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Peptides for Cancer Research: Immunotherapy & Beyond

Modern oncology is being reshaped by a class of molecules most people associate with skincare or muscle recovery. Peptides -- short chains of amino acids -- are now at the center of some of the most promising cancer research in decades.

Modern oncology is being reshaped by a class of molecules most people associate with skincare or muscle recovery. Peptides -- short chains of amino acids -- are now at the center of some of the most promising cancer research in decades. From personalized vaccines that teach your immune system to hunt tumors, to drug-delivery vehicles that bypass healthy tissue entirely, peptides are opening doors that traditional chemotherapy never could.

This guide breaks down what the science actually shows, where the clinical trials stand, and what you need to know about peptides in cancer research right now.

Table of Contents

Why Peptides Matter in Cancer Research

Cancer treatment has always been a balancing act. Chemotherapy kills tumor cells, but it also hammers healthy tissue. Radiation works, but it is blunt. Even monoclonal antibodies -- the gold standard of targeted therapy -- come with size-related limitations. They are large molecules that struggle to penetrate deep into solid tumors.

Peptides sit in a sweet spot between small-molecule drugs and large biologics. They are typically 5 to 50 amino acids long, which gives them several practical advantages over antibodies [1]:

  • Better tissue penetration. Their small size lets them reach tumor cells that antibodies cannot access.
  • Lower immunogenicity. Your immune system is less likely to attack peptides as foreign invaders.
  • Easier and cheaper to manufacture. Solid-phase peptide synthesis is well-established and scalable.
  • Flexible design. Scientists can modify sequences, attach drug payloads, or engineer them to target specific receptors.

The global peptide therapeutics market is projected to exceed $49 billion by 2026. While most approved peptide drugs treat metabolic or hormonal conditions -- semaglutide being the most well-known example -- oncology now represents one of the fastest-growing areas of peptide research, with more than 30 peptide vaccine candidates reaching Phase II clinical trials by mid-2025 [2].

How Anticancer Peptides Work

Anticancer peptides (ACPs) attack tumors through several distinct pathways. Understanding these mechanisms helps explain why researchers are so interested in combining peptide approaches with existing treatments.

Membrane Disruption

Cancer cells carry a different electrical charge on their surface compared to healthy cells. Normal cells keep negatively charged phospholipids tucked on the inside of their membranes. Cancer cells lose this asymmetry, exposing phosphatidylserine and other anionic molecules on their outer surface. Cancer cells also tend to have less cholesterol in their membranes, making them more vulnerable to disruption [3].

Cationic (positively charged) anticancer peptides exploit this difference. They bind selectively to cancer cell membranes, form pores, and trigger cell death -- while largely ignoring healthy cells.

Apoptosis Induction

Many ACPs activate programmed cell death pathways. They can trigger the intrinsic (mitochondrial) pathway by upregulating pro-death proteins like Bax while downregulating survival proteins like Bcl-2. Some peptides also activate the extrinsic apoptosis pathway through death receptors on the cell surface [3].

The antimicrobial peptide LL-37 illustrates this nicely. A fragment called FK-16, derived from LL-37's residues 17-32, induces both caspase-independent apoptosis and autophagic cell death in colon cancer cells. In lab studies, FK-16 was more effective against cancer cells than full-length LL-37, while leaving normal colon cells largely unharmed [4].

Angiogenesis Inhibition

Tumors need blood vessels to grow beyond a few millimeters. They hijack your body's blood vessel-building machinery by overproducing vascular endothelial growth factor (VEGF). Several peptides can block this process by interfering with VEGF signaling, killing endothelial cells that line blood vessels, or disrupting downstream pathways like c-Src/ERK [3].

Defensins, the body's natural antimicrobial peptides, turn out to have anti-angiogenic properties too. Human alpha-defensins bind to fibronectin and block integrin-mediated adhesion of endothelial cells, cutting off blood vessel formation through multiple pathways [5].

Immune System Activation

Some peptides work by waking up your immune system rather than directly killing cancer cells. They can activate natural killer (NK) cells, stimulate dendritic cells to present tumor antigens, or shift the balance of immune cell populations in the tumor microenvironment. This immunomodulatory approach overlaps with the logic behind peptide cancer vaccines, covered in the next section [1].

Peptide Cancer Vaccines: Teaching the Immune System

Peptide-based cancer vaccines represent one of the most active areas of oncology research. The concept is straightforward: give the immune system a piece of the tumor to study, so it can hunt and destroy cancer cells more effectively.

How Neoantigen Vaccines Work

Every tumor has mutations that produce abnormal proteins -- neoantigens -- found nowhere else in your body. Scientists can now sequence a patient's tumor DNA, identify these unique mutations, and synthesize short peptides (typically 20-30 amino acids) matching those neoantigen sequences. These peptides train cytotoxic CD8+ T cells to recognize and kill cells carrying those specific mutations [6].

Because neoantigens appear only on cancer cells, the immune response is highly selective. This is a major advantage over chemotherapy, which cannot distinguish cancerous tissue from healthy tissue.

Landmark Clinical Trial Results (2025)

Several neoantigen vaccine trials produced striking results in 2025:

Kidney cancer. A Phase I trial tested a personalized neoantigen vaccine in patients with high-risk, fully resected clear cell renal cell carcinoma. At a median follow-up of 40.2 months, none of the 9 participants had experienced a cancer recurrence. All patients generated T cell immune responses against the vaccine antigens, with no dose-limiting toxicities [7].

Pancreatic cancer. Memorial Sloan Kettering researchers partnered with BioNTech to test an mRNA-based neoantigen vaccine called autogene cevumeran. Each patient's vaccine contained mRNA encoding up to 20 target neoantigens. Eight of the 16 patients responded to treatment [8].

Multi-cancer Phase I (Mount Sinai). The PGV001 personalized multi-peptide vaccine was tested in 13 patients across multiple cancer types. At five-year follow-up, six patients survived, with three remaining tumor-free. This data prompted three additional trials in glioblastoma, urothelial cancer, and prostate cancer [9].

Peptide vs. mRNA Vaccine Platforms

Both peptide and mRNA platforms are being developed for cancer vaccines, and early data suggest they may have complementary strengths. Peptide-pulsed dendritic cell vaccines appear to produce higher per-epitope CD8+ T cell responses, likely because synthetic peptides load more efficiently onto class I presentation molecules. mRNA vaccines, by contrast, can target many neoantigens simultaneously but tend to generate CD4+-dominant responses [6].

The practical upside of peptide vaccines is simpler manufacturing. mRNA vaccines require specialized lipid nanoparticle delivery and cold-chain storage. Peptide synthesis is more established, though manufacturing personalized vaccines of either type still takes weeks.

Combination Strategies

Neoantigen vaccines are increasingly being tested alongside immune checkpoint inhibitors like pembrolizumab. The rationale is simple: the vaccine trains T cells to recognize the tumor, while the checkpoint inhibitor removes the "brakes" that tumors use to suppress immune attack. A Phase I trial is currently evaluating personalized neoantigen peptide vaccines with pembrolizumab in patients with advanced solid cancers [10].

Radiotherapy is another promising combination partner. Local radiation can trigger the release of tumor-associated antigens and damage-associated molecular patterns (DAMPs), which may amplify the vaccine-induced immune response [6].

Peptide-Drug Conjugates: Precision Drug Delivery

Peptide-drug conjugates (PDCs) are the oncology world's answer to a persistent problem: how do you get cytotoxic drugs to the tumor without poisoning the rest of the body?

The Design

A PDC has three parts: a tumor-homing peptide that recognizes cancer cells, a cytotoxic drug payload, and a linker that holds them together until the conjugate reaches its target. Once at the tumor site, the linker is cleaved -- often by enzymes overexpressed in the tumor microenvironment -- releasing the drug exactly where it is needed [11].

Advantages Over Antibody-Drug Conjugates

PDCs offer several practical advantages over the more established antibody-drug conjugates (ADCs):

FeaturePDCsADCs
Molecular sizeSmall (1-10 kDa)Large (150+ kDa)
Tumor penetrationHighLimited
ManufacturingChemical synthesisBiological production
ImmunogenicityLowModerate
CostLowerHigher
Half-lifeShorterLonger

The shorter half-life of PDCs is actually a double-edged sword. Rapid clearance means fewer systemic side effects, but it also means the drug may not stay in circulation long enough to reach every tumor cell.

PDCs in Clinical Trials

Lutathera (177Lu-DOTATATE) remains the only FDA-approved PDC-type therapy, approved in 2018 for somatostatin receptor-positive gastroenteropancreatic neuroendocrine tumors (GEP-NETs). It combines a somatostatin-targeting peptide with a radioactive lutetium-177 payload, delivering radiation directly to tumor cells expressing somatostatin receptors. The NETTER-1 trial showed significant improvements in progression-free survival compared to standard therapy [12]. In 2024, approval was expanded to pediatric patients aged 12 and older [13].

CBX-12 (Cybrexa Therapeutics) takes a different approach -- it targets the acidic pH of the tumor microenvironment rather than a specific receptor. Phase I trials completed enrollment in September 2024, showing activity in platinum-resistant ovarian cancer patients, including those with receptor-negative tumors. Phase II evaluation is underway [11].

ANG1005 uses a peptide that crosses the blood-brain barrier to deliver paclitaxel to brain metastases, achieving a 4.5-fold increase in brain drug uptake compared to paclitaxel alone [11].

AVA6000 (FAP-Dox) targets fibroblast activation protein (FAP) in the tumor stroma. Phase I data showed a 100-fold concentration difference between tumors and blood, suggesting highly selective delivery. Phase Ib cohorts are expanding into salivary gland cancer and triple-negative breast cancer [14].

Six PDCs are currently in Phase III trials, with approximately 96 in development across all stages [11].

Peptide Receptor Radionuclide Therapy (PRRT)

PRRT deserves special attention because it represents the most clinically validated peptide-based cancer treatment to date. The concept is elegant: attach a radioactive atom to a peptide that binds specifically to receptors overexpressed on tumor cells. The peptide finds the tumor; the radiation kills it.

How PRRT Works

The peptide component (typically a somatostatin analog like DOTATATE or DOTATOC) circulates through the body and binds to somatostatin receptors, which are overexpressed on neuroendocrine tumor cells. The attached radionuclide (lutetium-177 or yttrium-90) emits beta radiation, causing DNA double-strand breaks in the cancer cells and their immediate neighbors [12].

Before treatment, doctors use a companion diagnostic -- gallium-68 DOTATATE PET scan -- to confirm that the patient's tumor actually expresses somatostatin receptors. This ensures the therapy will reach its target.

Clinical Results

The NETTER-1 trial demonstrated that Lutathera plus octreotide reduced the risk of disease progression or death by 79% compared to high-dose octreotide alone in patients with midgut neuroendocrine tumors [12]. Quality of life and symptom control also improved significantly.

Beyond Neuroendocrine Tumors

Researchers are now exploring PRRT targeting other receptor types -- including bombesin receptors (overexpressed in prostate and breast cancers), cholecystokinin receptors (medullary thyroid cancer), and RGD-based peptides (targeting integrin receptors in various solid tumors). The success of Lutathera has validated the PRRT concept and opened the door for next-generation radiopeptide therapies.

Immune Checkpoint Peptides

Immune checkpoint inhibitors have transformed cancer treatment, but the currently approved drugs are all monoclonal antibodies -- large, expensive molecules that require intravenous infusion. Peptide-based checkpoint inhibitors could offer a smaller, cheaper, potentially oral alternative.

PD-1/PD-L1 Peptide Antagonists

The PD-1/PD-L1 axis is the most targeted checkpoint pathway in oncology. Tumor cells display PD-L1 on their surface, which binds to PD-1 on T cells and shuts down the immune attack. Blocking this interaction restores T cell function [1].

Several peptides have been designed to block PD-1/PD-L1 binding. AUNP-12, developed by Aurigene/Pierre Fabre, was one of the first peptide-based PD-1/PD-L1 inhibitors to enter clinical testing. These peptides aim to restore T cell activation and improve the effectiveness of immunotherapy at a fraction of the size and cost of antibody-based drugs.

Advantages of Peptide Checkpoint Inhibitors

Peptide checkpoint inhibitors penetrate tissue more easily than antibodies, which is relevant for solid tumors with dense stroma that antibodies struggle to access. They also clear from the body faster, which could reduce immune-related adverse events -- a significant problem with current antibody checkpoint inhibitors [1].

The trade-off is that shorter half-life may require more frequent dosing. Researchers are addressing this through modified peptide structures, depot formulations, and combination with nanoparticle delivery systems.

Cell-Penetrating Peptides in Oncology

Cell-penetrating peptides (CPPs) are short peptides (typically 5-30 amino acids) that can cross cell membranes efficiently. In cancer research, they are used as delivery vehicles to transport drugs, genes, or imaging agents directly into tumor cells [15].

Applications in Cancer

  • Drug delivery. CPPs conjugated to cytotoxic drugs can improve intracellular drug concentration in cancer cells while reducing systemic exposure.
  • Gene therapy. CPPs can deliver tumor-suppressor genes or small interfering RNAs (siRNAs) to silence oncogenes.
  • Vaccine adjuvants. CPPs help deliver tumor antigens to antigen-presenting cells, improving vaccine-induced immune responses.
  • Imaging. CPP-labeled imaging agents can improve tumor visualization during diagnosis or surgery.

Z12 Peptide

The Z12 peptide is a recent example of CPPs in immunotherapy. It promotes immune modulation at tumor sites by supporting the persistence of CD8+ effector T cells and activating Th1-polarized CD4+ T cells. A Phase I clinical trial (NCT04046445) is evaluating Z12-based vaccines in patients with stage IV colorectal cancer [15].

Peptides You Know -- And Their Cancer Research Connections

Several peptides commonly discussed in the health and wellness space have unexpected connections to cancer research. Here is what the science actually shows -- and what it does not.

LL-37 and Anticancer Activity

The antimicrobial peptide LL-37 -- the only human cathelicidin -- has shown direct anticancer effects in preclinical studies. Its fragment FK-16 kills colon cancer cells through p53-mediated apoptosis and autophagy while sparing normal colon epithelial cells [4]. Cathelicidin-deficient mice show increased susceptibility to colon tumorigenesis, suggesting a physiological role in cancer defense [16].

However, LL-37's relationship with cancer is complex. In some tumor types, it may actually promote growth. The research is still primarily preclinical.

GHK-Cu: Gene Expression and Cancer

The copper peptide GHK-Cu, best known for skin rejuvenation, has shown intriguing anticancer properties in gene expression studies. Broad Institute Connectivity Map data indicate that GHK reversed the expression of 70% of 54 overexpressed genes associated with aggressive metastatic colon cancer [17]. GHK upregulates several tumor suppressor genes including PTEN, BRCA1, and TP-73, and at nanomolar concentrations, it inhibited growth of neuroblastoma and lymphoma cells while stimulating healthy fibroblast growth [17].

The catch: GHK-Cu also promotes angiogenesis, which is something tumors need to survive. This makes it a complex molecule in the cancer context, and people with active cancer should approach it with caution.

BPC-157: The Angiogenesis Question

BPC-157 is widely discussed for tissue repair, but its relationship with cancer is nuanced. BPC-157 strongly promotes angiogenesis -- a property that helps wounds heal but could theoretically feed tumor growth. A single 2004 in vitro study found that BPC-157 inhibited melanoma cell growth and VEGF signaling [18], but no in vivo tumor studies have replicated this finding.

The honest assessment: there is not enough data to say BPC-157 is either safe or dangerous regarding cancer. Its strong pro-angiogenic properties represent a plausible theoretical risk, and anyone with active cancer or a high cancer risk should discuss it with their oncologist before use [19].

Semaglutide and Cancer Risk

Semaglutide and other GLP-1 receptor agonists are primarily metabolic drugs, but observational data have raised interesting questions about cancer incidence in patients taking them. Some studies suggest reduced rates of certain cancers in GLP-1 RA users, possibly related to weight loss, reduced inflammation, or direct cellular effects. However, the thyroid C-cell tumor signal in rodent studies (which prompted the boxed warning on GLP-1 drugs) is a reminder that metabolic peptides and cancer biology intersect in unpredictable ways.

Key Peptide Approaches Compared

ApproachMechanismClinical StageKey ExampleBest Suited For
Neoantigen vaccinesTrain T cells to target tumor-specific mutationsPhase I-IIPGV001, autogene cevumeranSolid tumors after surgery
Peptide-drug conjugatesDeliver cytotoxic payload to tumor cellsPhase I-IIILutathera, CBX-12, ANG1005Receptor-positive tumors
PRRTDeliver radiation via receptor-targeting peptideFDA-approvedLutathera (177Lu-DOTATATE)Neuroendocrine tumors
Checkpoint peptidesBlock PD-1/PD-L1 to restore T cell functionPhase I-IIAUNP-12Immune-responsive tumors
Cell-penetrating peptidesTransport drugs/genes across cell membranesPhase IZ12 vaccineDrug delivery platform
Direct anticancer peptidesKill cancer cells via membrane disruption/apoptosisPreclinicalFK-16 (from LL-37)Various cancers

Challenges and Limitations

Peptide cancer therapies face real obstacles that explain why -- despite decades of research -- only one peptide-based cancer treatment (Lutathera) has won FDA approval.

Stability and Half-Life

Peptides break down quickly in the bloodstream. Proteases chew them up, and the kidneys clear them rapidly. This means a peptide that works in a test tube may fail in the body. Solutions include cyclization (making the peptide circular), D-amino acid substitution, PEGylation, and nanoparticle encapsulation -- but each adds manufacturing complexity [1].

Manufacturing Personalized Vaccines

Personalized neoantigen vaccines require tumor sequencing, neoantigen prediction, peptide synthesis, and quality testing -- a process that currently takes weeks to over a month. For a patient with aggressive cancer, that timeline can be the difference between a treatment window and a missed opportunity [6].

Tumor Immune Evasion

Even a well-designed peptide vaccine can fail if the tumor changes its playbook. Cancer cells can downregulate the antigens being targeted, reduce MHC expression so T cells cannot "see" them, or recruit immunosuppressive cells (regulatory T cells, myeloid-derived suppressor cells) that shut down the immune response in the tumor microenvironment [1].

Predicting Which Neoantigens Will Work

Not every tumor mutation produces an effective vaccine target. Accurately predicting which neoantigens will trigger a strong T cell response remains a major bottleneck. Current AI models trained on millions of peptide entries are improving prediction accuracy, but the field still needs better tools [6].

The Pipeline: What's Coming Next

AI-Driven Peptide Discovery

Artificial intelligence is transforming anticancer peptide research. A 2025 review cataloged 68 AI models for anticancer peptide screening [20]. These tools can predict which peptide sequences will bind specific targets, cross cell membranes, or trigger immune responses -- work that previously took months of lab experiments. As datasets grow and models improve, the timeline from discovery to clinical candidate will continue to shrink.

Multifunctional Peptide Nanostructures

Researchers are engineering peptide-based nanostructures that combine multiple therapeutic functions in a single platform. These self-assembling systems can simultaneously trigger ferroptosis (iron-dependent cancer cell death), enable photothermal therapy (using laser light to heat and destroy tumors), and release chemotherapy drugs at the tumor site [2].

Next-Generation PDCs

The next wave of peptide-drug conjugates features "smart" linkers that respond to specific conditions in the tumor microenvironment -- pH changes, enzyme activity, or hypoxia. This improves the precision of drug release and reduces off-target effects [11].

Broader PRRT Applications

With Lutathera's success validating the concept, researchers are developing PRRT agents targeting receptors beyond somatostatin -- including bombesin receptors in prostate cancer, cholecystokinin receptors in thyroid cancer, and integrin receptors across multiple tumor types.

FAQ

Are peptide cancer treatments available now? Lutathera (lutetium-177 DOTATATE) is the only FDA-approved peptide-based cancer therapy, indicated for somatostatin receptor-positive gastroenteropancreatic neuroendocrine tumors. All other peptide-based cancer treatments are in clinical trials or preclinical development.

Can peptide supplements prevent cancer? No peptide supplement has been proven to prevent cancer in humans. Some peptides show anticancer activity in lab studies, but lab results do not translate directly to cancer prevention. Do not use any peptide as a substitute for evidence-based cancer screening or treatment.

Is BPC-157 safe if I have a cancer history? The evidence is insufficient to answer this question definitively. BPC-157's pro-angiogenic effects represent a theoretical concern for tumor growth, though limited in vitro data have shown anti-proliferative effects on melanoma cells. Talk to your oncologist before using any growth-promoting peptide if you have active cancer or a cancer history.

How do peptide cancer vaccines differ from COVID vaccines? Both aim to trigger an immune response, but cancer vaccines target tumor-specific neoantigens rather than viral proteins. Cancer vaccines are also highly personalized -- each patient's vaccine is tailored to their tumor's unique mutations. COVID vaccines use standardized sequences targeting the spike protein shared across viral variants.

What is the biggest obstacle to peptide cancer treatments? For personalized vaccines, manufacturing speed is the primary bottleneck. For other peptide approaches, stability and half-life in the body remain the core challenges. Getting a peptide to survive long enough in the bloodstream to reach its target -- without losing its structure or activity -- is an ongoing engineering problem.

Do anticancer peptides cause side effects? Lutathera's side effects include low blood cell counts, kidney effects, and rare cases of secondary blood cancers. Peptide vaccines in clinical trials have generally shown mild side effects (injection site reactions, fatigue, low-grade fever). Side effect profiles for investigational peptide therapies will become clearer as trials progress.

The Bottom Line

Peptides are not yet a standard cancer treatment, but they are no longer theoretical, either. One peptide-based therapy (Lutathera) is FDA-approved and saving lives. Personalized neoantigen vaccines are producing remarkable early results in kidney, pancreatic, and other cancers. Peptide-drug conjugates are advancing through late-stage trials with dozens more in the pipeline.

The science is moving fast. AI is accelerating peptide discovery. Manufacturing is improving. Clinical trial designs are getting smarter. The gap between "promising preclinical data" and "medicine your doctor can prescribe" is narrowing -- though it has not closed yet.

If you or someone you know is facing a cancer diagnosis, the most useful thing to know is this: clinical trials involving peptide-based treatments are actively recruiting patients across multiple cancer types. Ask your oncologist whether any are relevant to your situation.

For a broader look at how peptides interact with the immune system, see our guides on best peptides for immune support and best peptides for inflammation.

References

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  2. These ten peptide breakthroughs of 2025 define global medical trends for 2026. Intelligent Living. 2025. Link

  3. Li G, et al. Anti-cancer peptides: classification, mechanism of action, reconstruction and modification. Open Biol. 2020;10(7):200004. PMC7574553

  4. Ren SX, et al. FK-16 derived from the anticancer peptide LL-37 induces caspase-independent apoptosis and autophagic cell death in colon cancer cells. PLoS One. 2013;8(5):e63641. PMID: 23700428

  5. Xu D, Lu W. Defensins: a double-edged sword in host immunity. Front Immunol. 2020;11:764. Link

  6. Zhang X, et al. Advances in neoantigen-based cancer vaccines. Front Immunol. 2025. PMC12784945

  7. Braun DA, et al. A neoantigen vaccine generates antitumour immunity in renal cell carcinoma. Nature. 2025;637:417-424. Link

  8. Neoantigen vaccines keep kidney, pancreatic cancer at bay. National Cancer Institute Cancer Currents. 2025. Link

  9. Personalized cancer vaccine proves promising in a Phase 1 trial at Mount Sinai. Mount Sinai Newsroom. 2025. Link

  10. Ott PA, et al. A phase I pilot study of personalized neoantigen peptide-based vaccine in combination with pembrolizumab in advanced solid tumors (PNeoVCA). J Clin Oncol. 2024;42(16_suppl):TPS2700. Link

  11. Armstrong MT, et al. Peptide-drug conjugates: a new hope for cancer. J Pept Sci. 2025;31(5):e70040. PMC12254541

  12. Hennrich U, Kopka K. Lutathera: the first FDA- and EMA-approved radiopharmaceutical for peptide receptor radionuclide therapy. Pharmaceuticals. 2019;12(3):114. PMC6789871

  13. FDA approves lutetium Lu 177 dotatate for pediatric patients 12 years and older with GEP-NETs. U.S. Food and Drug Administration. 2024. Link

  14. Next-generation conjugates: small peptides to transform targeted cancer therapy. Bioconjugation Insights. 2025. Link

  15. Li W, et al. Advances and prospects of cell-penetrating peptides in tumor immunotherapy. Sci Rep. 2025;15:86130. Link

  16. Li D, et al. Host immune defense peptide LL-37 activates caspase-independent apoptosis and suppresses colon cancer. Cancer Res. 2012;72(24):6512-6523. PMID: 23100468

  17. Pickart L, Margolina A. Regenerative and protective actions of the GHK-Cu peptide in the light of the new gene data. Int J Mol Sci. 2018;19(7):1987. PMC6073405

  18. Tkalcevic VI, et al. BPC 157 inhibits cell growth and VEGF signalling via the MAPK kinase pathway in a human melanoma cell line. Melanoma Res. 2004;14(4):A33.

  19. PMC. Regeneration or risk? A narrative review of BPC-157 for musculoskeletal healing. 2025. PMC12446177

  20. Wu X, et al. Artificial intelligence-driven anticancer peptide discovery. iMetaOmics. 2025. Link