Adipotide
Also known as: FTPP, Fat-Targeted Proapoptotic Peptide, Prohibitin-Targeting Peptide 1, PTP-1, CKGGRAKDC-GG-D(KLAKLAK)2
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Key Facts: Adipotide
- Category
- Weight Loss
- FDA Status
- Not FDA Approved
- Clinical Status
- Investigational / abandoned - Not FDA approved for any use. Only human study (NCT01262664, MD Anderson, phase I in obese men with metastatic prostate cancer) was terminated in 2019 after enrolling 4 participants; no results posted. WADA: not named on the 2026 Prohibited List; as a substance with no regulatory approval for human use it falls under S0 (Non-Approved Substances), prohibited at all times.
- Banned in Sport (WADA)
- Not named on the WADA list, but WADA's S0 catch-all bans any substance without human therapeutic approval, which covers it. Prohibited at all times.
- Administration
- Subcutaneous injection
- Typical Dose
- No established human dose
- Frequency
- Once daily in animal studies
- Duration
- 28 days in the main monkey efficacy study; up to 63 days in dose-escalation
How does Adipotide work?
The molecule has two parts joined together. The targeting part, CKGGRAKDC, was found by screening peptides in living mice for ones that stick to fat-tissue blood vessels; it binds prohibitin on the endothelial cells lining white fat vasculature. The payload, D(KLAKLAK)2, is a known pro-apoptotic peptide that disrupts mitochondrial membranes once inside a cell, setting off programmed cell death. Kill the vessels and the fat tissue they supply is starved and resorbed. This is a destructive mechanism, not a metabolic nudge like GLP-1 drugs, and that matters for safety: prohibitin is not exclusive to fat vessels, and the kidney's proximal tubule cells turned out to be a clear off-target casualty in monkeys.
What does the research show?
The concept came from Kolonin and colleagues (Nature Medicine, 2004), who reported that ablating fat vasculature reversed obesity in mice. The key primate study is Barnhart et al. (Science Translational Medicine, 2011) from MD Anderson. Obese rhesus monkeys given 0.43 mg/kg/day subcutaneously for 28 days lost 7.4% to 14.7% of body weight (average 10.6%) while controls stayed roughly flat, with MRI and DEXA confirming fat loss and clear improvements in insulin resistance. Lean monkeys at the same dose did not lose weight. The cost: serum creatinine rose in a dose-dependent way above 0.25 mg/kg, and the authors documented kidney tubule injury with glucose and protein in the urine, dehydration at higher doses, and low phosphorus and potassium. Most of it reversed within 28 days, but one treated monkey in each study still had residual changes. A first-in-human phase I trial at MD Anderson in obese men with metastatic prostate cancer (NCT01262664) started in 2012, enrolled only 4 patients, and was terminated at the investigator's request in 2019 with no results posted. That is the whole human record. Nobody knows the safe human dose, and the kidney signal is the opposite of reassuring.
What doses have been studied?
Note: Animal study doses may not translate directly to humans.
Typical Dosingⓘ
Community experience
No established human dose
Not established (monkey studies used 0.10-0.75 mg/kg/day)
Once daily in animal studies
There is no published human dosing data. The only human trial was terminated after 4 participants without posting results. Anyone scaling up the monkey dose is guessing, and kidney injury appeared in monkeys at doses above 0.25 mg/kg/day. If used in research, kidney function monitoring (creatinine, urine glucose and protein) would be the bare minimum.
Research Dosingⓘ
Scientific studies
Doses observed in primate research. No human dose has been established or published.
Doses from Studies
0.43 mg/kg/day SC for 28 days
Preclinical Research - Barnhart et al., Sci Transl Med 2011 (obese rhesus monkeys) ↗
Duration
28 days in the main monkey efficacy study; up to 63 days in dose-escalation
Administration
Subcutaneous injection
When and how is Adipotide taken?
Best Time to Take
No evidence-based timing
Once daily in animal studies, typically 28-day cycles
Food Recommendation
With or without food
Why This Timing?
Monkey studies dosed once daily without any timing comparison. There is no human data to say morning or evening matters.
What are the side effects of Adipotide?
Not everyone experiences these effects. Individual responses vary based on dosage, duration, and personal factors.
- ●Kidney injury (proximal tubule damage) in all primate species tested
- ●Rising creatinine, dose-dependent
- ●Glucose and protein in the urine
- ●Dehydration and increased urine output at higher doses
- ●Low phosphorus and potassium
- ●Damage not always fully reversible (residual changes in some monkeys)
- ●No human safety data at all
- ●Destructive mechanism (kills blood vessel cells), with unknown off-target effects in people
References
- https://pubmed.ncbi.nlm.nih.gov/22072637/
- https://pmc.ncbi.nlm.nih.gov/articles/PMC3666164/
- https://clinicaltrials.gov/study/NCT01262664
- https://www.mdanderson.org/newsroom/obese-monkeys-lose-weight-on-drug-that-attacks-blood-supply-of-f.h00-158676579.html
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Frequently Asked Questions
What does Adipotide do?
Adipotide is an experimental peptide built to kill fat tissue by cutting off its blood supply. One half homes in on prohibitin, a protein on the blood vessels that feed white fat, and the other half is a cell-killing sequence that triggers those vessel cells to self-destruct. It produced striking weight loss in obese mice and monkeys, but it also caused kidney damage in every primate species tested, and its only human trial was terminated after enrolling 4 people with no results ever posted.
How does Adipotide work?
The molecule has two parts joined together. The targeting part, CKGGRAKDC, was found by screening peptides in living mice for ones that stick to fat-tissue blood vessels; it binds prohibitin on the endothelial cells lining white fat vasculature. The payload, D(KLAKLAK)2, is a known pro-apoptotic peptide that disrupts mitochondrial membranes once inside a cell, setting off programmed cell death. Kill the vessels and the fat tissue they supply is starved and resorbed. This is a destructive mechanism, not a metabolic nudge like GLP-1 drugs, and that matters for safety: prohibitin is not exclusive to fat vessels, and the kidney's proximal tubule cells turned out to be a clear off-target casualty in monkeys.
Is Adipotide FDA approved?
No, Adipotide is not currently FDA approved. Current status: Investigational / abandoned - Not FDA approved for any use. Only human study (NCT01262664, MD Anderson, phase I in obese men with metastatic prostate cancer) was terminated in 2019 after enrolling 4 participants; no results posted. WADA: not named on the 2026 Prohibited List; as a substance with no regulatory approval for human use it falls under S0 (Non-Approved Substances), prohibited at all times.
Is Adipotide banned in sport?
Not named on the WADA list, but WADA's S0 catch-all bans any substance without human therapeutic approval, which covers it. Prohibited at all times.
What are the side effects of Adipotide?
Reported side effects include: Kidney injury (proximal tubule damage) in all primate species tested, Rising creatinine, dose-dependent, Glucose and protein in the urine, Dehydration and increased urine output at higher doses, Low phosphorus and potassium. Individual responses vary based on dosage, duration, and personal health factors.
What is the typical dose of Adipotide?
Community-reported common dose: No established human dose (Once daily in animal studies). Range: Not established (monkey studies used 0.10-0.75 mg/kg/day). Administration: Subcutaneous injection. Community-reported doses. Not medical advice. Consult healthcare provider.
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