Adipotide (FTPP) 10mg

Adipotide (FTPP — Fat-Targeted Pro-Apoptotic Peptide) is a chimeric peptide designed to target and destroy the blood supply to white adipose tissue — an approach to fat loss that is mechanistically unique among all peptide and pharmaceutical weight loss strategies. Rather than reducing appetite, increasing fat oxidation, or altering hormonal signaling, Adipotide directly kills the endothelial cells of blood vessels supplying white adipose tissue depots, depriving fat cells of their vascular supply and inducing apoptotic fat cell death.

The targeting mechanism relies on a homing peptide that recognizes ANXA2 (Annexin A-2) expressed specifically on the vasculature of white adipose tissue, combined with a pro-apoptotic peptide (KLAKLAK sequence) that disrupts mitochondrial membranes when internalized into cells. ANXA2 expression on adipose vasculature is up-regulated in the context of metabolic obesity relative to the vasculature of other tissues — providing a degree of selectivity toward fat-associated blood vessels over general systemic vasculature. When Adipotide reaches its adipose vascular target, the pro-apoptotic domain kills the endothelial cells, the vessels collapse, and the dependent adipocytes die from ischemia.

Preclinical studies in obese non-human primates (rhesus macaques) demonstrated dramatic results: systemic Adipotide treatment produced 11% reduction in body weight over 4 weeks, with preferential loss of visceral and subcutaneous abdominal fat confirmed by MRI. This rate of fat loss far exceeded what could be achieved by caloric restriction in the study period and was accompanied by improvements in insulin sensitivity — a metabolic benefit independent of just the weight change. Importantly, the non-human primate data is one of the most directly translatable preclinical models for human metabolic disease, making these results particularly noteworthy.

The mechanism produces fat loss irrespective of caloric intake — adipose vasculature destruction works regardless of what the subject eats, making it fundamentally different from appetite-suppressing peptides whose efficacy depends on behavioral compliance with reduced intake. However, this mechanism also carries the potential for adverse effects: nephrotoxicity was observed in the NHP study at therapeutic doses (elevated creatinine, tubular injury on kidney biopsy), attributed to ANXA2 expression on renal tubular vasculature causing off-target renal vessel damage. This nephrotoxicity was reversible in most cases but represents a significant safety consideration.

Human Phase 1 safety data is not publicly available. Adipotide remains a preclinical/early research compound. Its significance lies in demonstrating proof-of-concept for adipose vascular targeting as a fat loss mechanism — a category of approach entirely distinct from all current pharmaceutical weight loss strategies. Research applications include mechanistic studies of adipose vasculature biology, proof-of-concept for vascular targeting peptide approaches, and preclinical fat loss model work.

Research compound — not for human use. The nephrotoxicity findings in NHP studies represent a significant preclinical safety concern that would require resolution before clinical development proceeds.