Last updated: March 2026
Adipotide (FTPP) doesn't suppress appetite — it destroys the blood supply to white fat tissue directly, triggering adipocyte apoptosis via mitochondrial disruption. Primate studies showed ~11% body weight and ~30% fat mass reduction in 28 days. Kidney toxicity has blocked human trials.
Adipotide uses a two-domain strategy: a targeting sequence that homes to white adipose tissue vasculature, and a proapoptotic sequence that destroys the endothelial cells of fat blood vessels. Cut off the blood supply — the fat cells die. This is fundamentally different from metabolic or appetite-based approaches.
The targeting domain of adipotide (sequence: CKGGRAKDC) binds to two receptors — annexin A2 (ANXA2) and prohibitin — that are selectively expressed on the luminal surface of white adipose tissue vasculature. These receptors are not significantly expressed on blood vessels of other tissues, providing tissue-specific targeting. The peptide reaches these receptors via systemic circulation and accumulates in white fat.
Once bound, the proapoptotic domain (D(KLAKLAK)2) disrupts mitochondrial membranes. This amphipathic peptide inserts into the inner mitochondrial membrane, dissipating the electrochemical gradient required for ATP synthesis. The result is rapid apoptosis of the endothelial cells lining the fat blood vessels. Without vascular supply, white fat cells undergo ischemic death.
In the Barnhart et al. (2011) rhesus monkey study, adipotide reduced white fat mass by ~30% while preserving lean body mass. MRI analysis showed selective reduction in subcutaneous and visceral white adipose depots. Brown adipose tissue and other organs were not significantly affected. This selectivity is attributed to the differential expression of ANXA2/prohibitin in white vs. brown fat vasculature.
The same ANXA2 receptor that adipotide targets in fat vasculature is also expressed in kidney tubular epithelial cells. This off-target binding causes nephrotoxicity — elevated serum creatinine, BUN elevation, and histological evidence of tubular damage were observed in treated monkeys. The toxicity appears dose-dependent, but a safe therapeutic window for humans has not been established, blocking progression to clinical trials.
All data from Barnhart et al., Science Translational Medicine, 2011 — obese rhesus monkeys treated with adipotide vs. saline control over 28 days. No human clinical data exists.
Safety data from primate studies only. Human incidence rates are unknown. Kidney toxicity is the primary safety concern that has blocked human trials.
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This page is for educational and research purposes only. Adipotide (FTPP) is an experimental compound with no completed human clinical trials. It has demonstrated kidney toxicity in primate studies. It is not approved by the FDA or any regulatory agency. This is emphatically not medical advice. Do not use this compound — its safety profile in humans is entirely unknown.