---
slug: bpc-157
title: BPC-157: Body Protection Compound
canonical: https://miscsubjects.com/a/bpc-157
---

If you have a disc that is wearing out, you are deciding between things that slow the wearing and things that claim to rebuild. BPC-157 is sold as the second kind. BPC-157 is a short chain of 15 amino acids copied from a protein found in human stomach juice. Around 150 animal papers, mostly rats, report it speeding repair in tendon, ligament, muscle, nerve, bone and gut. Five studies have been run in people, covering about 130 people in total, and none of them was a finished controlled trial in a torn or worn-out tissue. It has never been approved as a medicine anywhere. It is banned in sport at all times. Nobody has ever tested it on a spinal disc, in a rat or in a person.

One disclosure, because it should change how you read the rest. The operator of this site has a commercial interest in compounds described here. That is a reason to weigh what is on this page against the sources it cites rather than against its tone, and every claim below carries the source that supports it for exactly that reason.
## The two clocks running in your back

A disc has two parts. The soft centre (the *nucleus pulposus*) is a water-holding gel that takes the load. Around it is a tough ring of layered fibres that keeps the gel where it belongs. Degeneration is the gel losing water and the ring cracking, in that order, over years.

Three things drive that.

The first is blood supply, or the near-absence of it. A disc is the largest structure in your body with no blood vessels running into it. Nutrients seep in through the bone plates above and below, and waste seeps out the same way. Those plates harden and clog with age. Once they do, the centre of the disc is a long way from any food supply, and cells in the middle start dying of the thing every tissue dies of when the plumbing fails.

The second is water. The gel holds water because of long sugar-protein molecules packed inside it. Cells make those molecules; dying cells stop making them. Less of them means less water, less water means a flatter disc, and a flatter disc loads its ring unevenly.

The third is the tearing itself. The ring is under shear every time you bend. When the centre stops cushioning, the ring takes load it was never built for, splits, and lets gel push out into the space where nerve roots run. That is a herniation, and the leg pain that follows is a squeezed nerve root (*radiculopathy*).

What makes it break down faster: smoking, which narrows the same small vessels feeding the bone plates; sustained loading without recovery; obesity; a genetic hand you did not choose, which explains more of the variation than most people expect; and — this is the one worth knowing before you read the rest of this page — steroid injections, which reliably reduce pain and reliably make the tissue heal worse.

Set against that, regeneration in a disc means one of three things: cells surviving longer, cells making more of the water-holding molecules again, or the ring physically closing. Every claim made for BPC-157 in a back is a claim about the first two, made by way of the blood supply. Nobody claims it closes a torn ring.

## Made in the stomach, and it survives the stomach

The name is literal: Body Protection Compound. The 15-piece chain is a fragment of a larger protein that sits in human stomach juice, and its one genuinely odd physical property is that it does not fall apart in that juice for more than 24 hours. Almost no peptide survives a stomach. That single property is the only reason a swallowed form is discussed at all, and it points at the gut as the compound's home ground.

Nearly the whole research record traces to one group in Zagreb, Croatia, led by Predrag Sikirić, running since 1993 and now past 150 papers.

That cuts both ways. It is a coherent, decades-deep programme applying one consistent dosing scheme across dozens of tissues, and it is also most of the world's evidence coming from a single group with a stake in the answer. It is the reason independent trials in people matter more here than they would for a compound many labs had poked at.

## What the different kinds of proof can and cannot tell you

Before the evidence, one table, said once, so the rest of the page does not have to keep apologising for itself.

| Kind of study | What it can settle | What it cannot settle |
|---|---|---|
| Cells in a dish | That the compound touches a specific switch inside a cell | Anything about a whole animal, a dose, or a person |
| Rats and dogs | That it changes a real injury in a living body, and by how much | Whether the same thing happens in a human, at what dose, or with what harm |
| Small safety studies in people | That a given dose did not visibly hurt a few dozen people over days | Whether it works, for anything |
| Chart reviews and phone follow-ups | What people remembered when asked | Whether the compound or the passage of time caused it |
| Randomised placebo trials | Whether it works | Nothing else needed — this is the one that settles it, and for a torn tissue none has finished |
| Forum and social posts | What exposure people are actually running, and what harms turn up at that exposure | Whether it works. Not weakly — not at all |


## Five studies in people, and the biggest one about an injury was a round of phone calls

FDA compiled the total published human experience for its July 2026 review. It is short enough to print in full.

| Study | How it was taken, and how much | People | Design | What happened |
|---|---|---|---|---|
| Healthy volunteers, rectal | up to 2 mg/kg daily × 8 days | 24 | Safety only | Nothing serious; headache and wind most common |
| Ulcerative colitis (Ruenzi 2005) | 80 mg rectal daily × 2 weeks | ~53 split into groups, ~26 treated | Randomised; published only as a conference abstract | Difference between groups 1.6 points, range −4.84 to 1.62 — the range crosses zero, so no effect was shown |
| Knee pain (Lee & Padgett 2021) | 2–4 mg into the joint, 1–2 injections | 17 found, 16 reached | Looked back at charts, then rang people up | 14 of 16 (87.5%) said they felt better; no dummy injection, no pain score, no scan |
| Interstitial cystitis | 10 mg into the bladder | 12 | No comparison group | Nothing serious reported |
| Healthy volunteers, into a vein | 10 mg then 20 mg | 2 | Safety pilot | No harm seen |

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Two things fall out of that table and they are both worth sitting with.

The only randomised trial ever run on BPC-157 in a person was about an inflamed bowel, it exists only as a conference abstract, and the result range crosses zero — meaning the treated group and the untreated group cannot be told apart. And the only published report of BPC-157 doing anything for a musculoskeletal injury in a human is somebody reading old charts and then telephoning the people in them.

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Eleven of twelve people who got BPC-157 alone in that knee series said they improved a lot. There was no dummy injection, no random assignment, no standard pain questionnaire and no imaging. That is exactly the design that cannot separate a real drug effect from the well-known fact that sticking a needle into a sore knee makes people feel better for a while.

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Two registered trials matter. A 2015 safety and absorption study in 42 healthy volunteers in Mexico gave single swallowed doses of 1 mg, 3 mg or 6 mg, then 3 mg every eight hours for two weeks. It never posted results, and the results submission was formally cancelled in 2016. Nobody knows what it found.

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The trial that could actually settle the tissue-repair question started recruiting in February 2026. It is randomised, double-blind, placebo-controlled, injected under the skin once a day for 14 days alongside a standard rehab programme, in 120 people aged 18–45 who have a grade II hamstring tear confirmed on a scan within 72 hours of doing it. The two things being measured are days until they can play sport again and the change in the size of the injury on the scan from day 0 to day 14. It is expected to finish in February 2027.

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Until that reads out, there is nothing controlled in a human for any soft-tissue injury. Not weak data. None.

## Rats: what happened, in which tissue, at what dose

This is where nearly all the positive findings live. Read it as a picture of what the compound does in a living body when everything about the animal, the dose and the injury is controlled — and remember that the animals were young, healthy and injured on purpose, which is not your disc.

### A rat Achilles torn off the bone came back mechanically stronger

The join between tendon and bone is the hardest soft-tissue repair in the body and the one that most often fails. In rats whose Achilles tendon was surgically cut off the heel bone, BPC-157 raised the load the repair could take before failing, its stiffness and its springiness, all significantly above untreated animals. Under the microscope the collagen fibres were better lined up, there was more type I collagen — the strong, rope-like kind — and more blood vessels had grown in. Dose was 10 µg/kg, 10 ng/kg or 10 pg/kg into the belly cavity once a day, starting 30 minutes after surgery.

The same paper carries the finding most relevant to anyone who has already had a cortisone shot: the steroid 6α-methylprednisolone consistently made the healing worse, and BPC-157 substantially undid that damage.

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### Cut a ligament, crush a muscle, or sever the join between them — all three healed faster

The ligament model cut through the medial collateral ligament in rats and followed them 90 days. Treated animals came out ahead on four separate measures at once: how the leg worked, how strong the ligament was, how it looked to the eye, and how it looked under the microscope. Three different ways of giving it each worked — injection into the belly cavity at 10 µg/kg or 10 ng/kg daily, a cream at 1.0 µg per gram rubbed on, and plain drinking water at 0.16 µg/mL.

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The muscle model both cut through and crushed the rat calf muscle, and deliberately gave the animals a steroid to wreck the healing. The authors' finding is that BPC-157 completely reversed that steroid damage, given either by injection or as a cream, with the leg working normally again in treated animals.

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The place where muscle turns into tendon — a classic site of grumbling strain that never settles — got its own study. In treated rats the injured leg's stiffening resolved completely, while untreated animals stayed disabled. The muscle wasting seen in untreated animals was prevented. By days 28 to 42 the new tissue ran in the right direction instead of being bridged by scar. Both the microgram and the nanogram doses worked.

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The biggest recent study, from January 2025, pulled the quadriceps entirely off its bony anchors and then treated the rats only through their drinking water. The vastus muscles reattached as early as 21 days. Rectus femoris was back to normal anatomy at about 28 days. At three months the mature fibres ran parallel to the bone and sat right against it. Reattachment was tracked on ultrasound — the same imaging used on people.

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The review that swept this whole literature screened 544 papers and kept 36. Thirty-five of the 36 were animal or lab work. Across muscle, tendon, ligament and bone the results point the same way: better function, better structure, better mechanical strength. The same authors put the counterweight in the same breath — harm is possible from unregulated manufacturing, contamination, and the fact that safety in people is unknown.

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### A cut sciatic nerve regrew faster, which is the nearest thing to a nerve finding

Rats with a completely severed sciatic nerve got 10 µg/kg or 10 ng/kg into the belly cavity, into the stomach, locally at the repair site, or loaded straight into the tube bridging a removed segment. Self-mutilation of the dead-feeling limb — the standard sign that a rat's nerve pain is bad — did not happen in treated animals. Electrical testing showed stronger muscle signals. Weekly walking tests improved. Counting fibres under the microscope found more of them, thicker, with better insulation around them, at one to two months.

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Read what that is and is not. It is a nerve cut clean through and sewn back together. It is not a nerve being slowly squashed by a bulging disc or a tight tunnel in the wrist. No study of BPC-157 in a squashed or chronically compressed nerve has ever been published. The difference is not a technicality: a cut-and-repaired nerve has to regrow along a clear path, and a squashed nerve has to survive a mechanical problem that is still there. Different problems, different bottlenecks.

### Nobody has ever tested it on a disc

Two rat spinal-cord studies exist and both squash the cord itself, not a disc.

The 2019 study opened the spine at L2–L3 and compressed the tail end of the cord for 60 seconds, then gave a single injection into the belly cavity ten minutes later at 200 µg/kg or 2 µg/kg. Treated rats got progressively better tail movement, did not self-mutilate, and their spasticity had resolved by day 15, with less swelling and fewer dead motor nerve cells in the grey matter.

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The 2022 follow-up is the more interesting one, because it waited before treating. After a one-minute squash by a 60–66 g weight that definitely paralysed the tail, one group got 2 µg/kg into the belly cavity at ten minutes. A second got a 10 ng/kg dose into the stomach on day 4. A third drank 10 µg/kg in water from day 4 to day 30. Recovery was described as fast and lasting out to a full year, with only patchy swelling, minimal bleeding and no loss of nerve insulation at day 30. Treatment started four days late still worked — which matters, because nobody turns up at a clinic ten minutes after their back goes.

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Neither of those is a disc. There is no published study of BPC-157 in a herniated or worn-out disc, in any species. And the doses used in the spinal work run up to a hundred times the doses used in the tendon work, so you cannot even carry a number across.

The argument people make for the disc goes like this: the disc has almost no blood supply, its healing is therefore limited by blood supply, and BPC-157's main proposed action is growing new blood vessels — so it should help. That argument is coherent. It also has no animal model behind it, let alone a human one. Nobody has put this compound in a degenerating disc and looked.

There is one more wrinkle worth stating, because it runs the other way. A worn disc is not supposed to have blood vessels in it. Part of what goes wrong in a painful disc is that vessels and pain nerves grow *into* the cracked ring, from the outside in, and that ingrowth is one of the better-supported explanations for why some worn discs hurt and others do not. A compound whose headline action is growing new vessels is being proposed for a tissue where new vessel growth is part of the pain. Nobody has tested which way that lands.

## How the compound is supposed to build tissue back

Strip the marketing and the proposed action is a short chain you can check link by link.

BPC-157 raises the signals that grow new blood vessels at an injury. New vessels bring oxygen and repair cells to tissue that had neither. Alongside that, it pushes collagen production and gets tissue-building cells to crawl into the gap.

The receptor step has been worked out in detail. In the cells that line blood vessels, BPC-157 makes the cell pull VEGFR2 — the main docking point for the body's chief vessel-growing signal — inside itself, and then switches on the VEGFR2–Akt–eNOS chain over time. Block the pulling-inside step with a chemical called dynasore and the whole effect disappears, which means the pulling-inside is required, not incidental. Vessel density went up both in a dish and in living animals, and blood flow came back faster in muscle that had been starved of it.

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The crawling step has its own named mechanism. In tissue-building cells taken from rat tendon, BPC-157 dose-dependently added phosphate groups to two proteins, FAK and paxillin, which are the machinery a cell uses to grip a surface and haul itself along. The total amount of those two proteins did not change; only the switched-on fraction rose. The same study found the cells were not making more of themselves, so the effect is cells moving and surviving, not cells multiplying in number.

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A third mechanism sits underneath both. Tendon cells given BPC-157 at 0.5 µg/mL grew about seven times more growth hormone receptors by day three, measured both as the instruction and as the finished protein. The cell does not get more growth hormone. It gets better at hearing the growth hormone already going past.

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Nitric oxide — the gas that makes vessels widen — is pushed up in some situations and down in others, always paired with mopping up damaging free radicals. The Zagreb group reads that two-way behaviour as the whole point of the molecule: it pushes tissue toward normal rather than in one fixed direction. FDA reads the same observation as the reason no dose-response curve has ever been drawn for it. Both readings fit the data.

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Now map that chain onto your disc, honestly. Link one, new vessels: real, shown in cells and in rats, never in a disc. Link two, vessels feeding a starved tissue: real in muscle, never shown in a disc, and a disc is starved through hardened bone plates rather than through missing vessels, which is a different blockage. Link three, cells making the water-holding molecules again: never studied for this compound, in any tissue. The chain has a hole in the middle of it exactly where your problem is.

## The painkiller you are probably already taking runs the opposite way to expected

Most people who arrive with back pain are already on an anti-inflammatory, and most compounds interact badly with those. This one was studied as an antidote to them.

Diclofenac at 12.5 mg/kg into the belly cavity once daily for three days produced severe stomach, gut and liver damage in rats, raised bilirubin, AST and ALT, made the liver heavier, and caused prolonged drowsiness that progressed to liver-driven brain failure with brain swelling and damaged nerve cells. BPC-157 blocked that entire cascade at both the microgram and the nanogram dose, given either by injection or in drinking water.

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Read carefully, that is a gut-and-liver protection finding, not proof that combining the two heals a tendon better. What it does mean is that the medicine most likely to already be in the room is not, in rats, a documented problem.

The steroid interaction is the more useful one for a back. Two separate studies show BPC-157 undoing the damage a corticosteroid does to healing tendon and muscle. If you have had a cortisone injection into a joint or around a nerve root, the animal data says that shot measurably impaired the repair you went in for, and that this compound reversed that impairment in rats. That is the single most relevant animal finding on this page for a person with a degenerating spine, because so many people arrive having already had the shot.

## It is gone from your blood in about fifteen minutes

The only published measurements of what the body does to this compound come from rats and beagles.

Average time to clear half of it: 15.2 minutes. In dogs given it into a vein, 5.27 minutes. Peak level in the blood arrived three minutes after an injection into muscle. How much reaches the blood after an injection into muscle (bioavailability) was 14–19% in rats and 45–51% in dogs — wildly different between two species, and far from all of it. It leaves in urine and bile. Levels in kidney, liver, stomach wall, thymus and spleen went well above the level in blood.

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A compound cleared that fast cannot be working by keeping a steady level in your blood. Whatever it does, it does fast and locally, then sets off a slower tissue process that outlasts the exposure by weeks. Two practical things follow. First, that is the argument for splitting a daily dose rather than taking it all at once. Second, a once-a-week schedule has nothing behind it.

No measurement of any of this has ever been made in a person. Every number in this section is a rat or a dog, carried across species by assumption.

## Turning powder into a dose is arithmetic, not judgement

BPC-157 arrives as a freeze-dried white powder in a sealed glass vial, usually 5 mg or 10 mg. You add liquid to it. The liquid is bacteriostatic water — sterile water with 0.9% benzyl alcohol in it as a preservative, which is the thing that lets you put a needle into the same vial repeatedly over weeks. Plain sterile water dissolves the powder fine but has no preservative, so that vial is a one-time proposition.

The measuring device is a U-100 insulin syringe. U-100 means 100 units in a millilitre, so one unit on the barrel is 0.01 mL. Every conversion you will ever need comes from two lines:

- Micrograms per mL = total micrograms in the vial ÷ mL of water you added.
- Micrograms per syringe unit = that number ÷ 100.

Worked through: a 10 mg vial holds 10,000 mcg. You add 2 mL of bacteriostatic water. 10,000 ÷ 2 = 5,000 mcg per mL. 5,000 ÷ 100 = 50 mcg in one unit. A 250 mcg dose is therefore 250 ÷ 50 = 5 units on the barrel.

| Vial | Water added | Strength | Mcg per unit | Units for 250 mcg | Units for 500 mcg | Doses in the vial at 250 mcg |
|---|---|---|---|---|---|---|
| 5 mg (5,000 mcg) | 2.0 mL | 2,500 mcg/mL | 25 | 10 | 20 | 20 |
| 5 mg (5,000 mcg) | 2.5 mL | 2,000 mcg/mL | 20 | 12.5 | 25 | 20 |
| 10 mg (10,000 mcg) | 2.0 mL | 5,000 mcg/mL | 50 | 5 | 10 | 40 |
| 10 mg (10,000 mcg) | 3.0 mL | 3,333 mcg/mL | 33.3 | 7.5 | 15 | 40 |
| 10 mg (10,000 mcg) | 5.0 mL | 2,000 mcg/mL | 20 | 12.5 | 25 | 40 |

Adding more water does not add or remove peptide. The vial holds what it holds. More water only changes how many syringe units carry a given dose. More water gives you bigger, easier-to-read unit counts and a slightly bigger squirt going in. Less water gives you a smaller sting and finer lines to misread. Below about 5 units per dose, the error in reading a U-100 barrel starts to swamp the dose itself — which is the practical argument for putting 3 mL rather than 2 mL into a 10 mg vial.

Ruining the peptide by accident is easy. Let the vial come to room temperature first. Run the water slowly down the inside wall of the glass rather than blasting it onto the powder. Swirl until it dissolves. Never shake it — shaking tears at the surface where liquid meets air, which unfolds peptide chains and makes them clump together, and clumping is the exact thing FDA named as the trigger for the immune system reacting to it (immunogenicity).

## The clock starts the moment you add water

| State | Temperature | How long it actually lasts |
|---|---|---|
| Sealed, still a powder | 2–8 °C, out of the light | Months to years, to the maker's date; −20 °C for long holding |
| Mixed with bacteriostatic water | 2–8 °C | About four weeks — that limit is set by the preservative, not the peptide |
| Mixed, left on the counter | 20–25 °C | Hours to days; treat it as ruined |
| Mixed, then frozen | −20 °C | Do not. Freezing and thawing clumps the peptide |

Do the arithmetic against your own plan before you buy. A 10 mg vial at 250 mcg a day is 40 doses. Four weeks is 28 doses. You will throw away roughly a third of the vial, or you must buy a smaller one, or take more per day. There is no fourth option — refreezing it is the one thing that definitely damages it.

## Where the needle goes was never settled, because nobody asked the animals

Two placements compete and the animal work cannot referee between them, because rats were dosed into the belly cavity, into the stomach or rubbed on the skin, almost never at a specific human-style injection site.

- **Under the skin, near the sore part.** What most people do. The argument is a higher concentration where the repair is needed, which fits a 15-minute clearance and fits tissue levels running above blood levels.
- **Under the skin of the belly, anywhere.** Standard for gut, nerve and organ targets, and easier to do to yourself. The argument is that a compound reaching kidney, liver and stomach wall above blood level obviously travels, so the entry point may not matter.

The evidence tilts slightly toward the entry point not mattering. Several of the strongest structural results in the entire literature — the cut ligament, the muscle-tendon junction, the quadriceps reattachment, the sciatic nerve, the spinal cord — were produced in rats that simply drank the compound and still repaired a specific injury a long way from their gut. Nothing anywhere in the record shows a local injection beating a systemic one head to head.

Here are the doses that exist, all of them either from rats or scaled up from rats:

| Where the number comes from | The dose | How long |
|---|---|---|
| The standard rat tier | 10 µg/kg, 10 ng/kg or 10 pg/kg once a day | For as long as the study ran |
| The rat drinking-water equivalent | 0.16 µg/mL in water, about 12 mL per rat per day | For as long as the study ran |
| Scaling 10 µg/kg straight up to a 70 kg adult | about 0.7 mg per day | Not an established human dose. Just arithmetic |
| Given to humans into a joint, published | 2–4 mg per injection, 1–2 injections | One course |
| Given to humans by mouth, published (2015 Phase 1) | 1, 3 or 6 mg once; then 3 mg every 8 hours | Two weeks |

There is no validated human dose, no validated cycle length, no taper and no ceiling. USADA states it without softening: nobody knows whether a safe dose exists, or whether there is any way to use this compound safely for a named condition.

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Now notice what the table shows, because it is the single most overlooked fact about this compound. Every dose ever given to a human in a published study is measured in **milligrams**. Scaling the standard rat dose up to an adult lands at roughly 0.7 mg. The regimens circulating on forums and printed on vendor sites are measured in **micrograms** — a thousandth of a milligram — and land around 250 to 500 mcg. That is roughly a hundredth of anything ever formally given to a person. Nothing in the literature supports the microgram regimens. Nothing in the literature refutes them either. The dose question is not contested; it is simply open, and everyone taking it is guessing.

## The tablet and the vial are not the same product

Swallowed BPC-157 exists as capsules or tablets, commonly 500 mcg each, and the stomach-survival finding is what makes that format arguable at all. But surviving your stomach acid and getting into your bloodstream are two separate questions, and only the first has ever been shown in a person.

| | Tablet you swallow | Vial you mix and inject under the skin |
|---|---|---|
| What is actually proven about this route | Survives human stomach juice past 24 hours | In rats, 14–19% of an injection into muscle reaches the blood; in dogs, 45–51% |
| Animal evidence using this route | Substantial — the ligament, muscle-tendon junction, quadriceps reattachment, nerve and spinal cord studies all worked with the compound given by mouth or in water | Extensive, but nearly all of it into the belly cavity rather than under the skin |
| What has been given to humans this way | 1–6 mg by mouth in the 2015 Phase 1; 80 mg per enema in the colitis trial | 2–4 mg into a joint; 10–20 mg into a vein |
| Best-supported target | The gut, and any whole-body target where the rat drinking-water arm worked | Musculoskeletal — by convention, not by any head-to-head comparison |
| How much gets into a human's blood | Never measured | Never measured |
| What it costs you in practice | No needles, no mixing, no four-week clock | Needles, arithmetic, a fridge, and a four-week clock |

The evidence is friendlier to the swallowed route than the injection convention implies. Several of the strongest structural repair results in the whole corpus — ligament, muscle-tendon junction, muscle reattached to bone, delayed spinal cord recovery — came from rats drinking it in water. What nobody has is a measurement of how much of a swallowed dose gets into a human's blood, so choosing between the two forms rests on rat route data and on convenience, not on anything measured in a person.

## How long anything would take, if it worked

Timelines here are set by tissue biology, not by the compound. Collagen remodels at the speed collagen remodels. Nerves regrow at about a millimetre a day. Nothing changes that.

| Model | Time to the reported result |
|---|---|
| Squashed spinal cord, spasticity gone | 15 days |
| Quadriceps reattached to bone, vastus muscles | 21 days |
| Quadriceps reattached to bone, rectus femoris | ~28 days |
| Muscle-tendon junction, tissue running the right way | 28–42 days |
| Cut sciatic nerve, function and microscope findings | 1–2 months |
| Cut medial collateral ligament, full follow-up | 90 days |
| Hamstring tear Phase 2, injury size on scan | 14 days (the primary measure; reads out 2027) |

No human timeline has been established, because no controlled human trial has finished.

The one inference that is honest: these are collagen and nerve timescales — four to twelve weeks. Anything promising a result inside a fortnight is describing pain relief, not repair. That distinction has a consequence you can act on. Pain relief arrives before tissue has been rebuilt. If you feel better at day 10 and go back to loading your spine on that signal, you are loading a structure that has not changed.

## FDA's own toxicology is more specific than the safety talk around it

The Zagreb group's stated position is that BPC-157 is very safe, with no side effects in trials and a lethal dose never reached in toxicology work. FDA read the same body of work and described it differently.

In 28-day repeat-dose studies injecting into muscle, rats showed shortened clotting time and dogs showed lengthened clotting time on the same test — an unexplained effect on clotting that runs in opposite directions in two species. Blood ALT, glucose and triglycerides went up. No cancer-causing study of BPC-157 in either of its two chemical forms has ever been done. It did not damage DNA, and no birth-defect signal appeared when it was injected through gestation days 6–15.

FDA raised four objections. They are independent of each other, which means answering one leaves the other three standing.

| The objection | What it actually means |
|---|---|
| Not enough clinical safety information to describe the safety profile | The human safety file is too small to draw a picture from — not "reassuring so far", but too small to say anything |
| Real risk that the immune system reacts to it, made worse by clumping and by peptide impurities | Part of the risk comes from how it is made and handled, not from the molecule alone |
| No dose-response relationship established | The flat pattern where micrograms, nanograms and picograms all work reads to FDA as a weakness, not a feature |
| No molecular target identified | Despite the VEGFR2 and FAK work, no confirmed receptor has been pinned down |

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## The cancer question has a real answer and a real hole in it

The worry is mechanically sensible. A tumour cannot grow past a millimetre or two without recruiting new blood vessels. A compound whose headline action is growing new blood vessels could, in principle, supply them. An independent 2025 review states the worry and lands on the practical version of it: a cancer nobody has found yet.

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The Zagreb group published a formal rebuttal in the same journal. Their case is that BPC-157 strongly *blocked* vessel growth into the cornea, that it has shown anti-tumour activity both in living animals and in a dish, and that its nitric oxide effect is always paired with mopping up free radicals — that it pushes vessel growth toward the normal, self-limiting kind rather than driving it indiscriminately.

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Where that leaves you: no published rodent study shows BPC-157 speeding up tumour growth. No cancer-causing study exists. There is zero human cancer safety data. An active or suspected cancer is the one situation the mechanism itself argues against, and the missing study means the argument cannot be closed either way. If you have had a cancer, this is the question to take to your oncologist rather than to a forum.

## FDA said no, and its own advisory committee said yes by two votes

The regulatory position moved twice during 2026, and most summaries you will find online are stale.

| Date | What happened |
|---|---|
| Sept 2023 | FDA puts BPC-157 in Category 2 of the 503A bulk-substances list — significant safety risk, which bars compounding pharmacies from making it |
| 14 May 2026 | The revised interim list carries only six substances in Category 2. BPC-157 is in none of Categories 1, 2 or 3 — the nominations were withdrawn |
| July 2026 | FDA's own briefing document recommends against adding BPC-157 to the 503A list |
| 23 July 2026 | The Pharmacy Compounding Advisory Committee votes 8–6, with one abstention, to recommend adding it — against FDA's own staff |

If a page you are reading still says BPC-157 is FDA Category 2, it has not been updated since 14 May 2026.

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One detail in the meeting agenda changes what that vote means. The only condition FDA evaluated was ulcerative colitis. Tendonitis was among the uses put forward, and FDA declined to evaluate it because there was not enough information. A favourable vote about a bowel condition is not a favourable vote about tendon or disc repair, and it is being quoted as though it were.

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The committee itself was not persuaded of much. One panelist who voted yes described the thing being voted on as a black box. One who voted no pointed out that roughly 30% of people given a dummy treatment report improvement — sometimes even on objective measures — which is the entire difficulty with the uncontrolled reports the nomination rested on.

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Reporting on the meeting noted that a majority of the panelists voting yes had ties to the peptide industry.

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The vote creates no authority. It is advisory, FDA is not bound by it, and a formal rulemaking cycle realistically runs eight to twelve months.

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## There are two legal ways to compound a peptide and BPC-157 is on neither list

503A covers traditional compounding pharmacies. 503B covers registered outsourcing facilities, and it is a separate list with a separate standard: an outsourcing facility may not compound with a bulk substance unless that substance is on the 503B list, or the finished medicine is on FDA's drug shortage list at the time. BPC-157 is not on the 503B list, and the July 2026 vote concerned 503A only.

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That same page sets out what FDA expects of any lawfully compounded substance: a valid certificate of analysis, manufacture by an establishment registered under section 510 of the FD&C Act, and compliance with any applicable USP or National Formulary monograph. Grey-market BPC-157 meets none of the three.

## If you compete in anything, this is a strict-liability problem

BPC-157 is named explicitly on the WADA 2026 Prohibited List under S0, Non-Approved Substances, banned at all times — not just on competition day. S0 covers any substance with no current approval by any government health authority for human use anywhere, which is exactly what BPC-157 is.

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Strict liability means you are responsible for what is in your body regardless of intent and regardless of who recommended it. That applies at college, professional and masters level, in sports most people do not think of as drug-tested.

The Department of Defense goes further. Its Operation Supplement Safety programme lists BPC-157 on the Prohibited Dietary Supplement Ingredients List and states the position flatly: BPC-157 is not a dietary ingredient, it is an unapproved drug. That applies to service members however it is taken.

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## "Research use only" is a shipping label, not a legal category

Nearly all BPC-157 sold to the public is labelled a research chemical, not for human consumption. That phrase creates no lawful route to a person. It is a disclaimer attached to a product with no legal standing as a medicine, a food or a supplement in the United States. USADA names the tell directly: sites that print "research only" while also printing human dosing instructions are describing what they expect to happen.

The purity problem is the concrete risk, and it is bigger than the legal one. Independent testing of grey-market peptide samples finds mislabelling, wrong dosing or contamination in roughly 30%, and the contaminant classes are specific: bacterial toxins, incomplete chains that are missing pieces, leftover solvents, heavy metals, live microbes and breakdown products. Incomplete chains and clumping are the same two failure modes FDA named as the things that make an immune reaction more likely — which means the supply-chain risk and the drug risk are the same risk wearing two hats.

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> 30% contained incorrect amino acid sequences and two-thirds of samples fell below the 95% purity threshold.

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A certificate reading "99% by HPLC" does not clear a batch, and understanding why is worth two minutes. HPLC confirms the target peptide is there and measures how much of the total it is. It says nothing about what the other 1% consists of. An incomplete chain or a fever-causing bacterial toxin sits inside that remainder and never shows up. What you want is HPLC *and* mass spectrometry, done per batch, by a laboratory that is not the seller. A vendor's own certificate is not third-party testing, and a certificate photographed from a different batch is not a certificate at all.

## Which problems the evidence actually reaches

Every positive animal model in this literature is an acute surgical injury — a tendon cut through, a ligament severed, a muscle crushed, a tendon torn off bone, a nerve cut. There is no rat model of a fifteen-year grumbling tendon, and no reason to assume a repair signal helps tissue whose problem is failed remodelling rather than an unfilled hole.

| Your problem | What the animal data actually covers | How strong |
|---|---|---|
| Fresh tendon tear or rupture | Achilles cut through and torn off bone: strength to failure, stiffness, type I collagen all improved | Strongest animal case |
| Tendon pulling off bone | Achilles detachment and quadriceps reattachment, confirmed on ultrasound at 21–28 days | Strong in animals, nothing in humans |
| Ligament sprain | Medial collateral ligament cut through, 90-day follow-up, four measures | Strong in animals, nothing in humans |
| Fresh muscle strain | Calf muscle cut and crushed; the one Phase 2 trial targets a grade II hamstring | Animals plus one trial reading out 2027 |
| Pain where muscle becomes tendon | Its own rat model; stiffening resolved, wasting prevented | Strong in animals, nothing in humans |
| Healing spoiled by a cortisone shot you already had | Two studies show the steroid damage to tendon and muscle healing reversed | Animals, directly relevant, nothing in humans |
| You are on daily anti-inflammatories | Diclofenac damage to gut, liver and brain fully blocked | Animals; a protection finding, not a repair finding |
| Nerve cut and surgically repaired | Sciatic nerve: electrical signals, walking, insulation all improved | Moderate in animals, nothing in humans |
| Long-standing overuse tendon pain | No model exists. Every positive study is a fresh injury | Weak — the mechanism does not obviously apply |
| Carpal tunnel or other trapped nerve | No compression model exists | Absent |
| Herniated lumbar disc, sciatica | No disc model exists. Nearest thing is a squashed rat spinal cord at a 100× dose | Absent |
| Degenerative disc disease itself | Nothing. Not one study, in any species | Absent |

Three rows carry the weight and they are not the three people expect.

The cortisone-reversal row is the most useful finding in the entire animal literature, because a large share of people with a bad back arrive having already had a steroid injection that measurably worsened the healing they came in for. If any part of this compound's animal record applies to you, that is the part with the clearest logic behind it.

The long-standing-tendon-pain row is weak exactly where demand is highest.

And the two disc rows are empty. The problem people ask about most is the one with no animal model at all — and, as the next section shows, it is also one of the problems that generates the loudest success stories.

## Fifty people said what happened to them, and here is the count

Everything above this heading is evidence. Everything below it is testimony, and the difference is not a matter of degree.

This page holds 50 first-person accounts posted publicly between 2015 and 2026 — 40 on Reddit across r/Peptides, r/steroids, r/backpain, r/Sciatica, r/climbharder, r/PEDs, r/Biohackers, r/moreplatesmoredates, r/PeptideGuide, r/Peptidesource and r/Supplements, and 10 on X. Every one is self-reported by a person you cannot identify or question. Nobody assayed their vial, so the substance in the syringe is unknown in every single case. Nobody was randomly assigned. Almost nobody scanned the injury before and after. People who got better write posts more often than people who did not, so the set is filtered before you even read it.

It is here for one reason. No controlled trial in a human musculoskeletal injury has ever finished, so this is the entire record of people using it for the reasons you are considering it — and it is what you have already read by the time you got to this page.

### The count, with the denominator

Of the 50 accounts, 13 report no personal result at all — they are protocols, questions, general threads about the science, or one person's dosing accident. That leaves **37 accounts that state what happened to the person writing**. Here is the split:

| What they reported | Count | Share of the 37 |
|---|---|---|
| It helped — clear improvement they credit to it | 18 | 49% |
| Partly, or it faded, or they could not separate it from other things | 5 | 14% |
| Nothing happened | 10 | 27% |
| It made something worse | 4 | 11% |

Read that table twice. Half of the people who reported an outcome said it helped, and half did not. If you have seen this compound described online, you have almost certainly seen a version of that record where the 14 accounts reporting nothing or harm were left out. That version is a lie by selection, and it is the standard version.

Four more things the raw count hides.

The 10 "nothing happened" accounts are not shorter courses or smaller doses than the successes. Several ran six weeks or more at the same 500 mcg a day that the successes ran.

The 4 harm reports describe things the rat toxicology gives no reason to expect and the five human studies were far too small to catch: a joint that got worse and inflamed, vision going blurry over weeks, a finger swelling with fluid, and leg pain returning during treatment for a herniated disc.

One account reports a ten-fold dosing accident, which is a safety datapoint of its own and the reason the reconstitution arithmetic earlier on this page matters more than it looks.

And exactly one account in 50 reports an objective check by a clinician. One. Everybody else is reporting pain, movement and confidence — the three things most responsive to time, rest and expectation.

### The 18 who said it helped

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Two of those deserve a note rather than applause. The account crediting a clinician with saying the tear was gone is the single best entry in the whole set, and even that was a re-examination, not a repeat scan. And the account that asks itself "is this placebo?" also added collagen and more protein in the same window, which the writer says outright — that honesty makes it more useful than the confident ones, not less.

### The 5 who got part of a result, or lost it

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The last one is a pattern with no counterpart anywhere in the published literature: the effect fading on a steady dose, then not returning when the dose was raised. Nothing in the rat work predicts that. Nothing in the pharmacology explains it.

### The 10 who said nothing happened

These are the entries marketing copy leaves out. They are the same doses, the same durations, and several of them are longer courses than the successes.

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The standard reply offered inside these threads to a negative report is that the person got a bad vial. That reply cannot be checked — nobody in this set tested their product — and it is the exact mechanism by which a grey-market compound builds a record that can never fail. Every success counts as evidence; every failure counts as a counterfeit.

### The 4 who got worse

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The first of those is the one to read closely if you have a disc problem: leg pain returning and worsening during a course taken specifically to heal a herniated disc. That is the exact situation this page is about, and it is a harm report, not a success.

The second describes one joint improving while another got inflamed and worse in the same person, on the same dose, in the same course.

### The dosing accident, and where the numbers came from

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That is ten times the intended dose, caused by misreading a syringe barrel. Nobody was hurt. It is on this page because the numbers everyone uses have nothing under them, and the people using them say so plainly:

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Almost every account in the set describes 250 to 500 micrograms a day, under the skin, sometimes split into two or three shots, run for four to eight weeks. That band converged by copying, not by measurement. It is about a hundredth of the milligram doses used in every published human study.

### The 13 that report no outcome at all — including the six loudest posts here

Thirteen of the 50 accounts state no personal result. Seven are the protocols and dosing arguments already shown above. The other six are X posts, and they are worth looking at separately, because they are almost certainly the format in which most people first meet this compound.

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Read what those six actually are. Four are summaries of the animal literature written in the voice of personal endorsement — "repaired 5 different tissues", "no compound heals as many tissue types" — with a dose attached at the end and no report of the writer's own outcome anywhere in them. One is a person asking for an alternative. One is a person saying they never took it but wish they had.

They are in this count because leaving them out would be dishonest, and they are separated out because counting them as successes would be worse. The most confident writing about this compound contains the least first-hand information in it, and that is the single most useful thing this section can tell you.

### Where the accounts contradict the animal work

The animal record is strongest for fresh injuries and weakest — or empty — for long-standing tendon pain and for discs.

The forum record inverts that exactly. Long-standing elbow, wrist and shoulder tendon pain of one to five years' standing is the most common thing people treat. Herniated discs and sciatica — the problem with no animal model whatsoever — generate some of the most emphatic success reports on this page.

The single most emphatic disc account on this page — the sciatica report above, in which pain eased over six to seven weeks of injections after everything else had failed — is also the one with the least behind it, because no animal has ever been given this compound for a disc.

Two readings fit that and the accounts cannot separate them. Either the compound reaches structures the animal work never tested, or long-standing pain that comes and goes was going to improve anyway and the compound arrived during a good month. The disc reports are the clearest case, because a herniated disc shrinks on its own in a large share of people over roughly six to twelve weeks — which is exactly the window these protocols run. Somebody who starts a course at their worst week and finishes it feeling better has described the natural history of the condition, and would have written the same post taking nothing.

The swallowed route contradicts the pharmacology the same way. Surviving stomach acid is proven; getting into a human's blood from the gut is not. People report the two forms doing different jobs, which is precisely what you would expect if the tablet works locally in the gut and never reaches a tendon at all.

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### The stacking problem, which is the biggest hole in the whole set

Almost nobody takes this alone. TB-500 is combined with it so routinely that a large share of these accounts cannot attribute any outcome to either compound. Others add growth hormone, testosterone, surgery, physiotherapy, diet changes and rest inside the same weeks.

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The three most confident recovery stories on this page — the rotator cuff tear a clinician later called gone, the wrist rebuilt over seven vials, and the shoulder that felt 75% better in five days — were all run as BPC-157 plus TB-500, and two of them alongside structured rehab. Not one of them can tell you which part did the work.

That is not a small caveat. It means a good share of the 18 positive accounts are reports about a combination, run alongside the two interventions with the best evidence in all of musculoskeletal medicine — load management and time.

### What the counted record settles, and what it does not

It does not settle whether it works. Thirty-seven uncontrolled accounts filtered toward success are not weak evidence for a treatment effect; they are a different kind of object, and collecting three hundred more would change nothing about that. A 49% success rate in this set is not a 49% chance it works for you. It is a measurement of what people wrote down.

It does settle three things the published literature does not contain at all, and these are the reason it is worth counting rather than dismissing.

First, the real exposure. People are running 250–500 mcg a day under the skin for four to eight weeks, usually stacked with TB-500. No trial has ever studied that exposure. When somebody eventually does, this is the regimen they should test, and nobody would know it from the papers.

Second, harms at that exposure. Four of 37 accounts report getting worse — local swelling, a joint becoming more inflamed, blurred vision, and returning nerve pain. None of those appear in any published human safety dataset, because those datasets total about 130 people across five studies and would not detect a 1-in-10 problem if it existed.

Third, the mismatch. The two things people actually treat with it — long-standing tendon pain and lumbar disc disease — are the two the animal literature supports least and not at all, respectively.

The Phase 2 hamstring trial reading out in 2027 will answer the works-or-not question for one fresh injury in one muscle. Nothing currently running will answer it for a disc.

## What is settled about BPC-157, and what is not

| Status | Statement |
|---|---|
| Settled | It survives human stomach juice for more than 24 hours |
| Settled | It switches on the VEGFR2–Akt–eNOS chain and increases blood vessel density in a dish and in rodents |
| Settled | It improves mechanical strength and microscope appearance across many fresh rat injuries |
| Settled | It reverses the damage a corticosteroid does to tendon and muscle healing in rats |
| Settled | It blocks diclofenac-caused gut, liver and brain damage in rats |
| Settled | Half of it clears a rat's blood in about 15 minutes; 14–19% of an intramuscular dose reaches the blood in rats |
| Settled | It is on the WADA 2026 Prohibited List under S0, banned at all times, in and out of competition |
| Not shown | That it does anything for a musculoskeletal injury in a person — no controlled soft-tissue trial has finished |
| Not shown | That a swallowed dose reaches the bloodstream of a human |
| Not shown | That it feeds tumours — and equally not shown that it is safe if you have a cancer |
| Unknown | The right human dose. Every published human study used milligrams; everyone taking it uses micrograms |
| Unknown | Long-term safety, interactions with your other medicines, and why clotting time moves in opposite directions in rats and dogs |
| Unknown | Whether any of this reaches a spinal disc. Nobody has looked, in any species |

If you take one line from this page, take this one: the strongest argument for BPC-157 in a degenerating back is a chain of reasoning, and the strongest argument against it is that nobody has ever tested a single link of that chain in a disc. The animal work is real and it is good. It is also about tendons, ligaments, muscles and cut nerves in young rats injured on purpose, and your disc is none of those things.

*BPC-157 is not an approved medicine in any country. Everything sold to the public is grey-market and unverified. Nothing here is a dosing or treatment recommendation.*

The sibling objects for this page, each one inspectable on its own terms:

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