occurs when that balance tips toward excess production. The key players are myofibroblasts — specialized cells that contract wounds and secrete large amounts of extracellular matrix (ECM) proteins, primarily collagen types I and III. In healthy healing, myofibroblasts die off through apoptosis once the wound is closed. In fibrosis, they persist and keep producing matrix [3].

This pattern repeats across organs. Liver fibrosis involves activated hepatic stellate cells (a type of myofibroblast). Pulmonary fibrosis involves lung fibroblasts overproducing collagen. Cardiac fibrosis stiffens the heart muscle. Skin fibrosis produces keloids and hypertrophic scars. The cell types vary, but the underlying mechanism — myofibroblasts that will not stop — is remarkably consistent [1].

TGF-Beta: The Master Switch

Transforming growth factor beta (TGF-beta) is the most well-studied signaling pathway in fibrosis. It activates fibroblasts, drives their differentiation into myofibroblasts, and stimulates collagen synthesis through the Smad signaling cascade. Nearly every antifibrotic peptide under investigation targets TGF-beta directly or interferes with its downstream effects [2].

This makes TGF-beta a double-edged sword for drug developers. Block it completely and you impair normal wound healing and immune function. The goal is modulation — dialing down the overactive signaling without shutting it off entirely. Peptides are well-suited to this task because they can be designed for high specificity to particular components of the TGF-beta pathway [2].

For a broader look at peptides targeting inflammation (which often triggers fibrosis), see our guide on the best peptides for inflammation.

BPC-157: Collagen Remodeling Without Excess Scarring

BPC-157 is a 15-amino-acid synthetic peptide derived from human gastric juice. Its role in fibrosis research is nuanced: it promotes collagen synthesis during healing while simultaneously reducing excessive scar formation. That dual action makes it different from drugs that simply block collagen production.

What the Animal Studies Show

In three separate rat models — skin incisional wounds, colon-colon anastomoses, and sponge implantation angiogenesis assays — BPC-157 significantly increased granulation tissue formation, angiogenesis, and collagen production compared to controls [4].

A 2020 study in Frontiers in Pharmacology tested BPC-157 in a rat tendon-to-bone healing model. BPC-157 upregulated both collagen type I and type III expression, improved mechanical strength of the repair site, and — critically — reduced scar tissue formation [5].

How It Reduces Fibrosis

BPC-157 works through several overlapping mechanisms:

  • TGF-beta1 downregulation. BPC-157 reduces expression of TGF-beta1 and alpha-smooth muscle actin (alpha-SMA), the marker protein of myofibroblasts. By steering fibroblasts away from the myofibroblast fate, it prevents the excessive collagen deposition that causes fibrotic scarring [6].
  • MMP/TIMP ratio modulation. Matrix metalloproteinases (MMPs) break down collagen; tissue inhibitors of metalloproteinases (TIMPs) block them. BPC-157 adjusts the MMP-1/TIMP-1 ratio to favor orderly matrix turnover rather than accumulation [6].
  • Macrophage phenotype shift. BPC-157 shifts macrophage activity from the pro-inflammatory M1 phenotype toward the reparative M2 phenotype, which is associated with less fibrosis and better tissue remodeling [7].
  • VEGF-mediated angiogenesis. BPC-157 increases VEGF-A expression, promoting healthy blood vessel formation. Well-vascularized wounds tend to produce softer, less visible scars [6].

Limitations

Nearly all BPC-157 data comes from animal models. Only three pilot studies have examined BPC-157 in humans (for knee pain, interstitial cystitis, and IV safety/pharmacokinetics) [7]. The peptide is not approved for clinical use by any regulatory authority.

For a deeper look at BPC-157's tissue repair mechanisms, see our BPC-157 complete guide and our overview of peptides for wound healing.

Semaglutide and GLP-1 Agonists: The Metabolic Antifibrotic

Semaglutide was developed as a GLP-1 receptor agonist for type 2 diabetes and obesity. Its antifibrotic properties were, in many ways, a surprise — but they have now earned FDA approval.

The ESSENCE Trial and FDA Approval

In August 2025, the FDA granted accelerated approval for semaglutide (Wegovy formulation) to treat metabolic dysfunction-associated steatohepatitis (MASH) with moderate to advanced liver fibrosis (stages F2-F3) [8].

The data: compared to placebo, semaglutide increased steatohepatitis resolution without worsening fibrosis (63% vs. 34%) and reduced liver fibrosis without worsening steatohepatitis (37% vs. 23%) [8]. Earlier phase 2 data showed dose-dependent MASH resolution in 59% of treated patients vs. 17% on placebo [9].

Mechanisms in Fibrosis

Semaglutide's antifibrotic effects appear to work through both indirect and direct pathways:

  • Weight loss and metabolic improvement. By reducing fat accumulation in the liver and improving insulin sensitivity, semaglutide removes the metabolic drivers of MASH. Weight loss accounted for a major portion of the histological improvement — but not all of it [10].
  • Direct anti-inflammatory effects. Proteomic analyses identified 72 proteins significantly associated with MASH resolution and semaglutide treatment, with most related to metabolism and several directly implicated in fibrosis and inflammation [10].
  • TGF-beta pathway suppression. In animal models, GLP-1 receptor agonists reduced TGF-beta1 expression, inhibited epithelial-mesenchymal transition (a process where epithelial cells transform into fibroblast-like cells that produce collagen), and suppressed Smad3 and ERK1/2 signaling [11].
  • Weight-independent fibrosis improvement. In non-obese mouse models of MASH, semaglutide still improved fibrosis — suggesting disease-modifying mechanisms that go beyond metabolic correction [10].

Beyond the Liver

GLP-1 receptor agonists have shown antifibrotic effects in multiple organ systems:

  • Kidney: Liraglutide inhibited TGF-beta1-induced EMT in kidney cells and reduced renal fibrosis in animal models. Clinical data shows lower rates of macroalbuminuria and progression to end-stage kidney disease in patients taking GLP-1 agonists [12].
  • Heart: Preclinical studies show reduced cardiac fibrosis and improved ventricular remodeling [11].
  • Uterus: Semaglutide improved fibrosis and inflammation in intrauterine adhesion models [13].

Semaglutide's ability to reverse established cirrhosis remains unproven. But its approval for MASH with fibrosis marks a genuine milestone — the first GLP-1 agonist validated as an antifibrotic therapy. For the full pharmacology picture, see our semaglutide guide and our profile of tirzepatide, which also shows emerging metabolic-antifibrotic properties.

GHK-Cu: Restoring the Remodeling Balance

GHK-Cu is a naturally occurring copper-binding tripeptide. Plasma levels peak around age 20 (200 ng/mL) and decline to about 80 ng/mL by age 60 — a decline that correlates with reduced healing capacity and increased susceptibility to fibrosis [14].

Antifibrotic Mechanisms

GHK-Cu's approach to fibrosis is distinctive: rather than simply blocking collagen production, it restores balanced remodeling.

  • MMP modulation. GHK-Cu stimulates both collagen synthesis and collagen breakdown, maintaining the dynamic balance between production and degradation that prevents fibrosis. It modulates matrix metalloproteinase activity and their inhibitors [14].
  • TGF-beta pathway restoration. Using the Connectivity Map database, researchers found that GHK reverses gene expression changes associated with emphysematous lung destruction — specifically, it reactivates the TGF-beta pathway in contexts where it has become dysfunctional. Lung fibroblasts from COPD patients treated with GHK recovered their ability to contract and remodel collagen gels [15].
  • Broad gene modulation. Transcriptomic analyses show GHK-Cu affects over 4,000 human genes, upregulating those involved in tissue remodeling (collagen I, III) and downregulating pro-inflammatory pathways like NF-kappaB [15].

Organ-Specific Evidence

  • Lung fibrosis. GHK-Cu showed protective effects in bleomycin-induced pulmonary fibrosis models through anti-oxidative stress and anti-inflammation pathways [16].
  • Liver. GHK-Cu has demonstrated ability to improve liver tissue repair in animal models [14].
  • Skin. GHK-Cu reduces fibrosis in skin models by downregulating TGF-beta1 and other pro-fibrotic genes, promoting smoother healing with less scar formation [16].

GHK-Cu can increase collagen production by up to 70% in laboratory studies while simultaneously preventing the disorganized collagen deposition that causes fibrotic scarring [16]. The copper component is critical — it acts as a cofactor for lysyl oxidase and lysyl hydroxylase, enzymes that properly cross-link collagen for structural integrity.

For more on GHK-Cu's regenerative properties, see our GHK-Cu guide and our overview of best peptides for wound healing.

TB-500: Reducing Myofibroblasts at the Source

TB-500 is a synthetic fragment of thymosin beta-4, a naturally occurring 43-amino-acid peptide. Its antifibrotic effects center on one key property: it reduces myofibroblast numbers in wounds.

Myofibroblasts are the cells that produce excess collagen in fibrotic tissue. TB-500 decreases their accumulation through two mechanisms:

  1. Actin sequestration. By binding G-actin monomers, TB-500 modulates the cytoskeletal changes needed for fibroblast-to-myofibroblast differentiation [17].
  2. Anti-inflammatory action. TB-500 reduces inflammatory signaling that drives myofibroblast activation in the first place [17].

Organ Fibrosis Data

  • Skin wounds. In rat wound models, thymosin beta-4 increased re-epithelialization by up to 61% while producing less scar tissue than untreated controls. After 14 days, collagen fiber bundles in treated wounds were thicker and more organized, with visibly less scarring [18].
  • Lung fibrosis. Research has shown inflammation reductions in rodent models of pulmonary fibrosis [19].
  • Kidney fibrosis. The TB-500 metabolite Ac-SDKP reduced renal fibrosis in rodent models, decreasing collagen and fibronectin discharge and suppressing macrophage migration to damaged sites [19].
  • Liver fibrosis. A 2018 study reported antioxidant, anti-inflammatory, and antifibrotic properties of TB-500 in alcoholic liver injury [19].

The wound healing and antifibrotic data for TB-500 are consistent across multiple studies and organ systems, but they remain almost entirely preclinical. TB-500 is not approved for human use.

For information on combining TB-500 with other repair-promoting peptides, see our peptide stacking guide.

CJC-1295 and the GH/IGF-1 Axis

CJC-1295 is a synthetic analog of growth hormone-releasing hormone (GHRH) that stimulates pulsatile release of growth hormone (GH) and insulin-like growth factor 1 (IGF-1). Its connection to fibrosis research is indirect but relevant.

How GH/IGF-1 Affects Fibrosis

Growth hormone has well-documented effects on collagen synthesis. A single injection of CJC-1295 produced dose-dependent increases in GH (2- to 10-fold for 6+ days) and IGF-1 (1.5- to 3-fold for 9–11 days) [20]. That sustained elevation activates the GH-IGF-1 axis, which:

  • Boosts collagen synthesis needed for connective tissue repair
  • Promotes osteoblast activity and bone matrix formation
  • Accelerates wound healing and tissue remodeling [21]

The Fibrosis Question

The relationship between GH/IGF-1 and fibrosis is complicated. On one hand, increased collagen synthesis supports healing. On the other, the IGF-1 pathway cross-talks with TGF-beta — the central mediator of fibrosis. Whether sustained GH stimulation via CJC-1295 promotes healthy remodeling or tips toward excessive matrix deposition may depend on context: the tissue, the degree of existing damage, and the duration of stimulation [21].

This makes CJC-1295 more of a research tool for understanding GH-fibrosis interactions than a direct antifibrotic therapy. No studies have tested CJC-1295 specifically as a fibrosis treatment. Combined with ipamorelin (a growth hormone secretagogue), CJC-1295 is more commonly studied in contexts of recovery, body composition, and connective tissue repair.

Relaxin: The Dedicated Antifibrotic Peptide

If any peptide was "built" for fibrosis, it is relaxin. This hormone — best known for its role in pregnancy — has the most directly antifibrotic mechanism of any peptide in this guide.

Mechanism of Action

Relaxin works through its receptor RXFP1 to:

  • Limit collagen production in activated fibroblasts
  • Stimulate collagen degradation by increasing MMP-2 expression
  • Inhibit fibroblast differentiation into myofibroblasts
  • Reverse established fibrosis — not just prevent new scarring, but break down existing scar tissue [22]

That last point is rare. Most antifibrotic strategies prevent new collagen from accumulating. Relaxin has been shown to actively reverse it. In relaxin-knockout mice, recombinant relaxin treatment reversed established pulmonary, renal, and cardiac fibrosis by 40%–70% [23].

Clinical Trial History

Clinical translation has been difficult. Serelaxin (recombinant human relaxin-2) showed some benefits in acute heart failure trials — reducing dyspnea and markers of organ damage — but the pivotal RELAX-AHF-2 trial failed to demonstrate superiority over placebo for cardiovascular mortality [24]. A scleroderma trial was also largely unsuccessful, likely because most enrolled patients had end-stage disease that may have been beyond the point where relaxin could help [25].

The core problem: relaxin has a half-life of about 10 minutes. A 48-hour IV infusion simply does not provide the sustained exposure needed to reverse chronic fibrosis.

Next-Generation Approaches (2024–2025)

The field has not given up on relaxin — it has moved to longer-acting formulations:

  • AZD3427 (Phase 1, 2024): A long-acting relaxin-Fc fusion protein designed for weekly subcutaneous injection. In a 21-week study, it improved cardiac function (ejection fraction, cardiac output, stroke volume) and reduced vascular resistance with no adverse events [26].
  • AZD5462: An oral allosteric RXFP1 agonist — potentially the first pill-form relaxin therapy [27].
  • ML290: A small-molecule RXFP1 agonist that significantly reduced collagen content and alpha-SMA expression in mouse liver fibrosis models [28].
  • CircRNA-based delivery (2025): Circular RNA encoding human relaxin-2, delivered via lipid nanoparticles, achieved sustained expression with low immunogenicity and potent antifibrotic activity in mouse liver fibrosis — superior to recombinant protein [29].

Emerging Antifibrotic Peptides

Beyond the established players, several newer peptides are generating preclinical data:

ADSCP6

A peptide derived from adipose stem cells, ADSCP6 suppresses hypertrophic scarring by downregulating collagen type I and alpha-SMA in human scar fibroblasts. In a mouse wound model, topical ADSCP6 sped healing while reducing collagen content in the resulting scar [30].

E4 Peptide

Researchers at the Medical University of South Carolina found that the E4 peptide reverses fibrosis in human and mouse tissues by activating the urokinase pathway — binding to a cell membrane protein called enolase. E4 reversed fibrosis even in end-stage fibrotic lungs, and the results were reproduced in vivo [31].

ADP355

An adiponectin-derived peptide that showed antifibrotic effects on keloid fibroblasts and xenotransplanted keloid tissues — addressing the specific problem of raised, disfiguring scars [2].

BMP-7 Derived Peptides (THR-123, THR-184)

These peptides bind BMP receptor 1A and activate the Smad1/5 pathway — which antagonizes the pro-fibrotic TGF-beta/Smad3 axis. In mouse models of cardiac remodeling, they rescued ventricular hypertrophy and dysfunction. Delayed administration even partially reversed progressive remodeling [2].

B7-33

A synthetic relaxin-2 analog that selectively activates the RXFP1 receptor. Its antifibrotic properties have drawn interest for pulmonary and renal fibrosis research, where relaxin-2 has been shown to reduce fibrotic markers [32].

Peptide Comparison Table

PeptidePrimary Antifibrotic MechanismOrgan Systems StudiedClinical Status
BPC-157TGF-beta1 downregulation, MMP/TIMP balancingSkin, tendon, muscle, GIAnimal studies only
SemaglutideMetabolic correction + direct anti-inflammatoryLiver (MASH), kidney, heartFDA-approved for MASH with fibrosis
GHK-CuBalanced MMP modulation, gene expression resetLung, liver, skinPreclinical
TB-500Myofibroblast reduction, actin sequestrationSkin, lung, kidney, liverAnimal studies
CJC-1295GH/IGF-1 axis → collagen synthesisConnective tissue (general)Phase 1 (GH stimulation only)
Relaxin/SerelaxinRXFP1 → collagen degradation, MMP-2 upregulationHeart, kidney, lung, liverPhase 3 completed; next-gen in Phase 1
E4 PeptideUrokinase pathway activation via enolase bindingLungPreclinical
ADSCP6Collagen I / alpha-SMA downregulationSkin (hypertrophic scars)Preclinical

FAQ

Is there an FDA-approved peptide for fibrosis? Yes. Semaglutide (Wegovy) received accelerated FDA approval in August 2025 for treating MASH with moderate to advanced liver fibrosis (stages F2-F3). It is the first GLP-1 receptor agonist approved for a fibrotic indication.

Can BPC-157 reduce scar tissue? In animal studies, BPC-157 reduces scar formation during wound healing by downregulating TGF-beta1, balancing the MMP/TIMP ratio, and shifting macrophage activity toward a reparative phenotype. However, it has not been tested in human fibrosis trials and is not approved for clinical use.

What is the difference between fibrosis and a scar? A scar is fibrosis of the skin — excess collagen deposited during wound healing. Internal fibrosis follows the same mechanism but affects organs like the liver, lungs, kidneys, or heart. The biological process (myofibroblast overactivity, excess ECM deposition) is essentially the same regardless of location.

Can fibrosis be reversed, or only prevented? Some peptides — particularly relaxin — have shown the ability to reverse established fibrosis in animal models, not just prevent new scar formation. Semaglutide has demonstrated fibrosis improvement (though not complete reversal) in human MASH patients. Most current therapies are better at prevention than reversal.

Is GHK-Cu pro-fibrotic or antifibrotic? Neither exclusively. GHK-Cu promotes balanced collagen remodeling — it increases both collagen synthesis and organized collagen breakdown. In contexts where fibrosis is driven by dysfunctional remodeling (like COPD lungs), GHK-Cu restores normal function. This balanced approach makes it fundamentally different from drugs that simply block collagen production.

How does TGF-beta relate to fibrosis? TGF-beta is the primary signaling molecule that activates fibroblasts, drives their conversion into collagen-producing myofibroblasts, and stimulates ECM production. Nearly every antifibrotic peptide targets TGF-beta or its downstream pathways. The challenge is reducing overactive TGF-beta signaling without blocking the pathway entirely, which would impair normal wound healing.

Are peptides for fibrosis available to patients now? Semaglutide is available by prescription for its approved indications (diabetes, obesity, and MASH). Other antifibrotic peptides discussed here — BPC-157, TB-500, relaxin analogs, GHK-Cu — are either research compounds, not approved for human use, or in early clinical trials.

The Bottom Line

Fibrosis research has shifted from a problem with no good drug options to a field with multiple peptide-based strategies at various stages of development. Semaglutide's 2025 FDA approval for MASH with fibrosis marked a genuine turning point — proof that a peptide-class drug can produce measurable antifibrotic results in human patients.

The other peptides in this guide are at earlier stages but address fibrosis through distinct and potentially complementary mechanisms. BPC-157 rebalances collagen production. GHK-Cu resets dysfunctional gene expression. TB-500 reduces the myofibroblasts that drive scarring. Relaxin actively degrades excess collagen matrix. And newer peptides like E4 and ADSCP6 are opening entirely new pathways.

What makes peptides attractive for fibrosis — beyond their specificity and low toxicity — is that fibrosis is fundamentally a problem of dysregulated signaling. It is not an infection to be killed or a tumor to be excised. It is a normal repair process that has lost its off switch. Peptides, which evolved to modulate exactly these kinds of cellular signals, may be the most natural class of molecules to address it.

For related research, see our guides on peptides for wound healing, peptides for inflammation, and best peptides for gut health.

References

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