Adipotide (FTPP)
Aliases: FTPP · Fat Targeted Proapoptotic Peptide · KGGRAKD
Last verified: 2026-09-24
The short version
Adipotide is perhaps the most dramatic example of 'brilliant mechanism, bad drug'. The idea is genius: instead of making the body burn fat, you kill the vessels that feed fat tissue. In mice obesity literally vanishes; in monkeys ~11% of body weight in a month — better than most of today's drugs. And then the bill arrives: the kidneys. Adipose endothelium and renal tubules share receptor patterns, and the therapeutic window turned out too narrow for any clinical use. The gray market still sells it as the 'strongest fat-burning peptide', ignoring that development was shut down precisely because of toxicity — that is not a detail, it is the point of the story.
Identity & type
- Molecular type
- peptidomimetic
- Sequence / structure
- KGGRAKD-derived construct
- Molecular weight
- ~2.3 kDa
- Origin
- A synthetic homing peptide fused to a proapoptotic motif; targets the vasculature of white adipose tissue.
Mechanism of action
A peptidomimetic that binds prohibitin on the endothelial cells of white adipose tissue vasculature and induces their apoptosis → adipose ischemia → rapid resorption of fat cells; a synthetic construct (KGGRAKD peptide + proapoptotic domain motif).
not confirmed in humans
Dosing & routes
Official / clinical context
No approved documents exist and there never will be in this form; the program was terminated.
Regulator-approved labeling and published study designs — never a recommendation.
Community-reported practice
Occasionally appears in 'extreme' regimens: 0.5–2 mg SC daily, 2–4 weeks. Published reports are rare and unreliable; the risk of renal toxicity is systematically underestimated in the community.
Unverified self-reports. Not medical advice. Not endorsement.
Protocol — official vs community
Official / label
No approved protocol exists — development was discontinued. The single famous primate study used daily SC injections over ~4 weeks, producing ~11% body-weight loss.
Duration: ~4 weeks in the primate study; dose-dependent renal ischemia/tubular injury at higher doses terminated the therapeutic window.
The mechanism — apoptotic destruction of white-adipose vasculature — is the opposite of subtle. The renal toxicity that limits it is a mechanism-level problem, not a formulation issue.
Community (anecdotal)
Occasional gray-market listings cite 'research doses' extrapolated from the primate mg/kg data; no human protocol of any kind exists and none should be inferred.
- Cycle:
- No standardized pattern.
- Break:
- —
Community interest in adipotide is almost entirely theoretical — its toxicity profile and the absence of any human data keep actual use minimal. The honest entry is that the only documented regimen is the one that revealed the safety problem.
Human evidence
None. No registered human trial has ever been conducted.
Preclinical evidence
Good but terminal: two strong animal studies (mice, primates) with dramatic weight loss — and with the toxicity that stopped development.
Known risks
- Renal ischemia and tubular damage — demonstrated in primatescharacterized
- Hypotension and gastrointestinal symptoms in animal modelscharacterized
- Undefined quality and dosing of gray-market productscharacterized
Teal: characterized in clinical/labeling contexts. Amber: theoretical or reported outside controlled settings.
Unknowns & evidence gaps
- Everything in humans — never tested
- Whether any dose has an acceptable safety profile
Frequently asked questions
References
- Kolonin MG et al. Reversal of obesity by targeted ablation of adipose tissue. Nat Med, 2004
- Kim DH et al. Rapid weight loss and renal safety of adipotide in obese rhesus monkeys. Obesity, 2012