reviewed april 2026|next review october 2026|88 physicians psi has verified|592 published studies
Adipotide (FTPP)
Adipotide (FTPP) is a peptidomimetic that targets and destroys fat tissue blood vessels by binding prohibitin on adipose vasculature, producing dramatic weight loss in primate studies but with dose-limiting kidney toxicity that has stalled clinical development.
Evidence landscape: 592 published studies
Limited published studies. Mouse and primate data only. No human clinical trials.
- 18 Human
- 148 Animal
- 34 Reviews
- 392 Other research
Contains a targeting peptide that binds prohibitin on adipose vasculature, coupled to a pro-apoptotic sequence that kills fat tissue blood vessels, starving fat cells of blood supply.
Obese rhesus monkeys lost approximately 11% body weight in 4 weeks. The most aggressive fat loss result in published peptide research.
Significant kidney toxicity was observed. The prohibitin target is also present in renal proximal tubules. Development appears stalled.
PSI Assessment
Adipotide produced the most dramatic fat loss result in published peptide research: 11% body weight reduction in 4 weeks in obese monkeys. It works by a mechanism no other peptide uses: targeted destruction of the blood vessels that feed fat tissue. Without blood supply, fat cells die. The concept generated enormous media attention. But kidney toxicity is a fundamental problem. The same targeting mechanism that finds fat tissue blood vessels also damages kidney blood vessels. Development appears stalled because this safety challenge has not been solved.
The most aggressive fat loss approach ever studied in primates. 11% weight loss in 4 weeks. Development stalled by dose-limiting kidney toxicity.
Adipotide combines a targeting peptide (CKGGRAKDC) that binds prohibitin on adipose vasculature with a pro-apoptotic sequence (D(KLAKLAK)2) that destroys mitochondrial membranes in the targeted cells. The targeting is effective for fat tissue, but prohibitin is also expressed in kidney tubule cells. The resulting nephrotoxicity (kidney damage) is the central obstacle. No published approach to solving this off-target effect has been described.
What the evidence supports
Adipotide produces rapid fat loss in obese rhesus monkeys (approximately 11% body weight in 4 weeks) through targeted destruction of adipose tissue vasculature. The prohibitin-targeting mechanism selectively binds fat tissue blood vessels.
What is not yet established
How to eliminate dose-limiting kidney toxicity observed in primate studies. Safety or efficacy in humans. Whether vascular disruption of adipose tissue is a viable therapeutic approach given the renal damage. No clinical development program appears active.
Research Evidence
The findings below cover the targeting mechanism, the primate weight loss data, and the kidney toxicity that limits development.
Evidence by condition
Evidence dimensions for adipotide. Fat loss efficacy has primate data. Safety concerns dominate the development outlook.
| Condition | Mechanism | Animal evidence | Human evidence | Replication |
|---|---|---|---|---|
| Obesity/Fat Reduction |
In obese rhesus monkeys, adipotide produced approximately 11% body weight loss over 4 weeks with targeted reduction in abdominal fat. The weight loss was rapid and substantial compared to any other peptide-based approach.
The primate data is dramatic for the field. However, a single study in one primate species does not establish a viable therapeutic path, particularly with the observed toxicity.
The targeting peptide binds prohibitin on the surface of white adipose tissue blood vessels. The pro-apoptotic payload disrupts mitochondrial membranes upon internalization, killing the endothelial cells and collapsing the vascular supply to fat tissue.
The mechanism of action is well-characterized. The problem is not efficacy but off-target binding in kidney tubules.
Dose-limiting nephrotoxicity (kidney damage) was observed in the primate study. Prohibitin is expressed in renal proximal tubule cells, and the targeting peptide binds there as well.
The kidney toxicity is not an incidental side effect. It results from the same binding mechanism that produces the fat loss, making it inherently difficult to separate efficacy from toxicity.
18 Human|148 Animal|34 Reviews
View all 592 indexed studiesHow Adipotide (FTPP) Works
Adipotide is a dual-domain peptidomimetic containing a prohibitin-targeting sequence fused to a pro-apoptotic payload that destroys adipose tissue vasculature, causing fat cell death through blood supply deprivation.
Fat tissue needs blood vessels to survive, just like any other tissue. Adipotide is designed to find and destroy the blood vessels that feed fat cells. Without blood supply, fat cells die and are absorbed by the body. The problem is that the peptide can also damage blood vessels in the kidneys.
For a more detailed view of the biology, here is what researchers have observed at the molecular level.
The targeting domain (CKGGRAKDC) binds prohibitin on the surface of white adipose tissue endothelial cells. The cytotoxic domain (D(KLAKLAK)2) is a designed amphipathic peptide that disrupts mitochondrial membranes upon cellular internalization, triggering apoptosis. The compound enters cells through receptor-mediated endocytosis following prohibitin binding. Off-target toxicity occurs because prohibitin is also expressed in renal proximal tubule epithelium.
What is Adipotide (FTPP) being studied for?
Researchers are studying Adipotide (FTPP) across several health conditions. Each condition below is labeled with the strength of evidence that exists for that specific use, not for Adipotide (FTPP) overall. This means a compound can have human studies for one condition but only animal data for another.
Obesity/Fat Reduction
·Preclinical11% body weight loss in 4 weeks in obese rhesus monkeys through targeted destruction of adipose vasculature. The most dramatic fat loss result in published peptide research.
Limitations: One primate study. Dose-limiting kidney toxicity. Human studies have not been conducted. Development appears stalled. The toxicity arises from the same mechanism that produces efficacy, making it fundamentally difficult to resolve.
Safety and Regulatory Status
FDA Status: Not FDA-approved. Not in clinical development. Human studies have not been conducted.
Availability: Research compound only. Not available for human use through any channel.
Class context: Caused reversible but significant kidney toxicity in primate studies. Renal damage is the primary safety concern and the reason development appears stalled.
Significant safety concerns. Kidney toxicity in primate studies is dose-limiting and arises from the same prohibitin-targeting mechanism that produces fat loss. This compound is not available for human use.
Peptide Structure
Technical molecular data for researchers and clinicians.
Questions and Comparisons
Questions the evidence raises for a Adipotide (FTPP) discussion.
Comparison and Related Research
Adipotide represents a fundamentally different approach to fat loss compared to other weight management peptides.
Related compounds
Frequently Asked Questions
References
Each citation links to the original study on PubMed, the U.S. National Library of Medicine database.
- 1.First demonstration that a peptide targeting adipose tissue vasculature could reverse obesity in mice by destroying blood vessels that supply fat tissue, causing fat cell death from loss of blood supply.Kolonin MG et al., 2004 in Nat Med. View on PubMed
- 2.Showed that adipotide caused approximately 11% body weight loss in 4 weeks in obese rhesus monkeys with improved insulin sensitivity, providing the most advanced preclinical validation of targeted fat tissue ablation.Barnhart KF et al., 2011 in Sci Transl Med. View on PubMed
- 3.Characterized prohibitin as a surface marker on adipose tissue blood vessels and validated the concept of using peptide-guided vascular targeting to selectively destroy fat tissue.Kim DH et al., 2010 in J Drug Target. View on PubMed
- 4.Provided additional characterization of the adipose vasculature targeting mechanism, supporting the molecular basis for how adipotide selectively binds fat tissue blood vessels over other vascular beds.Daquinag AC et al., 2011 in Diabetes. View on PubMed
Medical Disclaimer
This content is for educational and informational purposes only and does not constitute medical advice. The information presented reflects published research as indexed by PSI and should not be used to make treatment decisions. Always consult a qualified healthcare provider before starting, stopping, or modifying any treatment.