Triple monoamine reuptake inhibitor (small molecule)

Tesofensine

A serotonin-noradrenaline-dopamine reuptake inhibitor researched for appetite suppression and obesity pharmacology.

Also referred to as: NS2330, triple monoamine reuptake inhibitor
Research use only. This page summarizes published scientific literature. It is not medical advice, not a recommendation, and not a claim that this compound treats, cures or prevents any condition. Nothing here is a suggestion to use it.

What Tesofensine is

Tesofensine (NS2330) is an oral small-molecule triple monoamine reuptake inhibitor that blocks presynaptic reuptake of serotonin, noradrenaline, and dopamine. It was originally explored in neurodegenerative indications and later redirected toward obesity after notable weight-loss signals emerged. A key randomized Phase II trial in adults with obesity reported dose-dependent weight reduction over 24 weeks, with additional human work on appetite and energy expenditure.

Mechanistic studies in diet-induced obese rodents link appetite suppression to indirect monoaminergic receptor pathways and restoration of low forebrain dopamine tone. More recent neuroscience work has examined hypothalamic GABAergic neuron silencing as part of its anti-obesity pharmacology.

Critical compliance note: tesofensine is not a peptide. Research-grade tesofensine is Research Use Only, is not an FDA-approved obesity drug product, and is not for human consumption. Clinical-trial mg amounts below are educational references to published studies, not instructions for use. Research chemical supply is not the same as a licensed medicine.

The record for Tesofensine spans both animal work and human trials. Those two kinds of evidence do not carry equal weight, and the amounts below come from different settings.

How it works

Tesofensine inhibits the serotonin transporter (SERT), norepinephrine transporter (NET), and dopamine transporter (DAT). Elevated synaptic monoamines influence hypothalamic and mesolimbic circuits that govern appetite, satiety, and reward valuation of food. Preclinical data implicate alpha-1 adrenergic and dopamine D1 pathway contributions to feeding suppression, while human studies show appetite reduction with a modest energy-expenditure component at studied oral doses.

The research context

Obesity pharmacologists, appetite-neurobiology labs, and monoamine-transporter chemistry groups are the main audience. It is often used as a benchmark oral central appetite suppressant when comparing newer anti-obesity mechanisms.

What the research examines

obesity pharmacotherapy researchappetite and satiety neurobiologymonoamine transporter pharmacologyenergy expenditure studieshypothalamic feeding circuits

Each tag marks a field where this compound appears in research. Appearing in a literature is not the same as working.

How it appears in the literature

Reported research amounts. These describe what was studied, not what anyone should do.

Research contextReported amountFrequencyRoute
Astrup et al. Phase II obesity trial oral daily doses250 mcg – 1 mgonce dailyoral
Lower clinical-research band emphasized for tolerability discussions250 mcg – 500 mcgonce dailyoral
See the full Tesofensine dosage chart, reconstitution math and calculator →

Handling & storage

Store solid research material tightly closed, dry, and protected from light at the supplier-recommended temperature. If dissolved for analytical work, prepare fresh standards or validated aliquots; this is a small molecule, not a reconstituted injectable peptide in clinical literature.

Notes on combined research

Published research usually evaluates tesofensine as monotherapy against placebo or standard care contexts rather than as part of injectable peptide stacks. Comparative frameworks versus GLP-1 agonists are conceptual (central appetite suppression versus incretin pathways), not established co-administration recipes.

Tesofensine questions

The landmark Phase II obesity trial studied 0.25-1.0 mg orally once daily. Those values describe investigational clinical research, not instructions for research-chemical use.

No. It is a small-molecule triple monoamine reuptake inhibitor. It appears in adjacent obesity-education content because researchers compare multiple anti-obesity mechanisms side by side.

No. Research-grade material is RUO and not for human consumption. It is not a substitute for any approved obesity medication.

By increasing synaptic serotonin, noradrenaline, and dopamine through reuptake inhibition, which alters central feeding and reward circuits. Animal data also point to specific adrenergic and dopamine receptor contributions.

Astrup et al. reported dose-dependent weight loss over 24 weeks with changes in body composition and quality-of-life measures versus placebo, alongside dose-related adverse effects.

Early development targeted neurologic indications such as Alzheimer's and Parkinson's disease before weight-loss signals prompted obesity-focused research.

Clinical literature uses oral dosing. Laboratory handling of research chemical powder follows analytical/small-molecule SOP, which is not the same as bacteriostatic-water reconstitution practices used for lyophilized peptides.

Read the research yourself

Each citation was checked against PubMed before it went on this page. If we cannot link it, we do not claim it.

Reference information only. The values below summarize amounts reported in published research literature and laboratory protocol discussions. They are not dosing recommendations, not medical advice, and not instructions for use in humans. All compounds referenced are for laboratory research use only and are not for human consumption.