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Research Monograph

Tesofensine (NS2330)

Also Known AsNS2330 · NS-2330 · Tesomet

Molecular Weight402.50 g/mol
Discovered2006
Citations4 peer-reviewed
Research Areas5 domains
Background

Originally developed by NeuroSearch A/S (Denmark) as a treatment for Alzheimer's and Parkinson's disease. During phase II CNS trials, pronounced weight loss was observed as a side effect, redirecting development toward obesity. Tesofensine is a triple monoamine reuptake inhibitor that blocks presynaptic uptake of norepinephrine, dopamine, and serotonin.

Mechanisms of Action

How Tesofensine Works

01

Norepinephrine Reuptake Inhibition

Potently blocks the norepinephrine transporter (NET), increasing synaptic norepinephrine concentrations. This drives thermogenesis via beta-adrenergic receptor activation in brown adipose tissue and elevates resting metabolic rate.

NETbeta-3 adrenergic receptorUCP1
02

Dopamine Reuptake Inhibition

Inhibits the dopamine transporter (DAT), raising dopaminergic tone in mesolimbic reward circuits. This modulates food reward salience and reduces hedonic eating behavior without producing amphetamine-like euphoria at therapeutic doses.

DATD1RD2Rnucleus accumbens
03

Serotonin Reuptake Inhibition

Blocks the serotonin transporter (SERT), enhancing serotonergic signaling in hypothalamic appetite centers. Increased 5-HT2C receptor activation in the arcuate nucleus promotes POMC neuron firing and suppresses appetite.

SERT5-HT2C receptorPOMC neuronsarcuate nucleus
04

Sympathetic Nervous System Activation

The combined monoamine reuptake inhibition produces a net sympathomimetic effect that increases energy expenditure through enhanced sympathetic outflow, elevated heart rate variability, and diet-induced thermogenesis amplification.

sympathetic nervous systembrown adipose tissuehypothalamic thermoregulation
Evidence-Graded Research Areas

Published Research

Strong
Moderate
Emerging
Preclinical

Obesity & Weight Management

Strong

The TIPO-1 and TIPO-2 phase II trials demonstrated dose-dependent weight loss of 6.5-12.8% over 24 weeks in obese subjects. The 0.5 mg dose produced approximately double the weight loss of sibutramine (comparator). Reductions in waist circumference, visceral fat, and fasting insulin were also observed.

Appetite Suppression & Satiety

Strong

Clinical data indicate a reduction in self-reported hunger scores and 24-hour energy intake by approximately 26% at the 0.5 mg dose. The mechanism is attributed to combined dopaminergic reward modulation and serotonergic hypothalamic signaling rather than a single neurotransmitter pathway.

Metabolic Rate Enhancement

Moderate

Indirect calorimetry in phase II subjects showed a 6% increase in resting energy expenditure relative to placebo. The thermogenic effect is primarily attributed to norepinephrine-mediated brown adipose tissue activation and sympathetic drive.

Neurodegenerative Disease

Moderate

Early phase II data in Alzheimer's disease (LENNART trial) showed improved cognitive scores on ADAS-Cog at 14 weeks. Parkinson's disease models showed preserved dopaminergic neuron integrity in 6-OHDA-lesioned rats. Development for CNS indications was deprioritized after the weight-loss findings.

Glycemic Control

Emerging

Secondary endpoints in obesity trials demonstrated improved fasting glucose, reduced HbA1c, and enhanced insulin sensitivity (HOMA-IR improvements) proportional to weight loss. The metabolic benefit appears largely weight-loss-mediated rather than a direct insulin-sensitizing mechanism.

Safety Profile

Phase II trials reported dose-dependent increases in heart rate (mean 7.4 bpm at 0.5 mg) and modest blood pressure elevation. Commonly reported adverse events included dry mouth, insomnia, constipation, and nausea. No serious cardiovascular events were reported in trial populations. Abuse liability assessments categorize tesofensine below Schedule II stimulants.

Handling & Storage

Tesofensine is supplied as an oral capsule form. Store at controlled room temperature (15-25°C) in the original container, protected from light and moisture. No reconstitution required.

References & Citations

Peer-Reviewed Literature

  1. 1

    Effect of tesofensine on bodyweight loss, body composition, and quality of life in obese patients: a randomised, double-blind, placebo-controlled trial

    Astrup A, Madsbad S, Breum L, et al.

    The Lancet, 2008PubMed 18996591DOI
  2. 2

    Tesofensine, a novel triple monoamine reuptake inhibitor, induces appetite suppression by indirect stimulation of alpha1 adrenoceptor and dopamine D1 receptor pathways in the diet-induced obese rat

    Axel AM, Mikkelsen JD, Hansen HH.

    Neuropsychopharmacology, 2010PubMed 20072117DOI
  3. 3

    The effect of the triple monoamine reuptake inhibitor tesofensine on energy metabolism and appetite in overweight and moderately obese men

    Sjödin A, Gasteyger C, Nielsen AL, et al.

    International Journal of Obesity, 2010PubMed 20440296DOI
  4. 4

    Tesofensine induces appetite suppression and weight loss with reversal of low forebrain dopamine levels in the diet-induced obese rat

    Hansen HH, Hansen G, Tang-Christensen M, et al.

    Pharmacology Biochemistry and Behavior, 2010PubMed 20599552DOI
Frequently Asked Questions

Tesofensine FAQ

What is tesofensine?

Tesofensine is a triple monoamine reuptake inhibitor originally developed for neurodegenerative diseases. It blocks the presynaptic reuptake of norepinephrine, dopamine, and serotonin. Phase II clinical trials demonstrated significant weight loss in obese subjects, making it one of the most potent anti-obesity compounds studied in clinical settings.

How does tesofensine differ from other weight-loss compounds?

Unlike single-target agents, tesofensine simultaneously modulates three neurotransmitter systems. This triple mechanism addresses appetite reduction (serotonin), food reward modulation (dopamine), and thermogenesis (norepinephrine) concurrently, which may explain the greater magnitude of weight loss observed compared to single-mechanism comparators.

What were the key clinical trial results?

In the phase II TIPO-1 trial published in The Lancet (2008), the 0.5 mg dose produced a mean weight loss of approximately 12.8% over 24 weeks, compared to 2.2% for placebo. This was accompanied by reductions in waist circumference, improvements in lipid profiles, and enhanced insulin sensitivity.

What is the purity of G26x Peptides tesofensine?

Our tesofensine is supplied at 99%+ purity, independently verified by Janoshik Analytical with a full Certificate of Analysis (COA) available for each batch.

How should tesofensine be stored?

Store at controlled room temperature (15-25°C) in the original container, protected from light and moisture. Tesofensine is chemically stable in capsule form and does not require refrigeration or reconstitution.

Available for Research

Tesofensine Products

All compounds 99%+ purity, verified by Janoshik Analytical. GMP-manufactured lyophilized powder.

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Oral Capsules
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Tesofensine 500mcg

500mcg × 60 Capsules

The appetite killer that boosts your mood — blocks reuptake of three feel-good neurotransmitters, eliminating hunger while giving you energy and focus. Oral, no injection.

  • Twice as effective as current weight loss drugs in clinical trials
  • Works through dopamine/serotonin/norepinephrine — triple reuptake
$182.99
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Disclaimer: This monograph is provided for educational and research purposes only. G26x Peptides products are sold exclusively as research chemicals. They are not intended for human consumption, therapeutic use, or as dietary supplements. All research should be conducted in compliance with applicable laws and institutional review board protocols. Information presented here is sourced from published peer-reviewed literature and does not constitute medical advice.