Adipotide

updated

Adipotide is a synthetic peptide that joins a fat-vessel homing sequence to a D-amino-acid proapoptotic sequence. In obese mice and in obese monkeys of three species it reduced white fat and improved insulin resistance, with reversible kidney tubule changes in the monkeys. No human outcome data exist: the one registered human study, which does not name adipotide, ended at 4 participants with no results posted.

Prohibitin-targeted proapoptotic peptidomimetic

  • PubChem lists Adipotide as CID 163360068, C111H206N36O28S2, molecular weight 2557.2, CAS 859216-15-2. The monkey paper defines it as CKGGRAKDC-GG-(D)(KLAKLAK)2.
  • In obese Old World monkeys of three species, the monkey paper reports rapid weight loss, improved insulin resistance and a marked fall in white fat on MRI and DEXA, with reversible changes in kidney proximal tubule function.
  • A 2012 letter argues the monkey weight loss may reflect a direct effect on food consumption, and a rodent paper of a peptide of this design found reduced food intake with no change in energy expenditure.
  • The one registered human study, NCT01262664, tested Prohibitin-TP01 in men with metastatic prostate cancer and obesity. It was terminated at the investigator's request after 4 participants enrolled, with no results posted, and the record does not name adipotide.
  • On 10 October 2026, an openFDA Drugs@FDA query for adipotide returned no match and a DailyMed search returned no label.
  • A PubMed search on 10 October 2026 for adipotide in titles and abstracts returned 3 records; none reports human data.

What is adipotide, and is it an approved drug?

Adipotide is a synthetic peptide that joins a fat-vessel homing sequence to a D-amino-acid proapoptotic sequence. On 10 October 2026, openFDA Drugs@FDA returned no match and DailyMed returned no label, so no FDA-approved adipotide product was found.

PubChem lists Adipotide as CID 163360068, C111H206N36O28S2, molecular weight 2557.2, CAS 859216-15-2, with synonyms that include Adipotide, HKPao and several vendor catalog codes. The monkey paper defines the molecule as CKGGRAKDC-GG-(D)(KLAKLAK)2: a fat-vessel homing sequence joined by a GG spacer to a D-amino-acid proapoptotic sequence. The PubChem systematic name shows D-amino-acid (2R) residues in the proapoptotic stretch. Prohibitin-targeting peptide is a descriptive name.

FTPP is a name collision. A PubChem name search for FTPP did not resolve to this compound, and neither did the bare targeting motif CKGGRAKDC. A PubMed search for FTPP in titles and abstracts on 10 October 2026 returned 14 records, and by title none is about this peptide. They include a PET probe, (4-[18F]fluorophenyl)triphenylphosphonium, and unrelated chemistry and engineering papers. No paper reviewed uses FTPP for adipotide.

An openFDA Drugs@FDA query for adipotide on 10 October 2026 returned no match, and a DailyMed search for the drug name adipotide returned no label. No FDA record was found in these two sources, so adipotide is not an FDA-approved drug or a labeled product. This says nothing about other regulators.

PubChem: adipotide identity

Chemical identity record

National Library of Medicine. PubChem compound record CID 163360068 (Adipotide).

PubChem lists Adipotide as CID 163360068, C111H206N36O28S2, molecular weight 2557.2, CAS 859216-15-2, with synonyms that include Adipotide, HKPao and several vendor catalog codes. The name FTPP did not resolve in a PubChem name search, and neither did the bare targeting motif CKGGRAKDC. The monkey paper defines the molecule as CKGGRAKDC-GG-(D)(KLAKLAK)2, and the PubChem systematic name shows D-amino-acid (2R) residues in the proapoptotic stretch. A PubMed search for FTPP in titles and abstracts on 2026-10-10 returned 14 records, and by title none is about this peptide.

Participants / model
Chemical identity, not a clinical population
Treatment
Defined synthetic peptidomimetic
Follow-up
Not applicable
Study design
NLM chemical record
Funding
not stated in the source

Prohibitin-targeting peptide is a descriptive name. FTPP is a name collision, and no paper reviewed uses it for adipotide.

Read the original source
FDA and DailyMed: no adipotide record, 10 October 2026

Regulatory record

U.S. Food and Drug Administration, openFDA Drugs@FDA query for adipotide, and DailyMed search for the drug name adipotide, run on 10 October 2026.

The openFDA Drugs@FDA query for adipotide returned no match, and a DailyMed search for the drug name adipotide returned no label. No FDA record was found in these two sources, so adipotide is not an FDA-approved drug or a labeled product.

Participants / model
Not a clinical population
Treatment
Not applicable
Follow-up
Searches run on 2026-10-10
Study design
Official FDA and NLM records
Funding
not stated in the source

This says nothing about other regulators.

Read the original source

What did the mouse and monkey studies find?

In obese mice, a proapoptotic peptide targeted to fat blood vessels ablated white fat and reversed obesity. In obese Old World monkeys of three species, adipotide produced rapid weight loss, improved insulin resistance and reduced white fat on MRI and DEXA, with reversible kidney tubule changes. The abstracts give no dose, route, group size or weight-loss figure.

The concept comes from a mouse paper by the founding group. In vivo phage display isolated the motif CKGGRAKDC, which homes to white fat blood vessels. The motif associates with prohibitin, a multifunctional membrane protein that the authors establish as a vascular marker of adipose tissue. A proapoptotic peptide targeted to prohibitin in the fat vasculature ablated white fat and reversed obesity in obese mice, which the authors describe as happening without detectable adverse effects. The abstract says prohibitin is also expressed in blood vessels of human white fat. It gives no dose or route.

The monkey paper names the molecule adipotide and tested it in obese Old World monkeys. The abstract reports targeted apoptosis within blood vessels of white adipose tissue, rapid weight loss, improved insulin resistance, and a marked reduction in white adipose tissue confirmed by magnetic resonance imaging and dual-energy x-ray absorptiometry. At experimentally determined optimal doses, monkeys from three different species displayed predictable and reversible changes in renal proximal tubule function. The abstract states no weight-loss figure, dose, route, group size or duration, so none is quoted here. The authors call adipotide a candidate drug for treating obesity in humans, not a tested one.

Neither paper tested a person. The kidney finding is the group's own, and the abstract does not say how large the changes were, how long they lasted, or whether any kidney tissue damage was seen.

Founding mouse paper: prohibitin-targeted peptide ablated white fat in obese mice

Animal study

Kolonin MG et al. Nat Med. 2004;10(6):625-32. PMID 15133506.

In vivo phage display isolated the motif CKGGRAKDC, which homes to white fat blood vessels and associates with prohibitin, which the authors establish as a vascular marker of adipose tissue. A proapoptotic peptide targeted to prohibitin in the fat vasculature ablated white fat and reversed obesity without detectable adverse effects, in the authors' words. The abstract says prohibitin is also expressed in blood vessels of human white fat.

Participants / model
Obese mice
Treatment
Targeted proapoptotic peptide; dose and route not stated in the abstract
Follow-up
not stated in the source
Study design
Preclinical study with in vivo phage display
Funding
not stated in the source

A mouse paper from the founding group. The abstract gives no dose or route.

Read the original source
Monkey paper: weight loss, improved insulin resistance and reversible kidney tubule changes

Animal study

Barnhart KF et al. Sci Transl Med. 2011;3(108):108ra112. PMID 22072637.

The paper names the molecule adipotide and tested it in obese Old World monkeys. The abstract reports targeted apoptosis within blood vessels of white adipose tissue, rapid weight loss, improved insulin resistance, and a marked reduction in white adipose tissue confirmed by magnetic resonance imaging and dual-energy x-ray absorptiometry. At experimentally determined optimal doses, monkeys from three different species displayed predictable and reversible changes in renal proximal tubule function. The authors call the molecule a candidate drug for treating obesity in humans.

Participants / model
Obese Old World monkeys, three species
Treatment
Adipotide; dose and route not stated in the abstract
Follow-up
not stated in the source
Study design
Preclinical study
Funding
not stated in the source

The abstract states no weight-loss figure, dose, route, group size or duration, and does not give the size or duration of the kidney changes or say whether kidney tissue damage was seen. The kidney finding is a reversible functional signal in monkeys.

Read the original source

Is the weight loss a fat effect or a food-intake effect?

It is disputed. A 2012 letter argued the monkey weight loss may reflect a direct effect on food consumption, and a rodent paper of a peptide of this design found reduced food intake with no change in energy expenditure. A separate mouse paper found a glucose effect that did not depend on weight.

A 2012 letter to the journal that ran the monkey paper argues that the reported weight loss may instead reflect a direct effect of adipotide on food consumption. The PubMed abstract is one sentence, and the citation shows an author reply was printed with it. It is a comment, not a data paper.

Independent rodent work points the same way. A paper that does not name adipotide tested a proapoptotic peptide designed to kill fat-vessel endothelium in lean and obese mice and rats treated for 4 or 27 days. It completely reversed high-fat-diet obesity in mice and lowered body weight in mice and rats on a high-fat diet, but not on a low-fat diet. Fat loss came with no change in energy expenditure and with reduced food intake, which occurred without signs of illness in a conditioned taste aversion test, and despite lower leptin. Because the abstract calls the molecule a proapoptotic peptide, this page refers to it as a peptide of this design. Dose and route are not stated in the abstract.

The same academic group reported a glucose effect that did not depend on weight. In obese mice on a high-fat diet, the peptide improved glucose tolerance on days 2 and 3 of treatment in a weight- and food-intake-independent way, compared with vehicle and with mice pair-fed to the treated group, and it lowered serum insulin and triglycerides. The authors read this as a role for adipose vasculature in glucose and lipid handling. The abstract calls the molecule peptide or PP and does not name adipotide, and it gives no dose or route.

2012 letter: weight loss may reflect food consumption

Narrative review

Criscione L. Sci Transl Med. 2012;4(131):131le2; author reply 131lr2. PMID 22539771.

A 2012 letter to the journal that ran the monkey paper argues the reported weight loss may instead reflect a direct effect of adipotide on food consumption. The abstract is one sentence, and the PubMed citation shows an author reply was printed with it.

Participants / model
Not a study population
Treatment
Not applicable
Follow-up
Not applicable
Study design
Published letter (peer-reviewed comment), not a data paper
Funding
not stated in the source

This is a comment, not a data paper.

Read the original source
Rodent paper: fat loss with reduced food intake, no change in energy expenditure

Animal study

Kim DH et al. Diabetes. 2010;59(4):907-15. PMID 20103704.

In lean and obese mice and rats treated for 4 or 27 days, a proapoptotic peptide designed to kill fat-vessel endothelium completely reversed high-fat-diet obesity in mice and lowered body weight in mice and rats on a high-fat diet, but not on a low-fat diet. Fat loss came with no change in energy expenditure and with reduced food intake, which occurred without signs of illness in a conditioned taste aversion test, and despite lower leptin.

Participants / model
Lean and obese mice and rats
Treatment
Proapoptotic peptide for 4 or 27 days; dose and route not stated in the abstract
Follow-up
4 or 27 days
Study design
Preclinical study
Funding
not stated in the source

The abstract calls the molecule a proapoptotic peptide and does not name adipotide, so the page says a peptide of this design.

Read the original source
Mouse paper: glucose tolerance improved independent of weight and food intake

Animal study

Kim DH et al. Diabetes. 2012;61(9):2299-310. PMID 22733798.

In obese mice on a high-fat diet, the peptide improved glucose tolerance on days 2 and 3 of treatment in a weight- and food-intake-independent way, compared with vehicle and with mice pair-fed to the treated group, and it lowered serum insulin and triglycerides. The authors read this as a role for adipose vasculature in glucose and lipid handling.

Participants / model
Obese mice on a high-fat diet
Treatment
Proapoptotic peptide; dose and route not stated in the abstract
Follow-up
Glucose tolerance measured on days 2 and 3 of treatment
Study design
Preclinical study with vehicle and pair-fed comparison groups
Funding
not stated in the source

The same academic group as the rodent food-intake paper. The abstract calls the molecule peptide or PP and does not name adipotide.

Read the original source

Has adipotide been given to people?

No published human data were found. The one registered study, NCT01262664, tested Prohibitin-TP01 in men with metastatic prostate cancer and obesity. It was terminated at the investigator's request with 4 participants enrolled and no results posted, and the record does not name adipotide.

ClinicalTrials.gov record NCT01262664, sponsored by M.D. Anderson Cancer Center, is titled as a first-in-man phase 1 of a single cycle of Prohibitin Targeting Peptide 1 in patients with metastatic prostate cancer and obesity. The drug is listed as Prohibitin-TP01, given by subcutaneous injection with dose escalation planned. The population is men with metastatic prostate cancer on androgen deprivation therapy with a BMI over 30. The primary aims are acceptable dose and biologic activity. Status is terminated at the principal investigator's request, actual enrollment is 4, start was 24 May 2012, completion is listed as 2 January 2019, the last update was posted on 4 January 2019, and no results are posted.

The record does not use the word adipotide or the sequence, so it cannot be called an adipotide trial without a primary source that ties the two names. Four participants and no posted results mean no human efficacy or safety conclusion can be drawn.

A PubMed search on 10 October 2026 for adipotide in titles and abstracts returned 3 records: the monkey paper, the 2012 letter, and a 2013 mouse paper that compares a prohibitin-targeted nanoparticle with adipotide. Adding human, humans, patients or volunteers returned 2 records, the monkey paper and the letter, and neither reports human data. Adding clinical trial or randomized controlled trial publication types returned 1 record, a 2017 metformin and GLP-1 paper that is unrelated by title. ClinicalTrials.gov returned no record for the query adipotide. In the records reviewed there is no human dose, no human pharmacokinetics, no human efficacy data and no published human safety data for adipotide.

NCT01262664: first-in-man phase 1, terminated at 4 participants, no results

Trial registry record

ClinicalTrials.gov record NCT01262664, sponsor M.D. Anderson Cancer Center. Last update posted 2019-01-04.

The record is titled as a first-in-man phase 1 of a single cycle of Prohibitin Targeting Peptide 1 in patients with metastatic prostate cancer and obesity. The drug is listed as Prohibitin-TP01 by subcutaneous injection with dose escalation. Status is terminated per the principal investigator's request, actual enrollment 4, start 2012-05-24, completion 2019-01-02, and no results are posted.

Participants / model
Men with metastatic prostate cancer on androgen deprivation therapy, BMI over 30
Treatment
Prohibitin-TP01 subcutaneous injection
Follow-up
Single cycle; started 2012-05-24, completion listed 2019-01-02
Study design
Registered first-in-man phase 1
Funding
Sponsor: M.D. Anderson Cancer Center

Primary aims were acceptable dose and biologic activity. The record does not use the word adipotide or the sequence, so it cannot be called an adipotide trial without a primary source that ties the two names. No results are posted.

Read the original source
Searches, 10 October 2026: no human data for adipotide

PubMed search record

PubMed search run on 10 October 2026: adipotide[tiab], 3 records. Related PubMed searches and a ClinicalTrials.gov query run the same day.

A PubMed search for adipotide in titles and abstracts returned 3 records: the monkey paper, the 2012 letter, and a 2013 mouse paper that compares a prohibitin-targeted nanoparticle with adipotide. A search adding human, humans, patients or volunteers returned 2 records, the monkey paper and the letter, neither reporting human data. A search adding clinical trial or randomized controlled trial publication types returned 1 record, a 2017 metformin and GLP-1 paper that is unrelated by title. ClinicalTrials.gov returned no record for the query adipotide. In the records reviewed there is no human dose, no human pharmacokinetics, no human efficacy data and no published human safety data for adipotide. No record reviewed states that development was discontinued.

Participants / model
Records returned, not a population
Treatment
Not applicable
Follow-up
Searches run on 2026-10-10
Study design
Literature and registry searches
Funding
not stated in the source

A search result shows what the databases returned on that date. It is not proof that no unindexed study exists. The only registry fact is the terminated study NCT01262664.

Read the original source

Does adipotide cause fat loss by targeting fat tissue blood vessels?

In obese mice and monkeys only. The kidney signal is real in the monkey paper. No record reviewed states that development was discontinued; the only registry fact is one human study terminated at the investigator's request after 4 participants.

Sellers describe adipotide, also sold as FTPP, as causing fat loss by targeting the blood vessels of fat tissue, and point to monkey data, a kidney signal and discontinued development.

The fat-loss claim is supported in obese mice and obese monkeys, with the food-intake question described above. The kidney signal appears in the monkey paper as reversible changes in renal proximal tubule function. The word discontinued has no primary source among the records reviewed: no company statement or regulator record was found. The one registry fact is that a single human study of Prohibitin-TP01 was terminated at the principal investigator's request after 4 participants, and that record does not name adipotide.

Vials sold as adipotide or FTPP are not tied to the PubChem structure by any analytical record reviewed, so what a given vial contains is not established.

Monkey paper: weight loss, improved insulin resistance and reversible kidney tubule changes

Animal study

Barnhart KF et al. Sci Transl Med. 2011;3(108):108ra112. PMID 22072637.

The paper names the molecule adipotide and tested it in obese Old World monkeys. The abstract reports targeted apoptosis within blood vessels of white adipose tissue, rapid weight loss, improved insulin resistance, and a marked reduction in white adipose tissue confirmed by magnetic resonance imaging and dual-energy x-ray absorptiometry. At experimentally determined optimal doses, monkeys from three different species displayed predictable and reversible changes in renal proximal tubule function. The authors call the molecule a candidate drug for treating obesity in humans.

Participants / model
Obese Old World monkeys, three species
Treatment
Adipotide; dose and route not stated in the abstract
Follow-up
not stated in the source
Study design
Preclinical study
Funding
not stated in the source

The abstract states no weight-loss figure, dose, route, group size or duration, and does not give the size or duration of the kidney changes or say whether kidney tissue damage was seen. The kidney finding is a reversible functional signal in monkeys.

Read the original source
2012 letter: weight loss may reflect food consumption

Narrative review

Criscione L. Sci Transl Med. 2012;4(131):131le2; author reply 131lr2. PMID 22539771.

A 2012 letter to the journal that ran the monkey paper argues the reported weight loss may instead reflect a direct effect of adipotide on food consumption. The abstract is one sentence, and the PubMed citation shows an author reply was printed with it.

Participants / model
Not a study population
Treatment
Not applicable
Follow-up
Not applicable
Study design
Published letter (peer-reviewed comment), not a data paper
Funding
not stated in the source

This is a comment, not a data paper.

Read the original source
NCT01262664: first-in-man phase 1, terminated at 4 participants, no results

Trial registry record

ClinicalTrials.gov record NCT01262664, sponsor M.D. Anderson Cancer Center. Last update posted 2019-01-04.

The record is titled as a first-in-man phase 1 of a single cycle of Prohibitin Targeting Peptide 1 in patients with metastatic prostate cancer and obesity. The drug is listed as Prohibitin-TP01 by subcutaneous injection with dose escalation. Status is terminated per the principal investigator's request, actual enrollment 4, start 2012-05-24, completion 2019-01-02, and no results are posted.

Participants / model
Men with metastatic prostate cancer on androgen deprivation therapy, BMI over 30
Treatment
Prohibitin-TP01 subcutaneous injection
Follow-up
Single cycle; started 2012-05-24, completion listed 2019-01-02
Study design
Registered first-in-man phase 1
Funding
Sponsor: M.D. Anderson Cancer Center

Primary aims were acceptable dose and biologic activity. The record does not use the word adipotide or the sequence, so it cannot be called an adipotide trial without a primary source that ties the two names. No results are posted.

Read the original source
Searches, 10 October 2026: no human data for adipotide

PubMed search record

PubMed search run on 10 October 2026: adipotide[tiab], 3 records. Related PubMed searches and a ClinicalTrials.gov query run the same day.

A PubMed search for adipotide in titles and abstracts returned 3 records: the monkey paper, the 2012 letter, and a 2013 mouse paper that compares a prohibitin-targeted nanoparticle with adipotide. A search adding human, humans, patients or volunteers returned 2 records, the monkey paper and the letter, neither reporting human data. A search adding clinical trial or randomized controlled trial publication types returned 1 record, a 2017 metformin and GLP-1 paper that is unrelated by title. ClinicalTrials.gov returned no record for the query adipotide. In the records reviewed there is no human dose, no human pharmacokinetics, no human efficacy data and no published human safety data for adipotide. No record reviewed states that development was discontinued.

Participants / model
Records returned, not a population
Treatment
Not applicable
Follow-up
Searches run on 2026-10-10
Study design
Literature and registry searches
Funding
not stated in the source

A search result shows what the databases returned on that date. It is not proof that no unindexed study exists. The only registry fact is the terminated study NCT01262664.

Read the original source

How is adipotide meant to work?

A homing sequence carries a proapoptotic sequence to the blood vessels of white fat, where the authors report targeted cell death and fat loss in obese mice and monkeys. A published letter and independent rodent work point to reduced food intake as an alternative explanation.

In mice, the motif CKGGRAKDC homes to white fat blood vessels and associates with prohibitin, which the authors establish as a vascular marker of adipose tissue. Adipotide joins that motif by a GG spacer to a D-amino-acid proapoptotic sequence, and in obese monkeys the authors report targeted apoptosis within blood vessels of white adipose tissue.

Two findings complicate the fat-vessel account. A 2012 letter argues the weight loss may reflect a direct effect on food consumption, and a rodent paper of a peptide of this design found reduced food intake with no change in energy expenditure. A separate mouse paper found improved glucose tolerance on days 2 and 3 that did not depend on weight or food intake, compared with pair-fed mice.

Founding mouse paper: prohibitin-targeted peptide ablated white fat in obese mice

Animal study

Kolonin MG et al. Nat Med. 2004;10(6):625-32. PMID 15133506.

In vivo phage display isolated the motif CKGGRAKDC, which homes to white fat blood vessels and associates with prohibitin, which the authors establish as a vascular marker of adipose tissue. A proapoptotic peptide targeted to prohibitin in the fat vasculature ablated white fat and reversed obesity without detectable adverse effects, in the authors' words. The abstract says prohibitin is also expressed in blood vessels of human white fat.

Participants / model
Obese mice
Treatment
Targeted proapoptotic peptide; dose and route not stated in the abstract
Follow-up
not stated in the source
Study design
Preclinical study with in vivo phage display
Funding
not stated in the source

A mouse paper from the founding group. The abstract gives no dose or route.

Read the original source
Monkey paper: weight loss, improved insulin resistance and reversible kidney tubule changes

Animal study

Barnhart KF et al. Sci Transl Med. 2011;3(108):108ra112. PMID 22072637.

The paper names the molecule adipotide and tested it in obese Old World monkeys. The abstract reports targeted apoptosis within blood vessels of white adipose tissue, rapid weight loss, improved insulin resistance, and a marked reduction in white adipose tissue confirmed by magnetic resonance imaging and dual-energy x-ray absorptiometry. At experimentally determined optimal doses, monkeys from three different species displayed predictable and reversible changes in renal proximal tubule function. The authors call the molecule a candidate drug for treating obesity in humans.

Participants / model
Obese Old World monkeys, three species
Treatment
Adipotide; dose and route not stated in the abstract
Follow-up
not stated in the source
Study design
Preclinical study
Funding
not stated in the source

The abstract states no weight-loss figure, dose, route, group size or duration, and does not give the size or duration of the kidney changes or say whether kidney tissue damage was seen. The kidney finding is a reversible functional signal in monkeys.

Read the original source
2012 letter: weight loss may reflect food consumption

Narrative review

Criscione L. Sci Transl Med. 2012;4(131):131le2; author reply 131lr2. PMID 22539771.

A 2012 letter to the journal that ran the monkey paper argues the reported weight loss may instead reflect a direct effect of adipotide on food consumption. The abstract is one sentence, and the PubMed citation shows an author reply was printed with it.

Participants / model
Not a study population
Treatment
Not applicable
Follow-up
Not applicable
Study design
Published letter (peer-reviewed comment), not a data paper
Funding
not stated in the source

This is a comment, not a data paper.

Read the original source
Rodent paper: fat loss with reduced food intake, no change in energy expenditure

Animal study

Kim DH et al. Diabetes. 2010;59(4):907-15. PMID 20103704.

In lean and obese mice and rats treated for 4 or 27 days, a proapoptotic peptide designed to kill fat-vessel endothelium completely reversed high-fat-diet obesity in mice and lowered body weight in mice and rats on a high-fat diet, but not on a low-fat diet. Fat loss came with no change in energy expenditure and with reduced food intake, which occurred without signs of illness in a conditioned taste aversion test, and despite lower leptin.

Participants / model
Lean and obese mice and rats
Treatment
Proapoptotic peptide for 4 or 27 days; dose and route not stated in the abstract
Follow-up
4 or 27 days
Study design
Preclinical study
Funding
not stated in the source

The abstract calls the molecule a proapoptotic peptide and does not name adipotide, so the page says a peptide of this design.

Read the original source
Mouse paper: glucose tolerance improved independent of weight and food intake

Animal study

Kim DH et al. Diabetes. 2012;61(9):2299-310. PMID 22733798.

In obese mice on a high-fat diet, the peptide improved glucose tolerance on days 2 and 3 of treatment in a weight- and food-intake-independent way, compared with vehicle and with mice pair-fed to the treated group, and it lowered serum insulin and triglycerides. The authors read this as a role for adipose vasculature in glucose and lipid handling.

Participants / model
Obese mice on a high-fat diet
Treatment
Proapoptotic peptide; dose and route not stated in the abstract
Follow-up
Glucose tolerance measured on days 2 and 3 of treatment
Study design
Preclinical study with vehicle and pair-fed comparison groups
Funding
not stated in the source

The same academic group as the rodent food-intake paper. The abstract calls the molecule peptide or PP and does not name adipotide.

Read the original source

What is known about the safety of adipotide?

No human safety data exist for adipotide. In the one primate paper, monkeys of three species showed reversible changes in kidney proximal tubule function at the doses the authors chose, and the abstract gives no size, duration or tissue findings.

The kidney finding is a reversible functional signal in monkeys, and the abstract does not say whether kidney tissue damage was seen. The founding mouse paper describes ablation of white fat in mice without detectable adverse effects, in the authors' words. The monkey paper is the only primate study among the records reviewed.

A separate mouse study raises a kidney question for fat-targeting peptides in a different formulation. In leptin-deficient ob/ob mice, liposomes carrying an adipose targeting sequence and the drug tesaglitazar did not take up more in adipose than in other tissues, took up more in the kidneys, and did not significantly change metabolic parameters. That tested a liposome carrying a different drug, and the abstract does not give the sequence of the targeting sequence, so it is a kidney-uptake caution and not an adipotide result.

In people, nothing can be concluded. The one registered study enrolled 4 participants and posted no results, and a PubMed search on 10 October 2026 found no human dose, pharmacokinetic, efficacy or safety data. Vials sold as adipotide are also not tied to the PubChem structure by any analytical record reviewed, so identity and purity of a given vial are unknown.

Monkey paper: weight loss, improved insulin resistance and reversible kidney tubule changes

Animal study

Barnhart KF et al. Sci Transl Med. 2011;3(108):108ra112. PMID 22072637.

The paper names the molecule adipotide and tested it in obese Old World monkeys. The abstract reports targeted apoptosis within blood vessels of white adipose tissue, rapid weight loss, improved insulin resistance, and a marked reduction in white adipose tissue confirmed by magnetic resonance imaging and dual-energy x-ray absorptiometry. At experimentally determined optimal doses, monkeys from three different species displayed predictable and reversible changes in renal proximal tubule function. The authors call the molecule a candidate drug for treating obesity in humans.

Participants / model
Obese Old World monkeys, three species
Treatment
Adipotide; dose and route not stated in the abstract
Follow-up
not stated in the source
Study design
Preclinical study
Funding
not stated in the source

The abstract states no weight-loss figure, dose, route, group size or duration, and does not give the size or duration of the kidney changes or say whether kidney tissue damage was seen. The kidney finding is a reversible functional signal in monkeys.

Read the original source
Founding mouse paper: prohibitin-targeted peptide ablated white fat in obese mice

Animal study

Kolonin MG et al. Nat Med. 2004;10(6):625-32. PMID 15133506.

In vivo phage display isolated the motif CKGGRAKDC, which homes to white fat blood vessels and associates with prohibitin, which the authors establish as a vascular marker of adipose tissue. A proapoptotic peptide targeted to prohibitin in the fat vasculature ablated white fat and reversed obesity without detectable adverse effects, in the authors' words. The abstract says prohibitin is also expressed in blood vessels of human white fat.

Participants / model
Obese mice
Treatment
Targeted proapoptotic peptide; dose and route not stated in the abstract
Follow-up
not stated in the source
Study design
Preclinical study with in vivo phage display
Funding
not stated in the source

A mouse paper from the founding group. The abstract gives no dose or route.

Read the original source
Targeted liposomes in ob/ob mice: more uptake in kidneys than in fat

Animal study

Bauknight DK et al. PLoS One. 2019;14(11):e0224917. PMID 31725756.

In leptin-deficient ob/ob mice, liposomes carrying an adipose targeting sequence and the drug tesaglitazar did not take up more in adipose than in other tissues, did take up more in the kidneys, and did not significantly change metabolic parameters.

Participants / model
ob/ob mice
Treatment
Adipose targeting sequence conjugated to liposomes carrying tesaglitazar
Follow-up
not stated in the source
Study design
Preclinical biodistribution study
Funding
not stated in the source

This tested a liposome carrying a different drug, not adipotide, and the abstract does not give the sequence of the targeting sequence. It is a kidney-uptake caution for fat-targeting peptides in a different formulation, not proof of anything about adipotide.

Read the original source
NCT01262664: first-in-man phase 1, terminated at 4 participants, no results

Trial registry record

ClinicalTrials.gov record NCT01262664, sponsor M.D. Anderson Cancer Center. Last update posted 2019-01-04.

The record is titled as a first-in-man phase 1 of a single cycle of Prohibitin Targeting Peptide 1 in patients with metastatic prostate cancer and obesity. The drug is listed as Prohibitin-TP01 by subcutaneous injection with dose escalation. Status is terminated per the principal investigator's request, actual enrollment 4, start 2012-05-24, completion 2019-01-02, and no results are posted.

Participants / model
Men with metastatic prostate cancer on androgen deprivation therapy, BMI over 30
Treatment
Prohibitin-TP01 subcutaneous injection
Follow-up
Single cycle; started 2012-05-24, completion listed 2019-01-02
Study design
Registered first-in-man phase 1
Funding
Sponsor: M.D. Anderson Cancer Center

Primary aims were acceptable dose and biologic activity. The record does not use the word adipotide or the sequence, so it cannot be called an adipotide trial without a primary source that ties the two names. No results are posted.

Read the original source
Searches, 10 October 2026: no human data for adipotide

PubMed search record

PubMed search run on 10 October 2026: adipotide[tiab], 3 records. Related PubMed searches and a ClinicalTrials.gov query run the same day.

A PubMed search for adipotide in titles and abstracts returned 3 records: the monkey paper, the 2012 letter, and a 2013 mouse paper that compares a prohibitin-targeted nanoparticle with adipotide. A search adding human, humans, patients or volunteers returned 2 records, the monkey paper and the letter, neither reporting human data. A search adding clinical trial or randomized controlled trial publication types returned 1 record, a 2017 metformin and GLP-1 paper that is unrelated by title. ClinicalTrials.gov returned no record for the query adipotide. In the records reviewed there is no human dose, no human pharmacokinetics, no human efficacy data and no published human safety data for adipotide. No record reviewed states that development was discontinued.

Participants / model
Records returned, not a population
Treatment
Not applicable
Follow-up
Searches run on 2026-10-10
Study design
Literature and registry searches
Funding
not stated in the source

A search result shows what the databases returned on that date. It is not proof that no unindexed study exists. The only registry fact is the terminated study NCT01262664.

Read the original source

Why does adipotide sit in D tier?

Adipotide has a coherent mouse and monkey story, but the evidence stops there. The monkey paper reports reversible kidney tubule changes, a letter and a rodent paper raise food intake as an explanation for the weight loss, and the one registered human study ended at 4 participants with no results.

The fat-loss story rests on a mouse paper and one monkey paper whose abstracts give no dose, route, group size or weight-loss figure. A published letter and an independent rodent paper both raise reduced eating as an explanation, and the monkey paper reports reversible kidney tubule changes at the doses it chose.

There is no regulator record and no human efficacy or safety data. The one registered human study did not name adipotide, enrolled 4 participants and posted no results. D is where the site places research chemicals whose promotion outruns the data, such as dihexa and j147.

Monkey paper: weight loss, improved insulin resistance and reversible kidney tubule changes

Animal study

Barnhart KF et al. Sci Transl Med. 2011;3(108):108ra112. PMID 22072637.

The paper names the molecule adipotide and tested it in obese Old World monkeys. The abstract reports targeted apoptosis within blood vessels of white adipose tissue, rapid weight loss, improved insulin resistance, and a marked reduction in white adipose tissue confirmed by magnetic resonance imaging and dual-energy x-ray absorptiometry. At experimentally determined optimal doses, monkeys from three different species displayed predictable and reversible changes in renal proximal tubule function. The authors call the molecule a candidate drug for treating obesity in humans.

Participants / model
Obese Old World monkeys, three species
Treatment
Adipotide; dose and route not stated in the abstract
Follow-up
not stated in the source
Study design
Preclinical study
Funding
not stated in the source

The abstract states no weight-loss figure, dose, route, group size or duration, and does not give the size or duration of the kidney changes or say whether kidney tissue damage was seen. The kidney finding is a reversible functional signal in monkeys.

Read the original source
2012 letter: weight loss may reflect food consumption

Narrative review

Criscione L. Sci Transl Med. 2012;4(131):131le2; author reply 131lr2. PMID 22539771.

A 2012 letter to the journal that ran the monkey paper argues the reported weight loss may instead reflect a direct effect of adipotide on food consumption. The abstract is one sentence, and the PubMed citation shows an author reply was printed with it.

Participants / model
Not a study population
Treatment
Not applicable
Follow-up
Not applicable
Study design
Published letter (peer-reviewed comment), not a data paper
Funding
not stated in the source

This is a comment, not a data paper.

Read the original source
Rodent paper: fat loss with reduced food intake, no change in energy expenditure

Animal study

Kim DH et al. Diabetes. 2010;59(4):907-15. PMID 20103704.

In lean and obese mice and rats treated for 4 or 27 days, a proapoptotic peptide designed to kill fat-vessel endothelium completely reversed high-fat-diet obesity in mice and lowered body weight in mice and rats on a high-fat diet, but not on a low-fat diet. Fat loss came with no change in energy expenditure and with reduced food intake, which occurred without signs of illness in a conditioned taste aversion test, and despite lower leptin.

Participants / model
Lean and obese mice and rats
Treatment
Proapoptotic peptide for 4 or 27 days; dose and route not stated in the abstract
Follow-up
4 or 27 days
Study design
Preclinical study
Funding
not stated in the source

The abstract calls the molecule a proapoptotic peptide and does not name adipotide, so the page says a peptide of this design.

Read the original source
NCT01262664: first-in-man phase 1, terminated at 4 participants, no results

Trial registry record

ClinicalTrials.gov record NCT01262664, sponsor M.D. Anderson Cancer Center. Last update posted 2019-01-04.

The record is titled as a first-in-man phase 1 of a single cycle of Prohibitin Targeting Peptide 1 in patients with metastatic prostate cancer and obesity. The drug is listed as Prohibitin-TP01 by subcutaneous injection with dose escalation. Status is terminated per the principal investigator's request, actual enrollment 4, start 2012-05-24, completion 2019-01-02, and no results are posted.

Participants / model
Men with metastatic prostate cancer on androgen deprivation therapy, BMI over 30
Treatment
Prohibitin-TP01 subcutaneous injection
Follow-up
Single cycle; started 2012-05-24, completion listed 2019-01-02
Study design
Registered first-in-man phase 1
Funding
Sponsor: M.D. Anderson Cancer Center

Primary aims were acceptable dose and biologic activity. The record does not use the word adipotide or the sequence, so it cannot be called an adipotide trial without a primary source that ties the two names. No results are posted.

Read the original source
FDA and DailyMed: no adipotide record, 10 October 2026

Regulatory record

U.S. Food and Drug Administration, openFDA Drugs@FDA query for adipotide, and DailyMed search for the drug name adipotide, run on 10 October 2026.

The openFDA Drugs@FDA query for adipotide returned no match, and a DailyMed search for the drug name adipotide returned no label. No FDA record was found in these two sources, so adipotide is not an FDA-approved drug or a labeled product.

Participants / model
Not a clinical population
Treatment
Not applicable
Follow-up
Searches run on 2026-10-10
Study design
Official FDA and NLM records
Funding
not stated in the source

This says nothing about other regulators.

Read the original source
Searches, 10 October 2026: no human data for adipotide

PubMed search record

PubMed search run on 10 October 2026: adipotide[tiab], 3 records. Related PubMed searches and a ClinicalTrials.gov query run the same day.

A PubMed search for adipotide in titles and abstracts returned 3 records: the monkey paper, the 2012 letter, and a 2013 mouse paper that compares a prohibitin-targeted nanoparticle with adipotide. A search adding human, humans, patients or volunteers returned 2 records, the monkey paper and the letter, neither reporting human data. A search adding clinical trial or randomized controlled trial publication types returned 1 record, a 2017 metformin and GLP-1 paper that is unrelated by title. ClinicalTrials.gov returned no record for the query adipotide. In the records reviewed there is no human dose, no human pharmacokinetics, no human efficacy data and no published human safety data for adipotide. No record reviewed states that development was discontinued.

Participants / model
Records returned, not a population
Treatment
Not applicable
Follow-up
Searches run on 2026-10-10
Study design
Literature and registry searches
Funding
not stated in the source

A search result shows what the databases returned on that date. It is not proof that no unindexed study exists. The only registry fact is the terminated study NCT01262664.

Read the original source

Studies and sources

PubChem: adipotide identity

Chemical identity record

National Library of Medicine. PubChem compound record CID 163360068 (Adipotide).

PubChem lists Adipotide as CID 163360068, C111H206N36O28S2, molecular weight 2557.2, CAS 859216-15-2, with synonyms that include Adipotide, HKPao and several vendor catalog codes. The name FTPP did not resolve in a PubChem name search, and neither did the bare targeting motif CKGGRAKDC. The monkey paper defines the molecule as CKGGRAKDC-GG-(D)(KLAKLAK)2, and the PubChem systematic name shows D-amino-acid (2R) residues in the proapoptotic stretch. A PubMed search for FTPP in titles and abstracts on 2026-10-10 returned 14 records, and by title none is about this peptide.

Participants / model
Chemical identity, not a clinical population
Treatment
Defined synthetic peptidomimetic
Follow-up
Not applicable
Study design
NLM chemical record
Funding
not stated in the source

Prohibitin-targeting peptide is a descriptive name. FTPP is a name collision, and no paper reviewed uses it for adipotide.

Read the original source
Founding mouse paper: prohibitin-targeted peptide ablated white fat in obese mice

Animal study

Kolonin MG et al. Nat Med. 2004;10(6):625-32. PMID 15133506.

In vivo phage display isolated the motif CKGGRAKDC, which homes to white fat blood vessels and associates with prohibitin, which the authors establish as a vascular marker of adipose tissue. A proapoptotic peptide targeted to prohibitin in the fat vasculature ablated white fat and reversed obesity without detectable adverse effects, in the authors' words. The abstract says prohibitin is also expressed in blood vessels of human white fat.

Participants / model
Obese mice
Treatment
Targeted proapoptotic peptide; dose and route not stated in the abstract
Follow-up
not stated in the source
Study design
Preclinical study with in vivo phage display
Funding
not stated in the source

A mouse paper from the founding group. The abstract gives no dose or route.

Read the original source
Monkey paper: weight loss, improved insulin resistance and reversible kidney tubule changes

Animal study

Barnhart KF et al. Sci Transl Med. 2011;3(108):108ra112. PMID 22072637.

The paper names the molecule adipotide and tested it in obese Old World monkeys. The abstract reports targeted apoptosis within blood vessels of white adipose tissue, rapid weight loss, improved insulin resistance, and a marked reduction in white adipose tissue confirmed by magnetic resonance imaging and dual-energy x-ray absorptiometry. At experimentally determined optimal doses, monkeys from three different species displayed predictable and reversible changes in renal proximal tubule function. The authors call the molecule a candidate drug for treating obesity in humans.

Participants / model
Obese Old World monkeys, three species
Treatment
Adipotide; dose and route not stated in the abstract
Follow-up
not stated in the source
Study design
Preclinical study
Funding
not stated in the source

The abstract states no weight-loss figure, dose, route, group size or duration, and does not give the size or duration of the kidney changes or say whether kidney tissue damage was seen. The kidney finding is a reversible functional signal in monkeys.

Read the original source
2012 letter: weight loss may reflect food consumption

Narrative review

Criscione L. Sci Transl Med. 2012;4(131):131le2; author reply 131lr2. PMID 22539771.

A 2012 letter to the journal that ran the monkey paper argues the reported weight loss may instead reflect a direct effect of adipotide on food consumption. The abstract is one sentence, and the PubMed citation shows an author reply was printed with it.

Participants / model
Not a study population
Treatment
Not applicable
Follow-up
Not applicable
Study design
Published letter (peer-reviewed comment), not a data paper
Funding
not stated in the source

This is a comment, not a data paper.

Read the original source
Rodent paper: fat loss with reduced food intake, no change in energy expenditure

Animal study

Kim DH et al. Diabetes. 2010;59(4):907-15. PMID 20103704.

In lean and obese mice and rats treated for 4 or 27 days, a proapoptotic peptide designed to kill fat-vessel endothelium completely reversed high-fat-diet obesity in mice and lowered body weight in mice and rats on a high-fat diet, but not on a low-fat diet. Fat loss came with no change in energy expenditure and with reduced food intake, which occurred without signs of illness in a conditioned taste aversion test, and despite lower leptin.

Participants / model
Lean and obese mice and rats
Treatment
Proapoptotic peptide for 4 or 27 days; dose and route not stated in the abstract
Follow-up
4 or 27 days
Study design
Preclinical study
Funding
not stated in the source

The abstract calls the molecule a proapoptotic peptide and does not name adipotide, so the page says a peptide of this design.

Read the original source
Mouse paper: glucose tolerance improved independent of weight and food intake

Animal study

Kim DH et al. Diabetes. 2012;61(9):2299-310. PMID 22733798.

In obese mice on a high-fat diet, the peptide improved glucose tolerance on days 2 and 3 of treatment in a weight- and food-intake-independent way, compared with vehicle and with mice pair-fed to the treated group, and it lowered serum insulin and triglycerides. The authors read this as a role for adipose vasculature in glucose and lipid handling.

Participants / model
Obese mice on a high-fat diet
Treatment
Proapoptotic peptide; dose and route not stated in the abstract
Follow-up
Glucose tolerance measured on days 2 and 3 of treatment
Study design
Preclinical study with vehicle and pair-fed comparison groups
Funding
not stated in the source

The same academic group as the rodent food-intake paper. The abstract calls the molecule peptide or PP and does not name adipotide.

Read the original source
NCT01262664: first-in-man phase 1, terminated at 4 participants, no results

Trial registry record

ClinicalTrials.gov record NCT01262664, sponsor M.D. Anderson Cancer Center. Last update posted 2019-01-04.

The record is titled as a first-in-man phase 1 of a single cycle of Prohibitin Targeting Peptide 1 in patients with metastatic prostate cancer and obesity. The drug is listed as Prohibitin-TP01 by subcutaneous injection with dose escalation. Status is terminated per the principal investigator's request, actual enrollment 4, start 2012-05-24, completion 2019-01-02, and no results are posted.

Participants / model
Men with metastatic prostate cancer on androgen deprivation therapy, BMI over 30
Treatment
Prohibitin-TP01 subcutaneous injection
Follow-up
Single cycle; started 2012-05-24, completion listed 2019-01-02
Study design
Registered first-in-man phase 1
Funding
Sponsor: M.D. Anderson Cancer Center

Primary aims were acceptable dose and biologic activity. The record does not use the word adipotide or the sequence, so it cannot be called an adipotide trial without a primary source that ties the two names. No results are posted.

Read the original source
Targeted liposomes in ob/ob mice: more uptake in kidneys than in fat

Animal study

Bauknight DK et al. PLoS One. 2019;14(11):e0224917. PMID 31725756.

In leptin-deficient ob/ob mice, liposomes carrying an adipose targeting sequence and the drug tesaglitazar did not take up more in adipose than in other tissues, did take up more in the kidneys, and did not significantly change metabolic parameters.

Participants / model
ob/ob mice
Treatment
Adipose targeting sequence conjugated to liposomes carrying tesaglitazar
Follow-up
not stated in the source
Study design
Preclinical biodistribution study
Funding
not stated in the source

This tested a liposome carrying a different drug, not adipotide, and the abstract does not give the sequence of the targeting sequence. It is a kidney-uptake caution for fat-targeting peptides in a different formulation, not proof of anything about adipotide.

Read the original source
FDA and DailyMed: no adipotide record, 10 October 2026

Regulatory record

U.S. Food and Drug Administration, openFDA Drugs@FDA query for adipotide, and DailyMed search for the drug name adipotide, run on 10 October 2026.

The openFDA Drugs@FDA query for adipotide returned no match, and a DailyMed search for the drug name adipotide returned no label. No FDA record was found in these two sources, so adipotide is not an FDA-approved drug or a labeled product.

Participants / model
Not a clinical population
Treatment
Not applicable
Follow-up
Searches run on 2026-10-10
Study design
Official FDA and NLM records
Funding
not stated in the source

This says nothing about other regulators.

Read the original source

Why is Adipotide in D tier?

D fits a research chemical whose evidence stops at animals. The mouse and monkey papers tell a coherent story, but the only primate paper also reports reversible kidney tubule changes, a letter and a rodent paper both raise reduced eating as an explanation for the weight loss, and the one registered human study ended at 4 participants with no results. There is no regulator record and no human efficacy or safety data.