The peptide that cuts the blood supply to white fat tissue — dramatic preclinical weight loss but kidney toxicity signals that stalled its clinical development.
Adipotide (FTPP — Fat-Targeted ProApoptotic Peptide) is an experimental peptide designed by Kolonin and Arap at MD Anderson. It combines two domains: a homing sequence that binds prohibitin on the vasculature of white adipose tissue, and a proapoptotic sequence that triggers cell death once bound. Net effect: selectively destroys the blood supply to white fat, which kills the fat cells behind it.
Preclinical data in obese primates was striking — 7–10% body weight loss with 27% fat mass reduction over 4 weeks. The dose-dependent kidney toxicity signal that effectively stalled clinical development comes from those rhesus macaque studies (Barnhart 2011, PMID 22072637); the early-phase human trial (NCT01262664) was discontinued and never published in peer-reviewed literature, so “human AKI” claims trace back to the primate data + sponsor program halt rather than a published human report.
Not FDA approved. Phase 1 trials on pause due to nephrotoxicity signal. Research chemical only; strongly not recommended outside of supervised research settings.
The homing domain binds prohibitin, a receptor selectively expressed on the endothelial cells of white adipose tissue vasculature. This is the molecular basis for tissue selectivity.
The proapoptotic domain triggers cell death in the bound endothelium. Fat tissue loses its blood supply, adipocytes starve and die, adipose tissue is reabsorbed.
Kidneys filter large quantities of blood and have a vascular bed that unfortunately expresses enough prohibitin-like targets for Adipotide to accumulate. Rhesus macaque studies (Barnhart 2011, PMID 22072637) documented dose-dependent AKI and rising creatinine at therapeutically relevant doses — that primate signal is the well-documented basis for the kidney concern and the major barrier to clinical development. Human exploration has remained limited and sparse in peer-reviewed literature.
| Benefit | Evidence |
|---|---|
| Weight loss (primate) | Barnhart 2011 Sci Transl Med: 11% weight loss in obese rhesus macaques over 28 days |
| Fat-mass specific loss | Preserved lean mass in primate studies — drop was specifically from white fat |
| Metabolic improvements | Improved insulin sensitivity in animal models |
| Human exploration | Limited early-stage human work has been reported but remains sparse in peer-reviewed literature; primary safety concern traces back to the primate AKI signal |
GLP-1 agonists (semaglutide, tirzepatide, retatrutide) have largely replaced the clinical interest in Adipotide. The safety margin is just much better.
Build your protocol, log every dose, monitor your body's response, and get reminders so you never miss a dose.
Start Tracking FreeGiven the kidney-injury signal in primate studies (and sparse human safety data), we don’t publish a recommended dosing protocol for Adipotide. Barnhart 2011 (PMID 22072637) dosed obese rhesus macaques at ~0.4 mg/kg/day for 28 days — community claims of “10 mg/kg/day” appear to be cumulative-across-cycle figures misread as per-day, and a true 10 mg/kg/day in a 100 kg adult would be ~200 vials per day, which is not physically plausible. Even at the actual ~0.4 mg/kg/day primate dose the AKI signal emerged. Modern GLP-1 agonists produce comparable weight loss with a radically better safety margin.
Standard lyophilized-powder reconstitution (2 mL BAC water per 10 mg vial) applies. See the general reconstitution pattern elsewhere in the library. Given the safety caveats above, we don’t provide a dose-volume table for Adipotide.
Pre-filled with a typical Adipotide (FTPP) setup. Edit any field — the draw updates live.
Insulin syringe — 100 units = 1 mL
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If you’re considering Adipotide for personal use, talk to a nephrologist first. Bloodwork before, mid-cycle, and after is non-negotiable. Semaglutide or tirzepatide give you equivalent fat loss without this concern — strongly consider those first.
Adipotide (FTPP) is a research peptide not approved by the FDA for human use. It is sold only as a research chemical, and StackTrax does not endorse or facilitate personal use.
Quality varies enormously among research-chemical suppliers. At minimum, look for:
StackTrax’s preferred partner NextGen Peptides does not currently carry Adipotide (FTPP)in their catalog, which is why you don’t see a direct purchase link here. Other major research-chemical suppliers carry it; we don’t specifically recommend one for this compound.
Build your protocol, log every dose, monitor your body's response, and get reminders so you never miss a dose.
Start Tracking FreeNo. Adipotide is not FDA approved. Phase 1 human trials were paused due to a nephrotoxicity signal, and the early-phase human trial (NCT01262664) was discontinued and never published in peer-reviewed literature. It is a research chemical only and strongly not recommended outside of supervised research settings.
It is a Fat-Targeted ProApoptotic Peptide (FTPP) designed by Kolonin and Arap at MD Anderson. It combines a homing sequence that binds prohibitin on the vasculature of white adipose tissue with a proapoptotic sequence that triggers cell death once bound. The net effect: it selectively destroys the blood supply to white fat, which kills the fat cells behind it.
In obese rhesus macaques, Barnhart 2011 (Sci Transl Med, PMID 22072637) showed 11% body weight loss with 27% fat mass reduction over 28 days, with preserved lean mass and improved insulin sensitivity. Human exploration has remained limited and sparse in peer-reviewed literature.
Dose-dependent kidney toxicity. Kidneys filter large quantities of blood and have a vascular bed that expresses enough prohibitin-like targets for Adipotide to accumulate. The Barnhart 2011 rhesus macaque studies documented dose-dependent AKI and rising creatinine at therapeutically relevant doses, and the early-phase human trial was discontinued. The primate signal is the well-documented basis for the kidney concern and the major barrier to clinical development.
Not really. The kidney-injury signal in primate studies (and sparse human safety data) means we don't publish a recommended dosing protocol. Even at the actual ~0.4 mg/kg/day primate dose, the AKI signal emerged. Contraindications include any pre-existing kidney disease, diabetes with nephropathy, dehydration, concurrent nephrotoxic drugs, pregnancy, or active cancer. Modern GLP-1 agonists (semaglutide, tirzepatide, retatrutide) produce comparable weight loss with a radically better safety margin — strongly consider those first.
Those figures appear to be cumulative-across-cycle numbers misread as per-day. A true 10 mg/kg/day in a 100 kg adult would be roughly 200 vials per day, which is not physically plausible. The Barnhart 2011 primate study actually dosed obese rhesus macaques at ~0.4 mg/kg/day for 28 days — and the AKI signal still emerged at that dose.
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StackTrax guides cover peptides and compounds that are not FDA-approved for the uses discussed. The dosing, reconstitution, and safety information is compiled from published research and community protocols for educational purposes only.
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