Adipotide
Chimeric peptidomimetic targeting white adipose vasculature
- Class
- Vascular-ablation peptide
- Half-life
- Unknown
- Route
- Subcutaneous (SubQ)
- Cadence
- Daily
- Evidence
- Animal data primarily
Overview
Adipotide is one of the most mechanistically radical weight-loss compounds ever tested — it doesn't suppress appetite or speed metabolism, it kills the blood vessels feeding your fat tissue. The idea: starve fat cells of their blood supply, they die, your immune system clears them, you lose weight. In obese monkeys, a 28-day course delivered ~11% body-weight loss with measurable fat-mass reduction on imaging. It never made it past early human testing.
The compound is a two-part molecule. The first half — a nine-amino-acid sequence called CKGGRAKDC — homes to prohibitin, a protein displayed on the surface of endothelial cells lining blood vessels in white fat. The second half — D(KLAKLAK)₂ — is a mitochondrial poison. When the whole molecule binds and gets internalized, it triggers apoptosis in those endothelial cells. The blood vessels collapse, the fat depot loses its nutrient supply, and fat cells undergo secondary death.
A Phase 1 trial was started in 2012 in obese men with castrate-resistant prostate cancer. It was terminated because of unacceptable kidney toxicity — the therapeutic window between a dose that worked and a dose that damaged kidneys turned out to be too narrow for safe use. Clinical development was permanently stopped in 2019. The peptide is still sold in research markets, but there is zero human safety or efficacy data in the public domain, and the primate data showed dose-dependent, reversible renal damage at effective doses.
Safety considerations
A few of the safety signals worth knowing — the full list, with dosing context and what to monitor, is inside AIx Core.
- Not approved for human use anywhere. The Phase 1 trial was terminated due to unacceptable nephrotoxicity — kidney damage at doses needed for efficacy. Clinical development permanently stopped in 2019.
- Dose-dependent, reversible renal tubular changes were the primary toxicity in the 2011 primate study (Barnhart). The researchers initially described these as 'predictable and reversible,' but the human trial could not find a safe therapeutic window.
- The proapoptotic domain (KLAKLAK) is inherently toxic to any cell that internalizes it — safety depends entirely on the homing peptide binding only to fat vasculature. Off-target binding to kidney, heart, or other organ vasculature could be catastrophic.
+ 3 more safety notes inside AIx Core →
Commonly monitored
Markers and signals people track when researching Adipotide.
- Serum creatinine and eGFR — dose-dependent renal toxicity was the dose-limiting factor in primates
- Body composition via DEXA or MRI — the primate studies used imaging to confirm fat-mass reduction
- Hydration status — increased urine output and mild dehydration reported at higher doses in monkeys
- Injection-site reactions
- Any signs of off-target vascular damage (unexplained pain, organ dysfunction)
Frequently asked questions
What is Adipotide?
Chimeric peptidomimetic targeting white adipose vasculature. Adipotide is one of the most mechanistically radical weight-loss compounds ever tested — it doesn't suppress appetite or speed metabolism, it kills the blood vessels feeding your fat tissue. The idea: starve fat cells of their blood supply, they die, your immune system clears them, you lose weight. In obese monkeys, a 28-day course delivered ~11% body-weight loss with measurable fat-mass reduction on imaging. It never made it past early human testing.
How is Adipotide administered?
Subcutaneous (SubQ), typically daily.
What is the half-life of Adipotide?
Unknown — No published human pharmacokinetic data; primate dosing was daily.
Is Adipotide approved for human use?
Adipotide is investigational — not approved by the FDA, EMA, or MHRA for human use at the time of writing.
What does the evidence show for Adipotide?
Evidence tier: Animal data primarily. Kolonin et al. 2004 (Nature Medicine, PMID 15133506): foundational mouse study using phage display to identify CKGGRAKDC homing to white-fat vasculature; diet-induced obese mice lost ~30% body weight over 4 weeks with the CKGGRAKDC-GG-D(KLAKLAK)₂ construct.
What is commonly monitored when researching Adipotide?
Commonly tracked markers + signals: Serum creatinine and eGFR — dose-dependent renal toxicity was the dose-limiting factor in primates, Body composition via DEXA or MRI — the primate studies used imaging to confirm fat-mass reduction, Hydration status — increased urine output and mild dehydration reported at higher doses in monkeys, Injection-site reactions, Any signs of off-target vascular damage (unexplained pain, organ dysfunction).
Related compounds
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