REGULATORYRFK Jr.: 14 peptides returning to Category 1 — FDA advisory committee July 2026TRENDINGHexarelin: ↑↑ Surging ��� Trends score 100 as of May 2026UPDATESemaglutide and tirzepatide compounding ended — shortage resolved Feb/May 2025REGULATORYBPC-157, TB-500, thymosin alpha-1, CJC-1295, ipamorelin: expected Category 1 reclassification pendingEVENTpep-talk con ��� First US Peptide Convention · August 2026 · Anaheim CAFDAFDA advisory committee meetings scheduled: late July 2026REGULATORYRFK Jr.: 14 peptides returning to Category 1 — FDA advisory committee July 2026TRENDINGHexarelin: ↑↑ Surging ��� Trends score 100 as of May 2026UPDATESemaglutide and tirzepatide compounding ended — shortage resolved Feb/May 2025REGULATORYBPC-157, TB-500, thymosin alpha-1, CJC-1295, ipamorelin: expected Category 1 reclassification pendingEVENTpep-talk con ��� First US Peptide Convention · August 2026 · Anaheim CAFDAFDA advisory committee meetings scheduled: late July 2026

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Peptide Library

Adipotide

FTPP / Prohibitin-TP01

Fat Loss & Body Composition

Adipotide (also known as FTPP or Prohibitin-TP01) is a chimeric peptide consisting of a prohibitin-targeting sequence fused to a pro-apoptotic peptide (D(KLAKLAK)2) that selectively destroys blood vessels supplying white adipose tissue, causing rapid and dramatic fat loss through vascular disruption. It was developed at the University of Texas MD Anderson Cancer Center and demonstrated remarkable fat reduction in obese rhesus monkeys, generating significant media attention. However, severe renal toxicity observed in primate studies has significantly tempered enthusiasm for its clinical development.

Mechanism of Action

Peptidomimetic that targets prohibitin on adipose vasculature. Binds to ANXA2 receptors on blood vessels supplying white adipose tissue, triggering targeted apoptosis of fat tissue endothelial cells. Causes selective fat tissue vascular disruption and subsequent fat cell death.

Research Protocols

For research purposes only. Not medical advice.

Research protocols in primates used 0.43mg/kg subcutaneously daily for 28 days. Resulted in 11% body weight loss. Human dosing not established. Very aggressive mechanism with significant renal toxicity risk.

Research Notes

Clinical Research Status

Adipotide demonstrated dramatic efficacy in a landmark 2012 primate study published in Science Translational Medicine, showing 11% body weight loss and 38% reduction in abdominal fat in obese rhesus monkeys over 28 days of treatment. Despite these impressive results, the severe kidney damage observed in treated animals has prevented progression to human clinical trials. No active clinical trial registrations for Adipotide in humans have been identified, and its development status remains uncertain with no recent publications from the original research group.

Key Published Findings

The targeting peptide CKGGRAKDC binds to prohibitin on the surface of blood vessels specifically in white adipose tissue, while the attached D(KLAKLAK)2 sequence disrupts mitochondrial membranes in endothelial cells, causing vascular collapse and subsequent adipocyte death. Treated monkeys showed dramatic reductions in body weight, BMI, abdominal circumference, and improvements in insulin resistance. Imaging studies confirmed selective destruction of adipose vasculature with corresponding fat tissue necrosis and reabsorption over the treatment period.

Safety Profile

The most significant safety concern is dose-dependent renal proximal tubule degeneration, likely due to prohibitin expression in kidney vasculature or renal filtration and accumulation of the peptide. Treated primates developed elevated BUN and creatinine levels, with histological evidence of tubular necrosis that was partially reversible upon treatment cessation. Additional concerns include the irreversible nature of vascular destruction in adipose tissue and the unknown long-term consequences of acute fat tissue necrosis on systemic inflammation and metabolic homeostasis.

Comparison to Related Compounds

Adipotide's mechanism is fundamentally different from all other fat loss compounds: rather than modulating metabolism, appetite, or lipolysis, it physically destroys the blood supply to fat tissue. GLP-1 agonists like semaglutide achieve comparable weight loss through appetite suppression without organ toxicity, making them far safer alternatives despite slower onset. The targeted vascular disruption approach was originally developed for cancer therapy (tumor angiogenesis inhibition) and represents a repurposing that may carry inherent toxicity risks in non-tumor tissue.

Community Observations

Despite significant interest generated by the primate study results, human self-experimentation with Adipotide is extremely rare due to legitimate fears of irreversible kidney damage. Online communities generally regard Adipotide as a cautionary example of dramatic efficacy coupled with unacceptable toxicity, often referenced in discussions about risk-reward calculations in experimental compound use. The compound is occasionally available from gray market peptide sources, but knowledgeable community members consistently advise against its use given the availability of safer alternatives for fat loss.

Half-Life

~30-60 minutes

Reconstitution

Bacteriostatic water (BAC)

Storage

Lyophilized

Refrigerate 2-8C. Protect from light.

Reconstituted

Refrigerate 2-8C. Use within 7 days.

US Legal Status

Research chemical (not FDA-approved)

Also Known As

FTPPProhibitin-TP01

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