Do Peptides Cause Cancer? A Compound-by-Compound Look at Angiogenesis, GH/IGF-1 and the Real Data

The short answer

No peptide sold for healing, muscle, fat loss or longevity has been shown to cause cancer in people. That sentence is true, and it is also less reassuring than it sounds, because for most of these compounds nobody has looked. BPC-157, TB-500, epitalon, most growth hormone secretagogues and nearly every research peptide have never been given to enough people for long enough to detect a cancer signal in either direction. FDA's July 2026 briefings on seven peptides repeatedly described the human safety data as limited or absent.¹

The question also hides four different questions. Some peptides are worried about because they grow new blood vessels, which tumours need. Some raise IGF-1, a growth factor linked to several cancers in large population studies. One is marketed as a telomerase activator, and telomerase is the enzyme most cancers switch on to keep dividing. And the GLP-1 medicines carry a boxed warning because they caused thyroid tumours in rodents. Each mechanism has different evidence behind it, and each applies to different compounds. This guide takes them one at a time, then compound by compound.

Everything below describes what studies found. It is not advice to take or avoid any compound, and it cannot tell you your own risk. The evidence grades come from our encyclopedia, where each compound's grade reflects the quality of all its human evidence, not just its cancer data.

Four mechanisms, four different questions

Cancer is cells growing when they should not. A substance can matter in two quite different ways: it can help start a cancer, by damaging DNA or switching on growth programs, or it can help an existing cancer grow and spread, by feeding it blood vessels, growth signals or the ability to keep dividing. Almost all the peptide concerns are of the second kind. They are about promotion, not initiation, which is why the people most exposed to the theoretical risk are those who already have a tumour, diagnosed or not.

• Angiogenesis and migration. Tumours cannot grow beyond a few millimetres without new blood vessels. Peptides that promote vessel growth or cell movement to heal wounds could, in principle, help a tumour do the same.
• The GH/IGF-1 axis. Growth hormone raises insulin-like growth factor 1, which tells cells to grow and not die. Higher natural IGF-1 is associated with several cancers.
• Telomerase. Most normal cells have a limited number of divisions because their chromosome tips shorten. Cancer cells get around this by switching on telomerase.
• GLP-1 receptors on thyroid C-cells. In rodents, GLP-1 drugs stimulate the calcitonin-producing C-cells of the thyroid and caused C-cell tumours, which is the basis of the boxed warning on every long-acting GLP-1 drug.

For each, the useful question is not "could it?" but "what has been measured in people?", and the answers range from a lot to nothing.

Angiogenesis and cell migration: BPC-157 and TB-500

BPC-157 Low is studied mostly for tissue repair, and one of its best-documented effects in animals is promoting the growth of new blood vessels, alongside interactions with standard angiogenic growth factors.² That is exactly the property that raises the cancer question. The research group behind most of the BPC-157 literature argues the opposite: in a 2025 exchange in the journal Pharmaceuticals, it described BPC-157 as controlling rather than simply stimulating angiogenesis, and as having anti-tumour effects in animal and cell studies.³ Both positions rest on laboratory and animal work. No study has followed people taking BPC-157 for cancer outcomes, and a 2025 independent review of BPC-157 for musculoskeletal healing concluded that human data are minimal and that it should be treated as investigational until proper trials exist.⁴

TB-500 and thymosin β4. TB-500 Low is a short synthetic fragment of thymosin β4, a natural protein that helps cells move by managing their actin. Thymosin β4 itself has a documented link to cancer biology, though as a marker rather than a cause. Tissue studies found it is abundant in fetal tissues, largely switched off in adult ones, and switched back on in some tumours; in colorectal cancer, high thymosin β4 went with the epithelial-mesenchymal transition that lets cancer cells spread.⁵ In 141 patients with differentiated thyroid cancer, higher thymosin β4 was associated with more advanced disease, lymph node spread and the BRAF V600E mutation.⁶ These studies show thymosin β4 tracks aggressive behaviour in some cancers. They do not show that injecting it, or the TB-500 fragment, causes or feeds a tumour, and no study has tested that in people. FDA's 2026 briefing described human data on TB-500 as non-existent.¹

Thymosin β4 does not even point one way. In multiple myeloma, a blood cancer, it was lower in cancer cells than in normal plasma cells, patients with higher levels lived longer, and raising it in mouse myeloma cells slowed their growth.⁷ The same molecule tracks aggressive behaviour in some solid tumours and looks protective in this one, which is a good reason to distrust simple claims either way.

The honest summary for both: a plausible mechanism, animal and tissue data pulling in different directions, and no human outcome data at all.

The GH/IGF-1 axis: secretagogues, growth hormone and MK-677

This is where the human data are strongest, but mostly indirect. Growth hormone secretagogues such as ipamorelin, CJC-1295 and sermorelin, and the oral secretagogue MK-677 Medium, all work by raising growth hormone, and growth hormone raises IGF-1. The question is what higher IGF-1 means for cancer.

The largest single answer comes from UK Biobank. In about 394,000 adults followed for an average of 6.9 years, each 5 nmol/L higher circulating IGF-1 was associated with an 8% higher risk of colorectal cancer, 11% higher breast cancer, 8% higher prostate cancer and 18% higher thyroid cancer, and with lower risks of ovarian and liver cancer.⁸ Those are associations with people's natural IGF-1, not the result of taking a drug, and the authors could not exclude that early, undiagnosed cancers affected the measurements. Still, they are why raising IGF-1 is treated as a caution in anyone with, or at high risk of, those cancers.

Genetics offers a partial check on that causality problem. A Mendelian randomisation study used 416 genetic variants that set people's IGF-1 levels from birth, so the comparison cannot be distorted by an existing tumour. Genetically higher IGF-1 was associated with colorectal cancer, with an odds ratio of 1.11 per standard deviation in UK Biobank and 1.22 in the BioBank Japan Project.⁹ That strengthens the case that IGF-1 itself, not something travelling with it, is part of the colorectal link, though it concerns lifelong genetic differences, not a few months of a drug.

Secretagogues raise IGF-1 substantially. In a two-year trial in healthy adults aged 60 to 81, MK-677 at 25 mg a day raised growth hormone and IGF-1 into the range of young adults.¹⁰ None of the secretagogue trials was large or long enough to measure cancer outcomes.

The closest thing to a long-term test is growth hormone itself, given to children for decades. The European SAGhE cohort followed children treated with recombinant growth hormone. It found raised cancer risks mainly in patients treated after a previous cancer, where cancer deaths rose with higher daily doses; in children treated for growth failure without other major disease there was no clear rise, although bone and bladder cancer and Hodgkin lymphoma needed further study. The authors concluded the results do not generally support a carcinogenic effect of growth hormone.¹¹ That is reassuring for otherwise healthy people and a warning for cancer survivors, and it comes from prescribed growth hormone under supervision, not from research peptides of unknown dose and purity.

A 2022 meta-analysis of 24 studies covering 254,776 people reached a similar conclusion: growth hormone treatment in childhood was not significantly associated with overall cancer incidence or cancer death, but it was associated with a higher risk of a second tumour (relative risk 1.77) in children who had already had cancer.¹² The pattern across both analyses is the same one the mechanism predicts. Raising the growth axis matters most where a tumour, or cells primed to become one, is already present.

Telomerase: epitalon

Epitalon Low (also spelled epithalon) is sold as an anti-ageing peptide on the claim that it switches on telomerase. That claim comes from a 2003 Russian study in which adding epithalon to human fetal fibroblasts in culture induced telomerase activity and lengthened telomeres.¹³ A 2025 study found the same in normal human cells, and in two breast cancer cell lines epitalon lengthened telomeres through a different, telomerase-independent route called ALT.¹⁴

Why that matters: in a landmark 1994 study, telomerase activity was found in 98 of 100 immortal cell populations and 90 of 101 tumour biopsies, but in none of 50 normal somatic tissues, which is why switching telomerase back on is considered a hallmark of cancer.¹⁵ Whether a peptide that nudges telomerase in a dish raises cancer risk in a person is untested. The animal studies that exist come from the same research group: in one rat study epithalon had virtually no effect on spontaneous tumours under standard lighting and reduced them under natural light.¹⁶ FDA's 2026 briefing noted that the carcinogenicity data consist of three similar mouse studies from one group, with no genotoxicity studies, and that the claims that epitalon prevents cancer are marketing claims, not findings.¹

GLP-1 drugs and thyroid C-cell tumours

The GLP-1 medicines are the one group here with large human datasets. Semaglutide High, tirzepatide High and their relatives carry a boxed warning because they caused thyroid C-cell tumours, including medullary thyroid carcinoma, in rodents, and they are contraindicated in people with a personal or family history of medullary thyroid carcinoma or with multiple endocrine neoplasia type 2.¹⁷¹⁸ The warning reflects what happened in rodents; whether it applies to people is the question the human studies below try to answer.

Human studies since 2023 have mostly been reassuring, with one notable exception. A French case-control study of 2,562 thyroid cancer cases found GLP-1 drug use for 1 to 3 years was associated with a higher risk of thyroid cancer (adjusted hazard ratio 1.58) and of medullary thyroid cancer (1.78).¹⁹ A Scandinavian cohort of about 145,000 GLP-1 users followed for a mean of 3.9 years found no increase in thyroid cancer against DPP-4 inhibitor users (hazard ratio 0.93), with confidence limits consistent with at most a 31% increase. In absolute terms thyroid cancer was rare in both groups: 1.33 cases per 10,000 person-years on GLP-1 drugs and 1.46 on DPP-4 inhibitors.²⁰ An international study of six databases found the same (hazard ratio 0.81), while noting that follow-up of about two to three years cannot rule out risk with long-term use.²¹

One reason the studies disagree may be how often people on these drugs are examined. Guidelines do not recommend routine thyroid screening when a GLP-1 drug is started, yet at one US academic health system 2,523 patients prescribed these drugs had thyroid ultrasounds between 2019 and 2024, and scans for them grew faster than for other patients from 2020 to 2023.²² Looking harder finds more small thyroid cancers whether or not a drug causes them, which can make a drug look riskier in studies that count diagnoses.

Across all cancers the picture points the other way. In about 86,000 adults with obesity or overweight, GLP-1 drug users had a 17% lower overall risk of the 14 cancers studied than matched non-users, with lower endometrial and ovarian cancer and meningioma, but a borderline higher risk of kidney cancer (hazard ratio 1.38) that needs longer follow-up.²³ Weight loss itself lowers the risk of many cancers, which may explain much of the benefit.

Retatrutide Medium is still investigational. It has no label yet and no cancer outcome data are available; the thyroid question above applies to it as a drug acting on the GLP-1 receptor, and its answer will come from longer follow-up.

The other peptides people ask about

Some peptides carry the opposite reputation. KPV Low, a tripeptide from the tail of α-MSH, prevented colitis-associated tumours in mice in a 2016 study, but only in mice that had the PepT1 transporter it uses to enter cells.²⁴ That is one mouse study of one kind of cancer, and nobody has tested KPV in people for any outcome. Humanin, a peptide encoded in mitochondrial DNA, blocks cell death, and an early review raised the possibility of a role in cancer development because it is also made in normal tissues such as the testis.²⁵ Neither observation says what taking these peptides would do; both show why "anti-cancer" and "pro-cancer" labels online usually outrun the evidence.

How to read a cancer claim about a peptide

Most of what circulates online about peptides and cancer mixes up kinds of evidence that answer different questions. Five distinctions sort out nearly every claim.

Cells, animals or people. A peptide that switches on telomerase in a dish, or grows blood vessels in a rat, has shown a mechanism. It has not shown a risk in people, and it has not ruled one out. Epitalon's telomerase data and BPC-157's angiogenesis data are both of this kind.

Starting a cancer or feeding one. Nothing in the evidence above suggests these peptides damage DNA the way carcinogens do. The plausible risk is growth of an existing tumour, including one nobody has found yet, which is why a cancer history changes the calculation so much.

Association or cause. Higher IGF-1 goes with more of some cancers, and thymosin β4 is higher in some aggressive tumours. Associations like these can run in either direction or share a hidden cause. Genetic studies, like the Mendelian randomisation work on IGF-1, are one of the few ways to test causation without a trial.

Relative or absolute risk. A hazard ratio of 1.58 sounds alarming. When the underlying rate is around one case per 10,000 people a year, even a real increase of that size means very few additional cancers, while the same ratio on a common cancer would matter far more.

Time. Most cancers take years to become detectable. A trial of 12 or 16 weeks cannot show a cancer effect in either direction, and even the GLP-1 cohorts, with two to four years of follow-up, say explicitly that they cannot rule out effects of long-term use. For most research peptides, there is no follow-up at all.

Compound by compound

Grades are our encyclopedia's, as of September 28, 2026, and describe each compound's whole evidence base. A high grade for semaglutide means its evidence is strong, not that it is free of risk.

What FDA said in July 2026

In its July 2026 briefings to the Pharmacy Compounding Advisory Committee, FDA did not claim any of the seven peptides causes cancer. Its safety findings were about missing evidence: limited and short nonclinical toxicology for BPC-157, with no information ruling out immune reactions to it; human-use information for TB-500 that it called non-existent; and for epitalon, no human safety data, three similar mouse studies of spontaneous tumours from one group and no genotoxicity studies.¹ The committee voted to recommend six of the seven for compounding anyway, and FDA had not acted on those votes as of September 25, 2026. A recommendation to allow compounding is not a finding that a substance is safe, and it says nothing about long-term cancer risk.

If you have had cancer, or are being treated

The mechanisms above matter most for people who already have a tumour, including one not yet found. That is why, for anyone with active cancer or a history of it, three categories deserve a conversation with the oncologist before anything else: compounds that raise growth hormone or IGF-1, including secretagogues and MK-677; compounds promoted for blood-vessel growth or tissue regeneration, such as BPC-157 and TB-500; and anything sold as a telomerase activator.

For GLP-1 medicines prescribed by a clinician, the label already defines who should not take them, and the human data are the best available for any compound on this page. For research peptides, the product is a second problem on top of the mechanism: identity, dose and purity are unverified, which makes any risk impossible to size. The absence of evidence of harm is not evidence of safety, and for most of these compounds that absence is all there is.

Frequently asked questions

Does BPC-157 cause cancer?

There is no evidence it does in people, because no study has looked. BPC-157 promotes blood-vessel growth in animal studies, which is why the question comes up; its main research group reports anti-tumour effects in animals and cells. Human data are minimal, so the risk is unknown rather than shown to be low.

Can TB-500 make cancer spread?

It has not been tested. TB-500 is a fragment of thymosin β4, and thymosin β4 is found at higher levels in some aggressive cancers, such as colorectal and thyroid tumours. That is an association in tumour tissue, not proof that injecting it feeds a tumour.

Do GLP-1 drugs like semaglutide cause thyroid cancer?

They caused thyroid C-cell tumours in rodents, hence the boxed warning. In people, large Scandinavian and international cohorts found no increase over two to four years, while a French case-control study found a higher risk after one to three years of use. Longer follow-up is still needed.

Does retatrutide cause cancer?

Retatrutide is still investigational, and no cancer outcome data are available yet. As a drug that acts on the GLP-1 receptor, the same thyroid question applies to it until longer follow-up is available.

Does MK-677 or a growth hormone secretagogue raise cancer risk?

They raise IGF-1, and higher natural IGF-1 is associated with more breast, prostate, colorectal and thyroid cancer in population studies. No secretagogue trial has been large or long enough to measure cancer outcomes, so the risk is theoretical but plausible, especially for people with a cancer history.

Is epitalon a cancer risk because it activates telomerase?

Unknown. Epitalon switched on telomerase in cultured human cells, and telomerase is active in most cancers, but no study has tested whether taking epitalon raises cancer risk in people. The animal tumour studies come from one group, and FDA noted there are no genotoxicity studies.

Related on Grey Peptides

• BPC-157 encyclopedia entry
• TB-500 encyclopedia entry
• Thymosin β4 encyclopedia entry
• MK-677 encyclopedia entry
• KPV encyclopedia entry
• Semaglutide encyclopedia entry
• The July 2026 PCAC votes and FDA's briefings
• Peptide side effects guide
• How we grade evidence

Sources

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7. Caers, J. et al. (2010). Thymosin beta4 in multiple myeloma: friend or foe. Annals of the New York Academy of Sciences, 1194, 125-129. PMID: 20536459
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9. Larsson, S. C. et al. (2020). Insulin-like growth factor-1 and site-specific cancers: A Mendelian randomization study. Cancer Medicine, 9(18), 6836-6842. PMID: 32717139
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17. Novo Nordisk. Wegovy (semaglutide) injection, US prescribing information: boxed warning, risk of thyroid C-cell tumors; contraindicated with a personal or family history of medullary thyroid carcinoma or MEN 2.
18. Eli Lilly and Company. Mounjaro and Zepbound (tirzepatide) injection, US prescribing information: boxed warning, risk of thyroid C-cell tumors.
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This article is for education. It is not medical advice, and it is not a guide to buying or using any peptide. If you have or have had cancer, talk to your oncologist before taking any compound discussed here.