Adipotide is unusual in this catalogue for having a human dose in the public record that almost nobody quotes, and a monkey dose that almost everybody does.
Both figures are real and correctly reported in their sources. They differ by a factor of about fourteen.
What the compound is
Adipotide is a peptidomimetic with the sequence CKGGRAKDC-GG-(D)(KLAKLAK)2: a targeting sequence that binds a receptor on the blood vessels serving white fat, joined to a pro-apoptotic sequence that kills the cell it is delivered to. The design intent is vascular — destroy the blood supply to fat tissue — rather than metabolic or appetite-mediated. That distinction matters later, because it is the part of the story the published literature argues about.
The one human record
Exactly one human trial has ever been registered, and it is not filed under the name the market uses. A ClinicalTrials.gov search for adipotide returns zero records. The trial is:
NCT01262664 — A First-in-Man, Phase I Evaluation of A Single Cycle of Prohibitin Targeting Peptide 1 in Patients With Metastatic Prostate Cancer and Obesity, sponsored by M.D. Anderson Cancer Center.
| Field | Registry value |
|---|---|
| Intervention | Starting dose of 0.03 mg/kg, injection under the skin, once each day, for 28 days |
| Phase | 1 |
| Design | Single group, open label, treatment |
| Condition | Prostate cancer |
| First posted | 17 December 2010 |
| Start date | 24 May 2012 (actual) |
| Completion | 2 January 2019 (actual) |
| Enrolment | 4 (actual) |
| Status | TERMINATED — "Terminated per PI's request" |
| Results posted | None |
Four patients over six and a half years, terminated, no results. That is the entire human record for this compound, and the 0.03 mg/kg daily for 28 days in the intervention field is the only human dose figure in it.
It is reported here as what the registry states — a Phase 1 starting dose, in men with metastatic prostate cancer and obesity, in a trial that did not complete. Nothing on this page is a recommendation.
The figure everyone actually quotes
The number on retail and forum pages is 0.43 mg/kg, and it has a real source: the 2011 Science Translational Medicine paper that put the compound on the map, A peptidomimetic targeting white fat causes weight loss and improved insulin resistance in obese monkeys.
That paper identifies 0.43 mg/kg given subcutaneously daily for 28 days as the optimal therapeutic dose in spontaneously obese rhesus macaques, and reports 0.25 mg/kg and 0.75 mg/kg groups alongside it.
Set the two records side by side:
| Registered human trial | Monkey study | |
|---|---|---|
| Dose | 0.03 mg/kg/day | 0.43 mg/kg/day (optimal) |
| Route | Subcutaneous | Subcutaneous |
| Duration | 28 days | 28 days |
| Species | Human | Rhesus macaque, plus two other species |
| Result | None posted | Weight loss, improved insulin resistance |
Same route, same schedule, a fourteen-fold difference in the dose, and only one of them measured in people. A Phase 1 starting dose is deliberately set well below the anticipated therapeutic level, so the gap is exactly what a first-in-man design would produce — which is the point. The monkey number is not the human number, and the trial designed to find the human number stopped after four patients.
What the monkey study also found
The part of that paper least often carried forward is in its own abstract: at experimentally determined optimal doses, monkeys from three different species displayed predictable and reversible changes in renal proximal tubule function.
The body of the paper is more specific. It describes the primary side effect as relatively mild, predictable and reversible renal injury and altered tubular function; reports slight-to-moderate dose-dependent elevations in serum creatinine during subcutaneous administration above a threshold dose; and notes that after the predetermined recovery period, one treated monkey in each study still showed a slight residual elevation in serum creatinine and urinary glucose. Separately, it reports that single doses up to 100 mg/kg — described as roughly 133-fold the corresponding therapeutic dose — did not result in lethality.
These are kidney effects observed at the dose that worked, not at an overdose. A page that quotes 0.43 mg/kg as the adipotide dose and omits this is quoting half of one sentence from a study it has not read past the abstract.
The mechanism is disputed in the literature
In April 2012 the same journal published a formal Comment on the monkey paper. Its argument, in the words of its own abstract: the reported effect "may instead reflect a direct effect of adipotide on food consumption."
That is a substantive disagreement about what the compound does, published in the same venue, seven months after the original. It does not establish that the Comment is right. It does establish that the fat-vasculature mechanism presented as settled fact on retail pages has been contested in the primary literature since 2012 and never resolved, because the human programme that would have resolved it enrolled four people.
The size of the evidence file, and a counting trap
A PubMed search for adipotide on 19 September 2026 returns seven records. Only four are about the compound:
| Record | What it is |
|---|---|
| 2011, Sci Transl Med | The rhesus macaque study |
| 2012, Sci Transl Med | The Comment on it |
| 2012, Diabetes | Glucose tolerance in obese mice, weight- and food-intake-independent |
| 2013, J Control Release | A comparison of nanoparticle-targeted and bioconjugate approaches |
The other three — a study of the GPER-selective agonist G-1, a paper on epigenetic age acceleration in adolescence, and a trial of metformin's effect on GLP-1 levels — have nothing to do with adipotide and are artefacts of PubMed's term mapping.
This is the same trap this site recorded in the FDA Drug Master File list on 18 September, where a substring search for BPC returned nine rows and not one was BPC-157. A search count is not an evidence count until the rows have been read individually. Four papers, one of which disputes another, and one terminated trial: that is the file.
Where this leaves the compound
Adipotide has no approved product anywhere, no label, no posted human result, a contested mechanism, a documented renal signal at its effective animal dose, and a development programme that stopped. Its most-quoted dose figure is from macaques; its only human figure is a starting dose from a trial that enrolled four people.
For how this catalogue grades figures of this kind, see how to read a dosing claim; the full index of what has been opened for each compound is the peptide dosage chart. The general point that the human record for these compounds is usually smaller than the search volume implies is covered in peptide side effects.
Sources
- ClinicalTrials.gov, NCT01262664, full protocol section via API v2. Identification, status, design, arms and interventions modules. Read 19 September 2026.
- ClinicalTrials.gov term queries "adipotide" and "prohibitin targeting" (1 record total). Read 19 September 2026.
- Barnhart KF et al. A peptidomimetic targeting white fat causes weight loss and improved insulin resistance in obese monkeys. Sci Transl Med, 9 November 2011. DOI 10.1126/scitranslmed.3002621. Full text via PMC3666164; abstract, dose-finding and renal sections. Read 19 September 2026.
- Comment on "A peptidomimetic targeting white fat causes weight loss and improved insulin resistance in obese monkeys". Sci Transl Med, 25 April 2012. DOI 10.1126/scitranslmed.3003760. Read 19 September 2026.
- PubMed E-utilities search for "adipotide", 7 records, each summary read individually. Read 19 September 2026.