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Tesofensine

Also known as: NS2330, NS 2330, Tesomet (tesofensine + metoprolol fixed-dose combination)
Moderate evidence FDA: research-only WADA: Not specifically listed by name, but as a stimulant-type monoamine-reuptake inhibitor it is plausibly captured under WADA's S6 stimulants class in-competition — athletes should treat it as prohibited and confirm.
Last updated · 2026-06-19

Tesofensine (development code NS2330) is a small-molecule triple monoamine-reuptake inhibitor — it simultaneously blocks the presynaptic reuptake of dopamine, noradrenaline and serotonin, raising the synaptic concentration of all three monoamines. It is not a peptide, despite appearing in peptide-protocol libraries; it lives in this compound library for completeness and is kept in the house format. Tesofensine was originally developed by the Danish biotech NeuroSearch as a treatment for Parkinson's and Alzheimer's disease. It failed in both neurological indications, but trial participants lost weight, which redirected the molecule toward obesity — where a 203-patient Phase II trial (the TIPO-1 trial, Astrup

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Molecular weight 408.92 Da
Half-life ~220 hours ~9
CAS number 195875-84-4
Route Oral
Where to buy Tesofensine →Swiss Chems · save 10% code aewpzbzd
02

Dosing

FREQUENCY 1x daily, oral
CYCLE LENGTH Studied continuously for 14-24 weeks in trials; no validated long-term protocol

0.5 mg/day once daily was the dose that produced the strongest weight loss with an acceptable safety margin in the Phase II TIPO-1 trial; 1.0 mg/day added little extra weight loss but markedly more adverse events and is not favored. The very long ~9-day half-life means the drug accumulates over weeks to steady state, so effects (and side effects) build gradually. These are trial-derived research figures, NOT validated medical dosing — there is no FDA-approved dose because the drug is not approved.

03

Mechanism

Triple monoamine-reuptake inhibitor that blocks the presynaptic reuptake of dopamine (DAT), noradrenaline (NET) and serotonin (SERT), raising synaptic levels of all three monoamines. Net effect is appetite suppression and increased satiety, with a smaller contribution from nighttime energy expenditure and fat oxidation. In diet-induced obese animals it normalises blunted forebrain dopamine and silences feeding-promoting GABAergic lateral hypothalamic neurons. Originally developed (as NS2330) by NeuroSearch for Parkinson's and Alzheimer's disease; repurposed for obesity after trial participants lost weight.

04

Research summary

Study Type Year Key Finding
Weight loss produced by tesofensine in patients with Parkinson's or Alzheimer's disease. Meta-analysis of four randomized, double-blind, multicenter trials (post-hoc weight endpoint) 2008 Pooled four randomized, double-blind, multicenter trials of tesofensine (n = 740) versus placebo (n = 228) run in Parkinson's or Alzheimer's disease, not in an obesity population
Subjective and objective effects of the novel triple reuptake inhibitor tesofensine in recreational stimulant users. Randomized, double-blind, single-dose crossover human abuse-potential study 2010 Single-dose, randomized, double-blind crossover abuse-liability study in 52 recreational stimulant users, comparing tesofensine with placebo, D-amphetamine (positive control), and bupropion and atomoxetine (negative/unscheduled controls)
Expression of concern--effect of tesofensine on bodyweight loss, body composition, and quality of life in obese patients: a randomised, double-blind, placebo-controlled trial. Editorial — unsigned Expression of Concern regarding a published randomised controlled trial 2013 The Lancet issued a formal Expression of Concern about the randomised, double-blind, placebo-controlled trial of tesofensine on bodyweight loss, body composition, and quality of life in obese patients
Under-reporting of adverse effects of tesofensine. Correspondence — letter to the editor (Comment) in The Lancet 2013 The Lancet published correspondence in 2013 under the title 'Under-reporting of adverse effects of tesofensine', placing adverse-event reporting for the compound into published dispute
05

Stacking & interactions

The clinically validated pairing — co-formulated as Tesomet specifically to blunt tesofensine's heart-rate/blood-pressure signal; the beta-blocker is a safety counterweight, not a synergistic fat-loss agent.

Speculative central-appetite (monoamine) + incretin (GLP-1) combination — no trial data, additive cardiovascular and GI risk.

Speculative central-appetite + dual incretin combination — no trial data, theoretical only.

Folk "dopamine/motivation" pairing seen in community stacks — no evidence and overlapping CNS stimulation; caution.

Stacks containing Tesofensine

Dopamine & Motivation

Semax + Tesofensine + GHK-Cu
06

Sourcing

Current prices

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0.25mg

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What bloodwork do I need?

Reference ranges are general guidelines. Consult your physician for interpretation.

PRE-CYCLE
  • CMP
  • CBC
  • Lipid Panel
  • Fasting Glucose
  • Fasting Insulin
  • Blood Pressure
  • Heart Rate
  • ECG (baseline, given HR effect)
DURING CYCLE
  • Blood Pressure
  • Heart Rate
  • CMP
  • Fasting Glucose
POST-CYCLE
  • CMP
  • Lipid Panel
  • Blood Pressure
  • Heart Rate
Safety & Regulatory Status
FDA STATUS research-only
WADA STATUS Not specifically listed by name, but as a stimulant-type monoamine-reuptake inhibitor it is plausibly captured under WADA's S6 stimulants class in-competition — athletes should treat it as prohibited and confirm.

Regulatory status for Tesofensine may change. Verify current status with your jurisdiction before use. This is not legal or medical advice.

Frequently Asked Questions

What is Tesofensine?
Tesofensine (development code NS2330) is a small-molecule triple monoamine-reuptake inhibitor — it blocks reuptake of dopamine, noradrenaline and serotonin, raising synaptic levels of all three. It was originally developed for Parkinson's and Alzheimer's disease, failed in those indications, and was repurposed for obesity after trial participants lost weight. In a 203-patient Phase II obesity trial (TIPO-1, Astrup, Lancet 2008) the 0.5 mg dose produced roughly twice the weight loss of then-approved drugs. It is NOT a peptide despite living in peptide protocol libraries, and it is not FDA-approved.
How does Tesofensine work?
It is a triple monoamine-reuptake inhibitor (dopamine + noradrenaline + serotonin). By blocking the dopamine transporter (human PET data show dose-dependent striatal occupancy up to ~80%) and the noradrenaline and serotonin transporters, it increases satiety and suppresses appetite. In diet-induced obese animals it restores blunted forebrain dopamine and silences feeding-promoting GABAergic neurons in the lateral hypothalamus. A smaller part of the effect comes from increased nighttime energy expenditure and fat oxidation.
How is Tesofensine dosed?
In clinical trials the effective obesity dose was 0.5 mg once daily orally; 0.25 mg was milder and 1.0 mg added little extra weight loss but more side effects. Its half-life is extremely long (about 9 days), so the drug accumulates over weeks. These are research-derived figures, not validated medical dosing — there is no FDA-approved dose because tesofensine is not approved. Consult a clinician.
Is Tesofensine FDA-approved?
No. Tesofensine is not FDA-approved. It reached Phase II trials for obesity with strong results but a Phase III program was never completed in the US or EU, and the pivotal Lancet trial later received an Expression of Concern over under-reported adverse events. It is sold only as a research chemical in the US. A fixed-dose tesofensine/metoprolol combination (Tesomet) has been studied for rarer indications such as hypothalamic obesity.
Is Tesofensine safe? What are the main side effects?
The most consistent objective signal is a dose-dependent rise in heart rate (about +7-8 bpm at 0.5-1.0 mg/day). Blood pressure was not significantly increased versus placebo at 0.25-0.5 mg in the obesity trial, but higher doses warrant monitoring. Common side effects were dry mouth, nausea, constipation, hard stools, diarrhea and insomnia. Because it raises dopamine, noradrenaline and serotonin, mood and sleep effects (insomnia, agitation, anxiety) are mechanistically expected, and a 2013 Lancet Expression of Concern flagged that adverse effects in the pivotal trial may have been under-reported. People with cardiovascular disease, arrhythmia, uncontrolled hypertension, anxiety disorders, or who take other serotonergic/stimulant drugs should avoid it.
What does the research on Tesofensine show?
For obesity the evidence is genuine but limited: the Phase II TIPO-1 trial (Astrup, Lancet 2008, 203 patients, 24 weeks) showed placebo-subtracted weight loss of about 4.5%, 9.2% and 10.6% at 0.25, 0.5 and 1.0 mg respectively. For its original indications the evidence is negative — randomized Parkinson's trials (early and advanced disease) and an Alzheimer's proof-of-concept trial all failed to show meaningful clinical benefit. Mechanistic support comes from human PET dopamine-transporter data and animal lateral-hypothalamus studies. No Phase III obesity trial was completed, so the overall human evidence tier is moderate, not strong.

References

  1. Astrup A, Meier DH, Mikkelsen BO, et al.. Weight loss produced by tesofensine in patients with Parkinson's or Alzheimer's disease.. Obesity (Silver Spring, Md.) (2008). PMID: 18356831
  2. Schoedel KA, Meier D, Chakraborty B, et al.. Subjective and objective effects of the novel triple reuptake inhibitor tesofensine in recreational stimulant users.. Clinical pharmacology and therapeutics (2010). PMID: 20520602
  3. Expression of concern--effect of tesofensine on bodyweight loss, body composition, and quality of life in obese patients: a randomised, double-blind, placebo-controlled trial.. Lancet (London, England) (2013). PMID: 23561987
  4. Astrup A, Madsbad S, Breum L, et al.. Under-reporting of adverse effects of tesofensine.. Lancet (London, England) (2013). PMID: 23849924