Adipotide (FTPP)
Peptidomimetic (CKGGRAKDC-GG-D(KLAKLAK)2) that targets the blood vessels of white fat and induces their apoptosis; tested in obese monkeys (2011); no published human trial.
60-Second Scientific Briefing
Adipotide is a synthetic peptidomimetic designed to bind the blood vessels that supply white fat and trigger the death of their cells. The main published study (Sci Transl Med 2011) was in obese monkeys: they lost weight and insulin resistance improved, but kidney function changed. Not approved by the US FDA or any other regulator; it is a research compound.
What is Adipotide (FTPP)?
Pharmacological Classification & Molecular IdentityAdipotide is a synthetic peptidomimetic designed to bind the blood vessels that supply white fat and trigger the death of their cells. [1] Sci Transl Med, 2011 ↗
Verified Chemical & Regulatory Registry Identifiers
Mechanism of Action & Receptor Targets
Biological Pathway and Target BindingReceptor Selectivity: A targeting sequence (CKGGRAKDC) binds the vessels of white adipose tissue, and a pro-apoptotic sequence then kills the vessel cells, starving the fat tissue of blood supply. [1] Sci Transl Med, 2011 ↗
Regulatory & FDA Approval Status
Legal and Regulatory ClassificationsNot approved by the US FDA or any other regulator; it is a research compound. [1] Sci Transl Med, 2011 ↗
Adipotide (FTPP) is not approved for commercial sale, prescription therapy, or compounded medication distribution. It exists strictly within authorized scientific and clinical research frameworks.
Human Evidence & Clinical Trials
Clinical Study Readouts and Evidence SynthesesNo human clinical trial has been published. Sci Transl Med 2011: in obese Old World monkeys of three species, adipotide induced targeted cell death in the blood vessels of white fat, with rapid weight loss, reduced white fat on MRI and DEXA scans, and improved insulin resistance. At the doses found to be optimal, the monkeys showed predictable, reversible changes in kidney proximal tubule function. [1] Sci Transl Med, 2011 ↗
Clinical Evidence
No human clinical trial has been published. Sci Transl Med 2011: in obese Old World monkeys of three species, adipotide induced targeted cell death in the blood vessels of white fat, with rapid weight loss, reduced white fat on MRI and DEXA scans, and improved insulin resistance. At the doses found to be optimal, the monkeys showed predictable, reversible changes in kidney proximal tubule function.
Safety Profile & Clinical Limitations
Documented Adverse Events and Known UncertaintiesThe only safety data come from monkeys, in which kidney (proximal tubule) function changed at the doses studied. There are no human safety data. [1] Sci Transl Med, 2011 ↗
Effects in people, kidney safety, long-term consequences of destroying fat-tissue blood vessels and the quality of non-pharmaceutical material are unknown. [1] Sci Transl Med, 2011 ↗
Dose Approval Status
Commercial Dosing Status and Policy DirectivesNo dose is approved or established for humans, and no human dose-finding study has been published. [1] Sci Transl Med, 2011 ↗
Under Egypt Peptides medical governance policies, no personal dosages, titration intervals, cycles, stacking recommendations, or self-injection instructions may be provided for unapproved investigational compounds. Clinical study protocols represent controlled experimental research parameters exclusively.
What is Known vs. What is Unknown
Evidence Comparison and Clinical Evidence Boundaries✓ Confirmed Scientific Evidence
- Adipotide is a synthetic peptidomimetic designed to bind the blood vessels that supply white fat and trigger the death of their cells.
- Targets & Selectivity: A targeting sequence (CKGGRAKDC) binds the vessels of white adipose tissue, and a pro-apoptotic sequence then kills the vessel cells, starving the fat tissue of blood supply.
- No human clinical trial has been published. Sci Transl Med 2011: in obese Old World monkeys of three species, adipotide induced targeted cell death in the blood vessels of white fat, with rapid weight loss, reduced white fat on MRI and DEXA scans, and improved insulin resistance. At the doses found to be optimal, the monkeys showed predictable, reversible changes in kidney proximal tubule function.
- Safety considerations: The only safety data come from monkeys, in which kidney (proximal tubule) function changed at the doses studied. There are no human safety data.
? Unknown / Under Ongoing Investigation
- Effects in people, kidney safety, long-term consequences of destroying fat-tissue blood vessels and the quality of non-pharmaceutical material are unknown.
Verified Questions & Answers
10 Verified scientific answers with permanent anchor keysAdipotide is a synthetic peptidomimetic designed to bind the blood vessels that supply white fat and trigger the death of their cells.
- A peptidomimetic targeting white fat causes weight loss and improved insulin resistance in obese monkeys (Sci Transl Med, 2011-11-09)
A targeting sequence (CKGGRAKDC) binds the vessels of white adipose tissue, and a pro-apoptotic sequence then kills the vessel cells, starving the fat tissue of blood supply.
- A peptidomimetic targeting white fat causes weight loss and improved insulin resistance in obese monkeys (Sci Transl Med, 2011-11-09)
No. Not approved by the US FDA or any other regulator; it is a research compound.
- A peptidomimetic targeting white fat causes weight loss and improved insulin resistance in obese monkeys (Sci Transl Med, 2011-11-09)
No human clinical trial has been published. The main published study (Sci Transl Med 2011) was in obese monkeys: they lost weight and insulin resistance improved, but kidney function changed.
No human clinical trial has been published. Sci Transl Med 2011: in obese Old World monkeys of three species, adipotide induced targeted cell death in the blood vessels of white fat, with rapid weight loss, reduced white fat on MRI and DEXA scans, and improved insulin resistance. At the doses found to be optimal, the monkeys showed predictable, reversible changes in kidney proximal tubule function.
- A peptidomimetic targeting white fat causes weight loss and improved insulin resistance in obese monkeys (Sci Transl Med, 2011-11-09)
The only safety data come from monkeys, in which kidney (proximal tubule) function changed at the doses studied. There are no human safety data.
- A peptidomimetic targeting white fat causes weight loss and improved insulin resistance in obese monkeys (Sci Transl Med, 2011-11-09)
Effects in people, kidney safety, long-term consequences of destroying fat-tissue blood vessels and the quality of non-pharmaceutical material are unknown.
- A peptidomimetic targeting white fat causes weight loss and improved insulin resistance in obese monkeys (Sci Transl Med, 2011-11-09)
No dose is approved or established for humans, and no human dose-finding study has been published.
- A peptidomimetic targeting white fat causes weight loss and improved insulin resistance in obese monkeys (Sci Transl Med, 2011-11-09)
There is no approved product label, so no official storage instructions exist.
It is not named individually on the 2026 WADA Prohibited List. Under section S0 (non-approved substances), any pharmacological substance without a current approval by a government health authority for human therapeutic use is prohibited at all times. Athletes should confirm with their national anti-doping organisation.
- WADA Prohibited List (World Anti-Doping Agency)
Egypt Peptides publishes reviewed scientific reference monographs for documentation and research. The site does not give individual medical advice, preparation or injection instructions, combination protocols or off-label use instructions. Decisions about any medicine belong to the treating physician.
- A peptidomimetic targeting white fat causes weight loss and improved insulin resistance in obese monkeys (Sci Transl Med, 2011-11-09)
Authoritative Sources & Literature Registry
Regulatory dossiers, clinical trial registries, and published studiesA peptidomimetic targeting white fat causes weight loss and improved insulin resistance in obese monkeys ↗
https://pubmed.ncbi.nlm.nih.gov/22072637/