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Professor Peptides
Research compound

Adipotide

Also known as Adipotide · FTPP · fat-targeted proapoptotic peptide · CKGGRAKDC-GG-D(KLAKLAK)2 · prohibitin-targeting peptide

Targeted proapoptotic peptide that kills white adipose tissue vasculature

Last reviewed · Educational reference — not medical advice.

Formula
C111H206N36O28S2
Molecular weight
2,557.2 g/mol
Half-life
Not characterised in published human pharmacokinetic studies
Route
Subcutaneous injection in preclinical studies
CAS
859216-15-2
PubChem
163360068 (opens in new tab)
Status
Preclinical research peptide — development did not progress to approval
Sequence as recorded
CKGGRAKDC-GG-D(KLAKLAK)2
Mechanism
Two-part chimeric design: the CKGGRAKDC sequence homes to prohibitin on the vasculature of white adipose tissue, delivering the D(KLAKLAK)2 domain, which disrupts mitochondrial membranes and triggers apoptosis in those endothelial cells. Adipose tissue regresses because its blood supply is ablated.
01

Overview

Adipotide (also called FTPP, for fat-targeted proapoptotic peptide) is a chimeric molecule with two functional halves. The US National Library of Medicine indexes it under the concept name CKGGRAKDC-GG-D(KLAKLAK)2, which states the design directly.

The first half, CKGGRAKDC, is a homing sequence that binds prohibitin in the vasculature supplying white adipose tissue. The second, D(KLAKLAK)2, is a proapoptotic domain that disrupts mitochondrial membranes. The strategy is deliberately indirect: rather than targeting fat cells, it targets their blood supply, killing the vasculature so the adipose tissue it feeds regresses.

Adipotide became well known following primate work reporting substantial weight loss. It is important to be clear about why it did not become a drug: the same mechanism that prunes adipose vasculature is not confined to adipose tissue, and renal toxicity emerged as a central concern in the published record. This is a compound whose development stalled on safety, not on efficacy — which makes its continued sale as a research chemical for fat loss particularly ill-advised.

No approved indication exists in any jurisdiction, and no published human trial demonstrated an acceptable risk-benefit profile.

Research areasTargeted adipose vasculature ablationProhibitin targetingObesity pharmacologyProapoptotic peptide design
02

What the evidence shows

Separated by study type
HumanClinical trials and human studies
No published trial established an acceptable risk-benefit profile. Development did not lead to approval in any jurisdiction.
AnimalRodent and other animal models
Primate and rodent studies reported substantial adiposity and weight reduction via ablation of white adipose tissue vasculature, with renal toxicity a recurring concern in the published record.
In vitroCell and tissue studies
The homing and proapoptotic domains have defined, separately characterised activities.
03

Key studies & findings

1 study
  1. 1

    The US National Library of Medicine indexes adipotide under the concept CKGGRAKDC-GG-D(KLAKLAK)2, confirming the chimeric homing-plus-proapoptotic design.

    NLM supplementary concept mapping (PubMed)

04

Benefits & effects

2 documented

  • Substantial adiposity reduction in preclinical primate and rodent models

    PreclinicalVerified

  • Demonstrated targeted delivery via prohibitin homing sequence

    PreclinicalVerified
05

Side effects & safety

2 reported

Safety noteResearch compound for laboratory use only. Not approved for human use; no established human safety database outside the trials cited here.

Recorded in the cited literature No human safety data supporting any use.

  • Renal toxicity is the principal concern in the published record

    unknown

  • Mechanism ablates vasculature and cannot be assumed adipose-specific

    unknown
06

Limitations & open questions

This compound's development did not stall for lack of weight-loss effect — it stalled on toxicity, with renal effects the principal published concern. A mechanism that ablates blood vessels cannot be assumed to spare vasculature outside adipose tissue, and the resulting fat loss is achieved by destroying tissue rather than by altering metabolic signalling. It remains sold as a research chemical for fat loss despite that history, which inverts the actual risk picture. No human efficacy or safety trial supports such use.

07

Pharmacology

Adipotide is a large chimeric peptide (C111H206N36O28S2, MW approximately 2557.2, CAS 859216-15-2, PubChem CID 163360068). Its two disulfide-capable cysteines in the CKGGRAKDC homing sequence are integral to prohibitin binding. No human pharmacokinetic data are available.

08

Frequently asked questions

Why was adipotide never approved?

Toxicity, principally renal, is the recurring concern in the published record — not lack of weight-loss effect. It is a case where the efficacy signal was real and the safety profile was the obstacle.

How does adipotide cause fat loss?

Indirectly. It homes to prohibitin on the blood vessels that supply white adipose tissue and triggers apoptosis in those vessels. The fat tissue regresses because its blood supply is destroyed — it is tissue ablation, not metabolic modulation.

Is adipotide safe to use for fat loss?

There is no evidential basis for such use. A compound whose development was halted over toxicity concerns, with no approved indication and no supportive human trial, is not a fat-loss agent.