Adipotide, aka FTPP or Fat Targeted Proapoptotic Peptide, is a synthetically developed peptidomimetic compound containing pro-apoptotic elements. Adipotide was developed to inhibit the proliferation of cancer cells through starvation. Research has suggested the impact of the peptide in depriving adipocytes of blood supply, causing them to die and be reabsorbed. Adipotide has also been researched for its action in metabolic function, with initial studies performed on monkeys and rodents. According to the results, rodents presented a 30% reduction in body weight. After 4 weeks of daily exposure to Adipotide and 4 weeks of non exposure, ten rhesus-obese females exhibited a 39% decrease in fat deposits and 11% reduction in body weight, on average. Researchers continue to consider Adipotide for its potential as a metabolic agent. This is due to the reported death of fat cells and the reduction of adipose tissue in initial studies. Adipotide is a synthetic compound with the potential to mitigate adipocytes and reduce an the overall concentration of subcutaneous fat through inducing the termination of cells that supply adipocytes within the blood vessels. R. Pasqualini and Dr. W. Arap are responsible for creating Adipotide. They reported that Adipotide appeared to deprive adipocytes in the blood, causing their death and reabsorption. Research in the peptide is still in its initial preclinical phases.


Adipotide Peptide Research

Research suggests this peptide acts through the discriminatory killing of cells in the blood vessels that feed white adipose tissue. Adipotide may lead to the vessels’ shrinkage (atrophy) and inevitably the death of cells (apoptosis), thus, cutting off the blood supply to adipocytes. This, then, may lead to insufficient or no oxygen and blood supply (ischemic injury) to the adipocytes. Since the impact is not reversible, the death of fat cells may also be rendered inevitable. The stereo-chemical structure of this peptide, as presented by molecular analysis, has displayed the potential of Adipotide to bind to two particular receptors that are found solely in the blood vessels that feed white adipose tissue. ANXA-2 and Prohibitin are the particular receptors just mentioned. Because of these receptors’ tissue specificity, the peptide has no reported impact on brown adipose tissue, and may not impact the thermogenesis of adaptive, brown fat. The thermogenesis of brown fat is particularly important just following birth, as the organisms may not typically exhibit a large capacity for heat conservation since the ratio of the body’s surface area to its volume prefers higher levels of heat loss. White adipose tissue is considered to be only produced when consumed energy surpasses used energy.

BMI Obesity and Adiposity

As of now, obesity is assessed using the skinfold thickness (anthropometry), Body Mass Index (BMI), and densitometry. A BMI score of thirty (30) is set as the obesity threshold. A rise in adiposity puts impacted organisms at high risk for such potential conditions as hyperlipidemia, cancers\, hypertension, Non-Insulin Dependent Diabetes Mellitus (NIDDM), metabolic syndrome, myocardial infarction, and cerebrovascular accidents. The morbidity rate is determined by how the adipose tissue is distributed.

What Is Adipose Tissue?

Adipose tissue is made up of lipid-storing adipose cells (adipocytes), and the vascular section where preadipocytes and macrophages are found. Adipose cell hypertrophy results from an increase of lipid discharge, and the rise in adipose mass is considered to be caused by the subsequent hyperplasia of adipose cells. This increase is marked by an elevated differentiation of preadipocytes to adipocytes, as well as a large amount of invading macrophages. Such a transformation and maintenance of elevated adipose mass is held up by a constant blood supply to the fat tissue.

What Is Ischemic Injury?

Ischemic injury – the lack of oxygen and blood supply to the adipose tissue might prevent the transformation and encourage the death of those injured fat cells. That’s why a peptidomimetic like Adipotide may potentially lead to a decrease in adipose mass by producing ischemic injury (that is not reversible) to the fat cells in white adipose tissue.

Adipotide Peptide and Obesity

A study was conducted by M G Kolonin et al (2004)(1) with the purpose of presenting that a targeted triggering of cell death in the blood vessels’ white adipose tissue, of particular interest within the context of obesity research. The study used a murine model. The experiment used a peptide motif isolate whose sequence allowed it to discriminatorily target white adipose tissue vasculature. In the mice, phage display was utilized to separate the peptide motif so that it’s alone. The results of the study suggested that the peptide motif may be linked with prohibitin, a multifunctional membrane protein. It was suggested that prohibitin was a label of vascular white adipose tissue. Also indicated by the results was the hypothesis that the cell death-causing peptide’s targeting of white adipose tissue vasculature led to the removal of the adipose tissue mass. The reabsorption of the white adipose may have led to a regularization of the metabolic processes altogether. Monkeys and rodents are biologically different, and this leads to major difficulties in the translation of obesity research developed in rats into those for monkeys.

Adipotide Peptide and Weight

A team of researchers conducted a study (2011)(3) in which a ligand-directed peptidomimetic was assessed for its functions in monkeys with obesity. The ligand-directed peptidomimetic was also named Adipotide. The study’s results presented that Adipotide did appear to trigger cell death in white adipose tissue vasculature, resulting in an improved insulin function and an accelerated decrease in weight in the primates. The decrease in white fat mass was supported by dual-energy x-ray absorptiometry (DEXA) and Magnetic resonance imaging (MRI). Results displayed an apparent enhancement in the primates’ renal function. The research suggested that Adipotide peptide may have potential in obesity mitigating prototypes. In another study in 2011(2) in which vascular labels for various organs were assessed, the research involved filtering of the library of peptides in research models of cancer, with the goal of discovering ligand-receptors particularly for specific vascular beds. A survey of motifs stemming from biopsies yielded a non-random dispersion pattern which implied the possibility to target particular, systemic vascular beds. Deeper analysis through affinity chromatography , similarity search, and protein arrays uncovered four native ligand-receptors. Two native ligand-receptors were dispersed in multiple tissues. The other receptors displayed a restricted particular dispersion with RAGE/leukocyte proteinase-3 being held to the development of secondary malignant growth in the bone, and prohibitin/annexin A2 being held to white adipose tissue. This study indicated that the receptors expressed in the white fat vasculature may have been prohibitin and ANXA-2 (annexin A2).



  1. Kolonin, M. G., Saha, P. K., Chan, L., Pasqualini, R., & Arap, W. Reversal of obesity by targeted ablation of adipose tissue. Nature medicine, 2004.
  2. Staquicini, F. I., Cardó-Vila, M., Kolonin, M. G., … & Arap, W. Vascular ligand-receptor mapping by direct combinatorial selection in cancer patients. Proceedings of the National Academy of Sciences, 2011.
  3. Barnhart, K. F., Christianson, D. R., Hanley, P. W., … & Pasqualini, R. A peptidomimetic targeting white fat causes weight loss and improved insulin resistance in obese monkeys. Science translational medicine, 2011.


NOTE: These products are intended for laboratory research use only. This peptide is not intended for personal use. Please review and adhere to our Terms and Conditions before ordering.


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