Also known as FTPP · Prohibitin-targeting peptide-1 · CKGGRAKDC-GG-D(KLAKLAK)2
A fat-targeting proapoptotic peptide that destroys the blood supply of white fat — striking in animals, but discontinued in humans for kidney toxicity.
Research refreshed
Adipotide (FTPP, "fat-targeted proapoptotic peptide") is a chimeric peptide designed to attack obesity from an unusual angle: instead of curbing appetite, it kills the blood vessels that feed white fat. One end is a homing sequence (CKGGRAKDC) that binds prohibitin on the vasculature of fat tissue; the other is a proapoptotic peptide that triggers cell death once delivered. In obese primates it produced rapid, striking fat loss — but its clinical development was halted over kidney toxicity.
Adipotide is one of the boldest ideas in metabolic research: treat obesity like a tumor by cutting off its blood supply. Developed at MD Anderson Cancer Center by Renata Pasqualini and Wadih Arap, it is a chimera of two peptides. The targeting half, the cyclic nonapeptide CKGGRAKDC, recognizes prohibitin displayed on the endothelial cells of the vasculature that specifically supplies white adipose tissue. The payload half, a D-amino-acid proapoptotic sequence written D(KLAKLAK)2, is harmless outside cells but disrupts mitochondrial membranes once the targeting domain gets it inside — killing the fat’s blood vessels and, with them, the fat.
In obese rhesus monkeys the results were dramatic: rapid loss of body weight and fat over a few weeks of treatment. But translating it to people ran into a hard limit. The same peptide accumulates in the kidney, and clinical development was discontinued (around 2019) because of nephrotoxicity — the gap between the fat-reducing dose and the kidney-damaging dose proved too narrow. Adipotide is not FDA-approved and is not in active clinical development; it remains an instructive, cautionary research compound.
A two-domain peptide: a cyclic CKGGRAKDC motif homes to prohibitin on white-adipose-tissue blood vessels, delivering a D(KLAKLAK)2 proapoptotic sequence that disrupts mitochondrial membranes and triggers apoptosis of the vascular endothelium feeding the fat.
Behind every vial of Adipotide is the same exacting pipeline every research peptide runs — but the chemistry plays out differently for this molecule. Here is how Adipotide, specifically, is brought into being.
On paper, Adipotide is C111H206N36O28S2 — about 2,557.2 daltons of precisely arranged atoms. Before a single bond is made, the target sequence, salt form, and purity threshold are written down as the contract the finished material must meet.
Adipotide is built one protected residue at a time by solid-phase synthesis, each cycle a deprotection, a coupling, and a wash. It also carries cyclization and a disulfide bridge, extra steps beyond a plain chain that add both capability and cost.
The crude mixture — Adipotide plus its deletions and side products — is then separated on preparative HPLC, and where the cut is taken decides the difference between a genuinely pure peptide and a barely-passable one.
A real batch of Adipotide proves itself: identity confirmed by mass spectrometry against its ~2,557.2 Da, purity read directly off an analytical HPLC trace, water and counterion content measured. That batch-specific certificate of analysis is the only honest way to know what is actually in a vial of Adipotide — and a short, cold, accountable chain of custody is how that purity survives the trip to your bench.
Adipotide is a chimeric peptide: a disulfide-cyclized CKGGRAKDC targeting domain joined to an all-D-amino-acid D(KLAKLAK)2 proapoptotic sequence with a C-terminal amide. Assembling two chemically distinct domains, forming the disulfide correctly, and handling the D-residues make it demanding to synthesize and purify cleanly.
Don't judge a vial by its cake. A fluffy, good-looking lyophilized powder reflects bulking agents and freeze-drying parameters — not purity. Insist on a batch-specific certificate of analysis.
Adipotide (FTPP) is a fat-targeting proapoptotic peptide that kills the blood vessels supplying white fat, developed at MD Anderson and studied for obesity in animals.
A targeting sequence (CKGGRAKDC) homes to prohibitin on the vasculature of fat tissue and delivers a proapoptotic peptide that triggers those blood vessels to die — starving the fat rather than suppressing appetite.
Clinical development was discontinued (around 2019) because of kidney toxicity — the peptide accumulates in the kidney and the safe dose window proved too narrow. It is not approved.
No — it is a preclinical research compound, discontinued in clinical development and not FDA-approved. This page is a research and educational reference.
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