--- title: "Adipotide: Research & Evidence | BodyHackGuide" url: https://www.bodyhackguide.co/compound/adipotide description: "Adipotide: mechanism, clinical studies & side effects." lang: en --- Skip to content Compare notes on r/BodyHackGuide (https://reddit.com/r/bodyhackguide) Compare notes with other researchers. Join r/BodyHackGuide (https://reddit.com/r/bodyhackguide) Image: Adipotide molecular structure (https://pubchem.ncbi.nlm.nih.gov/rest/pug/compound/cid/163360068/PNG?image_size=300x300) # Adipotide Weight Loss (https://www.bodyhackguide.co/wiki#cat-weight-loss)Phase 1 Also known as: FTPP, Fat-targeted proapoptotic peptide, CKGGRAKDC-GG-D(KLAKLAK)2, Prohibitin-TP01, Prohibitin targeting peptide 1 Adipotide is an experimental chimeric peptide that joins a white-fat-homing motif to a cell-killing motif, developed in the laboratory of Wadih Arap and Renata Pasqualini to destroy the blood supply of white adipose tissue. The homing half, the cyclic peptide CKGGRAKDC, was isolated by phage display in mice and binds prohibitin on fat vasculature; the killing half, D(KLAKLAK)2, disrupts mitochondrial membranes once inside the cell (PMID: 15133506, PMID: 22072637). Price check No vendor listings yet We do not track a vendor for Adipotide yet. Compare other compounds: https://www.bodyhackguide.co/compare Half-life: No published human value Route: Subcutaneous MW: 2557.2 g/mol CAS: 859216-15-2 Last reviewed: Oct 21, 2026 ## Overview ### At A Glance Mechanism Two halves bolted together… Half-Life No published human value. The first-in-human trial planned pharmacokinetic sampling at 10 minutes, 30 minutes, 1 hour and 4 hours after dosing but was terminated with no results posted (ClinicalTrials.gov NCT01262664). The monkey studies used daily subcutaneous dosing chosen by body surface area scaling rather than from a measured half-life (PMID: 22072637) Routes Subcutaneous Potential Benefits Body weight loss of 7.4% to 14.7% over 28 days in obese rhesus macaques Average 38.7% fall in total body fat by dual-energy x-ray absorptiometry in treated macaques against 14.8% in controls Abdominal white adipose tissue volume fall of 27.0% by magnetic resonance imaging at the end of the macaque recovery period Insulin area under the curve fall of 36.2% and insulinogenic index fall of 48.5% in obese macaques Glucose tolerance improvement within two to three days, independent of weight and food intake, in obese mice About 30% weight reduction over four weeks in obese mice in the founding study Safety Notes Common Dose-dependent rise in serum creatinine above 0.25 mg/kg a day in monkeys (PMID: 22072637) Glucosuria and proteinuria in monkeys during dosing (PMID: 22072637) Falls in serum phosphorus and serum potassium in monkeys (PMID: 22072637) Increased urine output and mild dehydration at the highest monkey doses (PMID: 22072637) Reduced food intake in proportion to dose in obese monkeys (PMID: 22072637) Serious Dose-dependent kidney lesions at necropsy in lean monkeys, graded minimal to moderate (PMID: 22072637) Minimal tubular degeneration still present in three monkeys after a four-week recovery (PMID: 22072637) No human safety data exists: the single phase 1 trial was terminated with 4 participants and no posted results The D(KLAKLAK)2 half is cytotoxic to any cell it enters, and selectivity depends entirely on the homing motif (PMID: 24098573, PMID: 23345420) ### Mechanism of Action ### Two halves bolted together Adipotide is a chimeric peptide with a homing half and a killing half. The homing half is the cyclic nine-residue motif CKGGRAKDC, which the Arap and Pasqualini group pulled out of a phage display library screened in live mice because it concentrated in the blood vessels of white fat. That motif binds prohibitin, a multifunctional membrane protein, and the same work established prohibitin as a vascular marker of adipose tissue (PMID: 15133506). The killing half is D(KLAKLAK)2, an amphipathic sequence built from D-amino acids. The group that made it reports that the motif resists proteolysis and disrupts lipid bilayers (PMID: 23345420), and describes it as disrupting mitochondrial membranes after receptor-mediated internalisation into a cell (PMID: 22072637). Written out, the molecule is CKGGRAKDC-GG-D(KLAKLAK)2, with GG as a short spacer (PMID: 22072637). ### Why the two halves matter separately On its own, D(KLAKLAK)2 is indiscriminate. In fungal cells it causes vacuolar injury, mitochondrial swelling, loss of mitochondrial membrane potential, reactive oxygen species accumulation and caspase-like activity, and an antioxidant blocks those effects (PMID: 24098573). Against gram-negative bacteria the same motif disrupts the microbial surface bilayer and dissipates membrane potential (PMID: 23345420). The homing motif is what is supposed to keep that activity confined: the peptide is internalised by prohibitin-expressing endothelium in white fat, and the killer half then damages mitochondrial membranes inside those cells (PMID: 22072637). ### The target is present in human fat, not only rodent fat The prohibitin receptor system is not a rodent-only finding. A combinatorial peptide library screened directly in cancer patients recovered roughly 2.35 million motifs from biopsies and identified four native ligand-receptor pairs, one of which, prohibitin with annexin A2, had a restricted distribution in normal human white adipose tissue (PMID: 22049339). Later work showed that the prohibitin and annexin A2 interaction regulates fatty acid transport in adipose tissue in mice and in human cells, and that the pair forms a complex with the fatty acid transporter CD36 (PMID: 27468426, PMID: 34314388). Prohibitin also has roles inside the adipocyte: overexpressing it in mouse 3T3-L1 fibroblasts was enough to induce adipogenesis in cell culture (PMID: 22124450), and a 2026 knock-in mouse study of prohibitin-1 cysteine-69 reported sex-dependent effects on fatty acid uptake, mitochondrial capacity and insulin sensitivity (PMID: 42778065). ### Vascular ablation, appetite, or both The original mouse paper framed the effect as resorption of established white fat after apoptosis in its vasculature, with normalisation of metabolism (PMID: 15133506). The monkey work complicated that story. Weight loss in obese rhesus macaques happened alongside a fall in food intake that tracked the dose, and the authors wrote that they could not rule out mild nausea, though the selective pattern (fewer biscuits, enrichment foods still eaten) pointed them toward satiety rather than illness (PMID: 22072637). A published comment on that paper argued the weight loss may instead reflect a direct effect on food consumption, and the authors replied in the same issue (PMID: 22539771). A separate mouse study found that the proapoptotic peptide improved glucose tolerance within two to three days, before and independently of weight and food intake changes, with pair-fed controls, which suggests the vascular effect does something to metabolism that appetite suppression alone does not explain (PMID: 22733798). ### Kidney handling is part of the mechanism The monkey investigators proposed a reason the kidney is the organ that reacts. Renal D-amino acid oxidase is, by their account, the only known mammalian enzyme able to use the D(KLAKLAK)2 moiety as a substrate, which they suggest might be the rate-limiting catabolic step for adipotide in the kidney. They also raised a second, non-toxic explanation for one of their laboratory signals: cleared adipotide may compete with the cation transport system that secretes creatinine, which would raise serum creatinine without a matching rise in blood urea nitrogen, exactly the pattern they saw (PMID: 22072637). ### Later peptides in the same family The design has been revised by other groups. A 2025 study reported a mixed-chirality prohibitin peptide, PTP-r, made by substituting D-arginine into prohibitin-TP01; it reduced body weight in diet-induced obese mice and the authors attributed its action to mitochondrial uncoupling rather than to vascular ablation (PMID: 40591817). Nanoparticle versions have also been built: prohibitin-targeted nanoparticles carrying the same killer peptide reduced body weight in diet-induced obese mice, and in a head-to-head comparison the nanoparticle formulation worked at a lower dose than the adipotide bioconjugate (PMID: 22982237, PMID: 23871959). Prohibitin-targeted carriers have since been loaded with other payloads, including a microRNA and resveratrol combination tested in obese mice in 2026 (PMID: 42849641). None of these has human data. ### Pharmacokinetics No human pharmacokinetic result for adipotide has been published. The first-in-human trial was designed to draw blood for pharmacokinetics at 10 minutes, 30 minutes, 1 hour and 4 hours after the first and the day 22 dose, but the trial was terminated and no results were posted (ClinicalTrials.gov NCT01262664). In monkeys, the dosing was daily, which the investigators chose empirically rather than from a measured half-life, and they found the optimal dose scaled across species with body surface area (PMID: 22072637). ### Overview Adipotide is an experimental chimeric peptide that joins a white-fat-homing motif to a cell-killing motif, developed in the laboratory of Wadih Arap and Renata Pasqualini to destroy the blood supply of white adipose tissue. The homing half, the cyclic peptide CKGGRAKDC, was isolated by phage display in mice and binds prohibitin on fat vasculature; the killing half, D(KLAKLAK)2, disrupts mitochondrial membranes once inside the cell (PMID: 15133506, PMID: 22072637). The best evidence comes from obese rhesus macaques, where 0.43 mg/kg a day for 28 days produced 7.4% to 14.7% body weight loss and an average 38.7% fall in total body fat, alongside dose-dependent and largely reversible kidney injury (PMID: 22072637). The only registered human trial, a phase 1 study in men with metastatic prostate cancer and obesity, enrolled 4 of a planned 39 participants, was terminated and has posted no results (ClinicalTrials.gov NCT01262664). ### Potential Research Fields Obesity Adipose tissue vasculature Ligand-directed drug delivery Phage display peptide discovery Prohibitin biology Renal toxicology ## Chemical Information IUPAC Name Not yet available CAS Number 859216-15-2 Molecular Formula C111H206N36O28S2 Molecular Mass 2557.2 g/mol View on PubChem: https://pubchem.ncbi.nlm.nih.gov/compound/163360068 ## Dosing & Protocols ### Unlock the Dosing tab Enter your email to keep reading. It is free, and it opens these tabs on every compound page in this browser. - Route You also get the free peptide cheat sheet by email. Unsubscribe anytime. Have an account? Sign in (https://www.bodyhackguide.co/auth) ## Research ### Unlock the research summary - A summary of the key research - Safety and side effects - A link to the PubMed results ## Interactions ### Interaction Matrix ### Contraindications These are cautions drawn from the published animal work and from the one registered human protocol. They are not advice, and no clinical use of adipotide is established. **Kidney function was the gating concern in the human protocol.** The MD Anderson phase 1 trial required serum creatinine no more than 1.5 times the upper limit of normal or creatinine clearance of at least 60 mL/min, and a 24-hour urine collection showing under 2,000 mg of protein, with a narrow exception to 3,000 mg for participants with haematuria and no casts, eosinophiluria or electrolyte wasting (ClinicalTrials.gov NCT01262664). The reason is visible in the monkey data: dose-dependent proximal tubule injury and altered tubular function (PMID: 22072637). **Nephrotoxic drugs were excluded.** Participants in that trial had to abstain from non-steroidal anti-inflammatory drugs, intravenous vancomycin, aminoglycosides and other potently nephrotoxic drugs from the time of consent until 30 days after the last dose, with low-dose aspirin at 81 mg a day or less the only exception (ClinicalTrials.gov NCT01262664). **Obstructive uropathy.** The protocol excluded hydronephrosis that was bilateral or involved a solitary kidney unless a nephrostomy or stent was already in place (ClinicalTrials.gov NCT01262664). **Uncontrolled hypertension and uncontrolled diabetes.** Both were exclusions, and the protocol states plainly that the intent of the hypertension criterion was to exclude people who might have unrecognised kidney damage from chronic uncontrolled high blood pressure (ClinicalTrials.gov NCT01262664). **Cardiac and organ reserve.** The protocol required normal B-type natriuretic peptide and electrocardiogram, or an ejection fraction of 45% or more with no more than mild diastolic dysfunction, and excluded recent heart failure, unstable angina, stroke, pulmonary embolism or myocardial infarction, lung disease needing supplemental oxygen, and known chronic liver disease with fibrosis or synthetic dysfunction (ClinicalTrials.gov NCT01262664). **Dehydration.** Monkeys on the highest doses produced more urine and showed mild dehydration (PMID: 22072637). **Mechanism-based caution about non-fat prohibitin.** Prohibitin is not confined to fat vasculature. It regulates adipocyte differentiation in cell culture (PMID: 22124450), partners with annexin A2 and CD36 in fatty acid transport (PMID: 27468426, PMID: 34314388), and prohibitin-targeted nanoparticles were more antiproliferative against cell lines expressing the receptor, including cancer lines (PMID: 28635372). A ligand-directed cytotoxin is only as selective as its target's distribution. **No data in women, in people without cancer, in children, or in pregnancy.** The single human trial enrolled men with metastatic prostate cancer and obesity only (ClinicalTrials.gov NCT01262664). The primate efficacy work used rhesus macaques and baboons, and the paper gives the sex of the animals only for the dose-finding cohort and the two baboons, which were female (PMID: 22072637). Research Disclaimer This interaction data is compiled from published research and community reports. It may not be exhaustive. Always consult a healthcare professional before combining compounds. No listings found for Adipotide. ### Sign in to leave a review Reviews on BodyHackGuide are tied to verified user accounts and moderated before publishing. Sign in (free, no spam) to share your experience with Adipotide. ### Related Compounds View All (https://www.bodyhackguide.co/wiki) ### 5-Amino-1MQ Weight Loss Preclinical 5-Amino-1MQ (5-amino-1-methylquinolinium iodide) is a small-molecule inhibitor of nicotinamide N-methyltransferase (NNMT), an enzyme that transfers a methyl group from S-adenosyl-L-methionine (SAM) to nicotinamide to form 1-methylnicotinamide (1-MNA) and S-adenosyl-L-homocysteine (SAH). t½ ~6–12 hours (oral) 50 mg - 150 mg daily (oral or injection) Preclinical View Profile https://www.bodyhackguide.co/compound/5-amino-1mq ### BAM15 Weight Loss Preclinical BAM15 is a small-molecule mitochondrial protonophore uncoupler that was first described in 2014 as a tool compound for dissipating proton motive force selectively across the inner mitochondrial membrane without collapsing the plasma membrane electrochemical gradient ([Kenwood et al., 2014]). Research compound — no established human doses. 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Preclinical View Profile https://www.bodyhackguide.co/compound/lipo-c View Full Dosage Guide → Protocols, calculator & safety for Adipotide https://www.bodyhackguide.co/guides/dosage/adipotide ### Price check No vendor listings yet See the vendor scorecard (https://www.bodyhackguide.co/vendors/scorecard) ### Research Score 45 0 PubMed results ### Quality Indicators Data Completeness 63% Description Mechanism of Action Chemical Data Dosing Protocols Safety Profile PubMed Results Interactions Vendor Listings ### Quick Facts Half-Life Molecular Weight 2557.2 g/mol Administration Subcutaneous CAS Number 859216-15-2 Trial Phase Phase 1 ### Safety Profile High Risk Common Side Effects - • Dose-dependent rise in serum creatinine above 0.25 mg/kg a day in monkeys (PMID: 22072637) - • Glucosuria and proteinuria in monkeys during dosing (PMID: 22072637) - • Falls in serum phosphorus and serum potassium in monkeys (PMID: 22072637) - • Increased urine output and mild dehydration at the highest monkey doses (PMID: 22072637) - • Reduced food intake in proportion to dose in obese monkeys (PMID: 22072637) Stop Use If - Not an approved medicine and never shown to be safe in people - Any kidney impairment, proteinuria or obstructive uropathy: all were exclusions in the one human protocol - Concurrent nephrotoxic drugs, which the human protocol barred from consent until 30 days after the last dose - No data in women, in people without cancer, in children or in pregnancy Research Disclaimer This information is for educational and research purposes only. Not intended as medical advice. Consult a healthcare professional before use. ## Frequently Asked Questions What is adipotide? Adipotide is an experimental two-part peptide, written CKGGRAKDC-GG-D(KLAKLAK)2, designed to kill the blood vessels that supply white fat. The first part of adipotide is a cyclic peptide that was isolated by phage display in mice because it homes to white fat vasculature, where it binds a membrane protein called prohibitin (PMID: 15133506). The second part of adipotide is a D-amino acid sequence that disrupts mitochondrial membranes once the peptide has been taken into a cell (PMID: 22072637, PMID: 23345420). Adipotide came out of the laboratory of Wadih Arap and Renata Pasqualini, who have published most of the work on it since 2004. Has adipotide been tested in humans? Adipotide has one registered human trial and no published human results. The trial was a phase 1 dose escalation at the University of Texas MD Anderson Cancer Center in men with metastatic prostate cancer and obesity, with the drug recorded as Prohibitin-TP01 and given as a daily subcutaneous injection for 28 days (ClinicalTrials.gov NCT01262664). The adipotide trial planned up to 39 participants, enrolled 4, and was terminated with the reason recorded as a request from the principal investigator, with a completion date of 2 January 2019. No results have been posted for that trial, so nothing is known publicly about how adipotide behaved in those four men. What did adipotide do in monkeys? The monkey studies are the only substantial evidence published on adipotide. In the fixed-dose study, 10 obese rhesus macaques given 0.43 mg/kg a day for 28 days lost 7.4% to 14.7% of their body weight while 5 saline controls changed by +1.0% to -3.5%, and total body fat measured by dual-energy x-ray absorptiometry fell by an average of 38.7% against 14.8% in controls (PMID: 22072637). Abdominal white fat volume on magnetic resonance imaging fell 17.5% by the end of dosing and 27.0% by the end of the recovery period, and the area under the insulin curve fell 36.2%. Weight loss with adipotide continued for about three weeks after the injections stopped. What were the kidney findings with adipotide? The kidney is where adipotide caused measurable harm in primates. In a Good Laboratory Practice toxicology study, lean rhesus macaques given 0.25, 0.43 or 0.75 mg/kg daily for 28 days had dose-dependent kidney lesions at necropsy that were absent in controls, graded minimal to mild at the low dose and minimal to moderate at the high dose, and described as single-cell necrosis plus reactive or regenerative change (PMID: 22072637). Monkeys on adipotide also had dose-dependent rises in serum creatinine without a matching rise in blood urea nitrogen, falls in serum phosphorus and potassium, and glucosuria, proteinuria and more renal epithelial cells in the urine. Most of those changes reversed within 28 days of stopping adipotide, though minimal tubular degeneration persisted in three animals after a four-week recovery. The investigators proposed that renal D-amino acid oxidase, which they describe as the only known mammalian enzyme that can use the D(KLAKLAK)2 moiety as a substrate, might be the rate-limiting catabolic step for adipotide in the kidney. Does adipotide work by destroying fat vessels or by suppressing appetite? Whether adipotide works by destroying fat vessels or by suppressing appetite is unresolved. The original mouse paper described resorption of established white fat after apoptosis in its vasculature (PMID: 15133506), but in monkeys the weight loss with adipotide came alongside a dose-related fall in food intake, and the authors said they could not completely rule out mild nausea (PMID: 22072637). A published comment on that paper argued that the effect of adipotide may instead reflect a direct effect on food consumption, and the authors replied in the same issue (PMID: 22539771). One argument against pure appetite suppression is that in obese mice the peptide improved glucose tolerance within two to three days independently of weight and food intake, with pair-fed controls (PMID: 22733798), and another is that lean monkeys given the therapeutic dose of adipotide did not lose weight at all (PMID: 22072637). Is adipotide approved or available as a medicine? Adipotide is not an approved medicine anywhere that this guide could verify. A query of the FDA Drugs@FDA database through the openFDA API on 20 October 2026 returned no application, brand name or active ingredient record for adipotide. The registry record for the single human trial states that Prohibitin-TP01 is not FDA approved or commercially available and is being used for research purposes only (ClinicalTrials.gov NCT01262664). Development of adipotide has left no published human results in the years since the monkey paper appeared in 2011, while other groups have moved on to redesigned prohibitin-targeting peptides and nanoparticle carriers tested only in mice (PMID: 40591817, PMID: 42849641). What is still unknown about adipotide? Almost everything about adipotide in people is unknown. No human efficacy, safety or pharmacokinetic result for adipotide has been published, and no randomised trial of adipotide exists in any species. The primate efficacy evidence for adipotide rests on 2 treated animals in a dose-finding study and 10 in a fixed-dose study, all at one centre, reported in a single 2011 paper (PMID: 22072637). Whether the kidney injury seen in monkeys can be separated from the weight loss, and whether a human dose exists that does one without the other, are open questions for adipotide, which is why later work in this family has focused on redesigned peptides and targeted carriers (PMID: 40591817, PMID: 22982237). ## Research Tools ### Peptide Calculator Reconstitution & syringe units https://www.bodyhackguide.co/tools/reconstitution ### Reconstitution Guide How to mix, step by step https://www.bodyhackguide.co/guides/how-to-reconstitute-peptides ### Nasal Spray Calc mL per actuation https://www.bodyhackguide.co/tools/intranasal ### Half-Life Visualizer Decay curves https://www.bodyhackguide.co/tools/halflife ## You may also like ### Eloralintide (LY3841136) Weight Loss View product (https://www.bodyhackguide.co/buy/eloralintide) ### AOD-9604 Metabolic & Weight Loss View product (https://www.bodyhackguide.co/buy/aod-9604) ### Cagrilintide Metabolic & Weight Loss View product (https://www.bodyhackguide.co/buy/cagrilintide) ### Cardarine (GW501516) Metabolic View product (https://www.bodyhackguide.co/buy/cardarine) ## Related Compounds ### 5-Amino-1MQ Weight Loss Preclinical ### BAM15 Weight Loss Preclinical ### Eloralintide (LY3841136) Weight Loss Phase 3 ### Exenatide Weight Loss FDA-approved ### L-Carnitine Weight Loss Preclinical ### Lipo-C Free 2026 Peptide Cheat Sheet (PDF) 38 compounds and blends: vial sizes, BAC water volumes, dosing ranges and bloodwork markers. 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All rights reserved. · Terms (https://www.bodyhackguide.co/terms) · Privacy (https://www.bodyhackguide.co/privacy) ## Structured data ```json [ { "@context": "https://schema.org", "@type": "BreadcrumbList", "itemListElement": [ { "@type": "ListItem", "position": 1, "name": "Home", "item": "https://www.bodyhackguide.co/" }, { "@type": "ListItem", "position": 2, "name": "Compounds", "item": "https://www.bodyhackguide.co/compare" }, { "@type": "ListItem", "position": 3, "name": "Adipotide" } ] }, { "@context": "https://schema.org", "@type": "MedicalWebPage", "name": "Adipotide", "description": "Adipotide is an experimental chimeric peptide that joins a white-fat-homing motif to a cell-killing motif, developed in the laboratory of Wadih Arap and Renata Pasqualini to destroy the blood supply of white adipose tissue. The homing half, the cyclic peptide CKGGRAKDC, was isolated by phage display in mice and binds prohibitin on fat vasculature; the killing half, D(KLAKLAK)2, disrupts mitochondrial membranes once inside the cell (PMID: 15133506, PMID: 22072637). The best evidence comes from obese rhesus macaques, where 0.43 mg/kg a day for 28 days produced 7.4% to 14.7% body weight loss and an average 38.7% fall in total body fat, alongside dose-dependent and largely reversible kidney injury (PMID: 22072637). The only registered human trial, a phase 1 study in men with metastatic prostate cancer and obesity, enrolled 4 of a planned 39 participants, was terminated and has posted no results (ClinicalTrials.gov NCT01262664).", "lastReviewed": "2026-10-21T06:27:47.674Z", "url": "https://www.bodyhackguide.co/compound/adipotide", "author": { "@type": "Person", "name": "BioChonch", "url": "https://www.bodyhackguide.co/about", "jobTitle": "Founder & Lead Researcher", "sameAs": [ "https://reddit.com/r/BodyHackGuide", "https://reddit.com/r/BrainHackGuide", "https://reddit.com/r/Biohackingher" ], "worksFor": { "@type": "Organization", "name": "BodyHackGuide", "url": "https://www.bodyhackguide.co" } }, "reviewedBy": { "@type": "Person", "name": "BioChonch", "url": "https://www.bodyhackguide.co/about", "jobTitle": "Founder & Lead Researcher", "sameAs": [ "https://reddit.com/r/BodyHackGuide", "https://reddit.com/r/BrainHackGuide", "https://reddit.com/r/Biohackingher" ], "worksFor": { "@type": "Organization", "name": "BodyHackGuide", "url": "https://www.bodyhackguide.co" } }, "publisher": { "@type": "Organization", "name": "BodyHackGuide", "url": "https://www.bodyhackguide.co" }, "mainContentOfPage": { "@type": "WebPageElement", "cssSelector": "main" }, "about": { "@type": "Drug", "name": "Adipotide", "alternateName": [ "FTPP", "Fat-targeted proapoptotic peptide", "CKGGRAKDC-GG-D(KLAKLAK)2", "Prohibitin-TP01", "Prohibitin targeting peptide 1" ], "description": "Adipotide is an experimental chimeric peptide that joins a white-fat-homing motif to a cell-killing motif, developed in the laboratory of Wadih Arap and Renata Pasqualini to destroy the blood supply of white adipose tissue. The homing half, the cyclic peptide CKGGRAKDC, was isolated by phage display in mice and binds prohibitin on fat vasculature; the killing half, D(KLAKLAK)2, disrupts mitochondrial membranes once inside the cell (PMID: 15133506, PMID: 22072637). The best evidence comes from obese rhesus macaques, where 0.43 mg/kg a day for 28 days produced 7.4% to 14.7% body weight loss and an average 38.7% fall in total body fat, alongside dose-dependent and largely reversible kidney injury (PMID: 22072637). The only registered human trial, a phase 1 study in men with metastatic prostate cancer and obesity, enrolled 4 of a planned 39 participants, was terminated and has posted no results (ClinicalTrials.gov NCT01262664).", "activeIngredient": "Adipotide", "administrationRoute": "Subcutaneous", "mechanismOfAction": "Two halves bolted together Adipotide is a chimeric peptide with a homing half and a killing half. The homing half is the cyclic nine-residue motif CKGGRAKDC, which the Arap and Pasqualini group pulled out of a phage display library screened in live mice because it concentrated in the blood vessels of white fat. That motif binds prohibitin, a multifunctional membrane protein, and the same work established prohibitin as a vascular marker of adipose tissue (PMID: 15133506). The killing half is D(KLAKLAK)2, an amphipathic sequence built from D-amino acids. The group that made it reports that the motif resists proteolysis and disrupts lipid bilayers (PMID: 23345420), and describes it as disrupting mitochondrial membranes after receptor-mediated internalisation into a cell (PMID: 22072637). Written out, the molecule is CKGGRAKDC-GG-D(KLAKLAK)2, with GG as a short spacer (PMID: 22072637). Why the two halves matter separately On its own, D(KLAKLAK)2 is indiscriminate. In fungal cells it causes vacuolar injury, mitochondrial swelling, loss of mitochondrial membrane potential, reactive oxygen species accumulation and caspase-like activity, and an antioxidant blocks those effects (PMID: 24098573). Against gram-negative bacteria the same motif disrupts the microbial surface bilayer and dissipates membrane potential (PMID: 23345420). The homing motif is what is supposed to keep that activity confined: the peptide is internalised by prohibitin-expressing endothelium in white fat, and the killer half then damages mitochondrial membranes inside those cells (PMID: 22072637). The target is present in human fat, not only rodent fat The prohibitin receptor system is not a rodent-only finding. A combinatorial peptide library screened directly in cancer patients recovered roughly 2.35 million motifs from biopsies and identified four native ligand-receptor pairs, one of which, prohibitin with annexin A2, had a restricted distribution in normal human white adipose tissue (PMID: 22049339). Later work showed that the prohibitin and annexin A2 interaction regulates fatty acid transport in adipose tissue in mice and in human cells, and that the pair forms a complex with the fatty acid transporter CD36 (PMID: 27468426, PMID: 34314388). Prohibitin also has roles inside the adipocyte: overexpressing it in mouse 3T3-L1 fibroblasts was enough to induce adipogenesis in cell culture (PMID: 22124450), and a 2026 knock-in mouse study of prohibitin-1 cysteine-69 reported sex-dependent effects on fatty acid uptake, mitochondrial capacity and insulin sensitivity (PMID: 42778065). Vascular ablation, appetite, or both The original mouse paper framed the effect as resorption of established white fat after apoptosis in its vasculature, with normalisation of metabolism (PMID: 15133506). The monkey work complicated that story. Weight loss in obese rhesus macaques happened alongside a fall in food intake that tracked the dose, and the authors wrote that they could not rule out mild nausea, though the selective pattern (fewer biscuits, enrichment foods still eaten) pointed them toward satiety rather than illness (PMID: 22072637). A published comment on that paper argued the weight loss may instead reflect a direct effect on food consumption, and the authors replied in the same issue (PMID: 22539771). A separate mouse study found that the proapoptotic peptide improved glucose tolerance within two to three days, before and independently of weight and food intake changes, with pair-fed controls, which suggests the vascular effect does something to metabolism that appetite suppression alone does not explain (PMID: 22733798). Kidney handling is part of the mechanism The monkey investigators proposed a reason the kidney is the organ that reacts. Renal D-amino acid oxidase is, by their account, the only known mammalian enzyme able to use the D(KLAKLAK)2 moiety as a substrate, which they suggest might be the rate-limiting catabolic step for adipotide in the kidney. They also raised a second, non-toxic explanation for one of their laboratory signals: cleared adipotide may compete with the cation transport system that secretes creatinine, which would raise serum creatinine without a matching rise in blood urea nitrogen, exactly the pattern they saw (PMID: 22072637). Later peptides in the same family The design has been revised by other groups. A 2025 study reported a mixed-chirality prohibitin peptide, PTP-r, made by substituting D-arginine into prohibitin-TP01; it reduced body weight in diet-induced obese mice and the authors attributed its action to mitochondrial uncoupling rather than to vascular ablation (PMID: 40591817). Nanoparticle versions have also been built: prohibitin-targeted nanoparticles carrying the same killer peptide reduced body weight in diet-induced obese mice, and in a head-to-head comparison the nanoparticle formulation worked at a lower dose than the adipotide bioconjugate (PMID: 22982237, PMID: 23871959). Prohibitin-targeted carriers have since been loaded with other payloads, including a microRNA and resveratrol combination tested in obese mice in 2026 (PMID: 42849641). None of these has human data. Pharmacokinetics No human pharmacokinetic result for adipotide has been published. The first-in-human trial was designed to draw blood for pharmacokinetics at 10 minutes, 30 minutes, 1 hour and 4 hours after the first and the day 22 dose, but the trial was terminated and no results were posted (ClinicalTrials.gov NCT01262664). In monkeys, the dosing was daily, which the investigators chose empirically rather than from a measured half-life, and they found the optimal dose scaled across species with body surface area (PMID: 22072637).", "legalStatus": "Not approved for human use (research chemical)", "warning": "For research purposes only. Not for human consumption." } }, { "@context": "https://schema.org", "@type": "FAQPage", "mainEntity": [ { "@type": "Question", "name": "What is adipotide?", "acceptedAnswer": { "@type": "Answer", "text": "Adipotide is an experimental two-part peptide, written CKGGRAKDC-GG-D(KLAKLAK)2, designed to kill the blood vessels that supply white fat. The first part of adipotide is a cyclic peptide that was isolated by phage display in mice because it homes to white fat vasculature, where it binds a membrane protein called prohibitin (PMID: 15133506). The second part of adipotide is a D-amino acid sequence that disrupts mitochondrial membranes once the peptide has been taken into a cell (PMID: 22072637, PMID: 23345420). Adipotide came out of the laboratory of Wadih Arap and Renata Pasqualini, who have published most of the work on it since 2004." } }, { "@type": "Question", "name": "Has adipotide been tested in humans?", "acceptedAnswer": { "@type": "Answer", "text": "Adipotide has one registered human trial and no published human results. The trial was a phase 1 dose escalation at the University of Texas MD Anderson Cancer Center in men with metastatic prostate cancer and obesity, with the drug recorded as Prohibitin-TP01 and given as a daily subcutaneous injection for 28 days (ClinicalTrials.gov NCT01262664). The adipotide trial planned up to 39 participants, enrolled 4, and was terminated with the reason recorded as a request from the principal investigator, with a completion date of 2 January 2019. No results have been posted for that trial, so nothing is known publicly about how adipotide behaved in those four men." } }, { "@type": "Question", "name": "What did adipotide do in monkeys?", "acceptedAnswer": { "@type": "Answer", "text": "The monkey studies are the only substantial evidence published on adipotide. In the fixed-dose study, 10 obese rhesus macaques given 0.43 mg/kg a day for 28 days lost 7.4% to 14.7% of their body weight while 5 saline controls changed by +1.0% to -3.5%, and total body fat measured by dual-energy x-ray absorptiometry fell by an average of 38.7% against 14.8% in controls (PMID: 22072637). Abdominal white fat volume on magnetic resonance imaging fell 17.5% by the end of dosing and 27.0% by the end of the recovery period, and the area under the insulin curve fell 36.2%. Weight loss with adipotide continued for about three weeks after the injections stopped." } }, { "@type": "Question", "name": "What were the kidney findings with adipotide?", "acceptedAnswer": { "@type": "Answer", "text": "The kidney is where adipotide caused measurable harm in primates. In a Good Laboratory Practice toxicology study, lean rhesus macaques given 0.25, 0.43 or 0.75 mg/kg daily for 28 days had dose-dependent kidney lesions at necropsy that were absent in controls, graded minimal to mild at the low dose and minimal to moderate at the high dose, and described as single-cell necrosis plus reactive or regenerative change (PMID: 22072637). Monkeys on adipotide also had dose-dependent rises in serum creatinine without a matching rise in blood urea nitrogen, falls in serum phosphorus and potassium, and glucosuria, proteinuria and more renal epithelial cells in the urine. Most of those changes reversed within 28 days of stopping adipotide, though minimal tubular degeneration persisted in three animals after a four-week recovery. The investigators proposed that renal D-amino acid oxidase, which they describe as the only known mammalian enzyme that can use the D(KLAKLAK)2 moiety as a substrate, might be the rate-limiting catabolic step for adipotide in the kidney." } }, { "@type": "Question", "name": "Does adipotide work by destroying fat vessels or by suppressing appetite?", "acceptedAnswer": { "@type": "Answer", "text": "Whether adipotide works by destroying fat vessels or by suppressing appetite is unresolved. The original mouse paper described resorption of established white fat after apoptosis in its vasculature (PMID: 15133506), but in monkeys the weight loss with adipotide came alongside a dose-related fall in food intake, and the authors said they could not completely rule out mild nausea (PMID: 22072637). A published comment on that paper argued that the effect of adipotide may instead reflect a direct effect on food consumption, and the authors replied in the same issue (PMID: 22539771). One argument against pure appetite suppression is that in obese mice the peptide improved glucose tolerance within two to three days independently of weight and food intake, with pair-fed controls (PMID: 22733798), and another is that lean monkeys given the therapeutic dose of adipotide did not lose weight at all (PMID: 22072637)." } }, { "@type": "Question", "name": "Is adipotide approved or available as a medicine?", "acceptedAnswer": { "@type": "Answer", "text": "Adipotide is not an approved medicine anywhere that this guide could verify. A query of the FDA Drugs@FDA database through the openFDA API on 20 October 2026 returned no application, brand name or active ingredient record for adipotide. The registry record for the single human trial states that Prohibitin-TP01 is not FDA approved or commercially available and is being used for research purposes only (ClinicalTrials.gov NCT01262664). Development of adipotide has left no published human results in the years since the monkey paper appeared in 2011, while other groups have moved on to redesigned prohibitin-targeting peptides and nanoparticle carriers tested only in mice (PMID: 40591817, PMID: 42849641)." } }, { "@type": "Question", "name": "What is still unknown about adipotide?", "acceptedAnswer": { "@type": "Answer", "text": "Almost everything about adipotide in people is unknown. No human efficacy, safety or pharmacokinetic result for adipotide has been published, and no randomised trial of adipotide exists in any species. The primate efficacy evidence for adipotide rests on 2 treated animals in a dose-finding study and 10 in a fixed-dose study, all at one centre, reported in a single 2011 paper (PMID: 22072637). Whether the kidney injury seen in monkeys can be separated from the weight loss, and whether a human dose exists that does one without the other, are open questions for adipotide, which is why later work in this family has focused on redesigned peptides and targeted carriers (PMID: 40591817, PMID: 22982237)." } } ] }, { "@context": "https://schema.org", "@type": "Organization", "@id": "https://www.bodyhackguide.co#organization", "name": "BodyHackGuide", "alternateName": "BHG", "url": "https://www.bodyhackguide.co", "logo": { "@type": "ImageObject", "url": "https://www.bodyhackguide.co/logo.png", "width": 512, "height": 512 }, "description": "Evidence-based research reference for peptides and nootropics. 273 compound profiles, interactive dosing calculators, vendor price comparisons, and trust-scored vendor reviews scored on a public, reproducible methodology applied to every vendor. 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