Adipotide (FTPP): what it is, what the animal studies found and why there are no human results

Adipotide is a designed molecule with two parts. The first is a nine-amino-acid peptide, CKGGRAKDC, that homes to the blood vessels of white fat. The second is a pro-apoptotic sequence, (KLAKLAK)2, made from D-amino acids, which disrupts mitochondrial membranes and kills the cell it enters. Joined by a two-glycine linker, the whole construct is written CKGGRAKDC-GG-D(KLAKLAK)2 ^[3]. Because half of it is built from D-amino acids rather than the natural L-forms, it is described as a peptidomimetic rather than a peptide, and the D-amino acids make it resistant to the enzymes that would normally break a peptide down.

The concept came from Wadih Arap and Renata Pasqualini’s laboratory at the MD Anderson Cancer Center in Texas, which uses in vivo phage display to find peptides that home to particular blood vessels. In 2004 the group reported that CKGGRAKDC binds prohibitin, a membrane protein they established as a marker of the blood vessels of adipose tissue, and that coupling it to the killer sequence caused white fat to be resorbed in obese mice ^[1]. The 2011 monkey paper gave the construct the name adipotide ^[3]. Online it is also sold as FTPP, for fat-targeted proapoptotic peptide, and the clinical trial called it Prohibitin-TP01 ^[8].

Adipotide therefore has nothing in common with the incretin and amylin peptides on this site, such as semaglutide, tirzepatide or cagrilintide, which reduce appetite through hormone receptors. Adipotide is a targeted cytotoxic agent: it is designed to destroy tissue. That is why its development path ran through a cancer centre and a cancer trial, and why the adipotide peptide sold by research suppliers is a different kind of product from anything else in the weight-loss category. See what research peptides are.

Fat tissue, like a tumour, depends on its blood supply. The 2004 study showed that prohibitin is displayed on the surface of endothelial cells lining the blood vessels of white fat, and that the CKGGRAKDC peptide binds it. Once the construct is bound and internalised, the (KLAKLAK)2 sequence triggers apoptosis in the endothelial cell. Loss of the vessels starves the fat tissue, which is resorbed. In mice, the authors reported resorption of established white fat, normalisation of metabolism and rapid reversal of obesity, which they described as being without detectable adverse effects ^[1]. A 2011 study of blood-vessel receptors in cancer patients later confirmed that a prohibitin and annexin A2 pairing is specific to white adipose tissue vasculature in humans, which is the basis for expecting the target to exist in people ^[2].

There is a competing explanation for the weight loss. A 2012 comment on the monkey study argued that the results might instead reflect a direct effect of adipotide on food consumption, since the treated monkeys ate less ^[4]. Reduced food intake could be a consequence of feeling unwell rather than of fat ablation, and the monkey paper itself reported that the treated animals developed kidney tubule dysfunction ^[3]. Whether the weight loss comes from killing fat vessels, from eating less, or from both, has not been settled in the published record.

A separate 2012 mouse study addressed a different question: whether destroying fat vasculature would impair glucose regulation by damaging fat tissue function. It found the opposite. The peptide rapidly improved glucose tolerance in obese mice on a high-fat diet, within two to three days, independently of weight loss and of food intake (a pair-fed control group ate the same amount without the peptide). Serum insulin and triglycerides fell, and gene-expression pathways in fat tissue that had been disrupted by the high-fat diet were reversed ^[5]. The authors proposed a role for adipose blood vessels in glucose homeostasis.

The evidence for adipotide weight loss comes from two animal studies, one in mice and one in monkeys; the adipotide monkeys study, in obese rhesus macaques, is the one that gave the compound its name. In the 2004 Nature Medicine paper, obese mice treated with the prohibitin-targeted pro-apoptotic peptide lost established white fat and their obesity reversed rapidly ^[1]. The paper does not report human data, and the phrase in its abstract about leading to targeted drugs for obese patients was a hope, not a result.

The 2011 Science Translational Medicine paper moved to primates, on the argument that differences between rodents and primates are a major reason rodent obesity treatments fail in people. Adipotide was given to spontaneously obese rhesus monkeys, and the paper reports targeted apoptosis in white fat blood vessels, rapid weight loss, improved insulin resistance, and a marked reduction in white adipose tissue confirmed by MRI and DXA scanning. It also reports that at the experimentally determined optimal doses, monkeys from three species showed predictable and reversible changes in renal proximal tubule function ^[3]. The kidney finding is the central safety fact about adipotide: the dose that worked also damaged the kidney, even if the damage reversed after treatment stopped.

Since then, the published work on this approach has been in mice. Researchers in Japan used the same fat-homing peptide motif to target drug-loaded nanoparticles to fat blood vessels in obese mice, as an alternative to a cytotoxic payload ^[7]. In 2025, an Australian group reported a new generation of prohibitin-targeting peptides, including one built from D-amino acids and substituted with D-arginine, that reduced body weight in diet-induced obese mice by inducing mitochondrial uncoupling and were described as having favourable preclinical safety profiles ^[6]. These are laboratory results in mice and are a different molecule from adipotide.

Adipotide has been given to people once, and not for obesity. A phase 1 trial at MD Anderson, registered as NCT01262664 and titled a first-in-man evaluation of a single cycle of Prohibitin Targeting Peptide 1 in patients with metastatic prostate cancer and obesity, aimed to find the highest tolerable dose in men with advanced prostate cancer who had no standard treatment options. The registry lists it as terminated at the principal investigator’s request, with four participants enrolled between a 2012 start and a 2019 primary completion date ^[8]. We found no published results from it.

The rationale for a cancer trial was the overlap between fat vasculature and tumour biology: prostate cancer is linked to obesity, and the same laboratory maps vascular receptors in cancer patients ^[2]. Whatever the reasoning, the outcome is that no human being has received adipotide in a trial designed to measure weight loss, and the only human exposure on record involved four cancer patients in a trial that was stopped. There is no adipotide dosage for humans, no human safety profile, and no human efficacy data.

This distinguishes adipotide from every other compound in the weight-loss category on this site. Investigational peptides such as retatrutide or survodutide have thousands of trial participants; the licensed drugs have outcome trials. Adipotide has mice, monkeys and a terminated four-person cancer study.

In mice, the 2012 glucose study saw improved glucose tolerance within two to three days of treatment ^[5], and the 2004 paper described obesity reversal as rapid ^[1]. The monkey study also described rapid weight loss ^[3]. These are animal timelines from short treatment courses; adipotide has no human timeline because it has no human weight-loss data. Claims on vendor sites about how long adipotide takes to work in people have no source.

The published abstracts of the mouse and monkey studies do not state doses in a form we can quote ^{[1] [3] [5]}; the monkey paper refers only to experimentally determined optimal doses at which kidney tubule changes occurred ^[3]. The human phase 1 trial was a dose-finding study whose purpose was to establish a tolerable dose, and it ended before doing so ^[8]. There is therefore no published adipotide dosage for humans, from any source.

Any adipotide dosage chart or protocol online is invented. This is not the usual caveat that trial doses are not recommendations; in this case there are no human trial doses to report. The animal data show that the effective dose in monkeys caused kidney damage ^[3], which is the opposite of a margin of safety. Our peptide calculator can do reconstitution arithmetic for any vial, but arithmetic on an unknown quantity of a cytotoxic peptide is not a dose.

The animal studies gave the construct by injection ^{[1] [3]}. Because the killer sequence is made from D-amino acids, the molecule resists digestion by proteases, which is part of the design, but no oral form has been studied. Research suppliers sell adipotide as a freeze-dried powder for reconstitution. Nothing about that product has been tested in any published study.

The adipotide side effects documented in the literature are from monkeys, and the main one is kidney injury. The 2011 paper reports predictable and reversible changes in renal proximal tubule function at the doses that produced weight loss, in monkeys from three different species ^[3]. The proximal tubule is the part of the kidney that reabsorbs filtered nutrients, and damage to it is a recognised form of drug toxicity. That this reversed in monkeys under laboratory care says nothing about what happens with repeated or uncontrolled dosing in people.

The 2012 comment raised a second concern: that the monkeys’ weight loss may have reflected reduced food consumption ^[4], which would be consistent with the animals feeling unwell. The 2004 mouse paper reported no detectable adverse effects ^[1], but mice and primates differed enough that the monkey study was needed in the first place ^[3]. The human trial, which was the only source of human safety information, was terminated with four participants and has no published results ^[8].

The nature of the molecule adds a category of risk that hormone-based peptides do not carry. Adipotide is designed to kill cells. Its selectivity depends on prohibitin being displayed only on fat vessels, and prohibitin is a widely expressed protein whose surface exposure on other vessels cannot be excluded in people. A product bought online adds the usual unknowns of content and purity on top. There is no human safety profile, no label and no regulator that has assessed it. The FDA’s statements on unapproved weight-loss peptides do not name adipotide, and there is nothing to add to them: it has never reached the stage where a regulator would have an opinion.

Adipotide vs semaglutide, or adipotide vs tirzepatide, is not a comparison of two treatments. Semaglutide and tirzepatide are licensed medicines with large trials; retatrutide, survodutide, mazdutide and eloralintide are investigational drugs with published human trials; cagrilintide has phase 3 results in combination. Adipotide has no human weight-loss trial. Its mechanism, destroying the blood supply of fat, is also different in kind from appetite suppression, and its animal toxicity is kidney damage rather than nausea.

Where the fat-vessel concept has continued, it has moved on from adipotide itself: to nanoparticle delivery ^[7] and to new prohibitin-targeting peptides ^[6], both still in mice. If any of that reaches human trials it will be under a different name. For an overview of the compounds that have been tested in people, see peptides for weight loss.

Adipotide is not approved as a medicine anywhere, has no marketing application on record that we could find, and has no active clinical development for obesity that we could identify as of September 2026. Its one registered human trial was terminated ^[8]. It is an experimental compound in the strict sense: something that exists in laboratories and in the vials of research suppliers, and nowhere else.

A research vial of adipotide is unlicensed material in every country. In the UK, see the UK legal status page; in the US, the US legal status page. The position in Europe, Canada and Australia is covered on those pages, and our legal status overview explains how each country treats peptides that are not medicines. Because adipotide is not derived from a human hormone and is cytotoxic by design, the usual argument that a research peptide is merely a copy of a licensed drug does not apply to it at all.

No storage data for adipotide have been published. Its D-amino-acid segment makes it more resistant to enzymatic degradation than a natural peptide, but that does not exempt it from the chemical instability of any peptide in solution. Research material is sold as a freeze-dried powder; general practice is to keep it cold, dry and away from light and to refrigerate it once reconstituted. See how to store peptides and the bacteriostatic water guide. Given what the molecule is designed to do, handling precautions appropriate to a cytotoxic compound would be the sensible default for anyone working with it in a laboratory.

PepFinder does not sell adipotide. If you are comparing research suppliers, see compare adipotide prices, read how to read a COA, and check our list of third-party tested suppliers. A certificate should report a measured mass consistent with the molecular weight of about 2557 g/mol; because the killer sequence is made of D-amino acids, a supplier that has synthesised the L-form by mistake would produce a molecule of the same mass that does not work as designed, so mass alone cannot confirm the product.

We track listings in the UK, the US, Canada, Australia and Europe. No published study has tested the content of adipotide sold online. Our guides to third-party peptide testing, spotting a fake supplier and peptide prices explained cover what to check, with the caveat that for adipotide the more important question is not whether the vial is genuine but that no genuine version has ever been shown to be tolerable in people.