Adipotide (FTPP)
A pro-apoptotic peptide that selectively destroys the vasculature supplying white adipose tissue, producing targeted fat loss without systemic metabolic effects.
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Compound Profile
Adipotide (FTPP)
Key Data
Research reference only
Research Focus
Preclinical data
⚠ Research & Educational Use Only. Adipotide (FTPP) is a research chemical documented here for scientific education. All information references peer-reviewed literature and preclinical/clinical study data. Not for human consumption. Not medical advice. Consult a licensed researcher or healthcare professional before any laboratory use.
- Uniquely targeted mechanism: destroys blood vessels feeding white adipose tissue, causing fat cell death through ischaemia
- In primate studies: 11% body weight reduction in 4 weeks without dietary restriction
- Selective for white adipose tissue vasculature - leaves visceral organs and lean tissue unaffected
- Adipotide (FTPP) is not FDA-approved for human use. It is a research chemical for scientific study only.
Research At a Glance
- Uniquely targeted mechanism: destroys blood vessels feeding white adipose tissue, causing fat cell death through ischaemia
- In primate studies: 11% body weight reduction in 4 weeks without dietary restriction
- Selective for white adipose tissue vasculature - leaves visceral organs and lean tissue unaffected
- Does not require caloric restriction to produce significant fat loss
In Plain English
Simple summaryAdipotide (FTPP, proapoptotic peptide) is a chimeric peptide developed at MD Anderson Cancer Center that selectively destroys blood vessels supplying white adipose tissue. It works by targeting prohibitin -- a protein highly expressed on the inner surface of blood vessels in fat tissue -- using a targeting sequence, then delivering a D(KLAKLAK)2 peptide that disrupts mitochondria and kills the cells it enters. The concept is elegantly targeted cell killing: identify a vessel marker unique to fat tissue, attach a mitochondria-disrupting warhead, and destroy the vessels that fat cells depend on. In obese rhesus monkeys, adipotide injections caused dramatic fat loss (average 11% body weight loss in 4 weeks) without affecting lean muscle mass, with metabolic improvements in insulin sensitivity.
- Uniquely targeted mechanism: destroys blood vessels feeding white adipose tissue, causing fat cell death through ischaemia
- In primate studies: 11% body weight reduction in 4 weeks without dietary restriction
- Selective for white adipose tissue vasculature - leaves visceral organs and lean tissue unaffected
The full scientific detail, mechanisms, citations, and dosing data, follows below.
What is Adipotide (FTPP)?
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Adipotide (FTPP - Fat Targeting Proapoptotic Peptide) is a chimeric peptide developed at MD Anderson Cancer Center that produces targeted destruction of the vasculature supplying white adipose tissue (WAT), resulting in fat cell death through ischaemic apoptosis. Its mechanism is fundamentally different from all other weight loss peptides - rather than reducing appetite or altering metabolism, it literally dismantles the blood supply that keeps fat cells alive.
The peptide's design is ingenious: it consists of two domains linked together. A targeting domain (CKGGRAKDC) that binds specifically to prohibitin expressed on the surface of white adipose tissue blood vessels, and a pro-apoptotic domain (KLAKLAK)₂ that disrupts mitochondrial membranes upon cellular internalisation. When adipotide reaches circulation, the targeting domain homes specifically to the vasculature of WAT - the peptide then penetrates into endothelial cells, where the KLAKLAK domain triggers mitochondrial disruption and apoptotic cell death. Without blood supply, the surrounding adipocytes undergo ischaemic apoptosis and are cleared by the immune system.
The selectivity of this targeting mechanism is remarkable. Despite the aggressive cytotoxic payload, the peptide preferentially accumulates in WAT vasculature rather than other tissues, due to the differential expression of prohibitin on adipose versus non-adipose endothelium. This selectivity has been validated in multiple rodent and primate models.
The landmark primate study published in Science Translational Medicine in 2011 remains the most cited research on adipotide. Obese rhesus monkeys treated for 28 days showed average weight loss of 11% with significant reduction in both subcutaneous and visceral fat. Importantly, this occurred without dietary restriction - the primates were fed ad libitum throughout. Insulin sensitivity improved beyond what weight loss alone would predict, suggesting additional metabolic effects.
The Achilles heel of adipotide research has been renal toxicity. In the primate study, some animals showed elevated serum creatinine and BUN, indicating transient kidney stress. This appears to be reversible upon cessation but has been the primary obstacle to human clinical translation. Research continues into modified versions with improved renal safety profiles.
Adipotide represents a fascinating proof of concept for "vascular targeting" approaches to adipose tissue reduction - a fundamentally different paradigm from the appetite-suppressing and metabolic-enhancing approaches of GLP-1 agents.
By the Numbers
Key Research Benefits
Documented effects observed in preclinical and clinical studies on Adipotide (FTPP). See all Metabolic & Weight peptides for comparison.
Side Effects & Risks
Adverse effects reported in the research literature. All data sourced from preclinical and clinical study reports. View all peptides' side effects →
Dosing Data from the Literature
Doses referenced below are sourced from published preclinical and clinical studies. Use the peptide dose calculator to convert these values to injection volume.
Adipotide research in non-human primates used doses of 0.5-1.0 mg/kg body weight once daily for 28 days. This produced approximately 11% weight reduction and significant visceral fat reduction.
Human-equivalent research doses extrapolated from primate data suggest approximately 0.03-0.1 mg/kg - however, no human clinical trials have been completed due to renal toxicity concerns identified in primate studies.
The renal toxicity observed in primates was reversible after cessation, but it represents the primary safety signal that has limited clinical translation. Researchers using adipotide in animal models monitor kidney function biomarkers (creatinine, BUN) throughout the protocol and maintain high fluid intake.
Administration in Research Settings
Standard reconstitution and administration methodology for laboratory research use.
Subcutaneous or intravenous administration in research models. Reconstitute with sterile saline or bacteriostatic water per vendor specifications. Administer once daily in animal research protocols.
Critical research consideration: monitor renal function markers throughout the protocol. Ensure adequate hydration (3-4x normal water intake in animal subjects). The peptide's mechanism of action begins within 24-48 hours of administration as blood vessel disruption in adipose tissue initiates.
Store lyophilised at -80°C for long-term stability; -20°C acceptable for 6 months.
What the research doesn't show
Adipotide showed serious nephrotoxicity (kidney damage) in the rhesus monkey study -- renal function declined in treated animals. This kidney toxicity is the primary obstacle to human development and has prevented the compound from advancing to clinical trials. The fat loss results are impressive but the kidney damage signal is significant enough that this compound's development path is genuinely uncertain.
Medical Expert Videos
Physicians, researchers, and pharmacologists explain Adipotide (FTPP), covering mechanisms of action, clinical context, and study findings.
Videos sourced from YouTube search. KnowYourPeptide does not endorse any individual creator. For research education only.
The Bottom Line
Adipotide (FTPP) has a growing body of preclinical evidence and a well-characterised safety profile in research settings. The most-studied application is: uniquely targeted mechanism: destroys blood vessels feeding white adipose tissue, causing fat cell death through ischaemia.
The most commonly reported side effect in research subjects is renal toxicity - the most significant concern; caused transient kidney function impairment in primate studies. It is a research chemical, not approved for human use.
Frequently Asked Questions
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Quick Reference
How It Compares
AOD-9604 and fragment 176-191 reduce fat through metabolic signaling (lipolysis, lipogenesis inhibition). Adipotide destroys the blood supply to fat tissue entirely -- a fundamentally different and more aggressive mechanism. Semaglutide and tirzepatide reduce fat through appetite suppression and metabolic effects. Adipotide's mechanism is unique in targeting the vasculature rather than the fat cells or their metabolic regulators.
Compare Adipotide (FTPP) side-by-sideResearch Use Only
This information is for educational research purposes only. This is not medical advice. Consult a qualified healthcare professional.