Adipotide: what the studies show, status and safety

Summary

Adipotide is not a metabolic drug but a cell-killing conjugate: an address tag that finds a protein on blood vessels in white fat, joined to a piece that destroys mitochondria. In monkeys it lowered weight and fat, and injured the kidneys in every dose group tested. Its only human trial closed after four patients, and no country has approved it.

Key findings at a glance

• The only human trial closed with four patients. It opened in 2012, was terminated in January 2019 at the investigator's request, and enrolled 4 of up to 39 planned participants. No results were posted and none were published ^[1], ^[2].
• Kidney injury appeared in every dose group of every animal study. In rhesus monkeys examined after the last dose, pathologists found dose-dependent damage that was absent in controls: individual dead cells (single-cell necrosis) and degeneration of the fine tubes that concentrate the urine ^[3].
• A sister compound with the same killing half did the same in humans. In a first-in-man study of BMTP-11, which carries the identical effector, the dose-limiting toxicity was explicitly renal, with protein and casts in the urine and rising creatinine ^[4].
• The targeting itself was never independently confirmed. The one quantitative biodistribution study of the address tag found no enrichment in fat tissue, no vessel-cell specificity, and increased uptake in the kidney ^[5].
• In obese monkeys the effect was measurable but temporary. In one controlled 28-day study, ten treated obese rhesus monkeys lost on average 10.6 per cent of body weight against five saline controls, and the loss began reversing after treatment ended ^[3].
• In mice the fat loss came from eating less, not from burning more. Energy expenditure did not change. A formal comment in the same journal argued the monkey result may reflect the same thing ^[6], ^[7].
• Nobody has applied for a lawful way to make it for people. Adipotide appears in no American bulk-substance list for pharmacy compounding, unlike BPC-157, ipamorelin or AOD-9604 ^[8].
• It is banned in sport at all times under the catch-all class for non-approved substances ^[9].

What it is

Adipotide is a chimeric peptidomimetic: a laboratory-built molecule that borrows the chemistry of peptides without being a natural one. It has two halves with two jobs, joined by a short linker.

The first half is a ring-shaped nine-unit motif, CKGGRAKDC. It was fished out of a random library in living mice in 2004, because it travelled to the blood vessels of white fat. Its binding partner was identified as prohibitin ^[10].

The second half, D(KLAKLAK)2, is built entirely from mirror-image amino acids. It punches holes in mitochondrial membranes and kills the cell that takes it up ^[3].

That mirror-image construction is deliberate. The body's peptide-splitting enzymes do not recognise it, so the killing half survives far longer than an ordinary peptide would ^[3].

The substance carries four names, which is a practical problem rather than a cosmetic one. The development owner called it Adipotide, the trial registry lists it as Prohibitin-TP01, the founding papers call it simply a proapoptotic peptide, and online trade uses FTPP ^[1], ^[3], ^[11].

Quick facts

How it works

The intended idea is to starve fat tissue rather than to change its metabolism. Fat cells need a dense blood supply; kill the vessels and the tissue shrinks. Everything else follows from that one design choice.

• The address half binds prohibitin. This membrane protein is enriched on the vessel lining of white fat in mice, and the motif was selected in living animals precisely because it went there ^[10].
• The killing half is not selective at all. D(KLAKLAK)2 destroys mitochondrial membranes in whatever cell internalises it. The safety of the whole molecule rests entirely on the address half being accurate ^[3].
• Prohibitin is not confined to fat. It is broadly expressed on immune, epithelial and vessel cells, and in the kidney it also sits in the narrow filtration slits between the cells that form the filter itself (the podocytes) ^[5], ^[10].
• The target does exist in humans. Selecting a peptide library directly in cancer patients returned prohibitin paired with annexin A2, distributed in white fat. That shows the address exists, not that the molecule works ^[13].
• The one independent check of the targeting failed. A group that measured where tagged carrier particles actually ended up in the body found no build-up in fat, no preference for vessel cells, and more uptake in the kidney. What dominated was ordinary engulfment by scavenger cells of the immune system, not targeting. The authors note that no earlier study had ever measured where the address tag goes ^[5].
• The mechanism was never settled. The authors of the monkey study wrote that a detailed mechanism remained to be elucidated, and that weight loss occurred alongside reduced food intake ^[3].

There is a plainer competing explanation. In mice, fat loss happened with no change in energy expenditure at all, driven only by eating less, and independently of leptin ^[6].

This is where Adipotide parts company with the peptides it is often listed beside. Appetite peptides and growth-hormone releasers act on receptors; this one acts by killing cells, and its nearest relatives are targeted cancer agents ^[3], ^[10].

What the studies found

Almost everything known comes from animals. PubMed held seven records for the name on 12 September 2026, none of them a clinical result ^[14].

Weight and fat in monkeys

Animal data The central study treated 15 spontaneously obese rhesus monkeys for 28 days, ten of them with the substance and five with saline, followed by 28 days of recovery. Treated animals changed weight by -7.4 to -14.7 per cent, an average of -10.6 per cent; controls ranged from +1.0 to -3.5 per cent ^[3].

Body mass index fell by an average of 10.0 per cent in treated animals, with individual animals between -3.7 and -17.3 per cent, against -3.5 to +3.3 per cent in controls. Waist circumference fell in nine of the ten treated animals and rose slightly in one. All three trends over time were statistically solid (mixed-effects model, p < 0.0001) ^[3].

Scans told the same story. Measured from the start of the study to the end of the recovery period, total body fat on X-ray scans fell 38.7 per cent in six treated animals, against 14.8 per cent in three controls (p < 0.0001). Abdominal fat volume on MRI fell 17.5 per cent by the end of dosing (p = 0.02), and 27.0 per cent by the end of recovery (p = 0.04) ^[3].

Animal data Two findings limit how far this travels. Weight, body mass index and waist circumference kept falling for three weeks after dosing stopped, then started to reverse. And lean monkeys given the same treatment did not lose weight, which means the effect was not a general one ^[3].

Blood sugar and insulin

Animal data In the same 15 monkeys, the insulin response to a glucose challenge fell by an average of 36.2 per cent against controls (p = 0.019). The insulinogenic index, which describes how briskly the pancreas releases insulin once glucose arrives, fell 48.5 per cent in treated animals while rising 33.8 per cent in controls (p = 0.006). Fasting glucose barely moved; these animals were not diabetic ^[3].

Animal data In obese mice, glucose tolerance improved quickly and, unusually, independently of weight and food intake. A pair-fed control group, given the same amount of food, did not show the effect. Serum insulin and triglycerides fell ^[15]. This is the strongest argument that something more than appetite was happening.

Food intake, the disputed point

Animal data In mice and rats the picture is unambiguous. Fat was lost only on a high-fat diet, not on a low-fat one, with no change in energy expenditure and no sign of nausea in a taste-aversion test. Leptin, the hormone fat tissue uses to signal fullness, fell, and so did a hunger-regulating signal in the brain (hypothalamic POMC expression), so the appetite effect was not running through leptin ^[6].

Animal data In the monkeys, the number of food biscuits eaten fell in proportion to the weight lost, while fruit, vegetables and nuts were still eaten. Energy expenditure could not be measured. The authors conceded that mild nausea as a contributor could not be completely ruled out ^[3].

A formal comment published in the same journal in 2012 pressed exactly this point, arguing that the result may instead reflect a direct effect on food consumption. The full text was not retrievable, so only the published abstract was used ^[7].

Where the molecule actually goes

Animal data, independent A separate group tagged carriers with the same address motif and measured, by flow cytometry and imaging, where they ended up. There was no enhanced uptake in fat tissue and no vessel-cell specificity, but there was increased uptake in the kidney. Engulfment by scavenger cells, not targeting, dominated ^[5].

Animal data, independent A head-to-head comparison in obese mice tested two ways of delivering the same killing peptide. Prohibitin-targeted nanoparticles lowered weight and leptin, and reduced fat in liver and muscle. The bioconjugate made of the same two parts, which is Adipotide itself, did not ^[16].

What is still unknown

• What the human body does with it. No pharmacokinetic data and no half-life have been published for any species. The human trial planned blood sampling on days 1 and 22; those data never appeared ^[3], ^[1].
• What a tolerable human amount would be. Establishing that was the primary aim of the terminated trial, and it was never reached ^[1].
• Whether the immune system reacts to it. Antibody testing was planned 30 days after the end of treatment and was never reported ^[1].
• Whether anything lasts. In monkeys the weight loss began reversing within the four-week recovery window, and no longer study exists ^[3].
• Basic toxicology. No published reproductive, genotoxicity or carcinogenicity data. Detailed single- and repeat-dose studies in 52 cynomolgus monkeys were announced in 2011 as forthcoming and could not be found in PubMed on 12 September 2026 ^[3], ^[14].
• What is in the material sold online. No laboratory analysis of a grey-market vial has been published ^[11].

Side effects and safety

There is no human safety record. Four patients received it, and nothing about them was ever reported. Everything below comes from animals, and it points consistently at one organ ^[1].

• The kidney is the target organ of toxicity. In rhesus monkeys examined a day after the last dose, kidney lesions were dose-dependent and absent in controls: single-cell necrosis, tubular degeneration and reactive regeneration ^[3].
• The damage did not depend on any weight effect. Lean rhesus monkeys, given the same treatment in the same programme, showed the kidney changes while losing no weight at all. Benefit and harm were not coupled ^[3].
• Recovery was incomplete in some animals. After four weeks without treatment, minimal tubular degeneration remained in one middle-dose and two high-dose monkeys ^[3].
• The blood and urine values matched what the microscope showed. Creatinine, the standard blood marker of kidney function, rose mildly to moderately with dose, without a matching rise in urea. Phosphate and potassium fell. The urine carried sugar, protein and shed kidney cells ^[3].
• Fluid balance shifted. Treated monkeys produced more urine, and mild dehydration was recorded at the highest dose levels, which the authors read as a sign of reduced filtration ^[3].
• Food intake fell. In monkeys this tracked the dose. In mice a taste-aversion test was negative, which argues against simple sickness ^[3], ^[6].
• Nothing appeared in the liver or the lipids. No abnormal fat accumulation was found in any monkey, and lipid profiles stayed normal ^[3].
• Very large single doses were not lethal. In tolerance work covering 52 cynomolgus monkeys, single doses around 133 times the level used for the weight effect did not kill the animals. This rests on one sentence in the primate paper, pointing to a publication that never appeared ^[3].

Two sentences from the same paper have to be read together. The authors sum the main side effect up as relatively mild, predictable and reversible kidney injury with altered tubular function. The detailed results show the injury not fully resolved in three of the recovery animals. Both are accurate; only the second is complete ^[3].

The strongest human signal comes from a relative. BMTP-11 carries the identical killing half with a different address tag. In its first-in-man study in men with metastatic prostate cancer, the limit on how much could be given was set by the kidney: dose-dependent kidney damage, with protein and cast-shaped deposits in the urine and rising creatinine in the blood. The kidney problem is therefore a property of the whole chemical class, and it has been seen in people ^[4].

The human trial treated the kidney as a risk organ from the outset. Entry required creatinine no more than 1.5 times the upper normal limit, or a clearance of at least 60 ml/min.

On top of that came a 24-hour urine collection holding less than two grams of protein. Patients with chronic uncontrolled high blood pressure were excluded, to screen out unrecognised kidney damage. Weekly laboratory checks and ECGs were planned. None of that exists outside a hospital ^[1].

Material traded online under the names Adipotide or FTPP carries the sellers' own labelling. They describe it as a non-sterile freeze-dried powder that would need sterile filtration before any animal experiment, and as not intended for administration to living organisms ^[11].

Why this page lists no doses

This page gives no amounts for Adipotide in any unit, for humans or for animals. The active half is a general cell poison. No amount is known that a human being tolerates, because the study meant to find one closed after four patients ^[1], ^[3].

Where a substance injures the kidneys of every dose group in every species tested, a figure on a reference page would read as an instruction rather than a citation. The sister compound sharing the same poison hit its dose limit at the kidney in humans ^[3], ^[4].

The single human study was also an oncology study in men with advanced prostate cancer and obesity who had no standard treatment left. That is the risk threshold against which any amount was judged, and it has nothing in common with anyone else's situation ^[1].

Development and approval status

Adipotide has never been approved in any market and never reached beyond a terminated phase 1 study. Register checks on 12 September 2026 found nothing anywhere ^[1].

• 2004 the address motif is fished out in living mice by phage display, a screening method in which viruses carry millions of different short peptides, and prohibitin is identified as its binding partner ^[10].
• December 2010 an exclusive worldwide licence for the homing-peptide technology is taken from a Texas cancer centre, and the trial is registered ^[2], ^[1].
• 2011 a subsidiary, Ablaris Therapeutics, is created for the obesity programme and raises 2.9 million US dollars ^[19].
• November 2011 the primate study is published ^[3].
• April and July 2012 a formal comment questions the interpretation, and the first patient is dosed three months later ^[7], ^[17].
• 2013 and 2014 the programme moves to the partner-based pipeline, with the cancer centre funding and running the study alone ^[2], ^[19].
• 2015 and 2016 the name appears only in the patent table, and in no filing after December 2016 ^[18].
• January 2019 the study is terminated at the investigator's request with four patients ^[1].

Five of these entries rest on register queries run alongside a control substance in the same database. A blank result therefore means absence, not a broken query ^[20], ^[21], ^[22], ^[23], ^[24].

The German entry rests on the full text of the narcotics annexes ^[25]. The British entry is weaker: the register could not be queried, so the status is inferred from the worldwide picture ^[26].

One finding deserves separate mention. Adipotide appears in no American list of bulk substances nominated for pharmacy compounding, while BPC-157, ipamorelin, AOD-9604 and kisspeptin all appear in the same document. Nobody ever asked for a lawful way to make it for people ^[8].

The wider legal picture is under are peptides legal and FDA-approved peptides.

Anti-doping

Adipotide is prohibited at all times, in and out of competition. It is not named on the 2026 list. It falls inside class S0, which covers any pharmacological substance with no current approval by a government health authority for human therapeutic use ^[9].

The wording names drugs under pre-clinical or clinical development or discontinued as examples. Discontinued development is exactly this substance's position, so the classification needs no interpretation. Substances in S0 are specified substances, which affects how a sanction is measured but not the ban itself ^[9].

Two mistakes are common. It does not belong in class S2 with peptide hormones and growth factors, because it is neither a hormone nor a mimic of one.

The second is its absence from the annex to the German anti-doping statute. That is a gap in a closed list, not a permission. The annex has no counterpart to the catch-all class, and medicines law applies regardless ^[27], ^[9].

No validated detection method for Adipotide has been published, which is not the same as being undetectable. The full picture is at peptides banned in sport.

Compared with related peptides

The comparison is instructive only as a contrast. The other four change signalling. Adipotide changes anatomy by killing cells, which places it chemically among ligand-directed cell-killing conjugates rather than among weight drugs ^[3], ^[10].

The second contrast is evidential. Each of the other four has at least one completed human study behind it. Adipotide has fifteen monkeys and an empty registry entry ^[1], ^[3].

AOD-9604 is the closest parallel in fate rather than in mechanism. Both are fat-directed programmes that never reached approval and still circulate in online trade. A 2026 review of the grey market for unapproved peptides covers AOD-9604 and eleven other substances, and does not mention Adipotide at all ^[28].

Common misconceptions

• "Adipotide is a fat-burning peptide." It burns nothing. It is a cell poison with an address tag; its relatives are targeted cancer agents, not metabolic drugs ^[3], ^[10].
• "The monkey study proved it melts fat selectively." That reading was formally disputed in the same journal. Treated monkeys ate less, energy expenditure could not be measured, and in mice the fat loss ran entirely through reduced food intake ^[7], ^[3], ^[6].
• "The kidney findings were mild and reversible, so they do not matter." The blood values were the mild part. Under the microscope there was single-cell necrosis, still visible after four weeks in three animals, and the same effector was dose-limiting at the kidney in humans ^[3], ^[4].
• "There are human data, the phase 1 study was completed." It was terminated, not completed, with 4 of up to 39 planned patients, no posted results and no publication ^[1], ^[2].
• "It was tested in people with obesity." It was tested in men with metastatic prostate cancer who also had obesity and no standard treatment left. Weight was a secondary measure in an oncology study ^[1].
• "It only hits fat tissue." The one independent quantitative study found no enrichment in fat and more uptake in the kidney, and prohibitin is expressed on many cell types ^[5].
• "It stopped for money reasons, not safety ones." No reason was ever published. What exists is a chronology and a kidney signal reproduced in every model ^[2], ^[18], ^[4].
• "FTPP and Adipotide are different substances." One substance, four names. Searching the trial registry for Adipotide returns nothing; the only human study is filed under the prohibitin name ^[1], ^[11].

Frequently asked questions

What is Adipotide?

It is a two-part synthetic molecule, not a hormone and not a metabolic drug. One half is an address tag that binds prohibitin, a protein found on the blood vessels that supply white fat. The other half destroys mitochondria and kills the cell it enters. The idea was to starve fat tissue rather than to change its metabolism.

Has Adipotide ever been tested in people?

Once, and the trial did not finish. A first-in-man study at a cancer centre opened in 2012 and closed in January 2019 with the status terminated, at the principal investigator's request. Four patients were enrolled out of up to 39 planned. No results were posted to the registry and none were published.

Is Adipotide approved anywhere?

No, and it never has been. Register checks on 12 September 2026 found no entry in the United States, the European Union, Germany, the United Kingdom, Australia, Canada or Switzerland. It is also missing from the American list of bulk substances nominated for pharmacy compounding. Nobody has ever applied for a lawful route to make it for people.

What did the monkey study of Adipotide actually show?

In 15 obese rhesus monkeys, ten treated and five controls, the treated animals lost on average 10.6 per cent of body weight over 28 days. Scans showed large falls in body fat. The same study found dose-dependent kidney lesions under the microscope. Lean monkeys showed the kidney changes without losing any weight.

Why is Adipotide considered dangerous?

Because its active half is a general cell poison. Its safety depends entirely on the address tag, and the one independent study of that tag did not confirm the targeting. Kidney injury appeared in every dose group of every animal study. In a sister compound carrying the same poison, it was the dose-limiting toxicity in humans.

Was the kidney damage from Adipotide reversible?

Partly. The paper's abstract calls the injury predictable and reversible, and most measurements did settle during a four-week recovery period. The detailed results are less tidy: minimal tubular degeneration was still present after those four weeks in one middle-dose and two high-dose monkeys. Both statements come from the same publication.

Is Adipotide the same as FTPP or Prohibitin-TP01?

Yes, all three names describe one substance. Adipotide was the development name, Prohibitin-TP01 the name in the clinical trial registry, and FTPP the abbreviation used in online trade. This matters in practice: searching the trial registry for Adipotide returns nothing, and the only human study appears only under the prohibitin name.

Is Adipotide banned in sport?

Yes, at all times. It is not named on the 2026 prohibited list. The catch-all class S0 covers any pharmacological substance with no current approval from a government health authority, explicitly including discontinued development compounds. That description fits exactly. It is absent from the German anti-doping statute's annex, which is not a permission of any kind.

Why did development of Adipotide stop?

No reason has ever been published, and it would be guesswork to name one. Only the sequence is documented. The licence holder wrote in 2013 that it was spending no internal resources on the programme, the name vanished from its filings after 2016, and the trial closed in 2019. Alongside that sits kidney toxicity reproduced in every animal model.

Cite this page

The facts on this page were checked on 12 September 2026, and every register behind the status table was queried on that day. Two things could still move: an unpublished toxicology paper could surface, and the British register entry rests on inference rather than a match.

myPeptides Research & Editing. (2026). Adipotide: what the studies show, status and safety. Version 1.0, 12 September 2026. myPeptides Peptide Register. Retrieved from https://mypep.app/peptides/adipotide

How pages in this register are compiled and graded is described under methodology; the full register is at peptides.

Last verified: 12 September 2026. Next review: on any publication of the announced toxicology data, on any new registered trial, or on any change to the anti-doping classification.