Adipotide
Evidence: CMetabolic / Weight Management
Key facts
- Research areaMetabolic / Weight Management
- Study records91 human
- Study-at-a-Glance1published summaries
- Last updated2026-07-30
Evidence Snapshot
What this grade covers
A for molecular identity; B for selected rodent and nonhuman-primate findings; C/D for registered first-in-human development context; E for established human weight loss, approval, safety, or dosing.
Regulatory Context
Investigational prohibitin-targeting peptidomimetic; not FDA-approved. A first-in-human phase 1 study was terminated and verified published results were not located.
In Plain English
A quick, research-focused overview. It does not replace, and cannot outrank, the detailed evidence below.
What is it?
Adipotide is a vascular-targeting proapoptotic peptidomimetic designed to bind prohibitin on white-adipose-tissue vasculature and deliver a mitochondria-disrupting sequence. Weight-loss findings come mainly from mouse and nonhuman-primate studies; a first-in-human trial was registered but terminated without verified published outcome results.
Why are researchers interested in it?
Adipotide combines the adipose-vasculature-homing motif CKGGRAKDC with a proapoptotic D(KLAKLAK)2 sequence. The targeting portion binds prohibitin associated with white-adipose vasculature, while the proapoptotic component disrupts mitochondrial membranes in targeted vascular cells, leading to loss of adipose blood supply in preclinical models.
What does the evidence look like?
Evidence grade D. Evidence types and limitations are separated below.
Biggest things to know
Renal proximal-tubule changes were reported in obese-monkey research.
Research Takeaway
Adipotide is a prohibitin-targeted proapoptotic peptidomimetic designed to direct a mitochondria-disrupting D(KLAKLAK)2 payload toward the vasculature of white adipose tissue; evidence from unconjugated KLAK peptides, generic prohibitin inhibitors, or other vascular-targeting constructs must not be treated as adipotide evidence.
Evidence boundary: Exact construct identity matters because both the targeting ligand and the proapoptotic payload determine the reported biological effect.
See all 6 evidence claims →Quick Summary
Adipotide is a vascular-targeting proapoptotic peptidomimetic designed to bind prohibitin on white-adipose-tissue vasculature and deliver a mitochondria-disrupting sequence. Weight-loss findings come mainly from mouse and nonhuman-primate studies; a first-in-human trial was registered but terminated without verified published outcome results.
Mechanism & Research Overview
Adipotide combines the adipose-vasculature-homing motif CKGGRAKDC with a proapoptotic D(KLAKLAK)2 sequence. The targeting portion binds prohibitin associated with white-adipose vasculature, while the proapoptotic component disrupts mitochondrial membranes in targeted vascular cells, leading to loss of adipose blood supply in preclinical models.
Mechanism pathway
Relationship-support labels describe the type and directness of the research available, not proof of safety or effectiveness. Indirectly supported, inferred and uncertain relationships are not equivalent to directly supported ones.
Step 1: Targeting component
- CompoundAdipotide
- Directly supported (Directly supported relationship)Biological targetProhibitinExtracellular Protein
- Leads toPathwayOther Defined PathwayPF14 is used because the frozen prohibitin-directed vascular-targeting component is a specialized targeting mechanism that does not fit any more specific governed Stage 28 pathway family.
Relationship details
- Adipotide → Prohibitin — Directly supportedThe CKGGRAKDC homing motif binds prohibitin associated with white-adipose vasculature.
Relevant tissue/system context: White-adipose vasculature
Step 2: Effector component
- CompoundAdipotide
- Directly supported (Directly supported relationship)Biological targetMitochondrial membraneMembrane / Lipid Target
- Leads toPathwayOther Defined PathwayPF14 is used because the frozen downstream mitochondrial-membrane-disruption component is a defined effector mechanism that does not fit any more specific governed Stage 28 pathway family.
- Contributes to
- Biological processLoss of adipose blood supply (preclinical)
Relationship details
- Adipotide → Mitochondrial membrane — Directly supportedThe D(KLAKLAK)2 proapoptotic component disrupts mitochondrial membranes in prohibitin-targeted vascular cells.
- Loss of adipose blood supply (preclinical) — contributes to the pathway (structural link, no support rating)Sources: adipotide-01-reversal-of-obesity-by-targeted-ablation-of-a
A biological process is not the same as a proven health or treatment outcome.
Relevant tissue/system context: White-adipose vascular endothelial cells
Evidence Claims
Individual scientific statements drawn from the sources cited below, each shown with the specific evidence boundary that statement does not establish.
Supported
Adipotide is a prohibitin-targeted proapoptotic peptidomimetic designed to direct a mitochondria-disrupting D(KLAKLAK)2 payload toward the vasculature of white adipose tissue; evidence from unconjugated KLAK peptides, generic prohibitin inhibitors, or other vascular-targeting constructs must not be treated as adipotide evidence.
Does not establish
Evidence boundary: Exact construct identity matters because both the targeting ligand and the proapoptotic payload determine the reported biological effect.
Sources: Reversal of obesity by targeted ablation of adipose tissue; A peptidomimetic targeting white fat causes weight loss and improved insulin resistance in obese monkeys; A comparative study between nanoparticle-targeted therapeutics and bioconjugates as obesity medication
Supported
In preclinical models, adipotide targets prohibitin-associated white-adipose vasculature and promotes vascular-cell injury/apoptosis, followed by loss of established white adipose tissue.
Does not establish
Evidence boundary: This is a preclinical mechanism and does not establish a safe or effective human fat-loss treatment.
Sources: Reversal of obesity by targeted ablation of adipose tissue; A peptidomimetic targeting white fat causes weight loss and improved insulin resistance in obese monkeys
Supported
In obese rhesus macaques, adipotide produced substantial reductions in body weight, BMI, abdominal circumference, and measured fat volume, with improvement in indices of insulin resistance during treatment.
Does not establish
Evidence boundary: These were nonhuman-primate studies; the magnitude of weight loss cannot be presented as expected human efficacy.
Supported
Nonhuman-primate studies identified dose-related renal tubular toxicity and changes including creatinine elevation, glucosuria, and proteinuria; many abnormalities improved after treatment stopped, but renal injury is a material safety signal.
Does not establish
Evidence boundary: Reversibility in experimental animals does not establish renal safety in humans.
Supported
A registered first-in-human Phase I study of Prohibitin-TP01 exists, but a trial registry entry is not evidence that adipotide has established human obesity efficacy.
Does not establish
Evidence boundary: Human-development status must be separated from completed, peer-reviewed clinical efficacy.
Supported
Adipotide should be described as an experimental compound without an established approved human obesity indication in this evidence package.
Does not establish
Evidence boundary: This claim does not attempt to characterize every jurisdiction; it defines the evidence boundary relevant to the MitoCore page.
Sources: A peptidomimetic targeting white fat causes weight loss and improved insulin resistance in obese monkeys; A first-in-man phase I evaluation of a single cycle of prohibitin targeting peptide 1 in patients with metastatic prostate cancer and obesity
Safety & Evidence Limitations
Considerations reported in the sources cited on this page — not a complete list of every possible risk, and not medical advice.
Safety Consideration
Renal proximal-tubule changes were reported in obese-monkey research.Safety Consideration
The mechanism intentionally injures targeted vasculature, creating substantial theoretical and observed safety concerns.Safety Consideration
No verified published human efficacy or safety results were located from the terminated phase 1 registry.Safety Consideration
Reduced food intake may have contributed to some primate weight-loss findings, according to published commentary.Safety Consideration
The catalog acronym FTTP should be retained only as a catalog spelling; FTPP is the literature acronym for fat-targeted proapoptotic peptide.Safety Consideration
Polyuria and dehydration accompany the reported renal proximal-tubule changes. Off-target vascular injury, apoptosis outside the intended adipose endothelium, and altered prohibitin/annexin-A2 biology are mechanism-level concerns. Hepatic, cardiac, neurologic, reproductive, developmental, immune, and oncologic effects are uncharacterized in humans. Immunogenicity, D-amino-acid impurity, aggregation, sterility, endotoxin risk, and repeated-course/long-term safety are unknown.
Research Areas Being Studied
Research areas discussed on this page reflect the Metabolic / Weight Management category and the sources cited below.
Findings Reported in Studies
Educational summary only — reported in cited studies, not a claim of proven benefit.
Show findings from 1 human study
- Vascular ligand-receptor mapping by direct combinatorial selection in cancer patients (2011):
Study Tables by Evidence Type
9 study records · 1 with a Study-at-a-Glance summary
- Human Studies & Clinical Data 1
- Animal / Cell / Preclinical Data 4
- Regulatory Documents & Official Trial Registries 2
Human Studies & Clinical Data(1)
Vascular ligand-receptor mapping by direct combinatorial selection in cancer patients
2011PMID 22049339
- Population / Model
- Human in vivo vascular ligand-receptor mapping study
- Dose / Duration / Finding
Human vascular-targeting research supported prohibitin as a vascular target for the CKGGRAKDC homing motif.
Safety note
This was target-mapping research, not an adipotide obesity efficacy trial.
Animal / Cell / Preclinical Data(4)
Peptide Designed to Elicit Apoptosis in Adipose Tissue Endothelium Reduces Food Intake and Body Weight
2010PMID 20103704 · DOI 10.2337/db09-1141
Study-at-a-Glance available
- Population / Model
- Dose / Duration / Finding
In diet-induced-obese mice and rats, a phage-display-derived peptide targeting prohibitin on white-adipose endothelium and fused to a proapoptotic sequence reduced body weight in animals on a high-fat diet, including complete reversal of high-fat-diet-induced obesity in mice, but did not produce the same effect in animals on a low-fat diet. Weight loss was accompanied by reduced food intake without a change in energy expenditure; food intake fell despite reduced circulating leptin, supporting a leptin-independent component of the feeding effect.
Show full finding
Key takeaway
In mice and rats, a peptide designed to trigger cell death in the blood-vessel lining of fat tissue reduced food intake and body weight in animals on a high-fat diet; this study did not test it in humans.
Study at a Glance
Study at a Glance
Plain-language summary of: Peptide Designed to Elicit Apoptosis in Adipose Tissue Endothelium Reduces Food Intake and Body Weight
A mouse and rat study of a peptide aimed at the blood vessels of fat tissue
Evidence status
What was being studied?
How a peptide that triggers cell death in the blood vessel lining of fat tissue changes food intake, energy use and appetite-related hormones in lab animals.
Who participated?
Lean and obese laboratory mice and rats. Humans were not studied.
How was the study done?
Animal experiment. Mice or rats were treated with the peptide for 4 or 27 days. Researchers measured daily energy intake and energy use in mice on a low-fat or high-fat diet and in rats on a high-fat diet. They also tested whether the peptide made the animals feel ill, and measured appetite-related gene activity and leptin levels. Only the abstract was reviewed.
Key results
In mice, the peptide completely reversed obesity caused by a high-fat diet. Mice and rats on a high-fat diet lost weight, but animals on a low-fat diet did not. The fat loss came with eating less and no change in energy use. The animals did not show signs of illness, and the eating reduction occurred even though circulating leptin was lower. The abstract gives no numerical effect sizes.
What does this mean?
Safety findings
Safety information was not available in the source reviewed. A taste-aversion test found no signs of illness in the animals, but that is not a safety assessment.
Important limitations
- Animal study (mice and rats); results may not apply to humans.
- Only the abstract was reviewed, and it gives no numeric effect sizes.
- The abstract does not report adverse effects beyond a conditioned taste aversion test for illness.
Sources
- Original study
- PubMed — PubMed
- Sources reviewed
- Abstract only — full text not reviewed.
This summary is a plain-language reading aid written by MitoCore. It does not replace the original study, which remains the authoritative source. Research information only, not medical advice.
A comparative study between nanoparticle-targeted therapeutics and bioconjugates as obesity medication
2013PMID 23871959 · DOI 10.1016/j.jconrel.2013.07.013
- Population / Model
- Dose / Duration / Finding
This study directly tested Adipotide (the KLA-conjugated prohibitin-targeting bioconjugate) head-to-head against a prohibitin-targeted nanoparticle formulation (KLA-PTNP) in diet-induced-obesity mice. At the low dose tested, KLA-PTNP—not Adipotide—produced significant body-weight reduction and a significant decrease in serum leptin; Adipotide itself did not reproduce this effect in this head-to-head comparison. This is a direct rodent comparative finding about Adipotide's own performance, not merely background context, though it remains a mouse model and does not provide human efficacy or safety evidence.
Show full finding
A peptidomimetic targeting white fat causes weight loss and improved insulin resistance in obese monkeys
2011PMID 22072637 · DOI 10.1126/scitranslmed.3002621
- Population / Model
- Obese rhesus monkeys
- Dose / Duration / Finding
The study reported weight loss and improved insulin-resistance measures in obese nonhuman primates.
Safety note
Renal proximal-tubule changes were reported and described as reversible after treatment withdrawal; nonhuman-primate findings do not establish human safety.
Reversal of obesity by targeted ablation of adipose tissue
2004PMID 15133506 · DOI 10.1038/nm1048
- Population / Model
- Obese mouse models
- Dose / Duration / Finding
A vascular-homing peptide linked to a proapoptotic sequence reduced white adipose tissue and body weight in mice.
Safety note
Mouse efficacy does not establish human benefit or safety; the mechanism intentionally injures adipose vasculature.
Regulatory Documents & Official Trial Registries(2)
A first-in-man phase I evaluation of a single cycle of prohibitin targeting peptide 1 in patients with metastatic prostate cancer and obesity
2010NCT01262664
- Population / Model
- Patients with advanced prostate cancer and obesity
- Dose / Duration / Finding
Official first-in-human phase 1 registry; the study is listed as terminated and verified peer-reviewed outcome results were not located.
Safety note
No public efficacy or safety conclusion should be inferred from the existence of the registry.
NCI Drug Dictionary: Prohibitin-Targeting Peptide 1
- Population / Model
- Dose / Duration / Finding
NCI's Drug Dictionary describes prohibitin-targeting peptide 1 (Adipotide/Prohibitin-TP01) as an investigational chimeric peptidomimetic that combines a prohibitin-targeting domain with a proapoptotic sequence and notes potential antineoplastic activity. NCI does not describe an FDA-approved product or an established human obesity indication.
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Review Articles / Secondary Sources(2)
Comment on “A peptidomimetic targeting white fat causes weight loss and improved insulin resistance in obese monkeys”
2012PMID 22539771
- Population / Model
- Dose / Duration / Finding
Published commentary questioned whether reduced food intake contributed to the primate weight-loss findings.
Safety note
Commentary highlights interpretive uncertainty and is not a separate efficacy experiment.
First Patient Dosed in Adipotide Phase I Study
- Population / Model
- Dose / Duration / Finding
Sponsor newsroom announcement describing dosing of the first patient in the Phase I Prohibitin-TP01/Adipotide study. Development-context material only -- not a peer-reviewed report of human weight-loss efficacy or outcome data, and registry status plus a company announcement do not by themselves establish published human efficacy.
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Anecdotal Reported Patterns — Not Medical Advice
Anecdotal Reported Patterns — Not Medical Advice
Reported dosing patterns are included for educational context only. They are self-reported, unverified, not medical advice, and not instructions for human use. Community-submitted patterns are not yet available in this Phase 1 prototype; this section is a placeholder reserved for moderated, aggregated community data.
Lab Markers to Discuss With a Clinician
Educational topics only — not self-monitoring instructions.
FAQ
Disclaimer
Educational information only. This page summarizes published and official research and does not provide medical advice, a recommendation, or instructions for human use.
Educational use only. This content is provided for informational and research-summary purposes only. It is not medical advice, not a treatment recommendation, not a dosing guide, and not a substitute for care from a licensed medical professional. Nothing here is intended to diagnose, treat, cure, prevent, or mitigate disease. Reported dosing patterns, when shown elsewhere on the site, must be labeled either as Study / Trial Dosing or Anecdotal Reported Patterns — Not Medical Advice. Community reports are self-reported, unverified, and not scientific proof.
Community-reported experiences, once enabled, must be displayed only as moderated, anonymized, or aggregated data. They are anecdotal, self-reported, unverified, and should never be presented as proof of safety, efficacy, or expected results.
Content status: Published. Last updated 2026-07-30.
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