Weight Loss Peptide –Adipotide(FTPP)

Adipotide, also known as FTPP (fat-targeted proapoptotic peptide) or prohibitin-TP01, is one of the most prominent examples of ligand-mediated peptide mimetics. Designed to target vascular markers in white adipose tissue (WAT), it can promote programmed cell death in adipose tissue microvessels, thereby impairing fat outflow and promoting the reduction of fat depots in mammalian research models.
Adipotide is a chimeric peptide consisting of a loop domain (CKGGRAKDC) fused to the proapoptotic D-amino acid oligomer D(KLAKLAK)2. The loop domain appears to bind to endothelial receptors (primarily prohibitin and annexin A2) present in white adipose tissue vessels. This mitochondrial-damaging D-peptide is subsequently internalized and can induce cell death in adipose-supported capillaries in mammalian research models.
Studies have shown that adipotide can selectively target these receptors. Preliminary data suggest that the annexin A2-arrestin-CD36 receptor complex can regulate fatty acid uptake by endothelial cells, and this peptide may inhibit this process.
Preliminary studies in diet-induced obese mice indicate that adipotide can significantly reduce white adipose tissue (WAT) mass. Over a four-week treatment period, mice exposed to FTPP experienced a reduction in total body weight of approximately 30% compared to the control group. The study found that the reduction in body fat also reduced calorie intake, while metabolic rate remained stable or even increased slightly.
Further observations show that improvements in glucose tolerance and insulin sensitivity can occur rapidly in these mouse models, suggesting that FTPP can modulate metabolic signaling independent of weight loss. These results provide a powerful platform for studying the mechanisms of ghrelin-fat signaling mediated by white adipose tissue (WAT) vessels.
In obese mouse models, 4 weeks of FTPP exposure reportedly resulted in a reduction in total body weight by approximately 11% and adipose tissue volume by 27–40%. Imaging techniques such as MRI and dual-energy X-ray absorptiometry (DEXA) confirmed significant atrophy of visceral and subcutaneous adipose tissue in these mice.
Furthermore, the study demonstrated a significant improvement in insulin sensitivity and a 50% reduction in insulin requirements, based on metabolic assessment. Since lean mice showed minimal changes in body weight at the same concentrations, these data suggest a treatable mechanism for obesity.