Most compounds in this cluster have a messy dose record: figures that circulate without sources, or sources that studied a different substance. Tesofensine has the opposite. Its human dose record is clean, narrow, consistently reported and easy to check — four oral doses, once daily, with weight and heart-rate figures published at each step over twenty years.
The interesting fact about tesofensine is not in the doses. It is in what the trial registry contains after all that work.
This page reports the published figures with their sources and dates. It is attributed journalism about a research record; it recommends nothing, and no figure here is offered as one for anybody to use.
It is not a peptide
Tesofensine is a small molecule: a triple monoamine reuptake inhibitor, blocking presynaptic uptake of noradrenaline, dopamine and serotonin. It is not a peptide, it is not peptide-adjacent, and its pharmacology has nothing in common with the compounds it shares a storefront with.
That matters for reading the dose figures. Peptide doses in this cluster are usually given as weight-scaled infusion rates in nanomoles, because that is how the studies were run. Tesofensine's are given in milligrams of a once-daily oral tablet, because it was developed as an ordinary oral CNS drug — first as NS 2330, for Parkinson's and Alzheimer's disease.
The site treats 5-amino-1MQ the same way, for the same reason: the class label on the storefront is wrong, and a reader working from it will misread the literature.
The whole published dose record, in one table
| Study | Population | Dose | Duration | Key result |
|---|---|---|---|---|
| Four RCTs, pooled (2008) | Parkinson's or Alzheimer's; 740 on drug, 228 placebo | 0.125, 0.25, 0.5, 1.0 mg oral once daily | 14 weeks | Weight change +0.5, −0.5, −0.9, −1.8, −2.8% (P = 0.015 for dose effect). Heart rate −0.4, +2.1, +4.2, +6.0, +6.8 bpm |
| TIPO-1, Phase 2 (2008) | 203 obese patients, BMI 30–40, energy-restricted diet | 0.25, 0.5, 1.0 mg oral once daily | 24 weeks | Weight loss 4.5%, 9.2%, 10.6% vs 2.0% placebo. Heart rate +7.4 bpm at 0.5 mg |
| Early Parkinson's (2007) | Patients with early PD | 0.25, 0.5, 1.0 mg | 14 weeks | UPDRS change −0.7, −1.3, −1.7; P = 0.64, 0.41, 0.27 — none significant |
| Motor-fluctuation PD | PD with motor fluctuations | 0.125, 0.25, 0.5, 1.0 mg | — | −7.1% off time at 0.25 mg (−68 min, P = 0.02) |
| Tesomet (2022) | 21 adults, hypothalamic obesity | 0.5 mg tesofensine + 50 mg metoprolol | 24 weeks | Additional weight change −6.3% (95% CI −11.3 to −1.3; P = 0.017) |
Four dose levels. One route. One frequency. Across two decades and three sponsors, nothing in the retrieved literature departs from that.
The obesity programme is a side effect that got promoted
The 2008 meta-analysis in Obesity is the hinge, and it is candid about what it is.
Four randomised, double-blind, multicentre trials had been run in Parkinson's and Alzheimer's disease — two in each — with 740 patients on tesofensine and 228 on placebo, taking oral drug once daily for fourteen weeks "without any weight loss program". That last clause is the point: nobody was trying to lose weight, and weight came off in a dose-dependent line.
In the obese subgroup, the proportion achieving at least 5% weight loss was 2.1% on placebo and 8.2%, 14.1%, 20.9% and 32.1% across the four ascending doses. The authors compared the effect to sibutramine and closed with the sentence that redirected the compound: "On the basis of these results, TE is now being developed for obesity management."
Meanwhile the indications it was actually being tested for did not respond. In early Parkinson's disease, none of the three doses moved the UPDRS score significantly; the largest adjusted mean difference, at 1.0 mg, was −1.7 with P = 0.27.
So the compound that reached the obesity literature is one that failed its original indication and produced weight loss while failing it. That is not a criticism — repurposing is ordinary, and this particular observation was well designed to notice. It is a fact about provenance that the efficacy figures alone do not convey.
The heart rate is the through-line, and the developers agreed
Read the fifth column of the table downward and the same signal appears in every study that measured it.
In the pooled 14-week trials: +2.1, +4.2, +6.0, +6.8 bpm across the ascending doses, against −0.4 on placebo, with P < 0.001 from 0.25 mg upward — and no blood-pressure effect.
In the 24-week obesity trial: +7.4 bpm at 0.5 mg, P = 0.0001, again with no significant systolic or diastolic change at 0.25 or 0.5 mg.
What happened next is the most informative thing in the whole record. The programme's answer was not to lower the dose. It was to add a beta-blocker.
Tesomet is a fixed combination of 0.5 mg tesofensine with 50 mg metoprolol. In the 24-week hypothalamic obesity study, the combination produced an additional mean weight change of −6.3% against placebo, and the paper reports "no significant differences in heart rate or blood pressure" between groups.
Two readings are available and both are honest. The combination solved the problem. And: the sponsor's own view of what 0.5 mg of tesofensine requires, in order to be given for six months, is a second drug managing its cardiovascular effect. Nothing on a research storefront supplies the second drug.
The adverse events in that study are worth stating in full, because they were mild and they were common: sleep disturbance in 50% on Tesomet against 13% on placebo, dry mouth 43% against 0%, headache 36% against 0%, in 21 patients of whom 18 completed.
The finding: thirteen studies, no Phase 3
ClinicalTrials.gov, read on 14 September 2026, returns thirteen registered interventional studies of tesofensine.
- Sponsors: Boehringer Ingelheim (the NS 2330 CNS trials), NeuroSearch (the obesity programme, including NCT00394667), Saniona (the metoprolol combination, hypothalamic obesity and Prader-Willi syndrome).
- Phases: every study is Phase 1, Phase 2, or Phase 1/2. There is no Phase 3 study in the registry.
- Status: eleven completed, two withdrawn — both Saniona open-label extension studies, one in Prader-Willi syndrome and one in hypothalamic obesity.
Set that against the Lancet authors' own closing sentence in 2008: the efficacy and safety findings "need confirmation in phase III trials".
Eighteen years later the registry contains no such trial. A 9.2% weight loss at 24 weeks is a strong Phase 2 result — better than what several approved products showed at the time — and the programme changed hands twice without ever running the study its own authors said it needed. Whatever the reason, the consequence for a reader is concrete: there is no confirmatory efficacy or safety dataset for tesofensine at any dose. Everything in the table above is Phase 2 or smaller, and the largest obesity study in it randomised 203 people.
What is not established
No approval, no labelling. FDA's Drugs@FDA application database returned no matching record and DailyMed returned no labelling, both queried 14 September 2026. There is no approved US indication and therefore no label-derived dose. This page makes no claim about other jurisdictions.
No long-term safety dataset. The longest studies in the retrieved record are 24 weeks, at n = 203 and n = 21.
No dose for anything but a tablet. Every published figure is an oral once-daily milligram dose. Nothing in the retrieved literature describes any other route, and no source states a dose for one.
Declining interest, not resolved questions. This term's search demand fell 61% year on year at the time it was queued. That is a fact about attention, not about evidence, and neither direction of that number tells a reader anything about the compound.
What a reader can check in ten minutes
Search ClinicalTrials.gov for tesofensine and sort by phase. Count the Phase 3 entries. Then open the Lancet abstract (PMID 18950853) and read its final sentence.
Then open the Tesomet study (PMID 35294397) and look at what is in the pill besides tesofensine, and why.
Related on this site
- Lipo-C dosage — a compounded weight-loss injection whose formula changes from pharmacy to pharmacy
- How to read a dosing claim — the checks that separate a sourced figure from a repeated one
- 5-Amino-1MQ dosage — another compound sold as a peptide that is not one
- Kisspeptin dosage — a full human dose record in units no vial label can carry
- Peptide side effects — what the adverse-event record does and does not contain
Sources and dates
PubMed records retrieved via NCBI E-utilities; registry data via the ClinicalTrials.gov API v2. All read 14 September 2026.
- Astrup A, Meier DH, Mikkelsen BO, Villumsen JS, Larsen TM. Weight loss produced by tesofensine in patients with Parkinson's or Alzheimer's disease. Obesity (Silver Spring). 2008;16(6):1363–9. DOI 10.1038/oby.2008.56. PMID 18356831.
- Astrup A, Madsbad S, Breum L, Jensen TJ, Kroustrup JP, Larsen TM. Effect of tesofensine on bodyweight loss, body composition, and quality of life in obese patients: a randomised, double-blind, placebo-controlled trial. Lancet. 2008;372(9653):1906–13. DOI 10.1016/S0140-6736(08)61525-1. PMID 18950853. ClinicalTrials.gov NCT00394667.
- Huynh K, Klose M, Krogsgaard K, et al. Randomized controlled trial of Tesomet for weight loss in hypothalamic obesity. Eur J Endocrinol. 2022;186(6):687–700. DOI 10.1530/EJE-21-0972. PMID 35294397.
- Hauser RA, Salin L, Juhel N, Konyago VL. Randomized trial of the triple monoamine reuptake inhibitor NS 2330 (tesofensine) in early Parkinson's disease. Mov Disord. 2007;22(3):359–65. DOI 10.1002/mds.21258. PMID 17149725.
- ClinicalTrials.gov API v2, intervention query "tesofensine" — 13 registered studies, sponsors Boehringer Ingelheim, NeuroSearch A/S and Saniona; phases Phase 1 and Phase 2 only; NCT05198362 and NCT05147415 withdrawn. Read 14 September 2026.
- openFDA Drugs@FDA endpoint and DailyMed SPL service, queried for tesofensine on 14 September 2026. Both returned zero records.