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Adipotide 10mg - Dragon Pharma

Dragon Pharma

Adipotide 10mg - Dragon Pharma

Injection · 10 mg · vial

In stock · ships within 24h Out of stock Ships from International · U.S Domestic
CompoundAdipotide
ClassProapoptotic Peptide
Half-lifeNot established
DetectionNot established
Liver toxicityLow, no human data
Water retentionNone
A freeze-dried 10 mg vial of a peptidomimetic also written as FTPP, or fat-targeting proapoptotic peptide. It carries a homing block for the blood vessels that feed white adipose tissue plus a domain that triggers apoptosis, so fat cells are starved rather than burned. The evidence is animal-only: obese rhesus macaques lost about 10.6 percent of body mass over 28 days of daily intravenous dosing, and the same study recorded dose-dependent changes in the renal tubules. No human efficacy data exist, human pharmacokinetics and a human dose are both unestablished, and clinical development was discontinued. Supplied by Dragon Pharma.
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Adipotide 10mg - Dragon Pharma
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$85.00
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Quality First

All products are manufactured under strict quality standards and independently tested before release. By purchasing, the buyer agrees to use these products in compliance with all applicable laws.

Product Overview

Dragon Pharma Adipotide arrives as a freeze-dried 10 mg vial of prohibitin-targeting peptide 1, a compound also written as prohibitin-TP01 or TP01, and as FTPP, short for fat-targeting proapoptotic peptide. Structurally it is not a natural hormone but a peptidomimetic built from two working parts: a homing sequence that recognises a protein on the endothelial cells of blood vessels inside white adipose tissue, and a proapoptotic domain that kills the cell it has docked onto. The result is not lipolysis in any ordinary sense.

What the mechanism destroys is the vasculature. Endothelial cells lining the vessels that supply white fat undergo apoptosis, the tissue loses perfusion, and the adipocytes that depended on that supply follow. Reviewed animal work is the whole evidence base: obese rhesus macaques treated for 28 days lost around 10.6 percent of body mass and required roughly half the insulin dose they needed before. The same study reported dose-dependent changes in the renal tubules, which captures the problem with the whole idea, because there was no clean separation between the effect that was wanted and the injury that came with it. The program that followed the phase I announcement in the early 2010s never produced peer-reviewed results, and development was halted.

Vial Arithmetic and Reconstitution

The powder is dissolved in bacteriostatic water dripped down the glass, and the vial is turned gently rather than shaken. Two strengths come out of a 10 mg vial, and each is arranged so that the 10 unit line on a U-100 barrel carries a round number of micrograms.

Doubling the diluent10 mg with 4 ml settles at 2.5 mg per ml; the small 5 mg vial matches it with 2 ml
Halving the diluent10 mg with 2 ml settles at 5 mg per ml; the 5 mg vial matches it with 1 ml
The 2.5 mg per ml strengthA 10 unit draw holds 0.1 ml and therefore 250 mcg of peptide
The 5 mg per ml strengthA 10 unit draw holds 0.1 ml and therefore 500 mcg of peptide
Animal protocol in the sourcesIntravenous dosing every day for 28 days in obese rhesus macaques; nothing about it transfers to people
Vendor research conventionNotes from vendors put 500 mcg to 1 mg a day subcutaneously forward as a convention, labelled unconfirmed and no recommendation
Human dose statusNothing validated, because no human dataset was ever produced

With a compound whose safety question is unresolved, the arithmetic matters less than the reason behind it. The source material is explicit that a human protocol does not exist, so any number quoted for the injected amount is a convention rather than a finding.

Animal Data and Research Protocols

The single protocol in the record is a monkey study, not a model of human use. Obese rhesus macaques received daily intravenous injections for 28 days, body mass fell by about 10.6 percent, insulin sensitivity improved to the point that roughly half the previous insulin dose was needed, and renal tubular changes appeared in a dose-dependent pattern. Every one of those four facts belongs to the same paper.

Because the effect depends on shutting down blood vessels, the safety debate is really about selectivity: how much of the vascular action lands outside white fat. Nothing in the sources answers that question for humans. This is also why the compound is referenced next to the rest of the fat-loss shelf rather than as part of it, and why no combination has ever been studied.

Fat-loss shelf, reading pair
Shelf comparison only; adipotide works on vessels, the others on metabolism, and nothing links them in the literature
Weight-management shelf
Contrast only: the incretin peptides and clenbuterol have human data behind them, while adipotide has neither data nor an active program
Observation shelf
Adipotide - requires kidney monitoring + MOTS-c 10 mg - mitochondrial angle
Grouped by topic on the shelf, not by evidence; no interaction data exist for the pair

What to Expect

  • Tenth of body mass in a monkey. The 10.6 percent loss came from 28 days of daily intravenous dosing in obese rhesus macaques, which is the striking number in the file and also a number that comes from animals.
  • Insulin sensitivity moved too. In the same study roughly half the previous insulin dose was sufficient, an effect that tracked with the mass loss.
  • It is not a lipolytic drug. The sequence runs from endothelial apoptosis to loss of perfusion to adipocyte death, so nothing is burned and the fat is starved of supply instead.
  • Narrow window in the animal data. Dose-dependent renal tubular changes showed up in the same treated animals, which means the effect and the damage rose together.
  • Limitation. There are no published human efficacy results; the announced phase I never delivered peer-reviewed data.
  • Limitation. Human half-life is unknown, a human dose does not exist and this vial is a research product.
  • Limitation. The substance is not named in the WADA Prohibited List, which reflects the absence of specific guidance rather than approval.

Side Effects and Management

This is the part of the file that stopped the program, and it should be read before the fat loss figures rather than after them.

Dose-dependent renal tubular changesKidney function sits at the centre of any research monitoring, and a deviation is a reason to stop. Seen in primates and clearly dose-related.
Risk to vessels outside the target tissueWith no human data, the selectivity question cannot be answered, so this stays an unknown risk by definition. It follows from how the peptide works.
Local irritation around the shotUse a fresh spot each time, keep the skin clean and dilute with bacteriostatic water. The usual local effect of the peptide class.
Dehydration and electrolyte shifts with fast weight lossWatch fluids and electrolytes if mass drops quickly. A theoretical measure, with no human data behind it.
No confirmed effect in peopleDo not plan around weight loss, because the only positive results come from animals. This is the direct consequence of the development status.

Renal Monitoring, Storage and No PCT

There is no post-cycle protocol here, because the compound does not touch the hormonal axis at all. The monitoring that follows from the source is one line long and entirely about the kidneys.

Onset of effect in animalsMeasured over 28 days of daily dosing in monkeys; no human timeline exists
Validated protocolNone. The only schedule in the sources is daily intravenous dosing in primates and it does not transfer to people
Low-dose cyclesDose-dependent renal toxicity makes a lower amount safer only in theory, because no human dose-response curve has been published
Follow-upRenal function is the one checkpoint that follows directly from the animal findings
StorageThe dry cake is refrigerated at 2-8 C out of the light; the diluted vial is also kept cold and is good for about 28 to 30 days, with freezing avoided
PCTNot applicable: this is not a hormonal compound and nothing is suppressed
This material is published for educational and research reference purposes only. The compounds described are research-grade materials supplied for laboratory work and are not presented here as medicines or as a treatment for any condition. Dosing information reflects published clinical and reference data for the active substances, not a recommendation or a prescription. Nothing on this page should be read as medical advice. Keep all products out of reach of children and follow the regulations that apply in your country.
What is Adipotide 10 mg from Dragon Pharma and how does it target fat?
It is a lyophilised 10 mg vial of prohibitin-targeting peptide 1, the research compound also called adipotide, prohibitin-TP01 or FTPP. The molecule has a homing block that binds a protein on the vessels inside white adipose tissue and a second domain that induces apoptosis, so the fat tissue loses its blood supply. Nothing is metabolised or burned in that process.
What does FTPP stand for?
FTPP is short for fat-targeting proapoptotic peptide, which describes both halves of the design: the targeting part that finds white fat vasculature and the proapoptotic part that kills the cell it has found. It is the same molecule as adipotide and as prohibitin-targeting peptide 1, so the three names appear interchangeably in vendor listings and papers.
How does Adipotide work?
Through the blood supply rather than through fat metabolism. The peptide docks onto endothelial cells of the vessels feeding white adipose tissue, the proapoptotic domain triggers cell death there, perfusion falls and the adipocytes that depended on it die. That is why the safety question is really about selectivity, since vascular tissue exists everywhere and not only in fat.
Has Adipotide ever been tested in people?
A phase I study was announced in the early 2010s, but no peer-reviewed human results were ever published, and by 2019 clinical development had been discontinued. There is therefore no human efficacy data, no human half-life and no human dose-response work. Everything quantified about this compound comes from animal research.
What happened to body fat in the treated monkeys?
In obese rhesus macaques given daily intravenous doses for 28 days, body mass fell by about 10.6 percent and insulin sensitivity improved enough that roughly half the earlier insulin dose was sufficient. Impressive numbers in a monkey, and still numbers from a monkey. No equivalent human measurement exists.
Why was Adipotide development stopped and does it affect the kidneys?
Kidney findings are the stated reason. The same primate study that produced the weight loss recorded dose-dependent changes in the renal tubules, so the desirable effect and the unwanted one rose together with no clean separation. With no human data to define an exposure that avoids that, the program was stopped rather than refined.
Is there a standard human dose of Adipotide, and how is a vial mixed?
There is no standard human dose, because no human dataset exists. Vendor notes put 500 mcg to 1 mg a day subcutaneously forward as a convention and label it unconfirmed. On mixing, a 10 mg vial taking 4 ml settles at 2.5 mg per ml, where a 10 unit draw carries 250 mcg; take 2 ml instead and the strength rises to 5 mg per ml, so the same draw carries 500 mcg.
Does Adipotide appear on the WADA Prohibited List, and where to buy it?
The name does not appear in the WADA Prohibited List and no separate anti-doping note covers it, which says only that the substance slipped under the radar rather than being cleared for use. Stock sits with the rest of the Dragon Pharma research peptides, and matching the batch number to the receipt is worth doing, because the trade name adipotide and the research name prohibitin-TP01 should describe the same vial.

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