Adipotide

Adipotide (also called FTPP or Prohibitin-TP01) is an experimental peptide drug (peptidomimetic) for obesity: it selectively destroys the blood vessels that supply white adipose tissue, triggering apoptosis of the attached fat cells. The compound has no regulatory approval and is not available for human use - the only published evidence comes from mouse and non-human primate studies, and a Phase 1 trial announced in 2012 never produced peer-reviewed results.

How does Adipotide work?

Adipotide is a bipartite (chimeric) peptide with the sequence CKGGRAKDC-GG-D(KLAKLAK)2:

• The first part (CKGGRAKDC) is a homing sequence that binds prohibitin, a membrane protein enriched on endothelial cells of white adipose vasculature.
• The second part (D(KLAKLAK)2) is a pro-apoptotic domain that, after internalization, disrupts mitochondrial membranes and triggers apoptosis.

The white-fat vascular endothelium dies, blood supply collapses, and the fat tissue is resorbed - a mechanism fundamentally different from incretin mimetics such as tirzepatide, which act through appetite and metabolism.

What does the evidence show?

Mouse study (2004)

The Kolonin group at MD Anderson Cancer Center showed in Nature Medicine in 2004 that daily adipotide in diet-induced obese mice produced roughly 30 % weight loss over 28 days, with no effect in lean animals. The paper established prohibitin as a vascular marker of white adipose tissue.

Primate study (2011)

Kirstin Barnhart and colleagues treated spontaneously obese rhesus macaques with 0.43 mg/kg adipotide subcutaneously for 28 days. Treated animals lost about 11 % body weight, BMI and waist circumference dropped, and insulin resistance improved measurably. The study was published in Science Translational Medicine in 2011 and remains the clinically most informative preclinical work to date.

Phase 1 trial (2012, never published)

In July 2012, Arrowhead Research announced the start of a Phase 1 trial in obese prostate-cancer patients at MD Anderson. Up to 39 participants and five dose levels were planned, but no peer-reviewed results were ever published - the clinical program is widely considered discontinued.

Safety profile

In all three non-human primate species studied by Barnhart et al., adipotide produced dose-dependent, reversible renal tubular changes - elevated creatinine, glucosuria, proteinuria, and increased renal epithelial cells in urine. This proximal tubule toxicity became the central hurdle for clinical development. No human safety data have ever been published.

Regulatory status and availability

• No FDA approval, no EMA approval.
• Not on the FDA 503A compoundable substances list; no legal source for human use.
• Listed on the WADA Prohibited List under category S0 (prohibited at all times).

For these reasons, there are no human dosing data and no approved vial formats for adipotide. If you want a general step-by-step overview of how lyophilized peptides are reconstituted for research purposes, see the peptide reconstitution guide.

Where does Adipotide fit in the peptide landscape?

Compared with tirzepatide and AOD-9604 - other peptides aimed at metabolism and weight - adipotide is conceptually elegant but never made it past preclinical work. A current overview of clinically successful peptides against obesity is available in the obesity overview at AOD-9604. All numbers above come from preclinical studies and are context only - not a dosing recommendation.

This article is for general information and education only. It is not medical advice and does not recommend the use or sourcing of adipotide.