Adipotide (FTPP)
Destroys fat tissue blood supply — with renal toxicity as the dose-limiting effect.
For research purposes only. These products are not intended to diagnose, treat, cure, or prevent any disease. By purchasing, you confirm these products will be used for legitimate research purposes.
About Adipotide (FTPP)
Adipotide is not a metabolic or appetite drug. It is a chimeric peptidomimetic that homes to the annexin A2–prohibitin receptor system on the blood vessels feeding white adipose tissue, carrying a pro-apoptotic domain that then destroys that vasculature. Fat cells die because their blood supply is cut off. That mechanism is ablative and it is worth understanding before comparing it to anything in the GLP-1 class, which works by signalling. The primate data is genuinely striking. Four weeks of treatment in obese rhesus monkeys produced a 28% reduction in body fat along with reduced food intake and improved insulin resistance. The dose-limiting problem is the kidney: monkeys across three species showed changes in renal proximal tubule function, which the investigators characterised as predictable and reversible at the optimal doses they identified. Reversible renal injury is still renal injury, and it is what stands between this compound and human use. No completed human trial exists, and there is no established human dose — meaning there is no way to know where the equivalent renal threshold sits in a person.
Key Benefits
- 28% reduction in body fat over 4 weeks in obese rhesus monkeys
- Improved insulin resistance alongside fat loss
- Targets adipose vasculature selectively rather than acting systemically on metabolism
- Reduced food intake as a secondary effect
Set a goal (top of the page) to see how Adipotide (FTPP) scores against it, and what the better-evidenced alternatives are.
Category Ratings
How to Take
Common Side Effects
- Renal proximal tubule dysfunction — the dose-limiting toxicity in primates, described as reversible at optimal doses
- Reduced food intake
- Dehydration risk secondary to altered tubular function
- No human safety data exists, so the human renal threshold is unknown
- Mechanism is destruction of blood vessels, which is not selective in principle
Legal & Regulatory Status
Research use only. Not FDA-approved and no completed human trial exists. Development stalled on dose-dependent renal toxicity observed in primates.
Safety and regulatory details for FDA-approved compounds are drawn from the official product label via openFDA; clinical development status reflects ClinicalTrials.gov. This information is provided for research reference, is not endorsed by the FDA, and may not be complete or current.
Research & Sources
- A peptidomimetic targeting white fat causes weight loss and improved insulin resistance in obese monkeys — includes the renal findings (PMC3666164)
- Prohibitin ligands in cell death and survival: mode of action and therapeutic potential (PMC7111013)
- Peptides and peptidomimetics as potential antiobesity agents — overview of current status (PMC6388543)
Sources are selected for reliability (peer-reviewed literature, openFDA, ClinicalTrials.gov) but this is a research summary, not medical advice, and may not be exhaustive.