Adipotide (FTPP)
Pro-apoptotic peptidomimetic (prohibitin-targeting)
A pro-apoptotic peptidomimetic referenced in adipose-tissue and metabolic research literature.
Also referenced as: FTPP, Fat-Targeted Proapoptotic Peptide
Overview
Adipotide (also called FTPP, prohibitin-targeting peptide-1) is a synthetic peptidomimetic combining a prohibitin-targeting sequence (CKGGRAKDC) with a pro-apoptotic amphipathic domain (KLAKLAK)2 via a linker. It was developed as an experimental agent to target the vasculature of white adipose tissue.
At a glance
What Adipotide (FTPP) does
Adipotide (also called FTPP or prohibitin-targeting peptide-1) is a peptidomimetic with a distinctive two-part 'homing missile' design, sequence CKGGRAKDC-GG-D(KLAKLAK)2. The first part is a targeting motif, identified by in-vivo phage display, that binds prohibitin, a receptor selectively displayed on the surface of endothelial cells that line the blood vessels feeding white adipose tissue. The second part, the D(KLAKLAK)2 sequence, is a pro-apoptotic peptide that disrupts mitochondrial membranes once it is internalized. So rather than acting on adipocytes' metabolism, Adipotide works by anatomically starving fat: it homes to the vasculature of white fat, triggers apoptosis of those blood-vessel endothelial cells, the capillaries regress, and the fat cells they supplied die from loss of blood supply. This is a fundamentally different, vascular-targeting mechanism from every other compound in this class.
The most notable evidence is a 2011 study in obese Old World monkeys (rhesus macaques), where Adipotide induced targeted apoptosis in white-adipose-tissue blood vessels and produced roughly 10.6% body-weight loss over 28 days, with MRI and DEXA confirming a marked reduction in white fat and with improved insulin resistance. However, the same primate work revealed dose-dependent renal tubular changes, and nephrotoxicity became the defining safety liability. Clinical development was discontinued around 2019 over these kidney-toxicity concerns. There is no established human efficacy or safety, and the renal risk is the central caveat for any discussion of this compound.
Effects reported in research
- Binds prohibitin on endothelial cells of white-adipose-tissue blood vessels (targeting mechanism).
- Delivers a pro-apoptotic D(KLAKLAK)2 peptide that disrupts mitochondrial membranes to kill targeted cells.
- Induces apoptosis of the vasculature supplying white fat, causing capillary regression (animal data).
- Fat cells die from loss of blood supply — an anatomical, vascular-targeting fat-loss mechanism, not a metabolic one.
- Produced ~10.6% body-weight loss over 28 days in obese rhesus macaques (2011 primate study).
- Reduced white adipose tissue confirmed by MRI and DEXA imaging in primates.
- Improved insulin resistance in the obese monkey model.
- Caused dose-dependent renal tubular (kidney) toxicity in primates — the key safety concern that ended clinical development around 2019. No established human efficacy/safety.
Effects listed reflect findings reported in the research literature — many in animal or in-vitro models. Listing an effect is not a claim of efficacy or a therapeutic indication in humans.
Mechanism of action
The CKGGRAKDC domain binds a prohibitin/ANXA2 receptor complex found on the endothelium (blood vessels) supplying white adipose tissue. Once localized, the D(KLAKLAK)2 domain disrupts mitochondrial membranes and triggers apoptosis, ablating the blood supply to fat depots. In animal studies this produced rapid loss of adipose tissue.
Mechanistic description reflects published research-literature understanding. Much peptide research is preclinical (in-vitro or animal-model); mechanism in humans may differ and is not established for many compounds.
What it's studied for
Research contexts in which Adipotide (FTPP) appears in the literature. Listing a research area is not a claim of efficacy or a therapeutic indication.
Key characteristics
- A peptidomimetic, not a simple linear peptide; class label here is approximate (it is not a GH fragment despite the group's field)
- Combines an adipose-vasculature-targeting motif with a pro-apoptotic (KLAKLAK)2 payload
- Caused marked fat loss in mouse and monkey studies
- A Phase 1 human trial was pursued; development was limited by dose-dependent kidney (renal) toxicity
- Not an approved drug
Reported research dosing reference only
Educational reference, not dosing guidance. The figures below summarize amounts reported in published research and research-community protocols, provided for educational and research context only. They are not medical advice, not a recommendation, and not instructions for human use. Adipotide (FTPP) is a research compound.
Reported research dosing comes from animal studies rather than established human protocols. Published rodent and primate work used body-weight-scaled daily dosing over short cycles. These are figures reported for research context only, not dosing guidance for humans.
- Rodent/primate studies: reported around ~0.43 mg/kg/day (referenced in the original targeted-apoptosis work) over ~4-week cycles
- Human protocol dosing is not established in the literature
Preclinical only; renal effects have been flagged in the literature. Reference figures for research context, not dosing guidance.
How it compares
Unlike the lipolytic GH fragments, adipotide does not stimulate fat metabolism; it destroys the blood vessels feeding fat tissue via a targeted pro-apoptotic mechanism.
Commonly studied alongside
Compounds frequently researched together with Adipotide (FTPP) in the literature. Cross-referenced for research context — not a usage or combination recommendation.
Compare and calculate
Side-by-side pages for the pairings the literature already documents for Adipotide (FTPP), plus the unit-conversion reference for a reconstituted vial. Factual comparisons of documented characteristics — not a recommendation to combine or use any compound.
Adipotide (FTPP) reconstitution calculator → Concentration, volume per measured amount and syringe units for a stated vial mass and diluent volume. A unit-conversion reference, not a dosing recommendation.
Handling & Stability
Lyophilized peptides are stored cold, protected from light, and reconstituted only at the time of intended in-vitro work.
- Avoid repeated freeze-thaw cycles
- Verify supplier lot and Certificate of Analysis
- Follow institutional lab-safety protocols
Analytical & COA Concepts
Reputable research suppliers publish a third-party Certificate of Analysis per batch. Key analytical concepts referenced in COAs include:
Category Context
Adipotide (FTPP) sits in the Metabolic & Mitochondrial area of the PeptiDex library.
- Entry type: Research compound reference
- Metabolic & Mitochondrial category hub →
- Browse the full library →
- Glossary of terms →
Where researchers source Adipotide (FTPP)
For researchers studying Adipotide (FTPP), third-party suppliers such as Practically Natty Peptides offer research-grade material, third-party tests every batch and provides Certificates of Analysis on request, and ship from the US.
PeptiDex does not maintain a direct supplier listing for this compound. The link above goes to a third-party research-supplier directory.
Frequently asked questions
What is adipotide (FTPP)?
Adipotide, also called prohibitin-targeting peptide-1 (FTPP), is a synthetic peptidomimetic with two domains: a homing motif (CKGGRAKDC) that targets white-adipose-tissue vasculature and a pro-apoptotic (KLAKLAK)2 moiety. It is studied as a targeted anti-obesity research agent that acts on the blood supply of fat tissue rather than on fat cells directly.
How does adipotide work mechanistically?
The homing peptide is reported to bind a prohibitin/annexin A2 complex on endothelial cells feeding white adipose tissue; the attached pro-apoptotic sequence then triggers apoptosis in those vessels. Disrupting the adipose blood supply causes the fed fat cells to regress, altering lipid uptake, glucose handling, and adipose signaling in models.
What research supports adipotide?
In a primate study, obese rhesus monkeys were reported to lose about 11% of body weight over 28 days with roughly 39% reduction in fat deposits. Rodent work reported similar targeted fat-mass loss. Because its mechanism affects vasculature, kidney-related effects have been a noted concern in the preclinical literature.
What is adipotide's structure and molecular weight?
Adipotide has the sequence CKGGRAKDC-GG-D(KLAKLAK)2, a cyclic homing motif joined to a dimeric pro-apoptotic peptide via a linker. Its molecular weight is approximately 2611 g/mol (molecular formula around C152H252N44O42). This composite peptidomimetic structure distinguishes it from simple linear peptides.
How is adipotide handled for research?
Adipotide is supplied as a lyophilized powder and reconstituted with sterile/bacteriostatic water for laboratory use. It is stored refrigerated or frozen as a solid and kept refrigerated once reconstituted. A COA with HPLC purity and mass identity is standard. It is a research compound with no approved therapeutic status.
Answers are educational summaries of research-literature context and do not constitute medical advice. See the Research Library, COA guide, and Storage & Handling guide for more.
References
Primary literature indexed in PubMed for Adipotide (FTPP). Listing a study records that it exists and is indexed — it is not a claim of efficacy, a therapeutic indication, or an endorsement of its conclusions. Much of this literature is preclinical (in-vitro or animal-model).
- A peptidomimetic targeting white fat causes weight loss and improved insulin resistance in obese monkeys
- Rapid and weight-independent improvement of glucose tolerance induced by a peptide designed to elicit apoptosis in adipose tissue endothelium
Each reference was checked against its PubMed record on 2026-07-28: the PMID resolves and the title, journal and year match. Where no indexed literature exists for a compound, PeptiDex says so rather than substituting a citation about a different molecule. See the editorial policy.