Adipotide

Adipotide, also called FTPP (fat-tissue-targeted proapoptotic peptide) or Prohibitin-TP01, is a synthetic peptide designed to shrink white fat by cutting off its blood supply rather than by acting on appetite or metabolism directly. It homes to a protein called prohibitin on the blood vessels feeding white adipose tissue and carries a cell-death-triggering sequence that causes those vessels, and the fat they feed, to break down. It produced striking, rapid weight loss in obese mice and rhesus monkeys, but it has only ever been tested in a small, terminated human Phase I trial in prostate cancer patients, not as a general obesity treatment, and it is not an approved drug.

Research snapshot

Category	Current information
Peptide category	Ligand-directed proapoptotic peptide (fat-vasculature-targeting)
Primary research interest	Targeted destruction of adipose-tissue blood vessels for rapid weight loss
Highest available evidence	Published animal research (mouse, rhesus monkey); one small terminated human Phase I trial with no published results
Human research available	Minimal — a single Phase I cancer-focused trial (NCT01262664, MD Anderson) terminated at 4 of a planned 39 participants, no published results
Development status	Investigational; broader obesity-focused development appears inactive with no confirmed reason identified
Regulatory status	Not approved anywhere
Last reviewed	September 27, 2026

Technical identity

Technical property	Information
Primary name	Adipotide
Alternative names	FTPP (fat-tissue-targeted proapoptotic peptide), Prohibitin-TP01, Prohibitin-targeting peptide 1, TP01
Peptide sequence	CKGGRAKDC-GG-D(KLAKLAK)2 — a fat-vasculature-homing nonapeptide (CKGGRAKDC) joined by a glycine-glycine linker to the synthetic proapoptotic peptide D(KLAKLAK)2
Amino-acid length	Homing nonapeptide (9 residues) plus GG linker and the D(KLAKLAK)2 proapoptotic domain
Molecular formula	C111H206N36O28S2 (per PubChem)
Molecular weight	Not independently re-derived from an authoritative source for this entry; regard any specific mass figure seen elsewhere online as unverified until confirmed against PubChem directly
CAS Registry Number	859216-15-2
PubChem CID	163360068
Chemical modifications	Bifunctional ligand-peptide construct: a targeting homing sequence joined by a GG linker to a proapoptotic effector sequence
Peptide class	Ligand-directed proapoptotic (vasculature-targeting) peptide
Primary biological target	Prohibitin, on the surface of adipose-tissue vascular endothelium
Developer or originator	Discovered by Kolonin, Pasqualini, Arap and colleagues (MD Anderson Cancer Center)
Development status	Investigational; one terminated Phase I human trial, no published results

What it is

Adipotide is a synthetic 9-plus-9 amino acid conjugate peptide, not a naturally occurring hormone. It combines a fat-vasculature “homing” sequence, CKGGRAKDC, with a well-known proapoptotic (cell-death-inducing) sequence, D(KLAKLAK)2, joined by a short glycine-glycine linker. It was developed by researchers at the University of Texas MD Anderson Cancer Center, led by Mikhail Kolonin together with Renata Pasqualini and Wadih Arap, who used a technique called in vivo phage display to search a mouse’s own bloodstream for peptides that would selectively attach to blood vessels in white fat. The team identified the CKGGRAKDC homing motif and, in a 2004 paper published in Nature Medicine, showed that attaching it to a proapoptotic peptide caused targeted destruction of white fat vasculature and rapid, reversible obesity reversal in mice.

The molecule works because the homing peptide binds prohibitin, a protein the same research group established as a marker present on the blood vessel lining specifically in white adipose tissue (and, separately, on some tumor vasculature, which is part of why an MD Anderson cancer research program later carried the compound into a human cancer trial). Because prohibitin is also expressed on blood vessels in human white fat, the original 2004 paper proposed this as a path toward a targeted human obesity drug, distinct from centrally acting appetite suppressants or metabolic drugs like GLP-1 agonists.

The compound subsequently moved through a licensing relationship in which Arrowhead Research/Arrowhead Pharmaceuticals held rights to it (under the name Adipotide) for an obesity indication, while MD Anderson separately ran a Phase I safety trial (under the name Prohibitin-TP01) in men with metastatic, castration-resistant prostate cancer and obesity, testing whether shrinking visceral fat could slow cancer growth. As of the date this entry was checked, this site found no evidence that Adipotide/FTPP has advanced beyond that single early-phase human trial, and no confirmed, specifically-named reason (safety failure, funding decision, or otherwise) for why broader development did not continue; the available evidence points to development having become inactive, but that should not be read as a confirmed formal discontinuation with a stated cause.

How does it work?

Plain-English explanation

Instead of telling fat cells to burn more energy or telling the brain to feel less hungry, Adipotide attacks the blood vessels that feed white fat tissue. Cut off a tissue’s blood supply and its cells die from lack of oxygen and nutrients; the body then reabsorbs that dead fat tissue. Because the peptide is designed to recognize a marker mostly found on fat-tissue blood vessels, it is intended to spare blood vessels elsewhere in the body.

Technical explanation

The homing domain, CKGGRAKDC, was selected by in vivo phage display for binding to white adipose tissue vasculature and was shown to associate with prohibitin, along with annexin A2 (ANXA2) identified in later mechanistic work from the same research group as a co-receptor involved in prohibitin trafficking and fatty acid transport regulation in adipose endothelium. The conjugated proapoptotic domain, D(KLAKLAK)2, is a well-characterized synthetic peptide that disrupts mitochondrial membranes and triggers apoptosis once it is internalized into a targeted cell, a “warhead” motif used in multiple other targeted-peptide research programs, not unique to Adipotide. The combined molecule is a ligand-directed, proapoptotic conjugate: the homing half provides tissue selectivity, and the warhead half does the killing once the peptide reaches its target.

Potential benefits and research applications

Rapid fat loss in obese mice (animal evidence)

What is being investigated: whether selectively destroying white fat vasculature causes rapid, reversible obesity reversal. How the effect might occur: prohibitin-directed apoptosis of adipose vasculature, cutting off blood supply to white fat. Evidence: the original 2004 Kolonin et al. Nature Medicine paper reported resorption of established white adipose tissue and normalization of metabolism in obese mice, described by the authors as rapid and without detectable adverse effects in that mouse work. Strength: has been shown in a peer-reviewed, controlled mouse study. Limitation: is a mouse result; effects and tolerability in mice do not establish either in primates or people.

Weight loss and improved insulin resistance in obese primates (animal evidence)

What is being investigated: whether the same targeted mechanism produces meaningful weight loss and metabolic improvement in a species closer to humans. How the effect might occur: the same prohibitin-directed vascular apoptosis mechanism as the mouse work. Evidence: a 2011 study (Barnhart et al., Science Translational Medicine) reported that obese rhesus monkeys receiving Adipotide lost an average of about 11 percent of body weight and about 27 percent of abdominal fat over 4 weeks of daily injections, with roughly 50 percent less insulin needed after treatment to achieve comparable glucose control, and untreated control monkeys showing no such changes. Strength: has been shown in a controlled, peer-reviewed non-human-primate study, the closest preclinical model to humans used for this compound. Limitation: the same study identified a dose-dependent, reversible reduction in kidney function as the treatment’s principal adverse effect in monkeys, described by the study’s authors as predictable and reversible in that setting, but this is a real, mechanism-linked safety signal that carried directly into the human trial design described below.

Slowing prostate cancer growth via fat reduction (early-phase human evidence, trial terminated)

What is being investigated: whether reducing visceral/white fat in obese men with advanced, castration-resistant prostate cancer could slow cancer progression, since adipose tissue is known to produce substances that can promote prostate cancer growth. How the effect might occur: the same prohibitin-targeted fat-vasculature-destruction mechanism, applied to reduce a fat-derived tumor-growth-promoting signal rather than for cosmetic weight loss. Evidence: MD Anderson Cancer Center sponsored a first-in-human Phase I dose-escalation trial (Prohibitin-TP01, ClinicalTrials.gov identifier NCT01262664) in men with metastatic prostate cancer and obesity (BMI over 30), giving daily subcutaneous injections for 28 days across up to five planned dose levels, three participants per level, with weight, BMI, waist/hip measurements, PSA, and kidney function tracked. Strength: is real, sourced, first-in-human clinical-trial evidence, which is more than exists for most peptides discussed on this site. Limitation: the trial’s registry record shows a status of “Terminated” with an enrollment of only 4 participants against an originally planned scope of up to 39, and this site did not locate a published results paper or a stated reason for termination in the sources reviewed; the trial’s outcome should be treated as unresolved and unpublished, not as a demonstrated failure or success.

What dosage information circulates?

Figures in this section summarize amounts and schedules reported in published research or circulating online. Their inclusion documents what is reported and does not establish that a regimen is verified, safe, effective, or appropriate.

Reported use or research objective	Route reported	Amount reported	Frequency reported	Reported duration	Evidence or source category
Prostate cancer / fat reduction (Phase I, terminated)	Not obtainable from the sources reviewed	No established or reliably sourced specific human milligram dosing figure was identified	Not obtainable from the sources reviewed	Not obtainable from the sources reviewed	Registered but terminated/unpublished human trial (NCT01262664)
Weight loss and insulin resistance (rhesus monkey)	Injection (route as used in primate study)	Specific per-kilogram dose not obtainable from the secondary summaries reviewed; not reproduced here to avoid mis-stating an unverified figure	Daily	4-week treatment period, with 4 additional weeks of post-treatment follow-up	Published animal research (Barnhart et al. 2011, Science Translational Medicine)
Obesity reversal (mouse)	Injection (route as used in mouse study)	Specific mouse dosing figures not independently re-verified for this entry	Short-course	Short-course	Published animal research (Kolonin et al. 2004, Nature Medicine)
General “research compound” framing, sold as “Adipotide” or “FTPP”	Subcutaneous injection	Informal daily amounts, commonly in the low single-digit milligram range	Daily	Not established	Widely repeated online, but its original source could not be verified

Amounts studied in human research

The MD Anderson Phase I trial (NCT01262664) administered Prohibitin-TP01 as a once-daily subcutaneous injection for up to 28 days, using a standard 3-participants-per-cohort dose-escalation design across up to five planned dose levels; the specific milligram amount used at each dose level was not disclosed in the trial registry summary reviewed for this entry, and no published results paper reporting those doses was located. No established or reliably sourced specific human milligram dosing figure was identified.

Amounts studied in animal research

The 2011 rhesus monkey study used daily injections of Adipotide over a 4-week treatment period, with an additional 4 weeks of post-treatment follow-up; the specific per-kilogram dose used in that primate study was not obtainable from the secondary summaries reviewed for this entry and is not reproduced here to avoid mis-stating a number this site could not directly verify against the original paper. The 2004 mouse study used the peptide in a similar short-course injection design; specific mouse dosing figures were likewise not independently re-verified for this entry.

Practitioner and community-reported protocols

Widely repeated online, but its original source could not be verified: research-chemical vendor sites selling “Adipotide” or “FTPP” describe informal daily subcutaneous injection amounts, commonly in the low single-digit milligram range, framed loosely against the animal studies described above. This site could not trace any specific circulating figure to a named clinical source, and no practitioner-reported (licensed clinical) protocol was identified for human use of this compound, consistent with its status as a peptide with only one small, terminated, unpublished-results human trial and no approved use. Given the kidney-function safety signal identified in the primate study and the compound’s ligand-directed, vasculature-destroying mechanism, self-administered use outside a supervised clinical trial carries risks that have not been characterized in any published human safety dataset.

Side effects, risks, and limitations

The clearest safety signal in the primary literature is renal (kidney): the 2011 rhesus monkey study identified a dose-dependent reduction in kidney function as the treatment’s principal adverse effect, described by the study’s authors as predictable and reversible in that setting, with treated monkeys reported to remain alert and without nausea or reduced food intake during the study. The human Phase I trial’s eligibility criteria required adequate baseline renal function and specifically excluded patients on potentially nephrotoxic drugs, a design choice that reflects the same kidney-focused safety concern carried over from the primate data. Beyond that, this site did not locate a published human adverse-event summary from the MD Anderson trial, since no results were published and the trial was terminated with only 4 of a planned 39 participants enrolled. Given the compound’s mechanism, deliberately triggering blood vessel destruction and localized cell death, there is an inherent theoretical concern about off-target vascular effects wherever prohibitin or related targets might be present outside white fat, though the trials described here did not report evidence of that occurring at the doses and durations tested.

Regulatory and developmental status

Adipotide/FTPP/Prohibitin-TP01 is an investigational compound with no approval anywhere for any use. It has never progressed past a single, small, first-in-human Phase I trial (MD Anderson Cancer Center, ClinicalTrials.gov NCT01262664), which began in 2012, is listed with a status of “Terminated,” enrolled only 4 of a planned 39 participants, and has no located published results as of the date this entry was checked. This site did not find a confirmed, specifically named reason for why broader obesity-focused development (under the Adipotide name, associated with Arrowhead Research/Arrowhead Pharmaceuticals) did not continue after the initial 2012 trial announcement; secondary industry commentary suggests the sponsoring company shifted resources toward other, more commercially advanced programs, but this site could not verify that as an official, stated reason for discontinuation, and no separate safety-driven discontinuation announcement was located either. The most accurate characterization is that development appears to have gone inactive rather than that it was formally discontinued for a confirmed, named cause.

Frequently asked questions

What is Adipotide?

A synthetic peptide (also called FTPP or Prohibitin-TP01) designed to destroy the blood vessels feeding white fat tissue, causing that fat to be reabsorbed by the body. It is investigational and not approved for any use.

How does it work?

One half of the molecule homes to a protein (prohibitin) found on blood vessels in white fat; the other half triggers cell death once the peptide reaches its target, cutting off blood supply to that fat tissue.

What dosage has been studied?

No established or reliably sourced specific human dosing figure was identified. A Phase I human trial used daily subcutaneous injections for up to 28 days across escalating, undisclosed dose levels; a 2011 primate study used daily injections for 4 weeks, but the specific per-kilogram dose was not independently verified for this entry.

Has Adipotide been tested in humans?

Yes, in one small, first-in-human Phase I trial at MD Anderson Cancer Center in men with metastatic prostate cancer and obesity. The trial (NCT01262664) is listed as “Terminated” with only 4 of a planned 39 participants enrolled, and no published results were located.

Is Adipotide a weight-loss drug people can get?

No. It has never been approved or marketed as an obesity treatment. Its only human testing was a small cancer-focused safety trial, not a general-population obesity trial, and that trial did not proceed to completion as originally planned.

Why did development stop?

No confirmed, specifically named reason was located in the sources reviewed for this entry. The human trial is listed as terminated with low enrollment and no published results, and broader obesity-focused development does not appear to have continued, but this site could not verify an official stated cause.

What side effects have been reported?

A dose-dependent, reversible reduction in kidney function was the principal adverse effect identified in the 2011 primate study. No published human adverse-event data from the terminated Phase I trial were located.

Is it approved anywhere?

No. It has no regulatory approval in any country for any indication.

What remains unknown?

Whether Adipotide would be effective or safe for obesity treatment in a broader human population; the actual doses used in the human Phase I trial and their results, since no results were published; and the specific reason human and commercial development did not continue past that one small trial.

Bottom line

Adipotide (FTPP / Prohibitin-TP01) is a genuinely clever, peer-reviewed piece of targeted-peptide science: a molecule designed to destroy fat-tissue blood vessels rather than act on appetite or metabolism, with real, published mouse and rhesus monkey data showing rapid weight loss and metabolic improvement. But its only human test was a small, cancer-focused Phase I safety trial that was terminated with just 4 of a planned 39 participants and no published results, and it is not an approved drug or an available obesity treatment. The primate data also identified a real, dose-dependent kidney-function signal that carried directly into that trial’s design. Whether the peptide could ever be both safe and effective in a general human population remains genuinely unanswered, not quietly resolved.