Adipotide

DNot approved; investigational (stalled)Mitochondrial, antioxidant and longevity compounds →FTPPprohibitin-TP01fat-targeted proapoptotic peptide
In one paragraphAdipotide is a two-part synthetic peptide: a homing sequence that binds a protein on the blood vessels of white fat, joined to a fragment that triggers cell death. Cut off the blood supply and the fat tissue shrinks. In obese monkeys it produced rapid weight loss and better insulin sensitivity — and dose-dependent, reversible kidney damage. A human phase 1 trial in prostate cancer was registered in 2010 and no result was ever published. It is sold online as a fat-loss peptide on the strength of the monkey study. It is not approved anywhere and is prohibited in sport.
Schematic 3D structure of Adipotide
25 residues · fat-vessel homing loop joined to a pro-apoptotic D-peptide · schematic
Overall gradeD No human evidence
Human trials0 published; a phase 1 in prostate cancer was registered and never reported
Outcomes graded3
Last reviewed10 September 2026
EvidenceWhat it isHow it worksUnknownsMolecule & PKRegulationQuestionsReferences

What the human research shows

The one grey-market fat-loss peptide with a genuinely striking animal result, and the one whose animal result came with a kidney warning in the same paper. No human has been reported taking it.

MetabolicCardioMuscleHealingNeuroImmuneSexualSkinAgeing

Evidence profile0–5

  • Metabolic & weightD0.0
  • Cardiovascular—0.0
  • Muscle & growth—0.0
  • Healing & repair—0.0
  • Neuro & sleep—0.0
  • Immune & inflammation—0.0
  • Sexual & hormonal—0.0
  • Skin & appearance—0.0
  • Ageing & longevity—0.0
No benefit outcome for Adipotide has both human evidence and a measurable effect, so the profile is empty. That is the finding, not a gap in the chart.
OutcomeGradeEffect sizeHuman studiesWhere the evidence comes from
Fat loss (humans)DNo human evidenceNot measurable0 publishedNo human efficacy or safety data exists in the literature. The registered phase 1 (prostate cancer, not obesity) has no published result.12
Fat loss (obese primates)DNo human evidenceNot measurablePreclinical onlyObese rhesus monkeys lost weight rapidly and improved insulin resistance, with imaging confirming loss of white fat — the result the product is sold on. Grade D because it is not human evidence.1
Kidney toxicity (primates)adverseDNo human evidenceNot measurablePreclinical onlyAt effective doses, monkeys of three species showed predictable, dose-dependent changes in proximal tubule function that reversed when treatment stopped. The mechanism — the homing sequence also binds in the kidney — is the reason development stalled and the reason human use without monitoring is reckless.1
AMultiple good human trials, consistentBSome human trials, mostly consistentCFew or weak human studiesDAnimal or anecdotal onlyeffect size · red = adverse

Literature searched to 10 September 2026. Human studies only; animal and cell work informs the mechanism section and nothing else.

What it is

Adipotide came from Wadih Arap and Renata Pasqualini's laboratory at MD Anderson, built from a technology that screens peptides for the blood vessels of specific tissues. The fat-vessel homing peptide binds prohibitin; the attached D-amino-acid KLAKLAK sequence disrupts mitochondria and kills the cell. Vessels die, fat starves.

The 2011 Science Translational Medicine paper in monkeys made headlines; a phase 1 trial in men with prostate cancer (to test safety and fat loss) was registered and quietly never reported. The compound has no sponsor advancing it today.

How it is thought to work

Targeted apoptosis of adipose endothelium. It does not act on appetite or metabolism directly; it removes the tissue's blood supply. That is also why it is not selective enough — prohibitin is expressed in kidney tubules, which is where the toxicity appeared.

What is still unknown

  • Everything about it in humans: dose, effect, and whether the kidney effect is reversible in people as it was in monkeys.
  • Why the phase 1 was never published.

The molecule and how long it lasts

Identity
Formula
C111H206N36O28S2
Molecular weight
2557.2 g/mol
CAS number
859216-15-2
PubChem
CID 163360068

PubChem record, read 23 September 2026.

Pharmacokinetics
Route
Injected as sold; monkeys only
Half-life
No human pharmacokinetic data

No pharmacokinetic study in people.

Regulatory status

European Union
Unauthorised medicinal product

No marketing authorisation anywhere. Supplying it for human use is an offence under national medicines law.

United States
Not approved

Investigational; one registered phase 1 with no reported result. Sold as a 'research chemical'.

United Kingdom
Unlicensed medicine

No MHRA licence.

Australia
Prescription-only / unapproved

Not on the ARTG; imports are seized.

Canada
Not authorised

No Drug Identification Number.

Sport (WADA)
Prohibited at all times

As a non-approved substance it falls under the non-approved-substances class, prohibited in and out of competition.

Questions people actually ask

Does adipotide work for fat loss?
In obese monkeys, dramatically. In humans, nobody knows: no result has ever been published. The monkey study also found kidney damage at effective doses.
Is adipotide safe?
The only safety data is from monkeys, where it caused dose-dependent kidney tubule damage that reversed on stopping. Whether that holds in humans, at grey-market doses, without monitoring, has never been tested.
Why was it never developed?
The kidney toxicity, most likely: the peptide that homes to fat vessels also binds in the kidney. A human phase 1 was registered in 2010 and no result appeared.

One page per claimed effect

References

  1. 1
  2. 2
    Searches of PubMed and ClinicalTrials.gov for adipotide in humans.LYO literature search, September 2026Seven PubMed results, none clinical; the registered phase 1 (prostate cancer) has no published result.

Change log

  • 2026-09-10Initial publication. Grade D: primate data only; kidney signal recorded.