Adipotide
| Category | Compounds |
|---|---|
| Also known as | FTPP, Prohibitin-TP01 |
| Last updated | 2026-04-14 |
| Reading time | 3 min read |
| Tags | metabolicfat-lossproapoptoticvasculatureresearch |
Overview
Adipotide, also referred to as FTPP (fat-targeted proapoptotic peptide), is a chimeric peptide designed to recognize a marker expressed on blood vessels feeding white adipose tissue and then deliver a proapoptotic signal. Unlike appetite-suppressing drugs, it aims to reduce fat mass by pruning the vascular network that supplies adipocytes, indirectly shrinking the depot.
Preclinical research in rodent and nonhuman primate obesity models has reported sizeable reductions in body weight and adiposity with preserved lean mass. These findings placed adipotide among the most discussed experimental fat-loss compounds, even though clinical development has been limited and it remains strictly a research peptide. It is often mentioned alongside AOD-9604, Tesofensine, and Cagrilintide in longevity and body composition communities.
Adipotide's mechanism — selective vascular pruning — is conceptually distinct from GLP-1 agonists like Semaglutide or amylin analogs like Cagrilintide. That uniqueness, together with renal safety signals observed in primate studies, is a recurring theme in public discussion of the peptide.
Structure / Chemistry
Adipotide is a bipartite peptide. One domain is a homing sequence (CKGGRAKDC) that binds prohibitin on the endothelium of white adipose vasculature; the other is a proapoptotic D-amino-acid sequence (KLAKLAK)2 that disrupts mitochondrial membranes once internalized. A short linker couples the two domains.
Mechanism of Action
The homing peptide directs circulating adipotide to endothelial cells lining adipose vasculature. Upon internalization, the KLAK motif permeabilizes mitochondrial membranes, triggering apoptosis of the targeted endothelial cells. Loss of local blood supply is thought to cause adipocyte atrophy and reabsorption, reducing fat-pad size.
Research Summary
| Area | Finding | Reference |
|---|---|---|
| Rodent obesity | Weight and adiposity reduction in obese mice | Kolonin et al., Nat Med 2004 |
| Primate obesity | Body weight decreases in obese rhesus monkeys | Barnhart et al., Sci Transl Med 2011 |
| Tumor vasculature | Parent targeting strategy in cancer models | Arap et al., Nat Med 2002 |
| Safety signals | Renal proximal tubule effects observed in primates | Barnhart et al., Sci Transl Med 2011 |
| Mechanism | Prohibitin expression on adipose endothelium | Kolonin et al., Nat Med 2004 |
Pharmacokinetics
Reported preclinical regimens used subcutaneous administration over a limited dosing window (often around 4 weeks) to avoid cumulative renal exposure. Plasma half-life is short, but pharmacodynamic effects persist because vascular remodeling takes time to reverse. Human pharmacokinetic data are not well established.
Common Discussion Topics
- Renal safety signals observed in nonhuman primates and what they imply for humans.
- Whether selective fat loss without caloric restriction would alter metabolic set-point.
- Contrast with incretin and amylin-based fat-loss research (Tirzepatide, Cagrilintide).
- The role of Leptin signaling in observed body-composition changes.
- Research-only status and lack of regulated human trials.
Related Compounds
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Related entries
- AOD-9604— A modified fragment of human growth hormone (amino acids 176-191) studied for fat metabolism and lipolysis without the diabetogenic, growth-promoting, or IGF-1-elevating effects of full-length hGH.
- Cagrilintide— Cagrilintide is a long-acting amylin analog investigated for weight management, often studied in combination with GLP-1 receptor agonists.
- FGF21— FGF21 is a liver-derived metabolic hormone of the fibroblast growth factor family that regulates energy balance, glucose handling, and macronutrient preference.
- Leptin— A 167-amino acid adipokine produced by white adipose tissue that signals energy reserve status to the hypothalamus, functioning as the body's primary long-term satiety hormone — with leptin resistance being a central feature of common obesity.
- Tesofensine— Tesofensine is a triple monoamine reuptake inhibitor studied for appetite suppression and weight loss, originally investigated for neurodegenerative disease.