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Weight loss · Daily shot

Adipotide

Gray market

Checked · 28 sources · 12 corrections on this page · No vendors · No affiliates · No one buys a word of it

0 human trials published

Preclinical · mice and monkeys

Gray market · No FDA ruling — not on any list

Sold as a research chemical.

Bottom line

A compound that stopped at four patients, with a kidney signal in monkeys at every dose that took fat off.

Also called
  • FTPP
  • Fat-Targeted Pro-apoptotic Peptide
  • Prohibitin-targeted peptidomimetic
  • CKGGRAKDC-GG-D(KLAKLAK)₂
Category
Peptide — Experimental Pro-Apoptotic Chimera
Class
Chimeric pro-apoptotic peptidomimetic
Structure
Homing domain + pro-apoptotic domain
Target
Prohibitin on adipose endothelium
Route (studied)
SubQ (one human Phase 1 trial) · SubQ (mice and monkeys)
Route (sold)
SubQ vials (research chemical)
FDA Status
Never progressed beyond preclinical
Human Trials
One small obesity trial (halted direction)
Primate Data
~11% body fat reduction in 4 weeks (rhesus)
Key Toxicity
Dose-dependent renal tubular injury
WADA Status
Not specifically named — prohibited at all times under S0 (no government has approved it for human use)
Cost & Access
Research-only

Also for weight loss

The other four questions

What does it do? Starves fat cells by killing the blood vessels that feed them. One part of the molecule docks onto a specific fat-vessel target; the other part ruptures those vessels from inside.
Who uses it? Nobody, in any approved setting: it is sold only as a research chemical (see Legal Status).
Does the evidence hold up? Obese mice and obese rhesus monkeys lost substantial body fat (Kolonin et al., 2004; Barnhart et al., 2011) — but the monkeys also showed dose-dependent kidney changes at the doses that worked (Barnhart et al., 2011). One human Phase 1 trial dosed four patients and was stopped (ClinicalTrials.gov NCT01262664).
Bottom line? A compound that stopped at four patients, with a kidney signal in monkeys at every dose that took fat off.

Dosing from the Literature

Published for fat loss: mouse and monkey doses, with kidney injury at every monkey dose that worked. Not published: any human dose; the one human trial’s registry record gives only its starting dose, 0.03 mg/kg a day, and posted no results.

The animal doses below are reproduced from the published preclinical literature, and the human row from the trial’s registry record, for historical / research reference. They are not a human use guide. No FDA-approved human dose exists, and the primate data document dose-dependent renal injury at every efficacy-positive dose tested.

Species / StudyDoseRoute / ScheduleNotes
Obese and ob/ob mice (Kolonin et al., 2004)Dose not stated in the paper readDaily subcutaneousTrial: targeting the pro-apoptotic peptide to prohibitin ablated white fat and reversed obesity, the authors report, “without detectable adverse effects.”
Obese mice and rats (Kim et al., 2010)3 mg/kgDaily subcutaneous, 4 or 27 daysTrial: an independent group; obesity reversed on a high-fat diet but not a low-fat one, through reduced food intake with no change in energy expenditure. No kidney measure.
Obese rhesus macaques (Barnhart et al., 2011)0.43 mg/kgDaily subcutaneous, 4 weeks, then 4 weeks offTrial: 15 monkeys, 10 treated. Weight −7.4 to −14.7% (controls +1.0 to −3.5%); total body fat −38.7% by the end against −14.8%. Serum creatinine rose dose-dependently above 0.25 mg/kg, with sugar and protein in the urine; most changes reversed within 28 days of stopping.
Lean rhesus monkeys, toxicology (Barnhart et al., 2011)0.25, 0.43 or 0.75 mg/kgDaily subcutaneous, 28 daysTrial: 15 monkeys in a Good Laboratory Practice study; those on 0.25 and 0.43 mg/kg did not lose weight.
Human Phase I (NCT01262664)Dose-escalation from 0.03 mg/kg a day (up to 5 levels)Daily SubQ × 28 daysTrial: four men with obesity and metastatic prostate cancer enrolled; terminated at the principal investigator’s request; results not published (ClinicalTrials.gov NCT01262664).
Dosing Disclaimer

The primate study that documents 7–15% weight loss in 4 weeks also documents dose-dependent kidney changes at those same doses. There is no published dose range in any species that produces the fat-loss phenotype without the parallel renal signal. Self-administration of Adipotide obtained through research-chemical channels, at community-cited doses, exposes the user to renal injury with zero clinical-grade safety monitoring. This is not a compound to experiment with.

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What It Is

Adipotide — also referred to as FTPP (Fat-Targeted Pro-apoptotic Peptide) or the prohibitin-targeted peptidomimetic — is a chimeric synthetic peptide designed to destroy white adipose tissue by killing the blood vessels that supply it. It was invented in 2004 in the laboratory of Renata Pasqualini and Wadih Arap at the University of Texas MD Anderson Cancer Center, with Mikhail Kolonin as first author. The approach translated a strategy that the same laboratory had developed for targeted tumor-vasculature ablation (fusing a tumor-vessel-homing peptide to a pro-apoptotic mitochondrial-disrupting peptide) into the adipose-tissue problem.

Structurally, Adipotide is a two-domain construct connected by a short linker: the N-terminal half is the homing peptide CKGGRAKDC (a disulfide-cyclized nonapeptide identified by in vivo phage display as a selective binder of white-fat vasculature); the C-terminal half is D(KLAKLAK)₂, a D-amino-acid amphipathic helical sequence that disrupts mitochondrial membranes once internalized into target cells. The two are joined by a short glycine-glycine linker. The overall molecule is therefore a ~30-amino-acid chimeric peptidomimetic, rather than a "natural" peptide.

The target of the homing sequence is prohibitin, a multifunctional mitochondrial and plasma-membrane protein — one review places it at the membrane, in the nucleus and in the mitochondria, with a different job in each (Peng et al., 2015; PMID 26091791). Prohibitin is expressed on the luminal surface of white adipose tissue microvasculature and functions as a vascular-bed-specific "zip code" for CKGGRAKDC-bearing peptides. Prohibitin expression is not confined to adipose vasculature — it is also found in mitochondria, in certain tumour vasculatures, and in the kidney, though no published study has shown that this is what makes adipotide nephrotoxic. In a human proximal tubule cell line, one group reports prohibitin in the mitochondria, where raising it protected the cells against oxidative injury and silencing it left them less able to survive it (Ye et al., 2015; PMID 26198983).

Adipotide is not a metabolic fat-loss drug in the usual sense. It does not alter lipolysis, lipogenesis, appetite, nutrient partitioning, or energy expenditure at the adipocyte (fat cell) level. It kills a specific vascular bed. Adipocytes in that bed die from ischemia, and the surrounding fat pad involutes. Regrowth requires re-vascularization; in obese rodents and primates, the compound produces durable fat-mass loss over weeks after dosing ends. This makes Adipotide pharmacologically unusual and interesting — but the same property that produces its effect (targeted vascular apoptosis) is the property that limits it (prohibitin is also present outside adipose).

Mechanism of Action

  • Vascular homing via prohibitin — The N-terminal CKGGRAKDC nonapeptide (a chain of 9 amino acids) binds prohibitin expressed on the luminal endothelium (the lining of blood vessels) of white adipose tissue microvasculature. Prohibitin was identified as the cognate receptor in the original 2004 Kolonin Nat Med paper via affinity chromatography and co-localization studies (Kolonin et al., Nat Med 2004; PMID 15133506). The binding is sufficiently tissue-selective that systemically administered CKGGRAKDC-fluorophore conjugates accumulate preferentially in adipose vascular beds.
  • Pro-apoptotic mitochondrial disruption — The C-terminal D(KLAKLAK)₂ sequence is an amphipathic α-helical cationic peptide. The KLAKLAK family was built from scratch in 1996 as antibacterial peptides "designed to be perfectly amphipathic in helical conformations"; in that paper, the more helical a sequence was in a membrane-like environment, the more toxic it was to mouse fibroblasts (Javadpour et al., 1996; PMID 8759631). Once internalized into the target endothelial cell, the helix inserts into the mitochondrial inner membrane, depolarizing it and releasing cytochrome c. The resulting caspase cascade drives endothelial apoptosis (programmed cell death). The D-stereochemistry provides resistance to cytoplasmic proteases during transit.
  • Endothelial apoptosis → vascular rarefaction — Loss of endothelial cells in the adipose microvasculature reduces blood flow to the tissue. Capillary density falls and the vascular "scaffold" that supports adipocyte viability collapses.
  • Adipocyte ischemic death — Deprived of their blood supply, adipocytes undergo ischemic necrosis and adjacent phagocytic cleanup. Fat pad mass decreases over days to weeks.
  • Durable body-composition change — Because adipocytes do not readily regenerate and the vascular scaffold must be rebuilt from remaining endothelial precursors, the body-composition change persists after compound washout. In primate studies, body fat did not recover to baseline during the 4-week follow-up after dosing ended.
  • Prohibitin and the kidney — Prohibitin is not adipose-exclusive, but in renal tubular cells the published work places it inside the cell rather than on its surface: in the human proximal-tubule line HK-2 it is a mitochondrial protein, where raising it protected the cells against oxidative injury and silencing it left them less able to survive it (Ye et al., 2015; PMID 26198983). The primate study that found the toxicity does not trace it to prohibitin: it reports dose-dependent, reversible changes in proximal-tubule function, and its authors discuss renal handling of the peptide instead — possible competition with tubular creatinine secretion, and renal D-amino acid oxidase as the only known mammalian enzyme that can use adipotide's D(KLAKLAK)₂ half as a substrate (Barnhart et al., 2011; PMID 22072637). The dose-limiting renal tubular injury is the finding; the step that delivers the payload to the kidney is not established.
  • Possible off-target effects in tumor vasculature — Some tumor types express CKGGRAKDC-binding prohibitin, and the laboratory's tumor work carries the same pro-apoptotic payload on different homing domains (D-WAT, D-CAN) rather than Adipotide's — a related but distinct therapeutic program.
  • Food intake fell too, and nobody has shown why — The intended mechanism is vascular-ablative, but in the monkey study the weight loss came with a drop in food intake, and the authors say further work is needed to tell satiety from a reduced demand for nutrients. In mice and rats, an independent group reports the fat loss happening through reduced food intake with no change in energy expenditure.

What the Research Shows

  • Original mouse obesity reversal (Kolonin 2004; PMID 15133506) — Obese ob/ob mice and diet-induced obese C57BL/6J mice received daily subcutaneous Adipotide. Body weight and fat mass decreased rapidly and durably; glucose tolerance and insulin sensitivity normalized. The authors reported normalization of metabolism "without detectable adverse effects" in mice; the kidney effects were found later, in monkeys (Barnhart 2011).
  • Rhesus macaque obesity (Barnhart 2011; Sci Transl Med; PMID 22072637) — Spontaneously obese rhesus macaques received Adipotide daily for 28 days. Body weight fell 7.4–14.7% over the 4 weeks of treatment (controls +1.0 to −3.5%); DEXA showed total body fat down 38.7% by the end of the study, 4 weeks after the last dose, against 14.8% in controls, and insulin resistance improved. Food intake fell along with the weight. The main side effect was on the kidney: dose-dependent rises in serum creatinine (blood urea nitrogen did not rise), sugar and protein in the urine, and changes in proximal tubule function that the authors call mild, predictable and reversible; most resolved within 28 days of stopping.
  • A published comment disputed the mechanism (Criscione, 2012; PMID 22539771) — Writing in the same journal, a reader argued the monkeys' weight loss "may instead reflect a direct effect of adipotide on food consumption" rather than the ablation of fat-tissue blood vessels; the authors replied in the same issue. The primate paper's own text says the weight loss "occurred concurrently with a reduction in food intake", and that lean monkeys given a therapeutic dose did not lose weight (Barnhart 2011; PMID 22072637).
  • A second laboratory, obese mice and rats, no kidney measurement — A group with no author from the MD Anderson program gave obese mice the same molecule, CKGGRAKDC-GG-D(KLAKLAK)₂, and reported glucose tolerance improving "rapidly and potently ... in a weight- and food intake-independent manner" — mice pair-fed to the treated group's food intake were the control for that — with serum insulin and triglycerides down against vehicle. The paper reports no kidney or urine measurement at all, so it neither confirms the renal signal nor clears it. The same group's earlier study of the same molecule, at 3 mg/kg subcutaneously, reports that it reversed high-fat-diet obesity in mice and cut body weight in mice and rats on a high-fat diet but not on a low-fat one, with the fat loss coming through reduced food intake rather than raised energy expenditure, and without signs of illness on a conditioned-taste-aversion test (Kim et al., 2010; PMID 20103704). That paper reports no kidney or urine measurement either.
  • Dose-ranging and toxicology refinements — Subsequent preclinical work explored dose-titration, formulation, and schedule modifications aimed at widening the therapeutic index. None of these substantially eliminated the renal toxicity at fat-loss-effective doses. One formulation line put the same KLAKLAK payload inside a prohibitin-targeted nanoparticle instead of conjugating it to the homing peptide, and reported a fall in body weight in diet-induced obese mice at a low dose where the Adipotide-style bioconjugate did not, with no detectable liver toxicity (Hossen et al., 2013; PMID 23871959).
  • Prostate cancer line of work — The published tumor work from that laboratory uses the same pro-apoptotic payload on adipose-stromal-cell homing domains, not Adipotide's prohibitin-homing peptide (D-WAT: Daquinag et al., 2016, PMID 26316391; D-CAN: Su et al., 2019, PMID 30361686). The only prostate-cancer use of Adipotide on record is the terminated Phase I below, which dosed four patients. This is a separate therapeutic program from the obesity application.
  • What the tumor papers actually used — The published tumor work from that laboratory joins the same KLAKLAK pro-apoptotic payload to different homing domains, not Adipotide's prohibitin-homing CKGGRAKDC. D-WAT, built on the cyclic domain CSWKYWFGEC, which homes to adipose stromal cells, depleted tumor stromal and perivascular cells and suppressed tumor growth in several mouse carcinoma models (Daquinag et al., 2016; PMID 26316391). D-CAN, also developed against adipose stromal cells, suppressed obesity-associated epithelial-mesenchymal transition and cancer progression in mouse prostate cancer models, and beat cisplatin alone when the two were combined (Su et al., 2019; PMID 30361686). No published study we could find gives Adipotide itself to a tumor model.
  • Limited clinical exploration — A Phase 1 dose-escalation study in obese men with prostate cancer began in May 2012 (ClinicalTrials.gov NCT01262664, listed as Prohibitin Targeting Peptide 1) and was stopped after four patients; no results have been published or posted, and the compound did not progress to advanced clinical development in the obesity indication.
  • The independent work never measured the kidney — One group outside the originating program published body-weight and glucose results with this molecule in mice and rats (Kim 2010; PMID 20103704, Kim 2012; PMID 22733798) and reports no kidney or urine measurement in either paper, so neither confirms the renal signal nor clears it.
Critical Context — Kidney Injury at Weight-Loss Doses

In obese monkeys, the kidney changes appeared at the doses that caused weight loss: serum creatinine rose, dose by dose, above 0.25 mg/kg (Barnhart et al., 2011). The 2004 mouse study reported no detectable adverse effects (Kolonin et al., 2004).

Human Data

The published human clinical experience with Adipotide is extremely limited.

  • Phase I dose-escalation in obese men with prostate cancer (NCT01262664) — Registered as NCT01262664, which records M.D. Anderson Cancer Center as lead sponsor with no collaborators, an actual start of May 24, 2012, four patients enrolled, and termination at the principal investigator's request. Designed as dose-escalation primarily to characterize safety and the primary body-composition end-point in obese men with prostate cancer. No results have been published or posted, and the compound did not advance to a Phase II or Phase III obesity program.
  • No dedicated non-oncology obesity trial published — Despite the striking rhesus macaque fat-loss data, no registered randomized placebo-controlled obesity trial in otherwise healthy obese adults has been published.
  • Community self-administration — Adipotide has appeared intermittently in gray-market research-chemical listings aimed at fat-loss self-experimenters. Community reports are sparse, often conflate Adipotide with unrelated compounds, and are anecdote, not signal.

Reconstitution & Storage

No label or guideline gives a strength, storage condition or shelf life for a product sold as adipotide. The published studies gave it by subcutaneous injection (Kolonin et al., 2004; Barnhart et al., 2011).

Side Effects & Risks

Important

In obese monkeys, adipotide caused dose-dependent changes in kidney tubule function at the doses that took fat off; most reversed within 28 days of stopping (Barnhart et al., 2011). No published human study reports its safety. Consult a licensed healthcare provider.

  • Renal tubular injury — the dose-limiting toxicity — Dose-dependent changes in proximal tubule function in all three monkey species studied: serum creatinine up (blood urea nitrogen was not), sugar and protein in the urine, and minimal-to-moderate tubular degeneration and single-cell necrosis in the kidney tissue. The authors call it relatively mild, predictable and reversible; most changes resolved within 28 days of stopping. It is not a theoretical risk: it appeared at the doses that caused weight loss.
  • Electrolytes — In the monkeys, serum phosphorus and potassium showed mild-to-moderate dose-dependent changes alongside the kidney findings (Barnhart et al., 2011).
  • Off-target delivery (theoretical) — Prohibitin is present outside adipose tissue, so the pro-apoptotic payload reaching non-target tissue is the stated worry; no published study has demonstrated that delivery in vivo, and the monkey study's authors did not conclude it (Barnhart et al., 2011; PMID 22072637).
  • Irreversible, cosmetically disproportionate fat loss — Because adipocytes killed by vascular destruction do not reliably regenerate, the fat loss may outlast the dosing; the longest published follow-up is the primate study's four weeks after the last dose, over which body fat kept falling. Disproportionate depletion of specific fat pads could create long-lasting cosmetic deformity.
  • Adipose hormone changes — Fat tissue is endocrine-active: it secretes leptin, adiponectin and other factors, and is a major site for the metabolism of sex steroids and glucocorticoids (Kershaw & Flier, 2004; PMID 15181022). Rapid adipose-tissue destruction could produce disordered leptin signaling and secondary metabolic consequences.
  • No human safety data — The one human trial dosed four patients and was terminated; no results are published (ClinicalTrials.gov NCT01262664).
  • Pregnancy and children — No study in either appears in the documents read for this page.
  • Drug interactions — None has been studied.
  • What is in a vial — Adipotide is sold as a research chemical; no analysis of such products appears in the documents read for this page.

Bloodwork & Monitoring

No trial, label or guideline sets monitoring for adipotide, and the one human trial published no results (ClinicalTrials.gov NCT01262664). The monkey study measured serum creatinine, blood urea nitrogen, phosphorus and potassium, urine glucose and protein, kidney tissue, body weight and DEXA body fat (Barnhart et al., 2011). The mouse and rat studies measured body weight, food intake, energy expenditure, glucose tolerance, serum insulin, lipids and leptin (Kim et al., 2010; Kim et al., 2012).

Commonly Stacked With

No study has tested adipotide with anything.

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Legal Status

Current Status — April 2026

Adipotide is not FDA-approved for any indication. It has not progressed beyond a limited Phase I dose-escalation in obese men with prostate cancer (NCT01262664) and is not currently in active clinical development for obesity or any other indication.

Adipotide is not specifically listed on the FDA Bulk Drug Substances Category 1 or Category 2 peptide lists. It exists in a regulatory gray zone similar to other preclinical experimental peptidomimetics: available for research use but not legally available for human clinical use in any jurisdiction.

Adipotide is not named on the WADA Prohibited List 2026, but S0 prohibits it at all times: no government has approved it for human therapeutic use (WADA Prohibited List 2026).

Adipotide was not among the 12 peptides FDA removed from Category 2 in April 2026, and FDA’s 503A categories list, updated May 14, 2026, does not name it (FDA 503A categories list, April 22 and May 14, 2026). No realistic regulatory path to US clinical availability exists absent a sponsor pursuing late-stage development — which, given the renal toxicity history and the maturation of GLP-1-class obesity pharmacology, is not commercially plausible.

Cost & Access

Adipotide is not approved for human use in any jurisdiction. It is available only through research-chemical suppliers for laboratory research purposes.

US 503A / 503B compounding pharmacies do not compound Adipotide. It was not among the 12 peptides FDA removed from Category 2 in April 2026 (FDA 503A categories list, April 22, 2026).

Kalios does not sell compounds.

References

  1. Kolonin MG, Saha PK, Chan L, Pasqualini R, Arap W. Reversal of obesity by targeted ablation of adipose tissue. Nat Med. 2004;10(6):625-632. PMID: 15133506. (The original Adipotide paper — describes CKGGRAKDC homing, prohibitin receptor identification, and ob/ob + DIO mouse obesity reversal.)
  2. Barnhart KF, Christianson DR, Hanley PW, Driessen WH, Bernacky BJ, Baze WB, Wen S, Tian M, Ma J, Kolonin MG, Saha PK, Do KA, Hulvat JF, Gelovani JG, Chan L, Arap W, Pasqualini R. A peptidomimetic targeting white fat causes weight loss and improved insulin resistance in obese monkeys. Sci Transl Med. 2011;3(108):108ra112. PMID: 22072637. (Rhesus macaque obesity study: 7–15% weight loss in 4 weeks, with reversible, dose-dependent changes in kidney tubule function.)
  3. Reitman ML. Magic bullets melt fat. Nat Med. 2004;10(6):581-582. PMID: 15170200. (Editorial commentary accompanying the 2004 Kolonin Nat Med paper, framing promise and mechanism.)
  4. Arap W, Pasqualini R, Ruoslahti E. Cancer treatment by targeted drug delivery to tumor vasculature in a mouse model. Science. 1998;279(5349):377-380. PMID: 9430587. (The methodology paper for tumor-vasculature-homing peptide discovery that the Adipotide program translated to adipose.)
  5. Ellerby HM, Arap W, Ellerby LM, Kain R, Andrusiak R, Rio GD, Krajewski S, Lombardo CR, Rao R, Ruoslahti E, Bredesen DE, Pasqualini R. Anti-cancer activity of targeted pro-apoptotic peptides. Nat Med. 1999;5(9):1032-1038. PMID: 10470080. (The foundational paper describing the D(KLAKLAK)₂ pro-apoptotic mitochondrial-disrupting sequence that Adipotide reuses.)
  6. ClinicalTrials.gov. A First-in-Man, Phase I Evaluation of A Single Cycle of Prohibitin Targeting Peptide 1 in Patients With Metastatic Prostate Cancer and Obesity (M.D. Anderson Cancer Center; terminated at the PI's request after 4 patients; started May 24, 2012; no results posted). NCT01262664. (Phase I dose-escalation; no results posted or published.)
  7. Kolonin MG, Sergeeva A, Staquicini DI, Smith TL, Tarleton CA, Molldrem JJ, Marchiò S, Pasqualini R, Arap W. Interaction between Tumor Cell Surface Receptor RAGE and Proteinase 3 Mediates Prostate Cancer Metastasis to Bone. Cancer Res. 2017;77(12):3144-3150. PMID: 28428279. (Related Kolonin / Arap / Pasqualini vascular-targeting program.)
  8. Daquinag AC, Tseng C, Salameh A, Zhang Y, Amaya-Manzanares F, Dadbin A, Florez F, Scherer PE, Kolonin MG. Depletion of white adipocyte progenitors induces beige adipocyte differentiation and suppresses obesity development. Cell Death Differ. 2015;22(2):351-363. PMID: 25342467. (Follow-up vascular-progenitor depletion work in adipose biology.)
  9. Kolonin MG, Pasqualini R, Arap W. Molecular addresses in blood vessels as targets for therapy. Curr Opin Chem Biol. 2001;5(3):308-313. PMID: 11479123. (Review framing the vascular-homing-peptide paradigm that underlies Adipotide.)
  10. Giordano RJ, Cardó-Vila M, Lahdenranta J, Pasqualini R, Arap W. Biopanning and rapid analysis of selective interactive ligands. Nat Med. 2001;7(11):1249-1253. PMID: 11689892. (Methodology for in vivo phage display, which identified CKGGRAKDC.)
  11. Hossen MN, Kajimoto K, Akita H, Hyodo M, Harashima H. Vascular-targeted nanotherapy for obesity: unexpected passive targeting mechanism to obese fat for the enhancement of active drug delivery. J Control Release. 2012;163(1):101-110. PMID: 22982237. (Related adipose-vascular-targeting therapeutic literature.)
  12. Daquinag AC, Dadbin A, Snyder B, Wang X, Sahin AA, Ueno NT, Kolonin MG. Non-glycanated Decorin Is a Drug Target on Human Adipose Stromal Cells. Mol Ther Oncolytics. 2017;6:1-9. PMID: 28607949. (Subsequent Kolonin-group adipose-targeting work.)
  13. Criscione L. Comment on "a peptidomimetic targeting white fat causes weight loss and improved insulin resistance in obese monkeys". Sci Transl Med. 2012;4(131):131le2. PMID: 22539771. (Published comment arguing the monkeys' weight loss may instead reflect a direct effect on food consumption; the authors replied in the same issue, at 131lr2.)
  14. Kim DH, Woods SC, Seeley RJ. Peptide designed to elicit apoptosis in adipose tissue endothelium reduces food intake and body weight. Diabetes. 2010;59(4):907-915. PMID: 20103704. (The same independent group, the same CKGGRAKDC-GG-D(KLAKLAK)₂ molecule at 3 mg/kg: high-fat-diet obesity reversed in mice, body weight down in mice and rats on a high-fat diet but not a low-fat one, through reduced food intake and not raised energy expenditure.)
  15. Kim DH, Sartor MA, Bain JR, Sandoval D, Stevens RD, Medvedovic M, Newgard CB, Woods SC, Seeley RJ. Rapid and weight-independent improvement of glucose tolerance induced by a peptide designed to elicit apoptosis in adipose tissue endothelium. Diabetes. 2012;61(9):2299-2310. PMID: 22733798. (A second laboratory, obese mice, the same CKGGRAKDC-GG-D(KLAKLAK)₂ molecule: glucose tolerance improved independently of weight and food intake. No kidney or urine measurement is reported.)
  16. Hossen N, Kajimoto K, Akita H, Hyodo M, Harashima H. A comparative study between nanoparticle-targeted therapeutics and bioconjugates as obesity medication. J Control Release. 2013;171(2):104-112. PMID: 23871959. (The same KLAKLAK payload inside a prohibitin-targeted nanoparticle, against the Adipotide-style bioconjugate, in diet-induced obese mice.)
  17. Javadpour MM, Juban MM, Lo WC, Bishop SM, Alberty JB, Cowell SM, Becker CL, McLaughlin ML. De novo antimicrobial peptides with low mammalian cell toxicity. J Med Chem. 1996;39(16):3107-3113. PMID: 8759631. (The de novo design of the KLAKLAK sequences Adipotide carries as its pro-apoptotic domain.)
  18. Peng YT, Chen P, Ouyang RY, Song L. Multifaceted role of prohibitin in cell survival and apoptosis. Apoptosis. 2015;20(9):1135-1149. PMID: 26091791. (Review of prohibitin's membrane, nuclear and mitochondrial locations, and the different job it does in each.)
  19. Ye J, Li J, Xia R, Zhou M, Yu L. Prohibitin protects proximal tubule epithelial cells against oxidative injury through mitochondrial pathways. Free Radic Res. 2015;49(11):1393-1403. PMID: 26198983. (Prohibitin in a human renal proximal tubule cell line: raising it protected the cells against oxidative injury, silencing it did the reverse.)
  20. Daquinag AC, Tseng C, Zhang Y, Amaya-Manzanares F, Florez F, Dadbin A, Zhang T, Kolonin MG. Targeted Proapoptotic Peptides Depleting Adipose Stromal Cells Inhibit Tumor Growth. Mol Ther. 2016;24(1):34-40. PMID: 26316391. (D-WAT: the same KLAKLAK payload on the CSWKYWFGEC homing domain, in mouse carcinoma models.)
  21. Su F, Ahn S, Saha A, DiGiovanni J, Kolonin MG. Adipose stromal cell targeting suppresses prostate cancer epithelial-mesenchymal transition and chemoresistance. Oncogene. 2019;38(11):1979-1988. PMID: 30361686. (D-CAN in mouse prostate cancer models — an adipose-stromal-cell homing domain, not Adipotide's prohibitin-homing one.)
  22. Wilding JPH, Batterham RL, Calanna S, Davies M, Van Gaal LF, Lingvay I, McGowan BM, Rosenstock J, Tran MTD, Wadden TA, Wharton S, Yokote K, Zeuthen N, Kushner RF. Once-Weekly Semaglutide in Adults with Overweight or Obesity. N Engl J Med. 2021;384(11):989-1002. PMID: 33567185. (STEP 1: −14.9% of body weight at 68 weeks, against −2.4% on placebo.)
  23. Jastreboff AM, Aronne LJ, Ahmad NN, Wharton S, Connery L, Alves B, Kiyosue A, Zhang S, Liu B, Bunck MC, Stefanski A. Tirzepatide Once Weekly for the Treatment of Obesity. N Engl J Med. 2022;387(3):205-216. PMID: 35658024. (SURMOUNT-1: −20.9% of body weight at 72 weeks on the highest dose.)
  24. Jastreboff AM, Kaplan LM, Frías JP, Wu Q, Du Y, Gurbuz S, Coskun T, Haupt A, Milicevic Z, Hartman ML. Triple-Hormone-Receptor Agonist Retatrutide for Obesity - A Phase 2 Trial. N Engl J Med. 2023;389(6):514-526. PMID: 37366315. (−24.2% of body weight at 48 weeks on the highest dose.)
  25. Kershaw EE, Flier JS. Adipose tissue as an endocrine organ. J Clin Endocrinol Metab. 2004;89(6):2548-2556. PMID: 15181022. (Review: the factors fat tissue secretes, and its role in the metabolism of sex steroids and glucocorticoids.)
  26. Waring WS, Moonie A. Earlier recognition of nephrotoxicity using novel biomarkers of acute kidney injury. Clin Toxicol (Phila). 2011;49(8):720-728. PMID: 21970770. (Review: serum creatinine as an insensitive marker of acute kidney injury, and urinary KIM-1 and NGAL as earlier indicators of tubular injury.)
  27. FDA. Bulk Drug Substances Nominated for Use in Compounding Under Section 503A of the FD&C Act (503A categories list), versions updated April 15, April 22 and May 14, 2026. fda.gov/media/94155/download. Read October 3, 2026. (Notice that 12 peptides would leave Category 2 because their nominations were withdrawn; their removal; GHK-Cu, except injectable, back in Category 1.)
  28. World Anti-Doping Agency. Prohibited List 2026 (in effect January 1, 2026). S0, Non-approved substances. wada-ama.org/sites/default/files/2025-09/2026list_en_final_clean_september_2025.pdf. Read October 3, 2026.

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Checked 18 Oct 2026