Adipotide
Weight Loss
In short
- A peptidomimetic designed to destroy the blood supply of white adipose tissue, causing fat cells to die from lack of perfusion.
- This is a fundamentally different and more aggressive mechanism than appetite suppression — it is targeted vascular ablation.
- Primate studies showed substantial fat loss and also DOSE-DEPENDENT KIDNEY TOXICITY.
- The renal toxicity is the reason development effectively stopped, and it is the central fact about this compound.
- No completed human trial. Not approved anywhere.
Structure
How it works
Adipotide consists of a targeting peptide that binds prohibitin and annexin A2 on the endothelium of blood vessels feeding white adipose tissue, linked to a pro-apoptotic peptide.
Once bound, the pro-apoptotic domain triggers death of those endothelial cells. The capillary network supplying the fat depot is destroyed, and the adipocytes it fed undergo apoptosis from ischaemia.
The targeting is what is supposed to make this selective. Whether the targeting is selective enough is exactly what the kidney findings call into question — the kidney is a highly vascular organ.
What the research shows
In obese rhesus monkeys, treatment produced roughly 11% weight loss over four weeks with reductions in fat mass and improved insulin sensitivity.
The same studies documented dose-dependent renal toxicity — changes in renal tubular epithelium and impaired kidney function.
A phase 1 trial in obese men with prostate cancer was initiated. No results establishing safety and efficacy in humans have been published.
Development did not continue.
Dosing in the literature
Figures below are quoted from published studies, with the species or population they were measured in. They are records of what was studied, not recommendations.
| Studied in | Amount | Route | Source |
|---|---|---|---|
| Rhesus monkey — obesity study | 0.43 mg/kg daily for 28 days | subcutaneous | PubMed |
Commonly reported ranges
These are amounts people report using. They are not from any study, have not been evaluated for safety, and are reproduced here only because they circulate widely and are better seen alongside the evidence than instead of it.
| Reported by | Amount | Route |
|---|---|---|
| Commonly reported | 0.5 mg/kg daily in short cycles | subcutaneous |
The primate dose is the only meaningful reference point, and the primate study is also where the kidney toxicity was documented — at the doses that produced the fat loss. Community protocols reproduce that dose. The toxicity is not a rare idiosyncratic reaction; it was dose-dependent and expected.
Handling and storage
Supplied as a lyophilised powder requiring reconstitution with bacteriostatic water. The powder is comparatively stable; once reconstituted it is refrigerated and used within weeks. Track the date you reconstitute each vial — the Inventory section does this, and it is the difference between knowing a vial is three weeks old and guessing.
Subcutaneous injection in short cycles is the community pattern.
Anyone using this should understand that renal function monitoring is the relevant precaution, and that the toxicity observed in primates was dose-dependent rather than incidental.
Side effects
The dominant and defining concern is renal toxicity. Primate studies showed dose-dependent changes in kidney function and renal tubular epithelium at therapeutic doses.
Other reported effects in animals include dehydration and reduced food and water intake.
No human safety database exists.
This is one of the few compounds in this library where a specific, serious, dose-dependent organ toxicity has been documented in a primate model at the doses that produce the desired effect. That combination is unusual and should carry a lot of weight.
Combinations
No interaction data. Combining with anything nephrotoxic — NSAIDs, certain antibiotics, high-dose creatine in dehydrated states — compounds the primary documented risk.
Adequate hydration is the one clearly relevant supportive measure.
Research status
Developed at MD Anderson by Arap and Pasqualini. The primate work was published in Science Translational Medicine in 2011 and attracted significant coverage.
A phase 1 trial was registered. Development has not advanced, and the renal findings are the widely understood reason.
Legal status
Not approved in any jurisdiction. Sold for research use only.
WADA status
Not specifically named on the Prohibited List. Falls under WADA class S0, which prohibits any pharmacological substance not currently approved by any governmental regulatory health authority for human therapeutic use. Treat it as prohibited in sport.
Conclusion
Adipotide works by killing the blood supply to fat tissue, and in the primate study that produced it, it also damaged kidneys in a dose-dependent way at the doses that worked.
Of everything in this library, this is the compound where the documented harm is most specific, most serious, and most directly tied to the effective dose.
Sources
Track your own Adipotide protocol
Peppers logs your doses, models your levels from this half-life, tracks your vials and tells you when you will run out. Free on iPhone.
Reference and educational information only. Not medical advice. Nothing here diagnoses, treats, or prescribes, and nothing here is a recommendation to use any compound. The compounds described are research chemicals and are not approved for human consumption. Legal and anti-doping status change — the review date above is when these claims were last checked. Talk to a qualified clinician about anything you intend to take.