adipotide peptide

• Homing Sequence (CKGGRAKDC): This domain “hunts” for specific proteins—prohibitin and annexin A2—that are expressed uniquely on the surface of blood vessels supplying white adipose tissue.
• Killer Domain ((KLAKLAK)₂): Once the homing sequence binds to the target, the cell internalizes the peptide. This second domain then disrupts the mitochondrial membranes within those specific vascular cells, triggering apoptosis.
• Outcome: Deprived of oxygen and nutrients due to vascular collapse, the fat cells die and are eventually reabsorbed and cleared by the body’s immune system
  Research Findings and Clinical Status
  • Efficacy in Primate Studies: In high-profile research, obese rhesus monkeys treated with Adipotide lost an average of 11% of their body weight in just 28 days. They also showed a 27% reduction in abdominal fat and marked improvements in insulin resistance.
  • Clinical Discontinuation: Although Phase 1 human trials began in 2012, clinical development was largely discontinued as of 2019.
  • Current Status (2026): It is primarily sold as a “Research Use Only” chemical. It is not FDA-approved for human consumption, and introduction into humans is strictly forbidden by law outside of authorized clinical settings. 
  Key Side Effects
  The most critical side effect noted in research is dose-dependent, reversible renal (kidney) injury. Specifically, studies in monkeys showed changes in renal proximal tubule function, though these effects generally reversed once the treatment stopped

  Adipotide vs. AOD-9604

  While both target fat, they function through entirely different pathways:

  Feature	Adipotide (FTPP)	AOD-9604
  Mechanism	Kills fat vasculature (apoptosis)	Enhances fat burning (lipolysis)
  Target	White fat blood vessels	Fat metabolism pathways (HGH fragment)
  Primary Effect	Direct fat cell death	Reduction of fat storage
  2026 Safety	Significant risk of kidney stress	Generally high safety profile