We use essential cookies (authentication, your saved goals/stack) by default. With your permission we'll also enable privacy-respecting analytics (Vercel Web Analytics, anonymous load-time metrics) and error-replay diagnostics (Sentry — DOM snapshots only when an error fires) so we can fix bugs faster. Learn more about cookies
Research peptide — not a dietary supplement
Adipotide (FTPP) is a research compound, not a regulated dietary supplement. It is typically administered by injection and sold “for research use only.” The evidence below is largely preclinical (animal and in-vitro) or early-stage, so no evidence score is assigned. This page is provided for transparency and education — it is not a recommendation to use. Consult a qualified healthcare provider, and be aware that purity, dosing, and legal status vary by jurisdiction.
What the evidence says
Most Adipotide (FTPP) studies are mechanism or observational rather than RCTs that measure a clinical effect — keep findings provisional.
Most evidence is from mixed-quality studies published 2004–2013.
Based on 5 studies
Confidence
LowBy outcome
Adipotide (FTPP) has an evidence score of 3.2/10 — emerging evidence based on 5 indexed studies. A proapoptotic research peptide that destroys the blood supply of white fat. It is a 'homing' peptide (CKGGRAKDC) that binds prohibitin on the vasculature of white adipose tissue, fused to a proapoptotic sequence that then kills those blood vessels — causing the fat they feed to be resorbed. The honest status: this is PRECLINICAL ONLY. Adipotide caused real, rapid weight loss in obese mice AND in obese monkeys, but in the monkey study it also caused dose-limiting kidney toxicity (changes in the renal proximal tubule). There has NEVER been a human trial of any kind — no safety, no efficacy, nothing. It is not an approved drug or a dietary supplement; it survives as a grey-market 'research use only' injectable with no quality control. Low score: a striking animal proof-of-concept shadowed by renal toxicity and zero human data. Representative study: PMID 15133506.
Semaglutide
Mostly mechanism / observationalAn FDA-approved GLP-1 receptor agonist (Ozempic/Rybelsus for type 2 diabetes, Wegovy for chronic weight management) with genuinely strong, large-RCT evidence for glycemic control and substantial weight loss, plus a cardiovascular-outcomes benefit. Honest appraisal: this is a real prescription medicine with real efficacy AND real risks — a boxed warning for thyroid C-cell tumors, pancreatitis and gallbladder risk, very common GI side effects, and growing concern about grey-market/compounded versions. It is included here for reference only, not as a supplement and not auto-recommended.
Last reviewed June 2026 · evidence from 5 studies · how we score
This information is for educational purposes only. It is not a substitute for professional medical advice. Always consult a qualified healthcare provider before starting, stopping, or changing any supplement or medication.
Adipotide (FTPP — Fat-Targeted Proapoptotic Peptide; CKGGRAKDC-GG-D(KLAKLAK)2)
A proapoptotic research peptide that destroys the blood supply of white fat. It is a 'homing' peptide (CKGGRAKDC) that binds prohibitin on the vasculature of white adipose tissue, fused to a proapoptotic sequence that then kills those blood vessels — causing the fat they feed to be resorbed. The honest status: this is PRECLINICAL ONLY. Adipotide caused real, rapid weight loss in obese mice AND in obese monkeys, but in the monkey study it also caused dose-limiting kidney toxicity (changes in the renal proximal tubule). There has NEVER been a human trial of any kind — no safety, no efficacy, nothing. It is not an approved drug or a dietary supplement; it survives as a grey-market 'research use only' injectable with no quality control. Low score: a striking animal proof-of-concept shadowed by renal toxicity and zero human data.
A striking preclinical proof-of-concept — a peptide that ablates white-fat vasculature and caused real, rapid weight loss in obese mice AND obese monkeys — but the pivotal primate study also showed dose-limiting renal proximal-tubule toxicity, there is not a single human trial of any kind, and it is sold only as an unregulated grey-market research chemical.
Adipotide — also called FTPP ('fat-targeted proapoptotic peptide') — is a two-part synthetic peptidomimetic, CKGGRAKDC-GG-D(KLAKLAK)2.
The first part (CKGGRAKDC) is a 'homing' peptide discovered by in vivo phage display in the Arap/Pasqualini/Kolonin lab; it binds prohibitin, a membrane protein that the same group established as a marker of the blood vessels (endothelium) of white adipose tissue.
The second part, D(KLAKLAK)2 (KLA), is a proapoptotic sequence that disrupts mitochondrial membranes and triggers programmed cell death once it is delivered inside a cell.
Bolted together, the construct delivers the cell-killing payload selectively to the vasculature that feeds white fat: the targeted blood vessels undergo apoptosis, the fat they supply loses its blood supply, and the adipose tissue is resorbed.
This is a fundamentally different mechanism from appetite suppressants or lipolytic agents — it ablates the tissue's supply lines rather than altering metabolism.
The foundational proof-of-concept (Kolonin et al., Nature Medicine 2004) showed that targeting this proapoptotic peptide to prohibitin in the adipose vasculature ablated white fat and produced rapid, weight-independent obesity reversal in obese mice.
A 2012 Diabetes study (Kim et al.) showed the same proapoptotic peptide rapidly improved glucose tolerance in obese mice independent of weight and food intake, implicating the adipose vasculature in glucose homeostasis.
The most-cited translation step (Barnhart, Christianson, Kolonin et al., Science Translational Medicine 2011) moved adipotide into obese Old World monkeys: treatment induced targeted apoptosis in white-fat blood vessels and produced rapid weight loss and improved insulin resistance, confirmed by MRI and DXA — BUT, and this is the load-bearing caveat, at the effective doses the monkeys showed predictable, reversible changes in renal proximal-tubule function.
That dose-limiting kidney signal is the central safety problem and the reason this entry stays low.
Here is the honest summary that the grey market omits: every result is from animals — mice and one monkey study; there has never been a published human trial of adipotide, not a phase-I safety study, not a pharmacokinetic study, nothing.
It is not approved by any regulator, it is not a lawful dietary-supplement ingredient, and material sold online is an unregulated 'research use only' chemical with no guarantee of identity, purity, or sterility — being injected for fat loss on the strength of animal data that also flagged kidney toxicity.
Adipotide is a genuinely interesting tool compound and a striking animal proof-of-concept for vascular-targeted fat ablation; it is not a longevity drug, not a supplement, and not something with any human safety record.
The CKGGRAKDC portion of adipotide is a homing peptide isolated by in vivo phage display that binds prohibitin, a membrane protein the Kolonin lab established as a marker of the endothelium (blood vessels) of white adipose tissue. This is what makes the construct selective for the supply lines of white fat rather than acting body-wide. Demonstrated in mice and monkeys — never characterised in humans.
Once homed, the fused D(KLAKLAK)2 (KLA) sequence disrupts mitochondrial membranes inside the targeted endothelial cells and triggers apoptosis (programmed cell death). The blood vessels feeding white fat die, so the fat loses its blood supply. This is tissue ablation, not metabolic modulation — a mechanistically distinct anti-obesity strategy shown only in animal models.
Following vascular ablation, established white adipose tissue is resorbed; in obese mice this normalised metabolism and reversed obesity, and in obese monkeys it produced rapid weight loss and improved insulin resistance. A related mouse study showed glucose tolerance improved within days, independent of weight loss — implicating the adipose vasculature itself in glucose homeostasis. All animal findings.
In the obese-monkey study, the effective doses produced predictable, reversible changes in renal proximal-tubule function — the dose-limiting toxicity of the compound. The proximal tubule reabsorbs filtered peptides, which plausibly concentrates the construct there. This kidney signal, not appetite or metabolic side effects, is the central safety constraint, and it has never been evaluated in humans.
How Adipotide (FTPP) works — from molecular targets to health outcomes. Click an edge to see supporting research.This visualization is in beta — pathways are being refined and expanded.
Tap node to isolate • Pinch to zoom • Tap edge for research
No legitimate or recommended human dose exists — adipotide has never been given to a human in a published study, so there is no validated dose, schedule, or safe exposure. We do NOT provide a dosing protocol. The only published dosing is in animals (subcutaneous daily cycles in obese mice and monkeys), and the monkey work explicitly defined doses by where renal toxicity began — animal dosing does not translate to a human dose and should not be read as guidance.
Can be taken without food
| Form | Type |
|---|---|
| 💊None — unapproved grey-market research chemical | Recommended |
There is no legitimate pharmaceutical form. Adipotide is a research peptidomimetic used in mouse and monkey studies; it is not a medicine or a dietary supplement.
Minimum: 1 weeks
Optimal: 4 weeks
Cycling: Not required
Note: No approved or validated timing — the compound has never been tested in humans. This library does not endorse or schedule its use.
Dose-response data unavailable. The current published research for Adipotide (FTPP) does not provide sufficient dose-specific outcome data to generate reliable dose-response curves.
Refer to the Dosage & Timing section above for recommended dose ranges based on available evidence.
There has never been a published human trial of adipotide — no safety study, no pharmacokinetics, no efficacy trial. Every effect listed here is from mice or monkeys and may not translate to people. The grey-market fat-loss use rests entirely on animal data.
In obese mice, targeted ablation of white-fat vasculature reversed obesity; in obese monkeys, adipotide produced rapid weight loss and a marked reduction in white adipose tissue confirmed by MRI and DXA. Genuine, striking preclinical effects — not demonstrated in humans.
Obese mice showed rapid, weight-independent improvement in glucose tolerance, and obese monkeys showed improved insulin resistance. An interesting metabolic signal tied to the adipose vasculature — but an animal-only finding.
At effective doses, monkeys developed predictable, reversible changes in renal proximal-tubule function — the dose-limiting toxicity of adipotide and the main reason it has not advanced. Reversible in the study, but it defines the therapeutic-window problem and is entirely uncharacterised in humans.
Because no human has ever been studied, the human safety profile — including whether the monkey renal signal occurs in people — is completely unknown. Grey-market injection compounds this with unverified product quality.
Avoid — there are no human trials, no approved use, and no quality-controlled product, and the only animal safety data flagged dose-limiting kidney toxicity. The animal evidence does not justify human self-experimentation.
Avoid entirely — the dose-limiting toxicity in animals was renal.
Avoid entirely — completely unstudied.
The dose-limiting toxicity of adipotide in monkeys was renal proximal-tubule injury. Combining it with anything else that stresses the kidneys is theoretically additive and has never been studied in humans — treat as potentially dangerous.
There are no human drug-interaction data of any kind. Interactions cannot be predicted because the compound has never been characterised in people.
Tip: This was the dose-limiting toxicity in monkeys (reversible in that study). Human risk is unknown and uncharacterised; there is no validated way to mitigate it because the compound is unapproved and untested in people.
Tip: No human has ever been studied — the side-effect profile in people is genuinely unknown. This is itself the warning.
Tip: Grey-market injectable material has no identity/purity/sterility guarantees; contamination and mislabelling are real risks.
The commonly studied dose of Adipotide (FTPP) is No legitimate or recommended human dose exists — adipotide has never been given to a human in a published study, so there is no validated dose, schedule, or safe exposure. We do NOT provide a dosing protocol. The only published dosing is in animals (subcutaneous daily cycles in obese mice and monkeys), and the monkey work explicitly defined doses by where renal toxicity began — animal dosing does not translate to a human dose and should not be read as guidance.. Individual needs vary — start at the lower end of the range and adjust based on how you respond.
Timing is flexible for Adipotide (FTPP) — consistent daily use matters more than the time of day. There is no validated human dosing schedule because the compound has never been tested in humans.
Adipotide (FTPP) should be used with caution — talk to a healthcare provider before taking it. The most commonly reported side effects are kidney (renal proximal-tubule) toxicity, unknown human side-effect profile, harm from an unregulated, impure or non-sterile product. Use caution if any of these apply to you: Not an approved medicine and not a regulated dietary supplement — unapproved grey-market research chemical; do not self-source; No human safety data exists — and the only animal-dose data showed dose-limiting kidney toxicity; Anyone with kidney disease or reduced renal function — the dose-limiting toxicity in animals was renal.
Tirzepatide
Mostly mechanism / observationalAn FDA-approved prescription medication (Mounjaro for type 2 diabetes, Zepbound for obesity and obstructive sleep apnea), not a dietary supplement. Honest appraisal: in head-to-head phase-3 trials it is the most effective approved weight-loss drug to date — up to ~21% body-weight loss over 72 weeks and superior to semaglutide — but it is a real medicine with real risks: a boxed warning for thyroid C-cell tumors, common GI side effects, and pancreatitis/gallbladder signals. Do not source or use it outside a prescription.