Adipotide

Mechanism of action

The CKGGRAKDC sequence binds prohibitin on the surface of endothelial cells specifically within white adipose tissue vasculature, concentrating the peptide there. The D(KLAKLAK)2 "killer" sequence then inserts into mitochondrial membranes of those endothelial cells, triggering apoptosis. Loss of the blood supply causes the downstream adipocytes to regress. The same prohibitin-targeting motif is also present in renal proximal tubule cells, which is the mechanistic origin of the nephrotoxicity.

Primary uses

• Obesity research (preclinical)
• Tumor-targeting peptide research (same technology platform)
• Community use should be considered extremely dangerous given the documented primate nephrotoxicity

Typical dosing

Regulatory status

Not approved. Strong preclinical data in obese rhesus monkeys (Barnhart et al., Sci Transl Med, 2011) showed ~11% body weight reduction and preferential fat loss over 28 days, but also produced nephrotoxicity (renal proximal tubule damage) in the monkey studies — which has prevented advancement into human trials despite enormous scientific interest.

Status as of this entry's last review, October 4, 2026. Approvals, compounding rules and sport rules change; the regulatory tracker is checked more often.

What we checked

Adipotide was tested in mice, rats and obese monkeys and was never given to people in a published study. This section adds what can be checked around its sources.

Identity, computed

The sequence is the one the 2011 monkey paper prints. It has a disulfide-closed ring and D-amino acids, so the site's calculator cannot give a reliable mass, and none is printed.

Regulatory status, read October 5, 2026

Drugs@FDA: 0 records for “adipotide”. EMA medicines list: 0 records for “adipotide”. Run for semaglutide, the same queries return 6 and 5 records (and the registry search 84 trials), so a zero here is an absence, not a broken search. Not named on the WADA 2026 and 2027 Prohibited Lists. As a substance with no current approval for human therapeutic use, it falls under section S0 (non-approved substances), which is prohibited at all times; the lists were read on September 27, 2026.

What the maker or sellers claim

Claim, from research-chemical sellers: adipotide melts fat in people. Its only primate study found kidney effects alongside weight loss, and no human study has been published.

What the animal studies show

In 2004 the MD Anderson group showed that a peptide homing to the blood vessels of white fat, fused to a pro-apoptotic segment, reversed obesity in mice (Kolonin et al., 2004). In obese rhesus monkeys, adipotide caused targeted cell death in fat-tissue blood vessels, rapid weight loss and better insulin sensitivity, with MRI confirming fat loss (Barnhart et al., 2011); at the optimal doses, monkeys of three species showed predictable, reversible changes in kidney proximal-tubule function. In obese mice, a related peptide improved glucose tolerance within days, before weight changed (Kim et al., 2012).

What we looked for and did not find

No human trial, no registry record and no pharmacokinetic data in people.

References

1. [pubmed] Barnhart KF, et al. "A peptidomimetic targeting white fat causes weight loss and improved insulin resistance in obese monkeys." Sci Transl Med, 2011;3:108ra112. PMID: 22072637.
2. [pubmed] Kolonin MG, et al. "Reversal of obesity by targeted ablation of adipose tissue." Nat Med, 2004;10:625-632. PMID: 15133506.
3. [pubmed] Kim DH, et al. "Rapid and weight-independent improvement of glucose tolerance induced by a peptide designed to elicit apoptosis in adipose tissue endothelium." Diabetes, 2012;61(9):2299-310. PMID: 22733798.

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