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    Research Use Only (RUO). For laboratory research only. Not for human or veterinary use.

    Research Use Only (RUO):Research classification with product and batch documentation where available.
    TESOFENSIN 500 mcg - Avenor Peptides

    Weight & Metabolism

    TESOFENSIN

    Strength: 500 mcg

    Tesofensin is studied around appetite and body weight, but it works differently from the GLP-1 compounds: it acts in the brain, on the signals that regulate hunger. It is a pill, not a peptide.

    €114,00
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    Batch documentationShips from Greece

    Free shipping: Greece from €50, Cyprus and Bulgaria from €100, France, Germany, Italy, Belgium, Netherlands and Spain from €200. Details

    This product is intended exclusively for laboratory research use. It is not intended for human consumption, diagnosis, treatment, or prevention of disease.

    Product information

    FormOral form
    Strength500 mcg
    SKUAVR-TESO-500MCG
    Stock statusIn stock
    COA / BatchSee the documentation state below
    StorageRefer to the label and available documentation details.
    Packaging / shippingControlled shipping preparation according to the available SKU variant.

    Documentation on request

    There is no published document for this specific SKU variant at the moment.

    Contact us about documentation

    Research overview

    What it is researched for

    Research focuses on topics such as:

    • appetite and feeling full
    • body-weight regulation
    • the brain's hunger signals

    Areas of research — not a promise of results.

    How this category is positioned

    The GLP-1 compounds press a "switch" in the gut. Tesofensin works higher up, in the brain. Same research topic, an entirely different route.

    Documentation & COA

    Batch documentation and COA, where available, are linked to the specific product batch and SKU.

    This product is intended exclusively for laboratory research use. It is not intended for human consumption, diagnosis, treatment, or prevention of disease.

    Product profile

    3

    monoamine transporters at once — norepinephrine, dopamine, serotonin

    ~234 hours

    half-life estimated in a population model (Lehr et al., 2007)

    18–77%

    dopamine transporter occupancy measured by PET (Appel et al., 2013)

    ≥98%

    active substance purity by HPLC

    Research context

    What it is

    Tesofensine is not a peptide. It is a small molecule that acts on the brain.

    It began as an experimental drug for neurological conditions. It failed there — but volunteers were losing weight. So it changed course.

    The technical detail

    Development code NS-2330. A reuptake inhibitor of three neurotransmitters: noradrenaline, dopamine and serotonin.

    How it works

    In the brain, three chemical messengers help set how hungry we feel.

    Tesofensine blocks their 'recycling', so they stay active longer. The satiety signal strengthens and appetite drops.

    The technical detail

    In 2024 it was shown to silence specific GABAergic neurons of the lateral hypothalamus, reducing the drive to eat (Perez et al., PLoS One).

    What the research shows today

    The pivotal study remains the 2008 phase II trial in the Lancet, with 203 participants.

    In 2022 a combination with a heart-rate agent was tested in a rare obesity caused by hypothalamic injury, adding further weight loss.

    −9.2%

    weight, wk 24, Lancet 2008

    +7.4

    beats/min (mid dose)

    203

    participants, phase II

    2008

    last large trial

    The loss was nearly double that of the drugs approved at the time — but the phase III for general obesity was never completed.

    What you should know

    The Lancet authors themselves kept a reservation: the findings need confirmation in phase III. That was never done for general obesity.

    There is a cardiovascular signal: at the mid dose heart rate rose by 7.4 beats per minute.

    It is sold online as a 'supplement', but it is a prohibited substance in sport (WADA, class S6).

    The technical detail

    Astrup et al., Lancet, 2008 (TIPO-1 trial); Tesomet combination, Huynh et al., 2022; urinary detection, Krug et al., 2026.

    Laboratory use

    Used in a controlled laboratory setting for in vitro inhibition studies at the dopamine (DAT), norepinephrine (NET) and serotonin (SERT) transporters, for comparative work against selective reuptake inhibitors, for structural and computational binding studies at the dopamine transporter, for LC-MS analytical method development and metabolite identification work, and for identity and purity confirmation by HPLC and mass spectrometry.

    Research Use Only — For laboratory research exclusively. Tesofensin is NOT approved as a medicine by the European Medicines Agency (EMA), the FDA, or the Greek National Organisation for Medicines (EOF). It is not a medicinal product, a dietary supplement, or a food. It is not intended for human or veterinary use, nor for the diagnosis, treatment, prevention or mitigation of any disease or condition. No dosing, protocols or administration guidance are provided. This is a psychoactive molecule with documented dose-dependent effects on heart rate and blood pressure; its development has not progressed beyond Phase II. It is listed under class S6 (stimulants) on the World Anti-Doping Agency's Prohibited List. The study data referenced here are presented for scientific information only and do not transfer to any non-research use. Sale is intended for research institutions and laboratories only.

    Structural data

    Class
    Triple monoamine reuptake inhibitor — norepinephrine, dopamine, serotonin
    Molecule type
    Small synthetic molecule (not a peptide), a tropane derivative
    Molecular formula
    C17H23Cl2NO
    Molecular weight
    ≈328.28 g/mol
    Development code
    NS-2330 (NeuroSearch A/S)
    ChEMBL identifier
    CHEMBL3989690
    InChIKey
    VCVWXKKWDOJNIT-ZOMKSWQUSA-N
    Naming stem (USAN)
    -fensine — designates a norepinephrine, serotonin and dopamine reuptake inhibitor
    Stereochemistry
    Single stereoisomer (four stereogenic centres)
    Development stage in the literature
    Reached Phase II; no completed Phase III programme
    Product form
    Oral capsule in sealed packaging
    Purity
    ≥98% (HPLC) — supplied with CoA

    Comparison

    Feature comparison

    FeatureTesofensin (this product)SemaglutideOrforglipron
    Where it actsIn the brain — blocks monoamine transporters at the synaptic cleftAt GLP-1 receptors (pancreas, gut, brain)At GLP-1 receptors
    MechanismTriple reuptake inhibition of norepinephrine, dopamine and serotoninGLP-1 receptor agonist (incretin pathway)GLP-1 receptor agonist (incretin pathway)
    Chemical natureSmall molecule, a tropane derivative (~328 g/mol)A 31-amino-acid peptideNon-peptide small molecule
    Route in the literatureOralMainly injectable (an oral form also exists)Oral
    Maturity of the evidenceReached Phase II — no completed Phase III programmeCompleted Phase III programmePhase III programme ongoing
    Recorded adverse-effect profileDose-dependent increases in heart rate and blood pressure; dry mouth, insomnia, nausea, mood changesPredominantly gastrointestinal (nausea, vomiting, diarrhoea)Predominantly gastrointestinal
    Regulatory statusNo EMA/FDA/EOF approval; listed under WADA class S6 stimulantsAn approved medicinal product in many countriesUnder regulatory evaluation
    Product formOral capsuleLyophilized powderCapsule / tablet

    Storage & handling

    • Capsules are stored at room temperature (approximately 15–25 °C) in a dry place.
    • Keep in the original sealed packaging until the point of laboratory use — refrigeration is not required.
    • Avoid exposure to humidity, direct sunlight and heat sources.
    • Avoid large temperature swings, which can affect the integrity of the capsule shell.
    • Handle using standard laboratory practice and appropriate personal protective equipment.
    • Keep away from children, out of food preparation areas, and in a clearly labelled container so it cannot be confused with a medicinal product.

    Documentation

    • Certificate of Analysis (CoA) per batch, with date and lot number.
    • Active substance purity analysis by HPLC — specification ≥98%.
    • Identity and molecular weight confirmation by mass spectrometry.
    • Research Use Only (RUO) declaration on the packaging.
    • Documents available on request for the specific batch you received.

    References

    References & documentation

    1. 1.Lehr T. et al. (2007). Population pharmacokinetic modelling of NS2330 (tesofensine) and its major metabolite in patients with Alzheimer's disease. Br J Clin Pharmacol, 64(1), 36-48.
    2. 2.Rascol O. et al. (2008). Tesofensine (NS 2330), a monoamine reuptake inhibitor, in patients with advanced Parkinson disease and motor fluctuations: the ADVANS Study. Arch Neurol, 65(5), 577-583.
    3. 3.Astrup A. et al. (2008). Weight loss produced by tesofensine in patients with Parkinson's or Alzheimer's disease. Obesity (Silver Spring), 16(6), 1363-1369.
    4. 4.Astrup A. et al. (2008). Effect of tesofensine on bodyweight loss, body composition, and quality of life in obese patients: a randomised, double-blind, placebo-controlled trial. Lancet, 372(9653), 1906-1913. [See also Expression of Concern, Lancet 2013;381(9873):1167, and Astrup A. et al., Under-reporting of adverse effects of tesofensine, Lancet 2013;382(9887):127.]
    5. 5.Doggrell S.A. (2009). Tesofensine — a novel potent weight loss medicine. Expert Opin Investig Drugs, 18(7), 1043-1046.
    6. 6.Bello N.T. & Zahner M.R. (2009). Tesofensine, a monoamine reuptake inhibitor for the treatment of obesity. Curr Opin Investig Drugs, 10(10), 1105-1116. (PMID: 19777399 — no DOI available)
    7. 7.Axel A.M. et al. (2010). 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. Neuropsychopharmacology, 35(7), 1464-1476.
    8. 8.Schoedel K.A. et al. (2010). Subjective and objective effects of the novel triple reuptake inhibitor tesofensine in recreational stimulant users. Clin Pharmacol Ther, 88(1), 69-78.
    9. 9.Bentzen B.H. et al. (2013). Anti-hypertensive treatment preserves appetite suppression while preventing cardiovascular adverse effects of tesofensine in rats. Obesity (Silver Spring), 21(5), 985-992.
    10. 10.Hansen H.H. et al. (2013). Tesofensine induces appetite suppression and weight loss with reversal of low forebrain dopamine levels in the diet-induced obese rat. Pharmacol Biochem Behav, 110, 265-271.
    11. 11.Appel L. et al. (2013). Tesofensine, a novel triple monoamine re-uptake inhibitor with anti-obesity effects: dopamine transporter occupancy as measured by PET. Eur Neuropsychopharmacol, 24(2), 251-261.
    12. 12.Perez C.I. et al. (2024). Tesofensine, a novel antiobesity drug, silences GABAergic hypothalamic neurons. PLoS One, 19(4), e0300544.
    13. 13.Li Y. et al. (2025). Structural basis for pharmacotherapeutic action of triple reuptake inhibitors. Nat Commun, 17(1), 61.
    14. 14.Krug O., Thomas A. & Thevis M. Investigations Into the Metabolism and Elimination of Tesofensine in Human Urine. Drug Test Anal.

    Category comparison

    Not sure which GLP-1 to choose?

    See the comparison

    Product information

    Frequently asked questions

    What does "triple monoamine reuptake inhibitor" mean?
    It means the molecule simultaneously blocks three transporter proteins at the synapse: the norepinephrine, dopamine and serotonin transporters. These transporters normally clear neurotransmitters back into the neuron. When they are blocked, all three neurotransmitters linger longer in the synapse. This is a mechanism that acts in the brain, not in the gut or the pancreas.
    How does it differ from GLP-1 molecules such as semaglutide?
    Fundamentally, on three levels. First, chemically: tesofensin is a small tropane molecule of ~328 g/mol, whereas semaglutide is a 31-amino-acid peptide. Second, mechanistically: GLP-1 molecules activate a hormone receptor in the incretin system; tesofensin blocks neurotransmitter transporters in the brain. Third, in terms of evidence: semaglutide has a completed Phase III programme and regulatory approvals, while tesofensin reached Phase II and holds no approval anywhere. These are not two versions of the same thing.
    What safety concerns are recorded in the literature?
    The principal concern is cardiovascular. The meta-analysis by Astrup and colleagues (Obesity, 2008), covering 740 participants, recorded a dose-dependent heart rate increase of up to 6.8 beats per minute relative to placebo. Subsequent reports also recorded significant blood pressure increases at the higher arms. Doggrell's evaluation (2009) additionally listed nausea, dry mouth, flatulence, insomnia and depressed mood, and called for further tolerability assessment. Beyond that, The Lancet published an expression of concern in 2013 regarding the 2008 Phase II trial, along with a letter titled "Under-reporting of adverse effects of tesofensine". These form part of the molecule's published record.
    Why was it originally developed for Alzheimer's and Parkinson's disease?
    Because both conditions involve loss of monoaminergic signalling, dopaminergic in particular. The hypothesis was that a molecule boosting all three monoamines might offset part of that loss. The programme advanced to Phase II trials — ADVANS by Rascol and colleagues (Arch Neurol, 2008) in advanced Parkinson's disease, and a 14-week study in 320 patients with Alzheimer's disease. Ultimately, as Bello and Zahner summarise (2009), the compound did not prove effective in those indications.
    How did it end up being studied in the body-weight field?
    As a side effect. Participants in the neurological trials showed unintended weight loss. Astrup and colleagues (Obesity, 2008) pooled four of those trials — 740 people on the compound, 228 on placebo — and demonstrated a statistically significant dose-dependent change in body weight over 14 weeks, with no dietary programme attached. That finding is what redirected the research.
    What did the imaging studies show?
    The PET study by Appel and colleagues (Eur Neuropsychopharmacol, 2013), using the [11C]βCIT-FE tracer, measured striatal dopamine transporter occupancy and found it varied dose-dependently between 18% and 77%. It is one of the few cases where the mechanism was confirmed directly in humans rather than inferred.
    Why is the half-life so long?
    The population pharmacokinetic model of Lehr and colleagues (Br J Clin Pharmacol, 2007) estimated a half-life of approximately 234 hours for the parent compound and 374 hours for the principal metabolite M1, arising from low apparent clearance combined with a large apparent volume of distribution. That is days rather than hours — which bears directly on how any laboratory study is designed.
    Is there recent mechanistic work?
    Yes. Perez and colleagues (PLoS One, 2024) showed the compound silences a subset of GABAergic neurons in the lateral hypothalamus, with a greater effect in obese than in lean rats. Li and colleagues (Nat Commun, 2025) resolved by cryo-electron microscopy the structure of the dopamine transporter bound to the molecule, showing it stabilises the transporter in an outward-facing conformation.
    What is the regulatory status of the molecule?
    It has not been approved by the EMA, the FDA or the Greek EOF, and it is not a medicinal product. ChEMBL records it at a maximum development phase of 2. It is additionally classified under class S6 (stimulants) on the World Anti-Doping Agency's Prohibited List and is banned in-competition (Krug et al., Drug Test Anal). That same paper notes it has been marketed online as a "dietary supplement" — a practice with no regulatory basis at all.
    Can it be used by humans or animals?
    No. The product is supplied exclusively for laboratory research. It is not intended for human or veterinary use, nor for in vivo application outside a controlled laboratory setting. No administration guidance, dosing or protocols are provided. Given the psychoactive nature of the molecule and its documented cardiovascular profile, this restriction is absolute.
    Do I receive a certificate of analysis?
    Yes. Every batch is accompanied by a CoA with HPLC purity analysis and mass spectrometry identity confirmation. It is available on request for the specific batch you received.