Adipotide (FTPP)

Structure: Two-peptide chimera. The targeting motif (CKGGRAKDC) binds prohibitin on the surface of adipose vasculature endothelial cells. This is fused to (KLAKLAK)2, a D-amino-acid pro-apoptotic sequence that disrupts mitochondrial membranes in the bound cells. The result is selective vascular pruning of white fat tissue.

Status: Research compound, not for human use.

• Adipotide has never been administered to humans in any approved clinical trial.
• The most cited preclinical work is in obese rhesus macaques (Barnhart et al., Science Translational Medicine, 2011). At efficacious doses, all primates developed reversible proximal renal tubule damage detectable by urinalysis. This dose-limiting nephrotoxicity has prevented human translation.
• Any product sold as "Adipotide" or "FTPP" online is research-grade, of unverified purity, and is being used by individuals outside any regulatory or medical framework.

Dosage (preclinical only, primates):

• 0.43mg/kg/day SubQ for 28 days produced ~11% body weight loss with reversible nephrotoxicity
• No human dose has ever been validated

Administration:

• SubQ in animal studies
• Not used in humans in any clinical setting

Key Notes:

• The mechanism is unique among fat-loss agents: it physically destroys the blood supply to adipose tissue rather than altering appetite, lipolysis, or thermogenesis. The fat does not return as quickly because the vascular bed itself is damaged.
• Renal tubular damage is the central safety issue. Proximal tubule cells also express prohibitin, and the peptide accumulates there during clearance. In primates the damage was reversible at the doses studied; chronic or repeat dosing has not been tested.
• Pharmacokinetics, immunogenicity, and long-term safety in humans are completely unknown.
• VitalMetrics does not endorse self-experimentation with Adipotide. This entry exists for educational completeness only. GLP-1 receptor agonists (semaglutide, tirzepatide, retatrutide) and GIP/GLP-1 dual agonists are dramatically better-supported tools for fat loss in humans.
• If a user nonetheless self-administers, the absolute minimum monitoring is urinalysis (proteinuria, glucosuria), serum creatinine, eGFR (preferably cystatin C-based), and a full electrolyte panel before, during, and after exposure.

References:

• Barnhart, K. F., Christianson, D. R., Hanley, P. W., Driessen, W. H., Bernacky, B. J., Baze, W. B., Wen, S., Tian, M., Ma, J., Kolonin, M. G., Saha, P. K., Do, K. A., Hulvat, J. F., Gelovani, J. G., Chan, L., Arap, W., & Pasqualini, R. (2011). A peptidomimetic targeting white fat causes weight loss and improved insulin resistance in obese monkeys. Science Translational Medicine, 3(108), 108ra112. DOI: 10.1126/scitranslmed.3002621
• Kolonin, M. G., Saha, P. K., Chan, L., Pasqualini, R., & Arap, W. (2004). Reversal of obesity by targeted ablation of adipose tissue. Nature Medicine, 10(6), 625-632. DOI: 10.1038/nm1048
• Daquinag, A. C., Zhang, Y., Amaya-Manzanares, F., Simmons, P. J., & Kolonin, M. G. (2011). An isoform of decorin is a resistin receptor on the surface of adipose progenitor cells. Cell Stem Cell, 9(1), 74-86. DOI: 10.1016/j.stem.2011.05.017