A serotonin-noradrenaline-dopamine reuptake inhibitor researched for appetite suppression and obesity pharmacology.
Pre-loaded with a typical Tesofensine vial. Change any value to match what you actually have.
What published research and laboratory protocols actually document for Tesofensine. Where a compound has no single microgram figure, we say so rather than inventing one.
| Reported amount | Frequency | Route | Where this figure comes from |
|---|---|---|---|
| 250 mcg – 1 mg | once daily | oral | Astrup et al. Phase II obesity trial oral daily doses Published study arms used 0.25, 0.5, and 1.0 mg daily for 24 weeks. These are clinical-trial exposures for investigational oral drug product, not RUO use instructions. |
| 250 mcg – 500 mcg | once daily | oral | Lower clinical-research band emphasized for tolerability discussions Lower daily amounts appear in benefit-risk discussions because higher exposures increased adverse-effect burden in trial literature. |
People searching this page also look for: tesofensine peptide dosage.
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.
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.
obesity pharmacotherapy research · appetite and satiety neurobiology · monoamine transporter pharmacology · energy expenditure studies · hypothalamic feeding circuits
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.
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.
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.
The questions people actually search for, answered plainly.
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.
Primary literature on Tesofensine. Open access where available.
Every citation above was programmatically checked against the NCBI PubMed database. Titles shown are the official indexed titles, not paraphrases.
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