What's on the label is the measured result — net peptide mass, not gross powder weight, plus RP-HPLC purity, on a lot-numbered COA for every batch.
Net peptide mass and RP-HPLC purity — a lot-numbered COA for every batch.
Net peptide mass + HPLC purity, per lot.
PCAC will review 7 peptides for the 503A bulks list, BPC-157, KPV, TB-500, MOTS-c, Emideltide, Semax, Epitalon. Read our briefing →
PCAC will review 7 peptides for the 503A bulks list. Read →
FDA PCAC reviews 7 peptides in July. Read →
Prohibitin-targeting adipose vascular peptide
PeptideXpo buyer fit
This PeptideXpo page is intentionally positioned for distributors, OEM buyers, and procurement teams comparing Adipotide (FTPP) inside a wider peptide catalog. It is not trying to be the deepest single-molecule monograph; the differentiated intent is assortment planning, export-ready documentation, fill-size comparison, and whether this SKU belongs in a broader buyer program.
Overview
Adipotide (also designated FTPP, FTTP, or prohibitin-targeting peptide 1 in the published literature) is a research peptidomimetic with a two-domain structure: a cyclic CKGGRAKDC homing motif that recognizes prohibitin on the endothelium of white-adipose-tissue blood vessels, fused via a GG linker to a D(KLAKLAK)2 pro-apoptotic sequence that disrupts mitochondrial membranes once delivered to its target tissue. The molecule was developed by Renata Pasqualini and Wadih Arap at the University of Texas MD Anderson Cancer Center as a vascular-targeting approach to obesity research, the homing motif targets the adipose-vasculature endothelium, and the apoptotic domain then triggers selective destruction of the adipose-supporting blood vessels in primate obesity models. PeptideXpo supplies Adipotide as a lyophilized powder at ≥99.0% HPLC purity. The complex disulfide-cyclized + D-amino-acid structure is demanding to synthesize and requires both peak-integration HPLC plus mass spec confirming the cyclized + modified mass on every batch. Sequence verification by LC-MS/MS is strongly recommended at first-time supplier qualification because the construct is sufficiently complex that cross-supplier identity confirmation is non-trivial without explicit sequence-level data.
Who buys this, and why
Most buyers in this category are 503A and 503B compounding pharmacies fulfilling metabolic and weight-management protocols, plus research labs investigating GLP-1 / GIP / GCG receptor pharmacology. The procurement decision usually hinges on three things: documented purity at scale, a regulatory team that can respond on destination-market questions in writing, and the ability to supply consistent counter-ion form (acetate by default) across recurring orders.
Primary buyer fit: academic and contract research laboratories.
Specifications
Documentation available on request
Regulatory note
Investigational peptidomimetic; CAS is not consistently registered across suppliers. Construct identity (cyclic disulfide + D-amino-acid pro-apoptotic domain) should be confirmed by LC-MS/MS sequence verification at first-time qualification. Sold for research use only.
Frequently asked questions
Adipotide combines a vascular-homing motif (the cyclic CKGGRAKDC peptide) with a pro-apoptotic effector (D(KLAKLAK)2) connected by a GG linker. The homing motif recognizes prohibitin displayed on the endothelium of blood vessels supplying white adipose tissue, a tissue-specific signature that distinguishes adipose vasculature from most other vascular beds. Once the homing peptide binds, the D(KLAKLAK)2 domain (a synthetic mitochondrial-membrane-disrupting amphipathic peptide built from D-amino acids for protease resistance) is delivered into the target endothelial cells where it triggers apoptosis. The vascular-targeting approach was novel for obesity research at the time of publication, destroying the support vasculature of adipose tissue rather than directly targeting adipocytes.
Adipotide's construct combines several features that complicate identity confirmation: (1) the N-terminal CKGGRAKDC is disulfide-cyclized (Cys1 to Cys9), creating a cyclic mass distinct from the linear precursor; (2) the central GG linker is straightforward but at the boundary between the two functional domains; and (3) the D(KLAKLAK)2 effector uses D-amino acids that don't change mass but do change biological behavior. Mass-spec alone confirms the overall mass but can't distinguish between, say, a non-cyclized linear precursor and the intended disulfide-cyclized product, nor can it distinguish L-amino-acid from D-amino-acid by mass. LC-MS/MS sequence verification covering both domains is the only test that confirms the construct as supplied matches the intended design.
The most-cited Adipotide primate study (Barnhart et al., Science Translational Medicine 2011) reported substantial weight reduction in obese rhesus macaques over 4 weeks of daily subcutaneous administration, with the loss concentrated in white adipose tissue mass rather than lean tissue. Histological analysis confirmed the proposed mechanism, selective destruction of adipose-vasculature endothelium with secondary adipocyte loss, distinguishing Adipotide from direct lipolytic agents that target adipocytes themselves. The therapeutic-development program did not advance to clinical trials because subsequent rodent studies surfaced renal-toxicity signals and concerns about long-term effects on adipose tissue's metabolic roles beyond fat storage. Adipotide remains a useful research tool for studying vascular-targeting therapeutic strategies and prohibitin biology, even though the obesity-drug program is discontinued.
