Adipotide
A peptidomimetic that targets prohibitin on the vasculature of white adipose tissue, inducing apoptosis of fat cells and rapid weight loss in primate models.
Also referenced as: FTPP, Prohibitin-Targeting Peptide
Also appears in: Metabolic
This name primarily lives in the research market and should not be read like an approved pharmaceutical product.
Primary lane: Weight Loss. Also surfaces under Metabolic for browsing and discovery.
FTPP, Prohibitin-Targeting Peptide
No FDA label signal · 2 trials · 19 PubMed results
Current evidence for Adipotide is limited to laboratory or animal studies — there are no name-matched human trials with reported results. Any claims about effects in people are not yet backed by clinical data.
Adipotide has no clinical trials that name it and 19 PubMed-indexed publications and is not FDA-approved. Current evidence is preclinical or mechanistic.
Re-checked nightly against the registries — tracked since 2026-07-09. No band changes yet.
Grades evidence strength, not efficacy or safety. Research-use context; not medical advice. Graded 2026-07-13 from PubMed, ClinicalTrials.gov, ISRCTN, openFDA, Health Canada, and OpenAlex — computed deterministically and refreshed nightly, with a retraction check. How we grade →
What is Adipotide?
Adipotide (also known as FTPP) is a synthetic peptidomimetic composed of two functional domains: a targeting sequence that binds to prohibitin — a protein expressed on the surface of blood vessels supplying white adipose tissue — and a pro-apoptotic sequence (KLAKLAK)₂ that disrupts mitochondrial membranes. By selectively destroying the blood supply to fat tissue, Adipotide causes fat cell death through ischemia.
How it works
- Vascular targeting — the targeting domain binds prohibitin, which is selectively expressed on the endothelium of white adipose tissue vasculature but not on vessels in other organs (Kolonin et al., Nature Medicine, 2004)
- Apoptosis induction — once internalized, the (KLAKLAK)₂ domain disrupts mitochondrial membranes in endothelial cells, triggering apoptosis (Ellerby et al., Nature Medicine, 1999)
- Adipose ischemia — destruction of the fat tissue vasculature starves adipocytes of blood supply, leading to fat pad shrinkage
Research status
Adipotide gained significant media attention after primate studies:
- Kolonin et al. (2004) demonstrated that prohibitin-targeting peptides selectively destroy white fat vasculature in mice, causing rapid weight loss (Nature Medicine, 10(6):625–632)
- Barnhart et al. (2011) showed that Adipotide treatment in obese rhesus monkeys caused significant weight loss (average 11% body weight) and improved insulin resistance over 28 days (Science Translational Medicine, 3(108):108ra112)
- The primate study also noted reversible renal toxicity (proximal tubule changes) that resolved after treatment cessation
No human clinical trials have been completed. An IND application was reportedly filed but no Phase I data has been published as of mid-2025.
Key considerations
- The primate data in Science Translational Medicine is unusually strong for a research peptide — most compounds lack any primate studies
- Renal toxicity observed in the monkey study raises safety concerns that have not been resolved in human trials
- The mechanism is inherently destructive (killing blood vessels) rather than metabolic modulation, which carries higher risk
- Available from a limited number of research vendors; synthesis is complex due to the chimeric two-domain structure
- Self-administration outside clinical oversight carries significant safety risk given the known renal toxicity signal