Adipotide Peptide (FTPP) – Research Overview
Adipotide (also known as FTPP or Fat-Targeted Proapoptotic Peptide) is an experimental synthetic peptidomimetic engineered to selectively target and eliminate white adipose tissue (fat cells). By inducing targeted cell death (apoptosis) in the blood vessels supplying fat cells, Adipotide has become a primary subject of study in obesity mitigation, metabolic regulation, and lipid research.
Quick Chemical Profile
- Molecular Formula: $C_{152}H_{252}N_{44}O_{42}$
- Molecular Weight: 2611.41 g/mol
- Synonyms: FTPP, Prohibitin-Targeting Peptide 1 (Prohibitin-TP01)
- Application: Laboratory Research Use Only
Mechanism of Action: How Adipotide Works
Adipotide functions through a dual-sequence design that targets the vascular supply of fat tissue rather than the nervous system or appetite centers.
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Targeted Binding: The peptide isolates a specific sequence (
CKGGRAKDC) via phage display that acts as a homing mechanism for prohibitin (PHB1) and annexin A2 (ANX2)—two proteins heavily expressed on the endothelial surface of white adipose tissue blood vessels. -
Mitochondrial Disruption: Once bound, the peptide introduces its proapoptotic payload, the D(KLAKLAK)2 sequence. This action disrupts mitochondrial membranes within the targeted vasculature.
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Apoptosis & Fat Burning: By cutting off the blood and nutrient supply to adipocytes (fat cells), the tissue undergoes programmed cell death (apoptosis). The body then metabolizes the stored fat to use as fuel.
Key Research & Clinical Insights
1. Significant Weight and Adipose Reduction
In landmark preclinical primate models, subjects presented with daily doses of Adipotide over four weeks demonstrated remarkable body composition changes without any alteration to diet or exercise routines:
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11% reduction in overall body weight.
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39% reduction in total fat deposits compared to baseline statistics.
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A noted reduction in food intake, prompting further research into how cellular fat loss interacts with systemic satiety signaling.
2. Rapid Improvement in Glucose Tolerance & Diabetes Markers
Preclinical trials on obese murine models highlighted Adipotide’s potent impact on metabolic markers, functioning independently of active weight loss.
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Homeostasis Acceleration: Within 2 to 3 days of presentation, subjects showed drastically improved glucose tolerance and a significant drop in baseline insulin and triglyceride levels.
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Mitochondrial Reversal: Microarray analysis revealed that Adipotide reversed high-fat-diet-induced damage to pathways governing oxidative phosphorylation and amino acid degradation within white adipose tissue.
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Lipid Modulation: The compound induced a shift in serum acylcarnitines, indicating an optimized mitochondrial metabolism of fatty acids.
3. Oncology and Vascular Mapping
Initial research into Adipotide’s homing mechanism stems from oncology studies mapping malignant tissue vasculature. Researchers isolated native ligand-receptors (such as integrin α4/annexin A4 and cathepsin B/apolipoprotein E3) to identify how specific vascular markers can be targeted to inhibit malignant cell growth by starving them of nutrient supplies.
Section 621 Disclaimer
Adipotide (FTPP) is available strictly for research and laboratory purposes only. It is not approved for human consumption, therapeutic, or clinical use. Please thoroughly review and adhere to our verified Terms and Conditions before completing your order.
Referenced Literature
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Thuaud, F., et al. (2013). Prohibitin ligands in cell death and survival. Chemistry & Biology, 20(3), 316–331.
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Kolonin, M. G., et al. (2004). Reversal of obesity by targeted ablation of adipose tissue. Nature Medicine, 10(6), 625-32.
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Salameh, A., et al. (2016). The prohibitin/annexin 2 interaction regulates fatty acid transport in adipose tissue. JCI Insight, 1(10), e86351.
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Barnhart, K. F., et al. (2011). A peptidomimetic targeting white fat causes weight loss and improved insulin resistance in obese monkeys. Science Translational Medicine, 3(108), 108ra112.
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Kim, D. H., et al. (2012). Rapid and weight-independent improvement of glucose tolerance induced by a peptide designed to elicit apoptosis in adipose tissue endothelium. Diabetes, 61(9), 2299-310.
Medical Reviewer: Dr. Marinov (MD, Ph.D.), Chief Assistant Professor in Preventive Medicine & Public Health. Expert in Nutrition, Dietetics, and Peptide Therapy Research.




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