Peptide Health Lab

Metabolic & GLP-1

Tesofensine

FOR RESEARCH PURPOSES ONLY

Also known as: NS 2330, NS-2330

Regulatory status
Research only
Evidence grade
Human RCT evidence

Last reviewed September 1, 2026 · 20 sources

What tesofensine is and how it works

Tesofensine, developed under the code NS 2330, is an orally administered small molecule that blocks the presynaptic reuptake of three monoamines at once: noradrenaline, dopamine and serotonin.[1] It is not a peptide, and it was not built as a weight-loss drug. Boehringer Ingelheim and NeuroSearch developed it for Parkinson's disease and Alzheimer's disease. A review of that programme records that the compound was ineffective as a treatment for those neurodegenerative conditions, and that a notable occurrence of unintended weight loss was observed in the people who received it.[9] The obesity programme was reverse-engineered from that observation, which is an unusual origin story and worth holding onto: the weight effect was first seen as a side effect in trials the drug lost.

The transporter blockade is measurable in living people. A positron-emission-tomography study measured mean striatal dopamine-transporter occupancy of 18% to 77% across multiple oral doses of 0.125 to 1 mg at anticipated steady state, and estimated that the maximum achievable occupancy was about 80%, half of it reached at roughly 0.25 mg and a plasma concentration of 4 ng/mL.[11] A 2025 cryo-electron-microscopy study that solved structures of the human dopamine transporter bound to five different triple reuptake inhibitors reported that tesofensine stabilises the transporter in an outward-facing conformation, unlike three of the other four compounds examined.[20] The mechanism, at the level of the target, is not in dispute.

How that blockade becomes appetite suppression has been worked out mostly in rodents. In diet-induced obese rats given tesofensine for 28 days, caloric intake and weight gain fell significantly more than in vehicle-treated rats, and both increased again once dosing was discontinued; the same study found lower striatal D2/D3 receptor availability that did not correlate with food intake or body weight, which the authors read as a pharmacological effect rather than the mechanism.[15] A 2024 study in mice and rats reported that tesofensine inhibits a subset of GABAergic neurons in the lateral hypothalamus, and that chemogenetically silencing those neurons enhanced its food-suppressing effect.[16] Those are rodent results. Naming the species is the point, because no human study has looked at either.

One pharmacokinetic fact governs everything else on this page. A population model built on 1,969 tesofensine and 1,714 metabolite concentrations from 320 patients estimated a half-life of 234 hours for the parent compound and 374 hours for its major metabolite M1, and found 62% higher exposure in women with reduced creatinine clearance than in men with normal renal function.[10] Exposure accumulates over weeks and clears over weeks.

What the research actually shows

The obesity trial everyone quotes — and the notice attached to it. A 24-week randomized, double-blind, placebo-controlled phase 2 trial at five Danish centres randomized 203 adults with a body-mass index of 30 to 40 to 0.25, 0.5 or 1.0 mg daily or placebo. Every arm, including placebo, was prescribed an energy-restricted diet. Mean weight loss was 2.0% on diet plus placebo and 4.5%, 9.2% and 10.6% on the three doses (p<0.0001), and heart rate rose 7.4 beats per minute in the 0.5 mg group (p=0.0001).[1] Two things about the famous number. The "10.6%" is the total loss in the 1.0 mg arm with the diet included, not the placebo-subtracted effect — those differences are roughly 2.5, 7.2 and 8.6 percentage points — and 1.0 mg was not the dose the investigators proposed carrying forward. Their own interpretation was that 0.5 mg "might have the potential" to produce twice the weight loss of the drugs then approved, and that the findings needed confirmation in phase 3 trials.[1]

In April 2013 the journal issued an Expression of Concern naming that trial, and the trial's authors published a reply three months later titled "Under-reporting of adverse effects of tesofensine".[2][3] The paper has not been retracted and nothing in the published record resolves the notice either way. It is not a footnote here, because that one trial is where nearly every tesofensine weight-loss figure in circulation comes from, and the concern attaches specifically to adverse-effect reporting.

The cleaner drug-only estimate is smaller. A meta-analysis pooled four randomized, double-blind, multicentre 14-week trials in patients with Parkinson's or Alzheimer's disease — 740 on drug, 228 on placebo, with no weight-loss programme of any kind. Weight change was +0.5% on placebo and -0.5%, -0.9%, -1.8% and -2.8% across 0.125 to 1.0 mg (P=0.015 for the dose effect); in the obese subgroup, 32.1% of patients on 1.0 mg reached at least 5% weight loss versus 2.1% on placebo. Heart rate rose 2.1 to 6.8 beats per minute, significant from 0.25 mg, with no blood-pressure effect observed in that pooled dataset.[4] Nobody in these trials was dieting, which makes this the drug's own contribution — and it is roughly 4% at the top dose, not 10%.

The mechanism in humans is appetite, not metabolic rate. In a randomized two-week trial, 32 overweight and moderately obese men housed in a respiration chamber showed higher satiety and fullness and lower prospective food intake than on placebo, and lost 1.8 kg more (P<0.0001) — but the investigators could demonstrate no significant effect on total 24-hour energy expenditure. They did find 4.6% higher night-time expenditure once adjusted for body composition, and 18 g more fat oxidation over 24 hours (P<0.001).[6] In the phase 2 appetite study, the randomized first part (n=158) found a dose-dependent rise in a composite satiety score at week 12 that correlated with 24-week weight loss (r=0.36, P<0.0001) — and the score fell back as weight loss progressed and returned to baseline after withdrawal.[5]

The original indications failed. In 261 patients with early Parkinson's disease, adjusted mean differences in total UPDRS score at 14 weeks were -0.7, -1.3 and -1.7 points (P=0.64, 0.41 and 0.27), and the authors concluded that at the doses tested the compound did not provide significantly greater benefit than placebo.[7] In advanced Parkinson's disease, modest improvements appeared at 0.5 mg and 0.25 mg but no dose-response relationship for efficacy could be established, while adverse reactions became more frequent at the higher doses.[8]

Where the evidence is weak

No phase 3 trial appears anywhere in the indexed literature. PubMed searches on 1 September 2026 for "tesofensine AND phase 3", "tesofensine AND phase III AND obesity", and "tesofensine AND Medix" returned, respectively, one record, eight records and zero records — and every one of the nine is a review, a commentary, or the 2008 phase 2 trial itself. A 372-patient phase 3 obesity trial is described in the licence holder's own corporate reporting; nothing about it appears in the peer-reviewed literature, so nobody outside the sponsor can read its methods, its endpoints, or its adverse-event tables. That is the single largest gap on this page, and it means the compound's entire published efficacy case rests on phase 2 work now nearly two decades old.

The flagship trial's Expression of Concern is unresolved. Overcorrecting is also a defect: the trial was not retracted, and the notice does not by itself establish that anything in it is wrong. But an open concern about adverse-effect reporting, on the trial that supplies the headline efficacy numbers, is a material limitation on how confidently those numbers can be read.[2]

"Tesomet is tesofensine" is the most dangerous misreading available. The hypothalamic-obesity work does not test tesofensine. It tests a fixed combination of 0.5 mg tesofensine and 50 mg metoprolol, a beta-1 blocker, in 21 adults over 24 weeks with safety as the primary endpoint; additional mean weight change was -6.3% (95% CI -11.3 to -1.3, P=0.017), and the trial reported no significant differences in heart rate or blood pressure between groups.[18] The beta-blocker is in that combination because of the cardiovascular signal described above. Telemetry in conscious rats showed that tesofensine dose-dependently raised heart rate and blood pressure, that metoprolol fully prevented those cardiovascular effects while leaving the hypophagic effect intact, and that an angiotensin-receptor antagonist only partly reversed the blood-pressure rise and did not touch the heart rate at all.[14] Reading "no heart-rate or blood-pressure difference" from the combination trial back onto tesofensine alone inverts the safety story: that result is what the beta-blocker was added to produce. An independent 2026 systematic review of seven randomized trials in acquired hypothalamic obesity also records that the combination was associated with reductions in both body weight and lean mass, and rates the certainty of that evidence as low.[19]

The cardiovascular signal has never been resolved against an outcome. Every randomized dataset that measured heart rate found a dose-dependent increase.[1][4] Blood pressure was not significantly raised at 0.25 and 0.5 mg over 24 weeks, and a review of the development programme reports significant increases at the highest dose tested.[9] No trial has measured cardiovascular events. "No cardiovascular effect" is not something these data support in either direction.

Nothing is known about durability. The longest randomized, placebo-controlled exposure in the published record is 24 weeks. The only longer dataset is part 2 of the appetite trial, which was open-label, single-group and uncontrolled (n=113); in the drug-free interval between the two parts the composite satiety score returned to baseline even though participants remained 7.2 kg lighter.[5] In rats, food intake and weight gain both climbed again after discontinuation.[15] PubMed searches on 1 September 2026 for "tesofensine AND weight regain" returned zero records, and for "tesofensine AND (52 weeks OR one year OR long-term)" returned 13, none of which is a controlled human trial running longer than 24 weeks.

Whole populations are unstudied. A PubMed search on 1 September 2026 for "tesofensine AND pregnancy" returned zero records, and a search for "tesofensine AND Prader-Willi" and one for "Tesomet AND Prader" each returned zero records as well — so any claim about the compound in Prader-Willi syndrome rests on material that is not indexed in PubMed and cannot be checked here. There is no label to fall back on for any of this, because there is no approval anywhere.

Why the badge above says human RCT for a compound whose programme stopped. The badge names the kind of evidence that tested the compound's typical claim, not a verdict on how the testing came out. Four randomized, double-blind, multicentre trials comparing tesofensine against placebo measured its effect on body weight before the obesity programme existed, and none of the four is the trial carrying the Expression of Concern.[4] That is genuinely randomized human evidence, and a lower badge would misdescribe it. What the badge cannot say is everything in this section: the trials were phase 2, the largest ran 24 weeks, the flagship one has an open notice against it, and the phase 3 programme that was supposed to settle the question has never been published. A grade is a description of study design. It is not an endorsement, and on this page it should be read with the research-only status and the paragraphs above it.

Legal and regulatory status

Tesofensine is not approved by the FDA for any indication. Verification at authoring time found no application in Drugs@FDA under the active-ingredient, generic-name or brand-name fields; no approved labeling in the structured product labeling database; and, in the National Drug Code directory, four records, every one of them a bulk-ingredient registration by an active-pharmaceutical-ingredient manufacturer rather than a finished drug product. Same-session control queries of identical shape for two anti-obesity comparators returned real records, which is what makes those null results a demonstrated absence rather than a malformed search. Nothing bearing this name has an authorised maker, an agreed indication, a labelled schedule, or a quality standard anyone is obliged to meet.

On Mexico, this page asserts neither an approval nor a rejection. Tesofensine is very widely described as "approved for obesity in Mexico", and that description does not survive checking. What can be verified is a sequence. The Mexican licensee filed a marketing application with COFEPRIS, the Mexican regulator. COFEPRIS's New Molecules Committee considered the molecule and, in February 2023, issued a favourable opinion — which the licence holder's own year-end report for 2025 describes verbatim as "a favorable non-binding opinion". COFEPRIS describes that committee, in its own words, as una instancia de consulta y opinión: a body of consultation and opinion. It is not the registration decision. The application was subsequently revised after regulator feedback and resubmitted on 20 February 2025, and the same licence-holder report states that the marketing authorisation application in Mexico "is currently under review". The definitive Mexican registry viewer is behind a CAPTCHA and was not queried for this page, so the honest limit of what was checked is: a committee opinion exists, it is advisory and non-binding, the application was still under review at the licence holder's most recent report, and no primary source consulted here shows either a granted registration or a refusal. The gap between "the advisory committee gave a favourable opinion" and "the regulator granted a marketing authorisation" is where essentially every "approved in Mexico" headline comes from. A foreign approval would not be an FDA approval in any case, and an advisory opinion is not even a foreign approval.

In tested sport, tesofensine is named on the 2026 World Anti-Doping Code International Standard Prohibited List — in force from 1 January 2026, retrieved from the World Anti-Doping Agency on 1 September 2026 via the United States Anti-Doping Agency's prohibited-list page — in section S6, stimulants, under S6.B specified stimulants, a section prohibited in competition only rather than at all times. The same classification appears verbatim in the indexed literature: the anti-doping laboratory that characterized the compound's urinary metabolism states in its own abstract that tesofensine is classified under S6 stimulants and is prohibited in-competition only.[13] That classification is revised annually, so the list in force on the day of a test is the only one that governs it, and no page written once can stand in for it. The same laboratory reported in 2026 that the compound has been marketed online as a dietary supplement promoted for weight management despite having no approved product anywhere, and characterised its urinary excretion after six volunteers each received 483 micrograms of such a product: four principal metabolites, peak concentrations of 1 to 4 ng/mL, and detection windows of up to 500 hours.[13]

Peptide Health Lab does not sell anything, does not tell anyone where to obtain anything, and takes no position on how unapproved material reaches anyone. What the regulatory status means for a reader is narrower and more useful: a compound whose development programme was discontinued for its original indications, whose one large obesity trial carries an open Expression of Concern, and whose phase 3 data have never been published, has not been through the filter that turns a promising phase 2 result into a known risk-benefit profile.[9]

Questions to bring to a provider

The useful conversation is comparative, because approved options with completed outcome trials exist for the goal most people bring to this compound.

  • Set against anti-obesity drugs whose phase 3 results are in the literature, what does an unpublished phase 3 programme leave a prescriber able to weigh here?[1]
  • Every randomized dataset on this compound found heart rate rising with dose. What existing cardiac or blood-pressure history would make that finding disqualifying rather than merely worth watching?[4]
  • Given a half-life of 234 hours for the parent compound and 374 for its metabolite, and 62% higher exposure with reduced renal function, how would renal function and any interacting medicine be assessed?[10]
  • This compound acts on the same monoamine systems as many psychiatric medicines. What does a current antidepressant, stimulant, or monoamine-oxidase inhibitor mean here?[8]
  • The satiety effect measured in the trial attenuated by week 24 and returned to baseline after withdrawal. What is the plan for the point at which it stops?[5]
  • If the interesting result was the hypothalamic-obesity trial, is it clear that the trial tested a fixed combination with a beta-blocker rather than tesofensine alone?[18]
  • The searched negative in the section above found nothing published on tesofensine exposure in a human pregnancy, and there is no label to carry any direction. Is pregnancy, intended pregnancy, or breastfeeding in the picture?
  • Material carrying this name outside a trial is not what any of these studies administered, and there is no approved manufacturer to make it so. How should that gap be weighed against the trial numbers on this page?[13]

A clinician who says "the phase 3 results have never been published, so let's use something that has been" is giving a defensible answer, not a conservative one.

Evidence by claim

Grades describe how strong the evidence is; the line under each grade describes what kind of studies it is. How we grade evidence.

Weight loss in adults with obesity, alongside an energy-restricted diet
Human RCT evidence human RCT · review

In a 24-week randomized, double-blind, placebo-controlled phase 2 trial of 203 adults, every arm followed an energy-restricted diet. Mean weight loss was 2.0% on diet plus placebo and 4.5%, 9.2% and 10.6% at 0.25, 0.5 and 1.0 mg (p<0.0001 versus diet plus placebo). The widely quoted "10%" is the total loss in the highest-dose arm, diet included; the placebo-subtracted differences are roughly 2.5, 7.2 and 8.6 percentage points. The trial's investigators wrote that these findings "need confirmation in phase III trials", and the trial carries an unresolved journal Expression of Concern.

[1] [2]

Weight loss without any diet programme
Human RCT evidence review

A meta-analysis of four randomized, double-blind, multicentre 14-week trials in patients with Parkinson's or Alzheimer's disease (740 on drug, 228 on placebo, no weight-loss programme) found weight changes of +0.5% on placebo and -0.5%, -0.9%, -1.8% and -2.8% across 0.125 to 1.0 mg (P=0.015 for the dose effect). In the obese subgroup the changes were -0.2% on placebo and up to -3.7%, and 32.1% of obese patients on 1.0 mg reached at least 5% weight loss versus 2.1% on placebo. This is a smaller effect than the obesity trial and it is the cleaner drug-only estimate, because nobody in it was dieting.

[4]

Appetite suppression as the mechanism of the weight loss
Human RCT evidence human RCT

In the randomized first part of a phase 2 trial (n=158), tesofensine produced a dose-dependent increase in a composite satiety score at week 12 that correlated with weight loss over 24 weeks (r=0.36, P<0.0001), but the score fell back as weight loss progressed and returned to baseline after withdrawal. In a separate randomized two-week trial in 32 overweight and moderately obese men, tesofensine produced higher ratings of satiety and fullness and lower prospective food intake than placebo. The satiety effect is real, randomized, and attenuating.

[5] [6]

Increased energy expenditure
Human RCT evidence human RCT

Largely not supported. In a randomized two-week trial in 32 men measured in a respiration chamber, the investigators could demonstrate no significant effect on total 24-hour energy expenditure compared with placebo. They did find higher expenditure during the night period (4.6%, P<0.05) once adjusted for body-composition change, and a 24-hour increase in fat oxidation of 18 g (P<0.001). Their conclusion was a pronounced effect on appetite and a slight effect on night-time energy expenditure — not a metabolic-rate drug.

[6]

The original indications — Parkinson's disease and Alzheimer's disease
Human RCT evidence human RCT · review

Negative or equivocal. A randomized trial in 261 patients with early Parkinson's disease found adjusted mean UPDRS differences of -0.7, -1.3 and -1.7 points at 14 weeks (P=0.64, 0.41 and 0.27) and concluded that the compound "did not provide significantly greater benefit than placebo". A randomized trial in advanced Parkinson's disease reported modest improvements at 0.5 mg and 0.25 mg but could not establish a dose-response relationship for efficacy while adverse reactions became more frequent at higher doses. A review of the programme states that the compound was ineffective for the neurodegenerative conditions and that unintended weight loss was the observation that redirected it.

[7] [8] [9]

Weight loss that lasts beyond 24 weeks
Anecdotal reports only human RCT · animal

Not established by any controlled trial. The only published data past 24 weeks come from part 2 of the appetite trial, which was open-label, single-group and uncontrolled (n=113), and in which the composite satiety score had returned to baseline during the drug-free interval despite participants remaining 7.2 kg lighter. In diet-induced obese rats, caloric intake and weight gain both increased again after treatment was discontinued. PubMed searches on 1 September 2026 for "tesofensine AND weight regain" returned zero records, and for "tesofensine AND (52 weeks OR one year OR long-term)" returned 13 records, none of them a controlled human trial longer than 24 weeks.

[5] [15]

Cardiovascular effects
Human RCT evidence human RCT · review

Randomized human trials measured heart rate and blood pressure, and they found a consistent, dose-dependent heart-rate increase: 7.4 beats per minute at 0.5 mg over 24 weeks in the obesity trial (p=0.0001), and 2.1 to 6.8 beats per minute across 0.25 to 1.0 mg over 14 weeks in the pooled neurology trials, significant from 0.25 mg. Blood pressure was not significantly raised at 0.25 and 0.5 mg over 24 weeks, and a review of the programme reports significant increases at the highest dose tested. No trial has measured cardiovascular events, so what these surrogate measurements mean clinically is unknown.

[1] [4] [9]

Weight loss in hypothalamic obesity — evidence for a combination, not for tesofensine alone
Human RCT evidence human RCT · review

The only randomized trial in this population tested a fixed combination of 0.5 mg tesofensine and 50 mg metoprolol against placebo in 21 adults for 24 weeks, with safety as the primary endpoint. Additional mean weight change was -6.3% (95% CI -11.3 to -1.3, P=0.017) and 8 of 13 on the combination reached at least 5% weight loss versus 1 of 8 on placebo. The trial reported no significant differences in heart rate or blood pressure between groups — which is a property of a combination containing a beta-blocker and must not be read across to tesofensine alone. An independent 2026 systematic review of seven randomized trials in acquired hypothalamic obesity records that the combination was associated with reductions in both body weight and lean mass, and rates the certainty of the body-composition evidence as low.

[18] [19]

Dopamine-transporter occupancy as the proximate mechanism in humans
Anecdotal reports only human observational

A positron-emission-tomography study measured mean striatal dopamine-transporter occupancy of 18% to 77% across multiple oral doses of 0.125 to 1 mg at steady state, estimated a maximum achievable occupancy of about 80%, and estimated that half of that was reached at roughly 0.25 mg and a plasma concentration of 4 ng/mL. The authors suggested the previously reported dose-dependent weight loss was in part mediated by this blockade. The grade beside this claim is the lowest of the three this library uses, and it reflects the design rather than the quality of the measurement: this was an open-label imaging study without randomization or a control group, so it is a mechanistic inference and not an efficacy result.

[11]

Abuse potential
Human RCT evidence human RCT

A single-dose randomized double-blind crossover study in 52 recreational stimulant users, with d-amphetamine as a positive control and bupropion and atomoxetine as negative controls, found tesofensine's subjective effects not significantly different from placebo and lower than or no different from the two negative controls. The authors concluded abuse potential is no greater than that of bupropion or atomoxetine. One dose, one session, in one population — this does not characterize repeated dosing.

[12]

FOR RESEARCH PURPOSES ONLY

Typical protocol range in the research

  • Phase 2 obesity trial in 203 adults with a body-mass index of 30 to 40, 24 weeks, five Danish centres, every arm on an energy-restricted diet

    0.25 mg, 0.5 mg, or 1.0 mg once daily [1]

  • Four randomized double-blind trials in patients with Parkinson's or Alzheimer's disease (740 on drug, 228 on placebo), 14 weeks, with no weight-loss programme of any kind, pooled in a meta-analysis

    0.125 mg, 0.25 mg, 0.5 mg, or 1.0 mg once daily [4]

  • Two-week mechanistic trial in 32 overweight and moderately obese men housed in a respiration chamber, using a higher short-term dose than the obesity programme carried forward

    2.0 mg daily for 7 days, then 1.0 mg daily for a further 7 days [6]

  • Combination arm, not tesofensine alone — the Tesomet trial in 21 adults with hypothalamic obesity, 24 weeks, where safety was the primary endpoint and the beta-blocker was part of the fixed combination

    0.5 mg tesofensine plus 50 mg metoprolol once daily [18]

No regulator anywhere has approved a tesofensine dose, and there is no label to describe. Two of these four entries are not what a reader usually means by a dose of tesofensine: one is a two-week mechanistic protocol at a higher dose than the obesity trials used, and one is a fixed combination with a beta-blocker whose results belong to the combination. Read every entry with its context attached.

Ranges are what published research reports, not a recommendation. PHL does not prescribe, and nothing here is personalized to you.

Side effects & safety signals

  • Increased heart rate

    Reported in every randomized dataset that measured it. In the 24-week phase 2 obesity trial, heart rate rose by 7.4 beats per minute in the 0.5 mg group (p=0.0001). In four pooled randomized trials in patients with Parkinson's or Alzheimer's disease, changes in heart rate after 14 weeks were -0.4, 2.1, 4.2, 6.0 and 6.8 beats per minute from placebo up to 1.0 mg, significant from 0.25 mg upward. · This is the signal that shaped the compound's development and the reason a beta-blocker was later put in a fixed combination with it. It is dose-dependent, it was present at the doses that produced the weight loss, and no trial has ever measured whether it translates into cardiovascular events. Any history of arrhythmia, uncontrolled hypertension, or heart failure is a reason to raise this with a clinician rather than reason past it.

    [1] [4]

  • Blood-pressure effects, which the trials do not settle

    In the 24-week obesity trial, the 0.25 mg and 0.5 mg groups showed no significant increase in systolic or diastolic blood pressure compared with placebo, and the pooled neurology trials observed no blood-pressure effect at any dose. A review of the development programme nonetheless reports significant blood-pressure increases at the highest dose tested, and telemetry in conscious rats found dose-dependent rises in both heart rate and blood pressure. · The honest summary is that blood pressure was not raised at the lower human doses studied and was raised at the top of the range, in an animal model and in at least one reading of the human programme. "No cardiovascular effect" is not a statement these data support.

    [1] [4] [9] [14]

  • Dry mouth, nausea, constipation, hard stools, diarrhoea, and insomnia

    The most common adverse events attributed to tesofensine in the 24-week phase 2 obesity trial, in which 161 of 203 randomized participants completed the study. · Reported as the characteristic tolerability profile of the compound in its largest published obesity trial. The completion rate is part of the picture: roughly a fifth of participants did not finish 24 weeks.

    [1]

  • Gastrointestinal and neuropsychiatric adverse events, more frequent at higher doses

    In the randomized advanced-Parkinson's trial, gastrointestinal and neuropsychiatric adverse events were more frequent with tesofensine than with placebo, especially at the higher dosages. In the 24-week randomized trial of the tesofensine-plus-metoprolol combination in hypothalamic obesity, sleep disturbance occurred in 50% on the combination versus 13% on placebo, dry mouth in 43% versus 0%, and headache in 36% versus 0%, and one participant had a combination-related serious adverse event, an exacerbation of pre-existing anxiety, that led to discontinuation. · A triple monoamine reuptake inhibitor acts on the same neurotransmitter systems that psychiatric medicines act on. The combination figures above belong to the combination, not to tesofensine alone, and are listed here because they are the most detailed adverse-event breakdown in the published record. A psychiatric history, or any current psychiatric medicine, is a reason to raise this with a clinician first.

    [8] [18]

  • An unresolved Expression of Concern about adverse-effect reporting in the flagship trial

    Not quantified · In April 2013 the journal that published the 24-week phase 2 obesity trial issued an Expression of Concern naming that trial. The trial's own authors published a reply in the same journal three months later, under the title "Under-reporting of adverse effects of tesofensine". The trial has not been retracted, and nothing in the published record resolves the notice in either direction. It attaches to the single trial that produces almost every weight-loss figure quoted about this compound, and it attaches specifically to how adverse effects were reported.

    [2] [3]

  • A half-life measured in hundreds of hours

    A population pharmacokinetic model built on 1,969 tesofensine and 1,714 metabolite concentrations from 320 patients estimated half-lives of 234 hours for tesofensine and 374 hours for its major metabolite M1, and found that women with a creatinine clearance of 35.6 mL/min had 62% higher exposure than men without renal impairment. An anti-doping excretion study in six volunteers detected the compound in urine for up to 500 hours. · This is a property, not an adverse event, and it changes how every adverse event above should be read: exposure builds for weeks and does not fall quickly when dosing stops, and renal function and sex both move it. Nothing published characterizes how that interacts with the many medicines that act on the same monoamine systems.

    [10] [13]

  • Abuse potential characterized only after a single dose

    In a single-dose randomized double-blind crossover study in 52 recreational stimulant users, the subjective effects of tesofensine were not significantly different from placebo, were lower than d-amphetamine 30 mg on all primary and most secondary measures, and were lower than or no different from bupropion and atomoxetine. The authors concluded abuse potential is no greater than that of bupropion or atomoxetine. · That is a reassuring result about one dose on one occasion in one population. It is not a finding about repeated dosing in a compound whose metabolite accumulates over weeks, and it is not a finding of no abuse potential.

    [12]

  • Motor stereotypies observed in rats

    In a 2024 rodent study the authors reported that tesofensine caused few, if any, head-weaving stereotypies at therapeutic doses, unlike phentermine. In a 2025 study from the same laboratory that quantified behaviour by sex, tesofensine elicited head-weaving in female rats only, to a lesser extent than the other dopaminergic agents tested, and was the agent most frequently associated with orolingual dyskinesia. · Rodent findings, from one research group, in two studies that do not say quite the same thing. No published human study has looked for either behaviour. This is listed because it is the only motor-side-effect signal in the literature at all, and it must not be read as a human finding.

    [16] [17]

  • No long-term safety data and no cardiovascular outcome trial

    Not established · The longest published randomized, placebo-controlled exposure is 24 weeks. The one longer dataset is an open-label, single-group, uncontrolled extension of that trial. PubMed searches on 1 September 2026 for "tesofensine AND cardiovascular outcomes" and for "tesofensine AND (mortality OR cardiovascular outcome)" returned four records between them, every one a review or a trial of the fixed combination, and no outcome trial of any kind. Absence of a finding is not a finding of safety.

    [5] [9]

  • Unverified identity and purity of material outside a trial

    Not quantified · There is no approved manufacturer of tesofensine anywhere, so nothing about the composition, concentration, or contaminant profile of material carrying this name outside a clinical trial is regulated or independently guaranteed. An anti-doping laboratory reported in 2026 that the compound has been marketed online as a dietary supplement promoted for weight management, and used one such product, at 483 micrograms per dose, to characterize urinary excretion in six volunteers. Every efficacy and safety number on this page was generated with sponsor-manufactured product under trial monitoring, and none of it transfers automatically to anything else.

    [13]

Published lists are never exhaustive, so report anything unexpected to a licensed provider.

Storage, handling & reconstitution

Lyophilized storage
Tesofensine is an orally administered small molecule, not a peptide. Every published human result was produced with a tablet manufactured inside a sponsor's quality system, and no lyophilized, freeze-dried, or injectable presentation of tesofensine appears anywhere in the published literature. There is therefore no freeze-dried form whose stability, expiry, or storage conditions any manufacturer or regulator has characterized, and general freeze-dried-peptide convention is not a tesofensine finding.
Reconstituted storage
No published study describes tesofensine in solution. The trial tablets were handled as investigational pharmaceutical material under a sponsor's quality system and used within a sponsor-assigned expiry. Nothing published assigns a shelf life, a storage temperature, or a beyond-use date to anything labelled tesofensine outside that system.
Reconstitution
Not applicable. Tesofensine was administered as an oral tablet in every published human study, so there is nothing to reconstitute. No published study describes a solution, a diluent, an injectable presentation, or a reconstitution procedure for this compound, and this page will not improvise one.
Handling notes
These two fields describe an absence of published data, not a set of conventions to follow. The pharmacology question that would matter most for anything held outside a trial is not storage but elimination: the published half-life for this compound and its major metabolite is measured in hundreds of hours, so exposure accumulates over weeks and clears over weeks, and no storage practice changes that.

The how-to guides cover the conventions behind these fields, and what the published stability data does and does not establish: Storage, Reconstitution, Handling.

Questions for your provider

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