Adipotide

Overview

Adipotide (FTPP) is a chimeric peptidomimetic developed in the Arap/Pasqualini lab (originally at MD Anderson) that couples a 9-residue homing motif (CKGGRAKDC) — isolated by in vivo phage display as a ligand for prohibitin on white-adipose-tissue vasculature — to the D-amino-acid pro-apoptotic domain D(KLAKLAK)2. It is an experimental research compound, NOT FDA-approved for any indication. A clinical-development program in prostate-cancer-associated obesity reached early-phase testing and was ultimately discontinued.

Mechanism of Action

The CKGGRAKDC domain binds prohibitin, a mitochondrial/plasma-membrane protein enriched on white-adipose endothelium (Kolonin et al., Nat Med 2004). Upon receptor-mediated internalization, the attached D(KLAKLAK)2 amphipathic motif disrupts mitochondrial membranes and induces apoptosis of adipose-vascular endothelial cells. The resulting vascular pruning starves white adipose tissue of blood supply, driving adipocyte loss and weight reduction in preclinical models.

Research Summary

Foundational proof-of-concept in obese mice (Kolonin et al., Nat Med 2004, PMID 15133506). A 4-week dosing study in spontaneously obese rhesus macaques showed substantial body-weight and fat-mass loss and improved insulin sensitivity but produced dose-dependent renal proximal-tubule toxicity (Barnhart et al., Sci Transl Med 2011, PMID 22072637). A small Phase 1 trial in obese prostate-cancer patients was initiated and later terminated; the program was permanently discontinued. No published human efficacy data. Grey-market human use is unstudied and carries documented nephrotoxicity risk.

Vendors selling Adipotide

Scored vendors carrying Adipotide, ranked by trust grade. Grades are computed from indexed Certificates of Analysis. Full $/mg pricing is on the comparison page.

Reported Side Effects

• Proximal-tubule nephrotoxicity (primate data)
• Dehydration
• Reduced appetite / nausea
• Fatigue
• Renal-function derangement requiring monitoring

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Research References

• Reversal of obesity by targeted ablation of adipose tissue (Kolonin, Saha, Chan, Pasqualini & Arap, Nat Med 2004) (2004)
• A peptidomimetic targeting white fat causes weight loss and improved insulin resistance in obese monkeys (Barnhart et al., Sci Transl Med 2011) (2011)

Frequently asked questions

Has Adipotide been independently lab-tested?

Disclosed Labs has collected 2 Certificates of Analysis (COA) for Adipotide from 2 independent testing labs. 2 vendors have submitted material for testing. Products average 98.8% tested purity across the corpus. Full testing data is available at https://www.disclosedlabs.com/peptides/adipotide/testing.

Where can researchers source Adipotide?

3 vendors with Disclosed Labs trust grades currently list Adipotide, including Profound Aminos, zztai Peptide Ltd, Certified Peptides. Compare live prices and lab-verified COAs at https://www.disclosedlabs.com/prices/adipotide.

How does Adipotide work?

The CKGGRAKDC domain binds prohibitin, a mitochondrial/plasma-membrane protein enriched on white-adipose endothelium (Kolonin et al., Nat Med 2004). Upon receptor-mediated internalization, the attached D(KLAKLAK)2 amphipathic motif disrupts mitochondrial membranes and induces apoptosis of adipose-vascular endothelial cells. The resulting vascular pruning starves white adipose tissue of blood supply, driving adipocyte loss and weight reduction in preclinical models.

What does the research say about Adipotide?

Foundational proof-of-concept in obese mice (Kolonin et al., Nat Med 2004, PMID 15133506). A 4-week dosing study in spontaneously obese rhesus macaques showed substantial body-weight and fat-mass loss and improved insulin sensitivity but produced dose-dependent renal proximal-tubule toxicity (Barnhart et al., Sci Transl Med 2011, PMID 22072637). A small Phase 1 trial in obese prostate-cancer patients was initiated and later terminated; the program was permanently discontinued. No published human efficacy data. Grey-market human use is unstudied and carries documented nephrotoxicity risk.