Tesofensine
An oral triple monoamine reuptake inhibitor, not a peptide, that produced roughly 10% weight loss in Phase 2 and a Mexican Phase 3 program but remains unapproved everywhere, with dose-related heart-rate increases and a Lancet expression of concern on its key trial.
Also referenced as: NS-2330, NS 2330, NS2330, Tesomet
Also appears in: Metabolic
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This compound has a genuine development or study trail, but it is not an approved routine drug.
Primary research area: Weight loss. Also surfaces under Metabolic for browsing and discovery.
Where the compound acts, as a browse axis. It is an editorial grouping for discovery, not a claim about labeled indications.
NS-2330, NS 2330, NS2330, Tesomet
No FDA label signal · 14 trials · 59 PubMed results
Tesofensine has name-matched human trials with published or reported controlled evidence, but is not FDA-approved. The research is real and ongoing — treat findings as developing rather than settled.
Tesofensine has 13 name-matched clinical trials (highest phase: Phase 2) and 59 PubMed-indexed publications and is not FDA-approved. 4 trials have posted results.
Re-checked nightly against the registries — tracked since 2026-10-28. No band changes yet.
Grades evidence strength, not efficacy or safety. Research-use context; not medical advice. Graded 2026-11-02 from PubMed, ClinicalTrials.gov, ISRCTN, openFDA, Health Canada, and OpenAlex — computed deterministically and refreshed nightly, with a retraction check. How we grade →
What is Tesofensine?
Tesofensine (development code NS 2330) is a synthetic small molecule, not a peptide: a phenyltropane carrying a 3,4-dichlorophenyl group that blocks the presynaptic transporters for dopamine, norepinephrine, and serotonin. It was discovered by the Danish company NeuroSearch and first taken into Phase 2 trials for Parkinson’s disease and Alzheimer’s disease, where it failed to show convincing efficacy but reliably caused weight loss. That side effect redirected the program toward obesity. NeuroSearch transferred the rights to Saniona (Denmark) in 2014, and Saniona’s licensee Productos Medix holds the commercial rights for Mexico and Argentina. Tesofensine appears in the research-peptide market as an oral appetite suppressant sold next to GLP-1 peptides, even though it has no structural or mechanistic relationship to them.
How it works
- Triple monoamine reuptake inhibition. Tesofensine and its active N-desmethyl metabolite (M1) inhibit the dopamine, norepinephrine, and serotonin transporters, raising synaptic levels of all three monoamines. In mouse pharmacokinetic-pharmacodynamic modeling, M1 was 4 to 5 times less potent at the dopamine transporter but reached roughly 8-fold higher trough steady-state concentrations, so it contributed to the overall effect in mice; the same authors note that human M1 concentrations are about 60% lower than the parent, so its contribution in people is probably smaller (Lehr et al., British Journal of Pharmacology, 2008;153(1):164–174).
- Measurable dopamine transporter occupancy at clinical doses. In a human PET study, striatal dopamine transporter occupancy rose from about 18% to 77% across 0.125 to 1 mg daily doses, with a projected maximum near 80% and half-maximal occupancy at roughly 0.25 mg (Appel et al., European Neuropsychopharmacology, 2014;24(2):251–261).
- Appetite suppression downstream of alpha-1 adrenergic and dopamine D1 signaling. In diet-induced obese rats, the hypophagic effect was almost completely reversed by the alpha-1 antagonist prazosin and partly by the D1 antagonist SCH23390, while alpha-2, D2, D3, and 5-HT2A/C blockers had no effect (Axel et al., Neuropsychopharmacology, 2010;35(7):1464–1476). A later rodent study tied the effect to silencing of feeding-promoting GABAergic neurons in the lateral hypothalamus (Perez et al., PLoS One, 2024).
- Mostly reduced intake, only a small thermogenic component. In a two-week respiration-chamber study of 32 overweight or moderately obese men given 2.0 mg then 1.0 mg daily (above the doses later carried forward), tesofensine increased satiety and fullness ratings and 24-hour fat oxidation, but total 24-hour energy expenditure was not significantly different from placebo; only nighttime expenditure rose, by about 4.6% (Sjödin et al., International Journal of Obesity, 2010;34(11):1634–1643; NCT00428415). In a sub-analysis of 158 TIPO-1 participants, a composite satiety score rose dose-dependently by week 12 and correlated with weight loss, then waned toward baseline by week 24 even as weight loss continued, returned to baseline after drug withdrawal, and rose again when 113 of them were re-exposed in an open-label phase (Gilbert et al., Obesity, 2012;20(3):553–561).
Research status
Neurology origins (2000 to 2008). The first human efficacy test was a nine-patient acute study of NS 2330 in relatively advanced Parkinson’s disease at the US National Institute of Neurological Disorders and Stroke (NCT00006077), which found no change in parkinsonian scores given alone or with levodopa (Bara-Jimenez et al., Movement Disorders, 2004;19(10):1183–1186). Boehringer Ingelheim then sponsored a Phase 2 program in early Parkinson’s disease (NCT00148486), levodopa-treated Parkinson’s with motor fluctuations (NCT00148512), and mild-to-moderate Alzheimer’s dementia (NCT00153010). In 261 patients with early Parkinson’s disease, none of three doses improved total UPDRS versus placebo at 14 weeks; decreased body weight and elevated heart rate were common at 1 mg (Hauser et al., Movement Disorders, 2007;22(3):359–365). The ADVANS study in advanced Parkinson’s disease found modest, dose-inconsistent improvements in UPDRS II+III and off time, with more gastrointestinal and neuropsychiatric adverse events at higher doses (Rascol et al., Archives of Neurology, 2008;65(5):577–583). The Alzheimer’s work, two four-week Phase 2a studies in 62 patients and a negative 14-week Phase 2b trial in 430 patients, was never published as a primary efficacy report; it is known only through pharmacokinetic and efficacy modeling (Lehr et al., AAPS Journal, 2010;12(2):117–129). Development for both neurologic indications was discontinued. A pooled analysis of the four Boehringer trials (740 on tesofensine, 228 on placebo) documented dose-dependent weight loss of up to 2.8% over 14 weeks without a weight-loss program, with heart rate significantly raised from 0.25 mg upward (+4.2 to +6.8 beats per minute) and no blood-pressure change (Astrup et al., Obesity, 2008;16(6):1363–1369).
TIPO-1 (Phase 2, obesity). The pivotal peer-reviewed evidence remains a 24-week, five-center Danish trial of 203 patients with BMI 30 to 40 on an energy-restricted diet (NCT00394667). Mean weight loss was 4.5%, 9.2%, and 10.6% at 0.25, 0.5, and 1.0 mg versus 2.0% with diet plus placebo; heart rate increased by 7.4 beats per minute at 0.5 mg, while systolic and diastolic blood pressure at the two lower doses did not differ significantly from placebo. Common adverse events were dry mouth, nausea, constipation, hard stools, diarrhea, and insomnia (Astrup et al., Lancet, 2008;372(9653):1906–1913). In April 2013 The Lancet issued an expression of concern on the paper after a Good Clinical Practice inspection by the Danish medicines regulator found that adverse events had not been collected and reported in line with the protocol (Lancet, 2013;381(9873):1167); the authors replied in a correspondence item titled “Under-reporting of adverse effects of tesofensine” (Lancet, 2013;382(9887):127). The expression of concern has not been resolved by a correction or retraction. A follow-on long-term safety study in 140 patients (NCT00481104) was completed in 2008 but has no peer-reviewed primary report.
Phase 3 in Mexico (Medix). Saniona’s licensee Productos Medix ran a 24-week, randomized, double-blind, placebo-controlled Phase 3 trial of 0.25 and 0.5 mg in 372 Mexican patients with obesity on diet and exercise. Topline results announced on 17 December 2018 reported approximately 10% weight loss at 0.5 mg, more than half of patients losing over 10%, no significant effect on blood pressure, and a “minor but statistically significant” heart-rate increase; those are Saniona’s words, repeated in its 2025 annual report and its January to June 2026 interim report. The trial does not appear among the 14 tesofensine and Tesomet studies registered on ClinicalTrials.gov and, as of October 2026, has not been published in a peer-reviewed journal; the only data source is company communication.
Mexican regulatory review (2023 to 2026), not an approval. Medix filed a new drug application with COFEPRIS, and in February 2023 the agency’s new-molecules technical committee issued what Saniona itself describes as a “favorable non-binding opinion.” That opinion was widely misreported as an approval. In early November 2024 Saniona disclosed that Medix had not received regulatory approval. Medix began revising the dossier on 10 February 2025 based on COFEPRIS feedback and resubmitted it on 20 February 2025. Saniona’s year-end 2025 report (February 2026), its 2025 annual report (April 2026), and its first-quarter 2026 report (May 2026) all describe the application as “currently under review,” and its January to June 2026 interim report (August 2026) says only that Medix “continues to pursue regulatory approval.” No tesofensine product is authorized for sale in Mexico, Argentina, or anywhere else.
Tesomet and the US pathway. Because the heart-rate signal was the main obstacle, Saniona built Tesomet, a fixed-dose combination of tesofensine 0.5 mg with the beta-1 blocker metoprolol 50 mg, after a rat telemetry study showed metoprolol fully prevented the cardiovascular sympathetic effects while leaving appetite suppression intact (Bentzen et al., Obesity, 2013;21(5):985–992). In a 24-week randomized trial of 21 adults with hypothalamic obesity (NCT03845075), Tesomet produced 6.3% placebo-adjusted weight loss with no between-group difference in heart rate or blood pressure; one treatment-related serious adverse event, worsening of pre-existing anxiety, led to discontinuation, and sleep disturbance was reported in 50% versus 13% on placebo (Huynh et al., European Journal of Endocrinology, 2022;186(6):687–700). A small Phase 2 in Prader-Willi syndrome (NCT03149445; nine adults and nine adolescents, three months) is reported by the company as showing a 5.4% weight reduction and reduced hyperphagia in adults, but has no peer-reviewed publication; an earlier Phase 2 of the combination in type 2 diabetes (NCT02737891) is likewise unpublished. Saniona states that the FDA has granted orphan drug designation for both hypothalamic obesity and Prader-Willi syndrome and confirmed a 505(b)(2) pathway, but the two US Phase 2b trials registered in late 2021 (NCT05147415, NCT05198362) were withdrawn before enrolling anyone, with the registry entries citing financial considerations, and Saniona describes the program as voluntarily paused for funding reasons while it seeks a partner. There is no active clinical trial of tesofensine or Tesomet anywhere, and no US marketing application has been filed.
Abuse liability. In 52 recreational stimulant users, single doses of tesofensine were not significantly different from placebo on subjective drug-liking measures, well below D-amphetamine 30 mg, and no greater than bupropion or atomoxetine (Schoedel et al., Clinical Pharmacology & Therapeutics, 2010;88(1):69–78).
Common dosage forms
In every clinical trial tesofensine was an oral tablet, in strengths from 0.125 to 1.0 mg; the strengths carried into Phase 3 were 0.25 and 0.5 mg, and Tesomet is a tablet combining 0.5 mg tesofensine with 50 mg metoprolol. Research vendors sell it as oral capsules or tablets in the 250 to 500 microgram range, sometimes labeled as a dietary supplement; it is not an injectable and is not supplied as lyophilized powder for reconstitution. A 2026 anti-doping study characterized urinary metabolites in six volunteers after a single 483 microgram dose of one such product sold as a “dietary supplement,” and detected the drug for up to 500 hours (Krug et al., Drug Testing and Analysis, 2026;18(9):1163–1173).
Key considerations
- Not a peptide, and not approved anywhere. Tesofensine is a tropane-class small molecule. It has no FDA approval, no clinical trial recruiting anywhere, and the often-repeated claim of a “2023 Mexican approval” is wrong: that was a non-binding committee opinion, the application was not approved in 2024, and the dossier resubmitted in February 2025 was still under COFEPRIS review in Saniona’s 2026 reporting. The Investigational status reflects that pending COFEPRIS marketing application and Saniona’s registered development program.
- Cardiovascular signal is dose-dependent and the reason the program stalled. Heart rate rose by about 7 beats per minute at 0.5 mg in TIPO-1, significantly from 0.25 mg in the pooled neurology trials, and by a “minor but statistically significant” amount in the company’s Phase 3 summary. Blood pressure was not significantly affected at 0.25 to 0.5 mg in those studies, but acute dosing raised both heart rate and blood pressure in rat telemetry. The developer’s own remedy was to co-formulate a beta-blocker, which is itself an acknowledgment of the issue.
- The best efficacy data carry an unresolved expression of concern. TIPO-1 is a single Phase 2 trial of 203 people whose adverse-event reporting failed a regulatory GCP inspection, and the Phase 3 that would supersede it has never been peer-reviewed or registered. Treat the “10% weight loss, comparable to GLP-1 agonists” framing accordingly; the GLP-1 comparison also ignores trial length (24 weeks versus 68 to 72 weeks) and population differences.
- Neuropsychiatric effects. Insomnia and sleep disturbance, dry mouth, constipation, and nausea recur across trials; neuropsychiatric adverse events were more frequent at higher doses in the advanced Parkinson’s program, and an anxiety exacerbation was the one treatment-related serious adverse event in the hypothalamic-obesity trial. Abuse liability testing was reassuring, but the compound is a dopamine transporter blocker and falls within WADA’s S6 stimulant class, prohibited in competition.
- Naming and category confusion. “Tesomet” is a combination product (tesofensine plus metoprolol) with a different cardiovascular profile and should not be conflated with tesofensine alone. Despite its origin in Alzheimer’s and Parkinson’s trials, every neurologic trial of tesofensine was negative or inconclusive, and there is no evidence of cognitive enhancement in healthy people; its appetite and metabolic-risk-factor effects are the only ones with clinical support.