FTTP is a chimeric peptide with a prohibitin-targeting “homing” domain and a pro-apoptotic domain. It binds vasculature of white adipose tissue, disrupting blood supply to adipocytes and inducing apoptosis, leading to targeted fat loss and improved metabolic parameters.
FTTP
Also known as: Adipotide; Prohibitin-Targeting Peptide
Overview
Benefits
- Targeted fat loss of visceral and subcutaneous fat
- Improved insulin sensitivity and glucose control
- Reduced cardiometabolic risk markers
- Non-invasive alternative to surgical reduction
Consider This Peptide If You Want To
- Seek targeted fat loss (e.g., abdominal)
- Aim to reduce visceral fat and improve metabolic health
Dosage & Administration
Dosage Guidelines
Recommended Dosage
• Amount:1 mg
• Frequency:daily
• Duration:14 days
• Rest Period:
• Time of Day:morning
• Ingestion:subcutaneous
Dosing should be individualized based on body weight and adjusted according to response. Regular monitoring of renal function is recommended due to potential nephrotoxic effects observed in preclinical studies.
Administration Routes:Subcutaneous Injection
Research Findings on Dosage:
Subcutaneous Injection: ● Commonly Reported Dosage: 0.5–10 mg/kg body weight, administered daily. ● Duration: 14–28 days, depending on study design and desired outcomes. Administration Notes: ● Dosing should be based on body weight and adjusted according to response and tolerability. ● Monitoring of renal function is recommended due to potential nephrotoxic effects observed in preclinical studies.
Mechanism of Action
Mechanism of Action
How this peptide works in the body
Targeted Binding to Adipose Vasculature: ● FTTP contains a homing sequence that specifically binds to prohibitin, a receptor abundantly expressed on the surface of endothelial cells in WAT vasculature. This selective binding ensures targeted delivery of the pro-apoptotic domain to adipose tissue. Induction of Apoptosis in Vascular Endothelial Cells: ● The pro-apoptotic domain of FTTP mimics the activity of BH3-only proteins, initiating the intrinsic apoptotic pathway.This leads to mitochondrial outer membrane permeabilization, cytochrome c release, and activation of caspases, culminating in endothelial cell apoptosis. Disruption of Adipose Tissue Blood Supply: ● Apoptosis of endothelial cells results in the collapse of the microvasculature within WAT, effectively starving adipocytes of oxygen and nutrients. This ischemic environment triggers secondary apoptosis of adipocytes. Reduction of Adipose Tissue Mass: ● The combined loss of vascular and adipocyte cells leads to a significant reduction in WAT mass. This effect is particularly pronounced in visceral fat depots, which are closely linked to metabolic diseases. Improvement in Metabolic Parameters: ● The reduction in visceral fat mass is associated with improved insulin sensitivity, decreased circulating free fatty acids, and enhanced glucose tolerance, contributing to overall metabolic health.
Consider Stacking With
- GLP-1 receptor agonists (e.g., Semaglutide)
- AMPK activators (e.g., AICAR)
- Mitochondrial support (e.g., CoQ10)
Side Effects & Cautions
Common Side Effects
- Mild injection site reactions (redness, swelling)
Cautions
- Not recommended with pre-existing kidney conditions
- Investigational in humans; safety/efficacy under clinical study
Rare Side Effects
- Potential nephrotoxicity observed in animal studies
Research & References
Research Highlights
● Targeted Fat Reduction (2012): FTTP induced significant weight loss in obese rhesus monkeys without affecting food intake. ● Metabolic Improvements (2013): Treated animals exhibited improved insulin sensitivity and lipid profiles. ● Selective Apoptosis (2014): Demonstrated specificity for adipose vasculature, sparing non-target tissues.
References
Kolonin, M.G., et al. (2004). Reversal of obesity by targeted ablation of adipose tissue. Nature Medicine, 10(6), 625–632. PMID: 15156200
Barnhart, K.F., et al. (2011). Selective apoptosis of adipose tissue vasculature and reduction in diet-induced obesity with an adipotide. Nature Medicine, 17(7), 911–915. PMID: 21685910