Preloaded Autoinjector | Adipotide (FTPP) | 3ml Pen | 10mg

The adipotide pen is a preloaded 3ml research autoinjector holding 10mg of the chimeric peptide FTPP in solution at 3.33mg/ml, approximately 1.30 mM. Two features set this molecule apart from anything else in a cartridge: a cyclising disulfide whose opening destroys the homing function, and a strongly cationic membrane-active domain built entirely from D-amino acids.

Specification Table

What Is Adipotide, and What Changes When It Ships in Solution?

It is a two-part chimeric peptide, a cyclic nine-residue homing motif joined by a Gly-Gly linker to a fourteen-residue membrane-disrupting domain, and in solution its two halves fail in completely different ways: the homing half depends on a disulfide that water can open, while the pro-apoptotic half is protease-proof but sticks to everything.

The homing domain is CKGGRAKDC, cyclised head to tail through a disulfide between its two cysteines. That ring is the targeting element: the motif was pulled out of in vivo phage-display vascular mapping (Arap 2002) and it recognises prohibitin on the vasculature of white adipose tissue. Reduction or intermolecular exchange of that single disulfide opens the ring, and an opened ring is a linear nonapeptide with no defined binding conformation. The consequence is unlike ordinary peptide degradation, where a modified molecule usually retains partial activity. Here the targeting either exists or it does not, and the mass barely changes when it stops existing: reduction adds 2 Da to a 2555 Da molecule, and a covalent dimer of two opened molecules lands at about 5110 Da.

The pro-apoptotic domain is the opposite problem. D(KLAKLAK)₂ is fourteen residues in all-D configuration, which is what makes it resistant to proteases while keeping the amphipathic helix that disrupts mitochondrial membranes. Nothing biological degrades it quickly, so its solution behaviour is physical. Seven lysines and one arginine against a single aspartate give a large net positive charge, and that charge does two things in a cartridge: it drives adsorption to negatively charged glass and to polymer surfaces, and it makes the peptide liable to precipitate on contact with polyanions. Phosphate buffer, heparin, nucleic acid and anionic detergents are all capable of dropping a cationic amphipathic peptide out of solution, which matters both for the fill formulation and for whatever the solution is added to downstream.

Beyond those two routes the sequence is quiet. There is no methionine, no tryptophan and no histidine, so oxidation outside the disulfide is minor. The aspartate in the homing domain sits next to lysine and can isomerise slowly to isoaspartate, a change that is invisible by mass because the isomer is isobaric. There is no asparagine, so deamidation does not apply.

No approved product exists, so no reference formulation, pH, preservative or stability dataset was ever reviewed by a regulator for this molecule. No dedicated solution-stability study was located in the peer-reviewed literature either. Everything above is inference from the sequence, and it should be treated as such.

Adipotide 10mg in 3ml: What Does Each Increment Carry?

Ten milligrams in 3 ml is 3.33 mg/ml, which at an estimated molecular weight of 2555 g/mol is approximately 1.30 mM, so a 0.01 ml increment carries 33 micrograms (about 13 nanomoles) and a 0.1 ml increment carries 333 micrograms (about 130 nanomoles).

Two cautions attach to those figures. The graduation resolution of this adipotide pen is not stated on the product record, so the 0.01 ml increment used here is the common insulin-pattern value rather than a confirmed property of the pen; the peptide calculator recomputes for any other graduation. More unusually, the molar figures inherit an uncertainty from the molecular weight itself. The 2555 g/mol value is calculated from the sequence rather than measured, and the literature does not settle a formula or a CAS number for this peptide, so every millimolar figure on this page carries roughly 2 to 3% uncertainty. Mass-based figures in milligrams do not.

Against the published work, adipotide 10mg in a 3 ml cartridge is a concentrated stock. In vitro apoptosis assays operate at micromolar peptide, so a 1.30 mM solution sits about a thousand times above them. The non-human primate work dosed by body weight, roughly 0.4 to 0.5 mg/kg per day subcutaneously in Barnhart 2011, which is a description of an animal study rather than a figure that transfers to a fixed-concentration device.

Adipotide Pen vs Vial: What Does the Format Suit?

The adipotide pen vs vial decision turns on surface losses: a preloaded cartridge removes the transfer steps where a strongly cationic peptide is most likely to disappear onto glass and plastic, while a lyophilized vial lets the laboratory choose a buffer that will not precipitate it.

For this molecule the reconstitution step is expensive in a way that is hard to see. Cationic amphipathic peptides adsorb to the vial wall, the syringe barrel and every pipette tip in the chain, and the loss is not recoverable and not visible. A cartridge filled once at manufacture removes those transfers and fixes the concentration at 3.33 mg/ml, at the cost of accepting an excipient system the buyer did not choose and cannot see. That trade is set out generally in the pen versus vial article and applies here with the surface chemistry weighted heavily. The six fields to confirm before ordering an adipotide pen are the same ones listed on the preloaded autoinjector category page: fill date, verified concentration, buffer and pH, graduation resolution, cartridge material and cold-chain history.

The lyophilized FTPP 5mg vial suits work where the buffer is part of the experiment. If a carrier protein or a low-binding additive is wanted to suppress adsorption, or a phosphate-free buffer is wanted to avoid precipitating the cation, that choice can only be made from a dry cake. Adipotide solution vs lyophilized is a question of who selects the counter-ion environment; with a pen, the filler did, and did not publish it.

The other side of the comparison is time. A dry cake holds the disulfide in a low-mobility state; a solution does not. For a molecule whose entire targeting function rests on one disulfide, the fill date is a more consequential number than it is for most peptides, and it is not stated. The sourcing guide for this compound covers what a certificate should show.

What the Product Record Does Not State

More is unstated for this compound than for most, and some of it is unstated in the literature rather than merely on the product record: there is no agreed CAS number, no verified molecular formula, no settled molecular weight, no published excipient system, no pH and no fill date.

The identity gap comes first. A CAS number circulating on vendor pages is not a registry entry, and a molecular weight of 2611 that cannot be derived from the published sequence is a warning about whatever else appears on the same document. The 2555 g/mol used here is a sequence calculation for the disulfide-cyclised free acid, and an amidated C-terminus would shift it by about one dalton. A certificate that reports an observed mass is more useful than one that reports a nominal one, because it says which form was actually made.

The formulation gap follows. Whether the fill contains phosphate matters directly, given the precipitation liability of a strongly cationic peptide. Whether it contains a carrier or a surfactant matters for how much peptide is still in solution rather than on the cartridge wall. The pH governs the disulfide exchange rate and the aspartate isomerisation rate. None of the three is published, and all three should be requested from the lot certificate of analysis before quantitative work rather than after an unexplained result.

Verifying the Adipotide Pen and Confirming What Is Inside

Inspect the solution in the adipotide pen against a white background before each draw for haze, particulate or visible fibres, because for a cationic amphipathic peptide the visible failure is precipitation rather than colour change, and it can appear within minutes of contact with the wrong buffer.

The analytical handles here are unusual, and the first thing to know is what will not work. The molecule has no tryptophan, no tyrosine and no phenylalanine, so there is no absorbance at 280 nm and no ultraviolet quantification of the kind that works for most peptides. Content has to come from backbone absorbance near 214 nm against a reference standard, from charged aerosol or evaporative light-scattering detection, or from amino acid analysis after hydrolysis.

Intact-mass LC-MS answers the disulfide question. An intact molecule reads about 2555 Da, the reduced open-ring form about 2 Da higher, and a covalent dimer near 5110 Da. What mass spectrometry cannot answer is stereochemistry: a batch in which the KLAKLAK domain had been assembled from L-amino acids instead of D would have exactly the same mass and very nearly the same chromatography, while being a different molecule with a different protease profile. Chiral amino acid analysis after hydrolysis is the measurement that settles it, and it is worth asking whether the supplier has run one.

Let the device reach ambient temperature before actuating, since cold solution is more viscous and spring-driven mechanisms deliver less against a viscous load. Gravimetric verification once per device, actuating onto a tared vessel and converting by solution density, is worth more than a nominal volume for any pen.

What Do the Adipotide Clinical Trials and Animal Studies Report?

The animal record is substantial and the human record is empty: two landmark animal papers, Kolonin 2004 in mice and Barnhart 2011 in obese rhesus monkeys, and a phase 1 study at MD Anderson that produced no published controlled efficacy or safety results.

Arap 2002 is where the homing motif came from, a phage-display map of the human vasculature that identified peptides binding to specific vascular beds. Kolonin 2004 in Nature Medicine put the motif to work: targeted ablation of the vasculature supplying white adipose tissue reversed obesity in mice, and the same paper identified prohibitin as the vascular receptor the motif recognises. Daquinag 2011 reviewed vascular targeting of adipose tissue as an approach, and Hossen 2012 examined delivery to obese fat.

Barnhart 2011 in Science Translational Medicine is the paper that matters most for anyone reading this page. In obese rhesus monkeys the peptidomimetic produced weight loss and improved insulin resistance, and it also produced dose-dependent, reversible changes in renal proximal-tubule function across three primate species. That renal finding is not incidental to the mechanism; a compound that works by inducing apoptosis in a targeted vascular bed is cytotoxic by design, and the kidney is where the study found the collateral effect.

Human adipotide clinical trials are the gap. A phase 1 study in obese men was undertaken at MD Anderson under an identifier given as NCT01262664, which could not be verified for this page, and it did not lead to later-phase development. No controlled human efficacy or safety results have been published, no human dose is established, and nothing has been published on any preloaded fixed-concentration device. The renal findings observed in primates were never cleared in people.

What Is the Safety and Regulatory Position?

Adipotide is approved nowhere, appears in no register of approved products in the United States, European Union, Japan, Australia or Canada, and public sources record that clinical development has been discontinued.

It is not an approved active ingredient and is not on any FDA 503A or 503B bulk-drug-substance list, so it cannot lawfully be compounded or sold for human use. The documented dose-dependent renal proximal-tubule dysfunction in primates makes it a high-concern substance rather than an ordinary research peptide, and the mechanism that produces the reported weight change in animals is the same mechanism that produces cytotoxicity. For athletes, no named WADA entry exists; as a non-approved pharmacological substance it falls under class S0, prohibited at all times.

No vendor solution has published identity, purity or stability data, and for this compound the identity question is sharper than usual given the unresolved molecular weight and CAS number. The adipotide pen is a laboratory research article and must not be given to humans or animals.

Published Literature

Each entry below was checked against publisher records or primary indexes. All concern the compound; nothing has been published on this delivery format.

1. Arap W, Kolonin MG, Trepel M, et al. Nature Medicine. 2002;8(2):121-127. DOI: 10.1038/nm0202-121 PMID: 11821895
2. Kolonin MG, Saha PK, Chan L, Pasqualini R, Arap W. Nature Medicine. 2004;10(6):625-632. DOI: 10.1038/nm1048 PMID: 15133506
3. Barnhart KF, Christianson DR, Hanley PW, et al. Science Translational Medicine. 2011;3(108):108ra112. DOI: 10.1126/scitranslmed.3002621 PMID: 22072637
4. Daquinag AC, Zhang Y, Kolonin MG. Trends in Pharmacological Sciences. 2011;32(5):300-307. DOI: 10.1016/j.tips.2011.01.004 PMID: 21349592
5. Hossen MN, Kajimoto K, Akita H, et al. Journal of Controlled Release. 2012;163(2):101-110. DOI: 10.1016/j.jconrel.2012.09.002 PMID: 22982237

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