Adipotide is an experimental 25-amino-acid peptide designed to kill the blood vessels that feed white fat. It was developed at the University of Texas M.D. Anderson Cancer Center as a possible obesity drug. In obese mice, rats and monkeys it caused rapid fat loss, but it also damaged the kidney tubules in monkeys.

The single most important fact: adipotide has never been shown to work or to be safe in people. Its only human trial, a small phase 1 dose-finding study in men with prostate cancer and obesity, enrolled 4 participants and was terminated without posted results. It is not approved anywhere. The name “FTPP” is a seller’s label; it does not appear in the peer-reviewed studies cited here, which call the compound adipotide or prohibitin-TP01.

This page summarizes what the animal studies, the trial registry and regulators report. It is for education only and is not medical advice.

Property	Detail
Class	Ligand-directed proapoptotic peptidomimetic (a “targeted cell-killing” peptide)
Sequence	CKGGRAKDC-GG-D(KLAKLAK)₂
Other names	Prohibitin-TP01, prohibitin targeting peptide 1
Target	Prohibitin on the blood vessels of white fat
Route studied	Subcutaneous injection, once daily
Doses studied	0.10–0.75 mg/kg/day in monkeys; 0.03 mg/kg/day starting dose in the human phase 1 trial
Half-life	No published pharmacokinetic data in animals or humans
Human evidence	One phase 1 trial (n = 4), terminated, no results posted
Main risk in animals	Dose-dependent kidney (proximal tubule) injury
US status	Not FDA-approved; not named in the DEA’s Schedule III list
WADA status	Prohibited at all times under S0 (non-approved substances)

What it is

Adipotide joins two pieces into one peptide (Barnhart et al., Sci Transl Med 2011):

Part	Sequence	What it does
Homing motif	CKGGRAKDC (cyclic)	Binds prohibitin on the inner lining (endothelium) of blood vessels in white fat
Linker	GG	Two glycines joining the two halves
Killing domain	D(KLAKLAK)₂	Made of D-amino acids (mirror-image forms that resist breakdown). Once taken into a cell, it disrupts mitochondrial membranes and triggers apoptosis (programmed cell death).

The killing domain came first. In 1999, researchers showed that short peptides pairing a tumor-vessel homing motif with D(KLAKLAK)₂ were selectively toxic to new blood-vessel cells and had anti-cancer activity in mice (Ellerby et al., Nat Med 1999).

The fat-homing motif was found in 2004. The team screened random peptides displayed on viruses (phage display) in living mice and recovered CKGGRAKDC, which homed to white fat vessels and bound prohibitin, a membrane protein (Kolonin et al., Nat Med 2004). A later screen in cancer patients found a prohibitin/annexin A2 receptor complex on the vessels of human white fat (Staquicini et al., PNAS 2011).

PubChem lists adipotide (CID 163360068) with the formula C₁₁₁H₂₀₆N₃₆O₂₈S₂ and a molecular weight of 2557.2 g/mol (PubChem).

The idea is different from appetite drugs. Instead of acting on the brain or gut, adipotide cuts off the blood supply of fat tissue, and the fat is then reabsorbed. It is unrelated to the growth-hormone fragments sold for fat loss, such as AOD-9604 and HGH Fragment 176-191.

How it works in the body

No study has published adipotide’s absorption, blood levels or half-life in any species. The monkey and human protocols both used daily injections (Barnhart et al., 2011; NCT01262664). The registered human trial planned blood sampling for pharmacokinetics, but no data were posted.

The monkey study authors noted that the kidney enzyme D-amino acid oxidase is the only known mammalian enzyme that can process the D(KLAKLAK)₂ portion. They suggested this may be the rate-limiting step in clearing adipotide through the kidney, which could help explain where its toxicity lands.

How the fat loss happens is not fully settled:

Vessel-targeted cell death. Monkeys showed apoptosis within blood vessels of white fat.
Less eating. Obese mice, rats and monkeys ate less on adipotide. In rodents this happened without a change in energy expenditure and despite lower leptin, a hormone that normally signals fullness (Kim et al., Diabetes 2010).
Obesity-specific effect. The peptide reduced body weight in mice and rats on a high-fat diet but not in those on a low-fat diet. Lean monkeys on 0.25 or 0.43 mg/kg/day did not lose weight.

Regulatory status

Not approved. Adipotide has no FDA or EMA approval for any use.
Development stalled. A 2025 review lists it as developed by Arrowhead Pharmaceuticals (through its subsidiary Ablaris Therapeutics) and its phase 1 program as discontinued in January 2019, with further development “limited for unknown reasons” (Liu et al., Cardiovasc Diabetol 2025).
Not a scheduled drug. It is not among the anabolic steroids named in 21 CFR 1308.13.
Banned in sport. WADA’s S0 class prohibits at all times any substance with no current government approval for human therapeutic use, including drugs under pre-clinical or clinical development or discontinued (WADA 2026 Prohibited List).

What the research shows

Rodents

In obese mice, the targeted peptide caused white fat to be reabsorbed and normalized metabolism, with rapid reversal of obesity and no detectable adverse effects reported (Kolonin et al., 2004). The monkey paper later summarized this as about 30% weight reduction in obese mice over 4 weeks.

A University of Cincinnati group gave 3 mg/kg/day subcutaneously to obese mice for 27 days and 1.5 mg/kg/day to obese rats for 4 days (Kim et al., 2010). Key findings:

the peptide completely reversed high-fat-diet obesity in mice;
weight loss came from reduced food intake, with no change in energy expenditure;
in a conditioned taste aversion test (a standard check for nausea-like illness), neither adipotide nor the control peptide changed flavor preference.

The same group found that glucose tolerance improved within 2–3 days in obese mice. The improvement was larger than in mice pair-fed to eat the same amount, so it was not explained by weight or food intake alone (Kim et al., Diabetes 2012).

Obese monkeys

The key study tested adipotide in obese Old World monkeys (Barnhart et al., 2011).

In a dose-finding pilot, 2 obese female rhesus macaques received rising daily doses (0.10, 0.25, 0.43, then 0.75 mg/kg) for 9 weeks while 2 received saline. The treated animals lost 15.4% and 20.4% of body weight; the controls did not change. From this, the authors chose 0.43 mg/kg/day as the “optimal” dose.

In the fixed-dose study, 15 obese rhesus macaques were randomized to adipotide 0.43 mg/kg/day (n = 10) or saline (n = 5) for 28 days, followed by 4 weeks off treatment:

Outcome	Adipotide	Saline
Body weight change, end of treatment	−7.4% to −14.7%	+1.0% to −3.5%
BMI change, end of treatment	−3.7% to −17.3%	−3.5% to +3.3%
Abdominal circumference, end of treatment	−6.5% to −14.3% in 9 of 10; +2% in 1	−6.3% to +6.9%
Total body fat by DEXA, end of study	−38.7% (mean)	−14.8% (mean)
Abdominal white fat by MRI	−17.5% end of treatment; −27.0% end of recovery	Not reported as a percentage
Insulin area under the curve during glucose testing	−36.2% vs control (p = 0.019)	Reference
Insulinogenic index (a marker of insulin resistance)	−48.5%	+33.8%

Weight, BMI and waist kept falling for 3 weeks after dosing stopped. Blood lipids stayed normal and free fatty acids trended down.

Treated monkeys ate fewer standard chow biscuits but still ate their enrichment foods. A published comment argued the weight loss may reflect a direct effect on food intake rather than fat-vessel destruction (Criscione, Sci Transl Med 2012).

Limits of the monkey data

The groups were small (10 treated animals in the main efficacy study).
Treatment lasted only 4 weeks in the controlled study.
Weight results are reported as ranges, not with confidence intervals.
Several authors held equity in or consulted for the developer companies (disclosed in Staquicini et al., 2011), and one author was affiliated with Ablaris Therapeutics.

Humans

The only human study was a first-in-human phase 1 trial at M.D. Anderson (NCT01262664):

Item	Detail
Population	Men with advanced (castrate-resistant) metastatic prostate cancer and obesity
Design	Open-label, single-group dose escalation; up to 5 dose levels, 3 participants per level
Dosing	Starting dose 0.03 mg/kg subcutaneously once daily for 28 days
Planned activity measure	Loss of 10% of baseline body weight at day 28
Enrollment	4 participants (actual)
Dates	Started May 2012; completed January 2019
Outcome	Terminated “per PI’s request”; no results posted

We found no peer-reviewed publication of results from this trial. There is no controlled human evidence on weight loss, fat loss, metabolic effects or safety.

Later work on the same target

Researchers have since tried to improve on adipotide in mice. A prohibitin-targeted nanoparticle carrying the D(KLAKLAK)₂ peptide reduced body weight at a low dose where the plain adipotide conjugate did not (Hossen et al., J Control Release 2013). A 2025 study replaced the killing domain with D-arginine versions to improve stability (Chan et al., J Am Chem Soc 2025). Both are mouse studies only.

Side effects and risks

All safety data come from animals. Human safety is unknown.

Kidney injury

Kidney toxicity was the main side effect in monkeys (Barnhart et al., 2011). The changes point to injury of the proximal tubule, the part of the kidney that reabsorbs glucose, phosphate and potassium:

slight-to-moderate, dose-dependent rises in serum creatinine at doses above 0.25 mg/kg;
mild-to-marked glucose in the urine and mild-to-moderate protein in the urine;
falls in blood phosphorus and potassium;
increased urine output, with mild dehydration at the highest doses.

In a 28-day formal (GLP) toxicology study in lean rhesus monkeys at 0.25, 0.43 and 0.75 mg/kg/day, animals examined 24 hours after the last dose had dose-dependent kidney lesions, including single-cell tubular necrosis (cell death). These were minimal to mild at the low dose and up to moderate at the high dose.

Most blood and urine changes reversed within 28 days of stopping. Some did not fully resolve: a slight creatinine and urine-glucose elevation persisted in one treated monkey in each efficacy study, creatinine stayed slightly raised in the high-dose toxicology group, and minimal tubular degeneration remained in some animals after recovery. The authors described the injury as “mild, predictable, and reversible,” but these were short studies in a small number of animals.

Other findings

In cynomolgus monkeys, single doses up to 100 mg/kg did not cause death; the detailed toxicology was said to be published elsewhere.
Monkeys showed no overt nausea, vomiting or food aversion.
No liver fat buildup was seen in the treated monkeys.

Unknowns that matter

Off-target vessel damage. The killing domain destroys any cell that takes it up. The homing motif concentrates it in fat vessels, but prohibitin is also found elsewhere in the body.
Long-term effects. No study has followed animals or people for months or years.
Product identity. Products sold as “adipotide” or “FTPP” outside research are not regulated for identity, purity, dose or sterility.

Key takeaways

A targeted cell-killing peptide. Adipotide links a fat-vessel homing motif to a mitochondria-disrupting D-peptide, aiming to starve white fat of its blood supply.
Striking results, but only in animals. Obese monkeys lost 7.4–14.7% of body weight in 4 weeks, with less body fat and better insulin response.
Kidney injury is the main known risk. Monkeys developed dose-dependent proximal tubule damage, and not every change fully reversed.
No human evidence. The only human trial enrolled 4 men, was terminated and posted no results.
Not approved and banned in sport. It has no FDA or EMA approval, and WADA prohibits it at all times under S0.
No known half-life. No pharmacokinetic data have been published in any species.

Sources

Barnhart KF, Christianson DR, Hanley PW, et al. A peptidomimetic targeting white fat causes weight loss and improved insulin resistance in obese monkeys. Sci Transl Med. 2011;3(108):108ra112. PubMed; PMC.
Kolonin MG, Saha PK, Chan L, et al. Reversal of obesity by targeted ablation of adipose tissue. Nat Med. 2004;10(6):625–632. PubMed.
Ellerby HM, Arap W, Ellerby LM, et al. Anti-cancer activity of targeted pro-apoptotic peptides. Nat Med. 1999;5(9):1032–1038. PubMed.
Staquicini FI, Cardó-Vila M, Kolonin MG, et al. Vascular ligand-receptor mapping by direct combinatorial selection in cancer patients. Proc Natl Acad Sci U S A. 2011;108(46):18637–18642. PubMed.
Kim DH, Woods SC, Seeley RJ. Peptide designed to elicit apoptosis in adipose tissue endothelium reduces food intake and body weight. Diabetes. 2010;59(4):907–915. PubMed.
Kim DH, Sartor MA, Bain JR, et al. Rapid and weight-independent improvement of glucose tolerance induced by a peptide designed to elicit apoptosis in adipose tissue endothelium. Diabetes. 2012;61(9):2299–2310. PubMed.
Criscione L. Comment on “a peptidomimetic targeting white fat causes weight loss and improved insulin resistance in obese monkeys”. Sci Transl Med. 2012;4(131):131le2. PubMed.
M.D. Anderson Cancer Center. A first-in-man, phase I evaluation of a single cycle of prohibitin targeting peptide 1 in patients with metastatic prostate cancer and obesity. ClinicalTrials.gov identifier NCT01262664. ClinicalTrials.gov.
Liu D, Chen W, Guo Z, et al. Advances and challenges of targeting epicardial adipose tissue (EAT) and perivascular adipose tissue (PVAT). Cardiovasc Diabetol. 2025;24(1):319. PubMed.
Hossen N, Kajimoto K, Akita H, et al. A comparative study between nanoparticle-targeted therapeutics and bioconjugates as obesity medication. J Control Release. 2013;171(2):104–112. PubMed.
Chan LY, Weger BD, Weger M, et al. Mixed-chirality prohibitin peptide: D-(RLARLAR)2 enhances stability and in vivo effects on obesity. J Am Chem Soc. 2025;147(28):24628–24642. PubMed.
National Center for Biotechnology Information. Adipotide, PubChem CID 163360068. PubChem.
World Anti-Doping Agency. The 2026 Prohibited List. WADA 2026 Prohibited List.
Code of Federal Regulations. 21 CFR 1308.13, Schedule III. 21 CFR 1308.13.

ADIPOTIDE (FTPP)