Peptides for Stretch Marks & Scarring

Stretch marks are scars. That sentence is worth saying plainly because it changes how you think about treating them. When skin stretches beyond its mechanical limit -- during pregnancy, rapid weight gain, growth spurts, or muscle building -- the collagen and elastin fibers in the dermis literally tear. What forms afterward is scar tissue, not normal skin. The collagen bundles are thinner, disorganized, and running in flat parallel rows instead of the basketweave pattern found in healthy dermis [1].

This is why most over-the-counter creams don't work. They sit on the surface while the damage lives one layer down.

Peptides offer a different approach. These short amino acid chains can signal fibroblasts (the cells that build your skin's structural framework) to produce new collagen and elastin, remodel damaged extracellular matrix, and reduce inflammation. Some are used topically. Others are being studied as injectables. A few are already in commercial skincare products.

Here is what the science actually says about each one -- where the evidence is strong, where it's preliminary, and where the marketing outpaces the data.

How Stretch Marks Form (And Why They're Hard to Fix)
The Peptides With Research Backing
Peptide Comparison Table
The GLP-1 Connection: Semaglutide and Skin Changes
Combination Strategies
What About Existing Scars?
Frequently Asked Questions
The Bottom Line
References

How Stretch Marks Form (And Why They're Hard to Fix)

Understanding stretch mark biology explains why peptides are relevant -- and why timing matters.

Stretch marks (striae distensae) develop in two distinct phases:

Striae rubrae (early stage). The marks appear red, pink, or purple. Under the surface, mast cells are degranulating, inflammatory mediators are active, and the dermis is undergoing acute mechanical failure. Collagen bundles have separated. Elastic fibers are fragmenting. But the tissue is still biologically active -- fibroblasts are attempting repair, blood vessels are present, and the extracellular matrix is being actively remodeled [1].

Striae albae (mature stage). Over months to years, the marks fade to white or silver. By this point, the damage is structural: the epidermis has thinned, rete ridges have flattened, and the dermal collagen has reorganized into dense, scar-like horizontal bundles. Blood supply has decreased. Fibroblast activity has slowed. The tissue resembles a mature atrophic scar [2].

This two-phase biology has a critical implication for treatment: peptides are far more likely to work during the rubrae phase, when the tissue is still actively remodeling and responsive to biochemical signals. Once marks mature into striae albae, the window for topical peptide intervention narrows significantly.

Three molecular problems define stretch marks:

Collagen disorganization. Normal skin has a dense, cross-linked basketweave of collagen types I and III. In striae, these bundles separate, and new collagen forms in thin, parallel, scar-like arrangements [1].
Elastin loss. Elastases released by mast cells and macrophages degrade elastic fibers. The remaining tropoelastin fragments cannot organize into functional elastic fibers, so the skin loses its ability to snap back [2].
Fibroblast dysfunction. Researchers have identified a "dormant phenotype" in fibroblasts from stretch mark tissue -- these cells are alive but underperforming, producing less collagen and elastin than fibroblasts from normal skin [3].

Any effective peptide treatment needs to address at least one -- ideally all three -- of these problems.

The Peptides With Research Backing

GHK-Cu: The Collagen Remodeler

What it is: GHK-Cu is a naturally occurring tripeptide (glycine-histidine-lysine) bound to a copper ion. Your body produces it. It's found in blood plasma, saliva, and urine at levels that decline with age -- from about 200 ng/mL at age 20 to roughly 80 ng/mL by age 60 [4].

Why it matters for stretch marks: GHK-Cu is arguably the best-studied peptide for collagen remodeling, and stretch marks are fundamentally a collagen disorder. The evidence breaks down across several mechanisms:

Collagen synthesis. In laboratory studies, GHK-Cu increased collagen production by up to 70%, outperforming both vitamin C and retinoic acid in a human comparative trial [4]. It stimulates synthesis of type I collagen (structural support) and type III collagen (tissue flexibility and repair) -- both of which are disrupted in striae.
Elastin production. GHK-Cu increases elastin and glycosaminoglycan synthesis and supports fibroblast function [5]. This directly targets the elastin loss that makes stretch marks permanent.
Matrix metalloproteinase (MMP) regulation. The peptide balances MMP activity, promoting beneficial tissue remodeling while preventing the excessive breakdown that leads to scarring [5].
Gene expression. Recent research shows GHK-Cu influences over 4,000 genes involved in tissue repair. It appears to reset the gene expression profile of aged or damaged skin cells toward patterns seen in younger, healthier tissue [5].
TGF-beta pathway. GHK activates both TGF-beta and integrin beta-1 pathways during tissue regeneration. In one study, fibroblasts with impaired remodeling capacity regained their ability to contract and reorganize collagen gel after GHK treatment [5].

Clinical evidence on skin: A 12-week trial of 71 women using GHK-Cu facial cream showed increased skin density and thickness with reduced sagging and fine lines. A separate study of 41 women using GHK-Cu eye cream for 12 weeks confirmed improved skin density and increased thickness [4].

The gap: No published clinical trials have tested GHK-Cu specifically on stretch marks. The evidence is extrapolated from wound healing and anti-aging studies. Given the peptide's documented effects on collagen remodeling and elastin synthesis, it's a strong candidate -- but the direct data doesn't exist yet.

Delivery format: Topical creams and serums (typically at 0.01-1% concentration). The copper ion aids skin penetration.

Matrixyl (Palmitoyl Pentapeptide-4): The Signal Peptide

What it is: Matrixyl is a five-amino-acid peptide attached to a 16-carbon fatty acid chain (palmitic acid) that helps it penetrate skin's lipid barriers. It's classified as a "matrikine" -- a messenger peptide that activates genes involved in extracellular matrix renewal [6].

How it works: Matrixyl tricks your skin into thinking it's been injured. This isn't as strange as it sounds. When collagen breaks down naturally, the fragments (matrikines) signal fibroblasts to produce more. Matrixyl mimics this fragment, triggering production of collagen types I, III, and IV, along with elastin, fibronectin, and glycosaminoglycans [6].

Clinical evidence: The wrinkle data is solid. In a 12-week randomized controlled trial of 93 women, Matrixyl significantly reduced wrinkle depth compared to placebo [6]. In a separate study, Matrixyl at just 3 ppm matched the wrinkle-reducing effects of retinol at 700 ppm -- with better skin tolerability [6].

For wound healing, a study published in ACS Omega found that Matrixyl accelerated wound closure in vivo, with collagen formation confirmed histologically on day 14 [7]. And a 2016 study evaluated palmitoyl pentapeptide for wound contractility and suggested it could help prevent scar formation by balancing wound healing with anti-fibrotic activity [7].

Relevance to stretch marks: The collagen-stimulating and elastin-boosting properties are directly relevant, since both are disrupted in striae. The palmitoyl modification improves skin penetration. And the anti-scarring data is particularly interesting -- if Matrixyl can prevent excessive scar formation in wounds, it may help prevent the scar-like collagen reorganization that defines mature stretch marks.

The gap: Like GHK-Cu, no controlled clinical trials have tested Matrixyl specifically on stretch marks. Some commercial products combine it with other actives for stretch mark treatment, but these haven't been validated in peer-reviewed research.

BPC-157: The Tissue Repair Peptide

What it is: BPC-157 is a 15-amino-acid peptide originally isolated from human gastric juice. It has been extensively studied in animal models for its ability to accelerate healing across multiple tissue types -- skin, tendon, muscle, bone, and gut [8].

Why the stretch mark connection: BPC-157's relevance comes from its broad tissue repair mechanisms:

Collagen synthesis. In rat skin incision models, topical BPC-157 promoted rapid development of reticulin fibers and collagen formation, with fully developed reticulin fibers within 10 days [9].
Wound closure. In alkali-burn wound models, BPC-157 treatment achieved nearly 80% wound closure by day 18, compared to 60% maximum in untreated animals. Histological examination showed better granulation tissue formation, re-epithelialization, dermal remodeling, and higher collagen deposition [10].
Angiogenesis. BPC-157 upregulates VEGF expression and accelerates blood vessel formation -- relevant because stretch marks in the rubrae phase still have active vasculature that supports tissue repair [10].
ERK1/2 signaling. The peptide works through the ERK1/2 signaling pathway and its downstream targets (c-Fos, c-Jun, egr-1), which regulate cell proliferation and tissue remodeling [10].

The catch: All BPC-157 skin healing research is preclinical. Zero randomized controlled trials have been conducted in humans for any skin condition, let alone stretch marks. The compound is not FDA-approved. While animal data is consistent and robust across multiple wound models and species (rats, pigs), the translation to human stretch mark treatment is entirely theoretical at this point [8].

How it's used: In research settings, BPC-157 has been tested both topically (as a cream) and systemically (injection). The topical route would be most relevant for stretch marks, but no human formulation has been validated.

Heptapeptide-7: The Newer Entry

What it is: Heptapeptide-7 (HP7) is a synthetic seven-amino-acid peptide modeled on natural wound healing sequences. It's a fragment of HB-107, a well-characterized wound healing peptide [11].

What the research shows: Ex vivo studies demonstrated that HP7 promotes keratinocyte proliferation and migration, collagen production by fibroblasts, and EGF-like (epidermal growth factor) activity. Microarray analysis of HP7-treated keratinocytes showed upregulated genes for cell division, growth factors, and ECM components [11].

Clinical data: A study of 32 women (mean age 54) found that topical application of HP7 improved forehead wrinkles and skin texture [11]. This is, however, a small study focused on photoaging rather than stretch marks.

Stretch mark relevance: HP7 is now being marketed specifically for stretch marks (Apothederm Stretch Mark Cream). Its fibroblast-stimulating properties are relevant to the dormant fibroblast problem seen in striae. Industry sources describe it as particularly beneficial for early-stage (red/pink) stretch marks, when fibroblasts are still responsive to signaling.

The gap: The clinical evidence is thin -- one small wrinkle study and manufacturer claims. No peer-reviewed clinical trials on stretch marks. HP7 is newer than GHK-Cu or Matrixyl, and the research base is correspondingly smaller.

Oral Collagen Peptides: The Systemic Approach

What they are: Hydrolyzed collagen peptides are collagen proteins broken down into smaller, absorbable fragments (typically 2-5 kDa). When taken orally, they're further digested into dipeptides and tripeptides that enter the bloodstream and reach the skin [12].

The clinical evidence for skin: This is actually one of the better-studied areas:

A double-blind, placebo-controlled trial of 69 women showed statistically significant improvements in skin elasticity after 8 weeks of 2.5g or 5.0g daily collagen hydrolysate supplementation [12].
A 2024 randomized trial found that 12 weeks of oral hydrolyzed collagen plus vitamin C increased collagen content in the papillary dermis, confirmed by high-resolution ultrasound [13].
A trial of 120 subjects reported a 40% increase in skin elasticity and improved collagen fiber organization in skin biopsies after 90 days of daily supplementation [14].

Stretch mark relevance: Improved skin elasticity is directly relevant to stretch mark prevention -- skin with more elastic collagen is less likely to tear under mechanical stress. One study found oral supplementation also reduced solar elastosis and improved collagen architecture, suggesting it supports structural repair in the dermis [14].

The gap: No clinical trials have specifically measured collagen peptide supplementation's effect on existing stretch marks. The evidence supports improved skin structure broadly, but the leap to "this treats striae" hasn't been validated. Oral collagen likely works best as a preventive strategy (during pregnancy, rapid growth, or bodybuilding) rather than a treatment for established marks.

Peptide Comparison Table

Peptide	Delivery	Key Mechanism	Evidence Level for Stretch Marks	Best For
GHK-Cu	Topical	Collagen remodeling, elastin synthesis, 4,000+ gene modulation	Strong indirect (collagen/wound data, no stretch mark trials)	Both early and mature marks
Matrixyl	Topical	Signal peptide triggering collagen I, III, IV + elastin production	Moderate indirect (wrinkle trials, wound healing data)	Early marks, prevention
BPC-157	Topical/Injectable	ERK1/2 pathway, angiogenesis, collagen deposition	Preclinical only (strong animal data, no human trials)	Theoretical -- research stage
Heptapeptide-7	Topical	Fibroblast activation, EGF-like activity, ECM gene upregulation	Limited (one small skin study, no stretch mark trials)	Early (rubrae) marks
Collagen Peptides	Oral	Systemic collagen/elastin support, fibroblast stimulation	Moderate (multiple skin elasticity trials, no stretch mark-specific data)	Prevention, overall skin health

The GLP-1 Connection: Semaglutide and Skin Changes

Here's something worth knowing: rapid weight loss from semaglutide and other GLP-1 receptor agonists can create a separate set of skin concerns. As fat volume decreases quickly, skin that was stretched may now be loose rather than scarred. This is a different problem from stretch marks, though the two often coexist.

GLP-1 agonists do have documented anti-inflammatory effects that extend beyond metabolism. Emerging research suggests these drugs may influence skin inflammatory pathways, and there are case reports of improved skin conditions in patients taking semaglutide or tirzepatide [15]. But no one has studied GLP-1 agonists as a stretch mark treatment, and using them for skin purposes would be entirely off-label.

Where the connection becomes practical: if you've experienced significant weight loss on a GLP-1 medication and have both loose skin and stretch marks, the peptide approach to stretch marks (collagen remodeling with GHK-Cu, structural support from oral collagen) could complement the skin-tightening strategies your dermatologist recommends.

Growth hormone-releasing peptides like CJC-1295 and Ipamorelin are sometimes discussed in the context of skin quality because growth hormone stimulates collagen synthesis and skin thickness. While the mechanism is sound -- GH does promote dermal collagen -- these peptides are not studied for stretch marks specifically, and their use carries significant hormonal considerations that go well beyond skin appearance.

Combination Strategies

No single peptide addresses every aspect of stretch mark pathology. Researchers and clinicians are increasingly interested in multi-peptide approaches:

Topical stacking. GHK-Cu for collagen remodeling combined with Matrixyl for signal-peptide stimulation is a common pairing in advanced skincare formulations. GHK-Cu targets the structural rebuilding while Matrixyl amplifies the production signals. For more on combining peptides safely, see our Peptide Stacking Guide.

Topical + oral. Using topical peptides (GHK-Cu or Matrixyl) alongside oral collagen supplementation (5-10g daily) covers both local repair and systemic support. The oral peptides improve overall skin elasticity from within, while topicals target specific areas.

Peptides + procedures. The most promising clinical approach combines peptides with procedures that create controlled micro-damage in the dermis:

Microneedling + peptides. Microneedling creates thousands of tiny channels in the skin, both triggering the body's wound healing response and dramatically improving peptide penetration. Applying GHK-Cu or Matrixyl immediately after microneedling may amplify both the procedure's collagen-stimulating effects and the peptide's delivery to the dermis.
Fractional laser + peptides. Similar principle -- the laser creates zones of controlled thermal damage that trigger remodeling, and peptides applied post-procedure support the repair process.

These combination approaches are based on sound biological reasoning and are used in clinical practice, but randomized controlled trials comparing peptide-enhanced protocols to procedures alone are still limited.

What About Existing Scars?

Stretch marks and other scars share similar biology: disorganized collagen, reduced elastin, impaired vascularization. The peptides discussed here are relevant to both.

For hypertrophic scars and keloids, the dynamics differ -- these involve excessive collagen production rather than insufficient production. BPC-157 research in wounds has shown it promotes organized collagen deposition rather than chaotic overgrowth, which could be relevant for scar remodeling [8]. GHK-Cu's MMP-balancing activity also helps break down excessive scar tissue while promoting organized replacement [5].

For atrophic scars (acne scars, surgical scars), the same collagen-stimulating peptides that target stretch marks apply. The related guide on Best Peptides for Skin Wound Healing covers this territory in more detail.

Frequently Asked Questions

Can peptides completely remove stretch marks? No topical treatment, including peptides, can completely erase mature stretch marks (striae albae). These are structural scars in the dermis. Peptides can improve their appearance by stimulating new collagen production, increasing skin thickness, and improving texture. Early-stage red or pink marks (striae rubrae) respond significantly better than old white marks because the tissue is still actively remodeling.

When should I start using peptides for stretch marks? As early as possible. During pregnancy, rapid weight gain, puberty, or bodybuilding -- before marks fully form -- is the ideal prevention window. If marks have already appeared, the rubrae (red/purple) phase offers the best treatment window. Oral collagen peptides can be started at any time as a general skin health strategy.

Which peptide should I try first? For topical use, GHK-Cu has the strongest overall research base for collagen remodeling and skin repair. It's widely available in skincare formulations. For a systemic approach, oral collagen peptides (5-10g daily) have the most clinical trial support for improving skin elasticity. Combining both is reasonable.

Are peptides safe during pregnancy? Oral collagen peptides are generally considered safe during pregnancy, as they're essentially a protein supplement. Topical peptides like GHK-Cu and Matrixyl are used in many cosmetic products without reported adverse effects, though large-scale pregnancy safety studies are limited. BPC-157 should not be used during pregnancy -- it has no human safety data at all. Always discuss any new supplement or topical with your obstetrician.

How long before I see results? Collagen remodeling is slow. Most clinical studies on peptide skincare show measurable improvements at 8-12 weeks of consistent use. Visible improvement in stretch mark appearance may take 3-6 months. Early-stage marks will respond faster than mature white marks.

Can I combine peptides with retinoids? Yes. Retinoids (tretinoin, retinol) stimulate collagen production through different pathways than peptides, making them complementary. Apply retinoid at night and peptide serum in the morning, or alternate nights. Retinoids are not safe during pregnancy.

The Bottom Line

Stretch marks are dermal scars, and no topical treatment -- peptide or otherwise -- will make them disappear entirely. But the research on peptides for collagen remodeling is substantial and growing.

GHK-Cu has the deepest evidence base: documented collagen synthesis, elastin production, MMP regulation, and gene-level reprogramming of skin repair mechanisms. Matrixyl has solid clinical trial data for collagen stimulation and wrinkle reduction, with emerging wound healing evidence. Oral collagen peptides have multiple randomized controlled trials showing improved skin elasticity and dermal collagen content. BPC-157 has impressive preclinical wound healing data but zero human trials. Heptapeptide-7 is promising but early.

The honest assessment: no peptide has been tested in a published randomized controlled trial specifically for stretch marks. The evidence is extrapolated from wound healing, anti-aging, and collagen biology research. That extrapolation is reasonable -- stretch marks are a collagen and elastin disorder, and these peptides target collagen and elastin -- but it is not the same as direct proof.

What you can do right now: if stretch marks are a concern, start with what has the strongest evidence foundation. GHK-Cu topically for targeted collagen remodeling. Oral collagen peptides for systemic skin support. And if you're working with a dermatologist on procedural treatments like microneedling or fractional laser, ask about incorporating peptides into the post-treatment protocol.

The science is moving in the right direction. Direct clinical trials for stretch marks are the missing piece -- and given the size of the market (stretch marks affect up to 90% of pregnant women and 70% of adolescent females), those trials will come.

References

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Ud-Din S, McGeorge D, Bayat A. Topical management of striae distensae (stretch marks): prevention and therapy of striae rubrae and albae. J Eur Acad Dermatol Venereol. 2016;30(2):211-222. PMC
Pierard GE, Nizet JL, Pierard-Franchimont C. Cellulite: from standing fat herniation to hypodermal stretch marks. Am J Dermatopathol. 2000;22(1):34-37. PubMed
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Seiwerth S, Sikiric P, Grabarevic Z, et al. BPC 157's effect on healing. J Physiol Paris. 1997;91(3-5):173-178. PubMed
Chang CH, Tsai WC, Lin MS, Hsu YH, Pang JH. Body protective compound-157 enhances alkali-burn wound healing in vivo and promotes proliferation, migration, and angiogenesis in vitro. Drug Des Devel Ther. 2015;9:3015-3023. PMC
Falla TJ, Dobke MK, Engleman MA, Schein PD. Efficacy of hexapeptide-7 on menopausal skin. J Drugs Dermatol. 2010;9(1):49-54. PubMed
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Reilly DM, Lozano J. A clinical trial shows improvement in skin collagen, hydration, elasticity, wrinkles, scalp, and hair condition following 12-week oral intake of a supplement containing hydrolysed collagen. Dermatol Res Pract. 2024;2024:8752787. PMC
Czajka A, Kania EM, Genovese L, et al. Daily oral supplementation with collagen peptides combined with vitamins and other bioactive compounds improves skin elasticity and has a beneficial effect on joint and general wellbeing. Nutr Res. 2018;57:97-108. ScienceDirect
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