The entire published adipotide dosage record is one monkey study and a human trial that enrolled four people and stopped. Everything else in circulation is filling that gap.
The short version
The monkey study gave 0.43 mg/kg under the skin, once a day, for 28 days. Ten treated animals lost 7.4% to 14.7% of body weight. Creatinine rose above 0.25 mg/kg. The human trial opened at 0.03 mg/kg, enrolled four people, and ended.
Adipotide is not a peptide in the ordinary sense. It is a peptidomimetic that homes to the blood vessels feeding white fat and then triggers cell death in them. The mechanism is striking, the primate data is striking, and the clinical program is four people long.
What the adipotide studies administered
| Study | Species | Dose | Route | Duration | n |
|---|---|---|---|---|---|
| Kolonin et al., 2004 | Mouse (obese) | — | — | — | — |
| Barnhart et al., 2011 — dose finding | Rhesus macaque (obese) | 0.10, 0.25, 0.43 and 0.75 mg/kg | Subcutaneous, daily | — | part of 15 |
| Barnhart et al., 2011 — main study | Rhesus macaque (obese) | 0.43 mg/kg | Subcutaneous, daily | 28 days, then 4 weeks off | 15 (10 treated, 5 control) |
| NCT01262664 — Phase 1 | Human (metastatic prostate cancer with obesity) | 0.03 mg/kg starting dose | Subcutaneous, once daily | 28 days planned | 4 enrolled; terminated |
A dash means we have no sourced figure for that cell and have not estimated one.
The first row is dashes because we could not reach the dose. The 2004 mouse paper is paywalled and its abstract contains no figure, and the widely repeated milligram-per- kilogram number for it does not trace to the paper.
The monkey study, which is the real data
Barnhart and colleagues randomized 15 obese rhesus macaques, 10 to adipotide and 5 to saline. Treated animals received 0.43 mg/kg subcutaneously every day for 28 consecutive days, followed by a four-week recovery period.
The monkeys receiving the therapy displayed marked weight loss that ranged from −7.4 to −14.7% of pretreatment body weight.
Barnhart et al., Science Translational Medicine, 2011That came with improvements in insulin resistance. Body mass index, abdominal circumference and imaged fat mass all fell in a dose-dependent way.
A dose-finding phase had tested 0.10, 0.25, 0.43 and 0.75 mg/kg first. That is a properly built study, and it is why this compound is discussed at all.
- Old World primates, which is the closest preclinical model to a person that anything in this library has been run in.
- A control arm, five animals on saline.
- A recovery period, four weeks off treatment with continued monitoring — which is how the reversibility of the kidney finding was established.
Research compounds with lot-matched testing
Third-party tested research compounds, each shipped with a batch-matched certificate of analysis showing HPLC purity and mass-spec identity — the documentation this site argues you should hold any supplier to.
The kidney signal
Slight-to-moderate dose-dependent elevations in serum creatinine were observed during subcutaneous administration of doses greater than 0.25 mg/kg.
Barnhart et al., Science Translational Medicine, 2011Most of the serum and urine changes reversed within 28 days of stopping treatment.
The effect dose and the signal dose overlap. The regimen that produced the weight loss, 0.43 mg/kg, sits above the 0.25 mg/kg threshold at which the creatinine changes started. This is not a compound where a low dose gives you the benefit and a high dose gives you the risk. In the only study with both, they arrived together.
Read that against the main study dose. The regimen that produced the weight loss, 0.43 mg/kg, sits above the threshold where the creatinine changes began. The effect and the signal are not at different ends of the dose range; they overlap.
The human trial, and what it does not tell you
A first-in-man Phase 1 opened in men with metastatic prostate cancer and obesity. The design planned up to five dose levels with three participants at each, starting at 0.03 mg/kg subcutaneously, once daily for 28 days.
Actual enrollment was four. The registry lists the study as terminated, with the reason given as the principal investigator's request. No results were posted.
- What is on record: the starting dose, the route, the schedule and the planned escalation.
- What is not: a maximum tolerated dose, any efficacy figure, or any safety readout at all.
- What is often claimed: that the trial stopped for kidney toxicity. The registry says only that the investigator requested it, so we do not report a reason.
We also screened every published paper tagged to adipotide. All of them are preclinical. No human adipotide results have been published anywhere.
What if you already have a number?
The only adipotide amounts on record are a monkey dose and a Phase 1 starting dose.
Turning a figure into a syringe volume is arithmetic, and the peptide calculator does it from the vial strength and the volume of diluent. That part always works.
Which is the trap. A calculator converts an unsourced number as cleanly as a sourced one. The output looks equally precise either way. A starting dose is where a safety study begins, which is the opposite of a conclusion.
What is checkable
Adipotide is a chimeric construct: a homing peptide joined to a pro-apoptotic sequence. That makes identity confirmation more important than usual, because the two halves can be synthesized correctly and joined incorrectly.
Mass spec on the intact molecule is the check that matters. How to read a COA, the complete guide and where to buy adipotide cover sourcing, and the peptide dosage chart places it beside the rest of the library.
Research compounds with lot-matched testing
Third-party tested research compounds, each shipped with a batch-matched certificate of analysis showing HPLC purity and mass-spec identity — the documentation this site argues you should hold any supplier to.
What to know now
- The monkey study used 0.43 mg/kg subcutaneously, daily, for 28 days, in 10 treated animals against 5 controls.
- Weight loss was 7.4% to 14.7% of pre-treatment body weight.
- Creatinine rose in a dose-dependent way above 0.25 mg/kg, and mostly reversed after stopping.
- The human Phase 1 opened at 0.03 mg/kg and enrolled four participants before terminating.
- No results were posted and no human adipotide data has ever been published.
- The 2004 mouse dose is not in the reachable record, so we do not publish one.
What we're watching
Results posting on the terminated Phase 1 would be the most informative event possible here, even from four participants. A terminated trial with nothing posted is the least useful state a clinical record can be in.
Beyond that, the mechanism has moved into targeted nanoparticle work rather than the free peptidomimetic. That is where any future dosing data is most likely to come from.
Frequently asked questions
What dose of adipotide was used in monkeys?
0.43 mg/kg subcutaneously, once daily, for 28 consecutive days, in 10 obese rhesus macaques against 5 controls. A dose-finding phase tested 0.10, 0.25, 0.43 and 0.75 mg/kg.
Has adipotide been given to humans?
A first-in-man Phase 1 trial opened at a starting dose of 0.03 mg/kg subcutaneously, once daily for 28 days. It enrolled four participants and was terminated. No results were posted and nothing has been published.
How much weight did the monkeys lose?
Between 7.4% and 14.7% of pre-treatment body weight over 28 days, with improved insulin resistance.
What was the kidney finding?
Slight to moderate dose-dependent rises in serum creatinine at doses above 0.25 mg/kg. Most of the changes reversed within 28 days of stopping.
Why is there no adipotide dose for humans?
Because the only human trial stopped after four participants without reaching a maximum tolerated dose. The starting dose is on record; nothing above it is.
References
- Barnhart, K. F., Christianson, D. R., Hanley, P. W., Driessen, W. H. P., Bernacky, B. J., Baze, W. B., Wen, S., Tian, M., Ma, J., Kolonin, M. G., Saha, P. K., Do, K.-A., Hulvat, J. F., Gelovani, J. G., Chan, L., Arap, W., & Pasqualini, R. (2011). A peptidomimetic targeting white fat causes weight loss and improved insulin resistance in obese monkeys. Science Translational Medicine, 3(108), 108ra112. https://doi.org/10.1126/scitranslmed.3002621
- Kolonin, M. G., Saha, P. K., Chan, L., Pasqualini, R., & Arap, W. (2004). Reversal of obesity by targeted ablation of adipose tissue. Nature Medicine, 10(6), 625–632. https://doi.org/10.1038/nm1048
- ClinicalTrials.gov. A first-in-man, phase I evaluation of a single cycle of prohibitin targeting peptide 1 in patients with metastatic prostate cancer and obesity (NCT01262664). Terminated; no results posted. https://clinicaltrials.gov/study/NCT01262664
- Hong, J., & Kim, Y. H. (2022). Fatty liver/adipose tissue dual-targeting nanoparticles with heme oxygenase-1 inducer for amelioration of obesity, obesity-induced type 2 diabetes, and steatohepatitis. Advanced Science, 9(33), e2203286. https://doi.org/10.1002/advs.202203286
- Hu, Q., Cao, H., Zhou, L., et al. (2021). Measurement of BAT activity by targeted molecular magnetic resonance imaging. Magnetic Resonance Imaging, 77, 1–6. https://doi.org/10.1016/j.mri.2020.12.006
The Phase 1 record was read directly from the trial registry. It lists the study as terminated at the investigator's request, with no results posted.