Adipotide (FTPP)

What it is

Adipotide, also called FTPP or prohibitin-TP01, is a peptide built on the principle of address plus active agent. The address is a short motif that was found in 2004 with a screening method in living animals and accumulates in white fat tissue. There it binds to prohibitin, a protein the researchers described as a vascular marker of fat tissue. Prohibitin is also present in the blood vessels of human white fat.

The second part is a peptide that, after uptake into the cell, destroys its mitochondrial membrane and thus triggers programmed cell death. The same cell-killing motif is used in cancer research, there with other addresses. The idea behind it: fat tissue needs blood vessels. Take away its supply and it shrinks.

How it is supposed to work

The simple story goes like this: adipotide cuts off the blood supply to belly fat, the fat shrinks, and because only the fat vessels carry the address, the rest of the body is spared. In the images from the primate study, the fat loss is indeed visible, measured by magnetic resonance and weekly body fat measurement.

The animal data themselves tell a more complicated story. The monkeys ate less during treatment. Lean monkeys lost no weight under the same dose. In rodents, the peptide worked only in animals on a high-fat diet, not in lean ones, and did so without any change in energy expenditure but with lower food intake. The metabolic rate could not be measured in the primate study. The same journal published a commentary attributing the weight loss to the reduced food intake. A second rodent experiment also showed that glucose tolerance improved independently of weight and food quantity. That the blood vessels of fat tissue play a role in glucose metabolism is thus supported. That the weight loss comes from vascular destruction alone is not.

What happened to the development

After the 2011 primate study, adipotide was hailed in the press as a breakthrough. A phase 1 trial started in 2012 at MD Anderson Cancer Center in men with advanced prostate cancer and obesity. The aim was to find the highest tolerable dose. The trial was terminated at the request of the principal investigator and officially closed in 2019, with 4 enrolled participants and no results posted. No publication on it exists.

This is part of the context: the primate study comes from a group whose university and lead authors have financial interests in the substance, including patents and consulting fees. The paper discloses this. There is no independent replication in monkeys. The principle is still being developed today, but in mouse models: a variant with a modified building block, published in 2025, acts by uncoupling the mitochondria.

What the studies show

Kolonin et al., Nature Medicine 2004

The foundational paper. Using a screening method in living animals, the motif CKGGRAKDC was found, which accumulates in white fat tissue and binds to prohibitin. Coupled to a cell-killing peptide, it reduced white fat in a mouse model and normalized metabolism. The endpoint was fat loss in the animal.

Barnhart et al., Science Translational Medicine 2011

The only primate paper and the basis of all advertising claims. Three Old World monkey species: dose finding in 4 obese rhesus monkeys over 9 weeks, main experiment in 15 obese rhesus monkeys over 4 weeks of treatment plus 4 weeks of recovery, safety testing in 15 lean rhesus monkeys over 28 days, further data from 52 cynomolgus monkeys, pilot experiment in 2 baboons. Endpoints were weight, body fat and safety. Both findings occurred: the fat loss and the effect on the kidneys.

Kim et al., Diabetes 2010 and 2012

Two independent rodent papers on the mechanism. The fat loss occurred without a change in energy expenditure but with lower food intake, and only in animals on a high-fat diet. Glucose tolerance, by contrast, improved quickly and independently of weight and food quantity, tested against pair-fed control animals.

Phase 1 trial NCT01262664

The only registered trial in humans, started on May 24, 2012, at MD Anderson Cancer Center in men with advanced prostate cancer and obesity. Up to 5 dose levels with 3 participants each were planned. The trial was terminated at the request of the principal investigator and closed in early 2019, with 4 enrolled participants and no results posted.

Where the data stop

For adipotide there is not a single peer-reviewed study in humans. Anyone claiming efficacy, tolerability or durability in humans is extrapolating monkey data. The longest treatment duration in these data is 9 weeks in 2 animals, and 4 weeks in the controlled experiment. For anything beyond that, there is nothing.

The mechanism is also more open than the advertising suggests. Weight loss in the animals was tied to overweight and went hand in hand with lower food intake. Whether vascular destruction itself is the reason has not been clarified. And prohibitin is not a molecule that occurs only in fat tissue. It is found in mitochondria, on cell membranes and in the cytoplasm of many cell types. What a cell-killing peptide does there has not been studied in humans. The one molecule with the same cell-killing building block that made it into a human study, a cancer drug with a different target address, had exactly the side effect already noticed in the monkeys: dose-dependent kidney toxicity as the dose-limiting finding, in 6 treated patients. In addition, the primate study comes from a group with patents and company shares and has never been independently replicated.

Status, approval and legal

Adipotide is not approved as a medicine anywhere in the world and is not legally marketable in Germany. Its development stage is preclinical. The only registered human study was terminated and closed in 2019. Offers on the internet are not tested, and the label “for research purposes only” does not change the legal situation. We therefore give no dosage information. For sport the situation is clear: class S0 of the 2026 Prohibited List bans at all times pharmacologically active substances that are not approved by any governmental health authority for human use, explicitly including substances in development and those whose development has been discontinued. According to this wording, adipotide falls under it.

Safety

The best-supported finding on safety is the effect on the kidneys. In the primate study, a dose-dependent disorder of the renal tubules occurred, with a rise in blood creatinine, sugar and protein in the urine, more renal epithelial cells in the urine, lower phosphate and potassium, and mild dehydration at the highest dose. Most changes reversed within 28 days after discontinuation; in the tissue examination, only minimal traces remained after recovery. A single animal per study still had elevated creatinine at the end. Single doses up to about 133 times the respective therapeutic dose were not lethal in monkeys. There are no data on side effects in humans, because the only human study was terminated without results. Outside a clinical trial, adipotide is not suitable for anyone. Anyone who has kidney disease, takes medicines that strain the kidneys, is pregnant or is breastfeeding is directly affected by the substance’s best-documented risk.

Sources

• Barnhart et al., Sci Transl Med 2011 (primate study)
• Kolonin et al., Nat Med 2004 (foundational paper)
• Kim et al., Diabetes 2010 (food intake and energy expenditure)
• Kim et al., Diabetes 2012 (glucose tolerance)
• Criscione, Sci Transl Med 2012 (commentary on the primate study)
• Pasqualini et al., Cancer 2015 (related molecule in humans)
• Chan et al., J Am Chem Soc 2025 (further development in a mouse model)
• ClinicalTrials.gov, NCT01262664 (terminated phase 1 trial)
• WADA Prohibited List 2026, BGBl. III Nr. 219/2025