Adipotide

FTPP (fat-targeted proapoptotic peptide), prohibitin-TP01, CKGGRAKDC-GG-D(KLAKLAK)2

Metabolic & weight

Awaiting medical reviewEN ES DE FR PT ZH+ Follow for updates

Summary

Class: Synthetic chimeric peptidomimetic: a 9-residue targeting sequence that binds prohibitin on fat-tissue blood vessels, linked to a cell-killing (pro-apoptotic) D-amino-acid sequence
Mechanism: Homes to the blood vessels that supply white fat and kills them, starving fat tissue so it shrinks — a "vascular targeting" approach borrowed from cancer research
Routes studied: Subcutaneous and intraperitoneal injection (mice, rats, rhesus monkeys); subcutaneous (community, rare)
Dose range reported: Mice: ~3 mg/kg/day. Rhesus monkeys: 0.43 mg/kg/day subcutaneous for 28 days. Community reports (very limited): 0.25–1 mg/day. No human dose exists
Half-life: Not characterised in humans; cleared within hours in animals
Storage: Lyophilised: refrigerate, protect from light. Reconstituted: refrigerate; D-amino-acid segment is protease-resistant but the targeting sequence is not
Regulatory status: Not approved anywhere; a planned human trial was registered but outcomes have not been published

Doses are as reported in studies or by the community — never recommendations.

1What it is

Adipotide is not a hormone fragment or a signalling peptide. It is a targeted toxin. Researchers at MD Anderson Cancer Center (Wadih Arap and Renata Pasqualini) had been developing peptides that seek out the blood vessels feeding tumours. In 2004 they applied the same idea to fat: a short sequence was found that binds prohibitin, a protein unusually exposed on the surface of blood vessels in white adipose tissue. They attached it to a synthetic peptide (D(KLAKLAK)2) that disrupts mitochondria once inside a cell. The result homes to fat-tissue vessels and kills them, and the fat tissue, cut off from supply, regresses.

It attracted attention in 2011 when a monkey study showed rapid weight loss, and it circulates in the community under the name "adipotide". It is one of the compounds on this site with the clearest known serious toxicity.

2How it's thought to work

Targeting. the CKGGRAKDC sequence binds prohibitin and a partner protein (annexin A2) on endothelial cells lining white-fat blood vessels. Prohibitin is inside cells in most tissues but surfaces on fat vasculature, which is why the targeting is selective.

Killing. once internalised, the D(KLAKLAK)2 segment disrupts mitochondrial membranes and triggers apoptosis of the endothelial cell.

Downstream. loss of vasculature causes fat-cell death and tissue regression, with secondary improvements in insulin sensitivity in treated animals.

The catch. prohibitin is also expressed in the kidney, which is where the toxicity shows up.

Proposed: a homing sequence that recognises a marker on the blood vessels feeding fat tissue, tied to a sequence that triggers cell death. The target is the blood supply rather than the fat cell. Primate work showed weight loss and kidney toxicity; it has not been through human trials.Schematic — not to scale

3What the research shows

Weight loss in obese mice

Obese mice treated for four weeks lost about 30% of body weight, with ablation of white fat vasculature, reduced fat mass and improved metabolic profile; lean mice were less affected (Kolonin 2004, Nat Med). [1]

Weight loss in obese rhesus monkeys

Spontaneously obese monkeys given 0.43 mg/kg/day subcutaneously for 28 days lost about 11% of body weight and 39% of abdominal fat by imaging over the treatment and follow-up period, with improved insulin sensitivity. Lean monkeys did not lose weight. Treated animals developed dose-dependent kidney injury (reduced glomerular filtration, raised creatinine, tubular changes) that was reversible after stopping (Barnhart 2011, Sci Transl Med). Food intake fell during treatment. [2]

Graded D/C

Targeting mechanism and prohibitin biology

Phage-display screening in mice identified the prohibitin-binding sequence and showed it homes to white fat vasculature after systemic injection (Kolonin 2004). Later work mapped prohibitin and annexin A2 as the vascular receptor pair in human tissue samples (Staquicini 2011), which is the main evidence that the target exists in humans — but binding is not the same as a demonstrated effect. [1][4]

Not gradednone published

Human trials

A Phase 1 trial in obese men with prostate cancer at MD Anderson was registered around 2011. No results have been published and the current status is unclear †. There is no human efficacy or safety data of any kind.

Fat loss, body recomposition in the community

Anecdotal reports exist; they are sparse compared with other peptides, and several describe stopping because of side effects or concern about kidney effects.

4Reported side effects and interactions

Literature-reported

Dose-dependent nephrotoxicity in monkeys — rising creatinine, reduced glomerular filtration rate, renal tubular damage on histology — reversible after cessation at the doses used. Dehydration-related signs. Reduced food intake. In mice, treated animals showed no reported liver or haematological toxicity, but the monkey kidney findings are the critical result.

Community-reported

increased thirst and urination, fatigue, nausea, lethargy, lower back or flank discomfort, reduced appetite. Several reports describe raised creatinine on blood tests.

Theoretical. the compound is a cytotoxic targeted toxin; any off-target prohibitin expression (kidney, and potentially others) is a site of possible injury. Effects on fertility, the heart (prohibitin is abundant in cardiac mitochondria) and long-term kidney function are unknown. Fat loss may be irreversible where vasculature is destroyed, which is both the intended effect and a concern.

Interactions. none studied. Anything else that stresses the kidney (NSAIDs, dehydration, contrast media, nephrotoxic antibiotics) would be a plausible compounding risk.

Markers researchers commonly monitor

Marker	Why it's watched
Serum creatinine and estimated GFR	the primary toxicity seen in primates; the only marker with direct experimental backing.
Blood urea nitrogen and electrolytes (sodium, potassium)	kidney function and dehydration.
Urinalysis including protein and microscopy	tubular injury.
Cystatin C	a more sensitive GFR marker where available.
Body weight, fat mass by imaging or DEXA	efficacy readouts used in the monkey study.
Fasting glucose and insulin	improved insulin sensitivity was reported in treated animals.
Appetite and fluid intake	reduced food intake and dehydration signs were part of the primate picture.

Free for everyone. Safety information is never behind a paywall.

5Reconstitution and handling

Typically supplied as powder in 5 mg or 10 mg vials. with , swirl gently, protect from light. Given the kidney findings in primates, the research literature itself treats this as a compound requiring renal monitoring at every dosing stage.

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6Commonly studied alongside

Nothing in the literature. In community discussion it is occasionally mentioned alongside other fat-loss peptides; there is no rationale or data for combination.

Informational cross-links. Not stack recommendations.

7Regulatory status by region

Region	Status (checked —)
United States	Not FDA-approved. Not on the 2023 Category 2 compounding list as far as this review could establish †
European Union	Not authorised
United Kingdom	Not licensed
Australia	Not approved
South Africa	Not registered
Sport	Prohibited by WADA (S0 — non-approved substances)

8Open questions

Is the kidney injury fully reversible after longer or repeated courses? Only a single 28-day course has been studied.
Does the targeting hold in humans — is prohibitin exposed on human fat vasculature in the same way?
What happened to the registered Phase 1 trial?
Is destroyed fat vasculature regenerated, and does fat return?
Does the pro-apoptotic segment reach any tissue beyond fat and kidney at the doses used — heart, testis and brain express prohibitin and have not been examined.

9References

1Kolonin MG et al. (2004). Reversal of obesity by targeted ablation of adipose tissue. Nat Med. PubMed · DOI
2Barnhart KF et al. (2011). A peptidomimetic targeting white fat causes weight loss and improved insulin resistance in obese monkeys. Sci Transl Med. PubMed · DOI
3Ellerby HM et al. (1999). Anti-cancer activity of targeted pro-apoptotic peptides. Nat Med. PubMed · DOI
4Staquicini FI et al. (2011). Vascular ligand-receptor mapping by direct combinatorial selection in cancer patients. Proc Natl Acad Sci U S A. PubMed · DOI
5Daquinag AC et al. (2016). Depletion of white adipocyte progenitors induces beige adipocyte differentiation and suppresses obesity development. Cell Death Differ. PubMed · DOI

† Being confirmed by our reviewers against current sources.

10Community

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Self-reported side effects Phase 2

Not enough data yet. 0 of the 50 members needed have logged this compound for 4+ weeks. We don't show anything below 50, so no one can be identified.

11Page history

25 Oct 2026Profile published — awaiting medical review

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