Tesofensine Research & Scientific Overview

Jump to: Structure | Mechanism | Studies | Pharmacokinetics | Protocols | Limitations | Lead Researcher | References

Tesofensine Molecular Structure & Chemical Properties

Tesofensine represents a novel triple monoamine reuptake inhibitor that has generated significant scientific interest since its initial development for neurodegenerative diseases revealed unexpected weight loss effects. Originally investigated for Alzheimer’s and Parkinson’s disease treatment in the early 2000s, tesofensine demonstrated limited efficacy for these neurological conditions but produced consistent weight loss as an unintended effect, particularly in overweight and obese participants. This observation prompted a strategic research pivot toward obesity pharmacotherapy, where tesofensine has demonstrated weight loss magnitudes approximately double those of previously approved anti-obesity medications in Phase II clinical trials. Unlike most appetite suppressants that act through single pathways, tesofensine’s simultaneous inhibition of norepinephrine, dopamine, and serotonin reuptake transporters creates a distinctive pharmacological profile with potential advantages for metabolic regulation and body weight control.

Chemical Structure

[IMAGE PLACEHOLDER] Insert 2D chemical structure image here Image URL: https://pubchem.ncbi.nlm.nih.gov/image/imgsrv.fcgi?cid=11370864&t=l Alt text: Tesofensine molecular structure diagram showing phenyltropane derivative Source credit: PubChem Position: Center-aligned below heading

2D molecular structure (Source: PubChem)

Technical Specifications

Tesofensine belongs to the phenyltropane class of compounds, characterized by a bicyclic tropane structure with a dichlorophenyl substituent. This structural configuration provides high affinity for monoamine transporters while conferring exceptional metabolic stability, resulting in the compound’s remarkably long plasma half-life compared to other reuptake inhibitors.

Tesofensine Mechanism of Action

Tesofensine exerts its biological effects through potent inhibition of presynaptic monoamine reuptake transporters, simultaneously blocking norepinephrine, dopamine, and serotonin reuptake. This triple monoamine reuptake inhibitor mechanism distinguishes tesofensine from single-target appetite suppressants and creates synergistic effects on appetite regulation, energy expenditure, and metabolic function. Current research indicates that tesofensine’s weight loss effects result from both reduced food intake through appetite suppression and potentially increased energy expenditure, though the relative contributions of these mechanisms continue to be investigated.

Primary Pharmacological Mechanisms

Norepinephrine Transporter Inhibition – Primary Appetite Suppression

Research has demonstrated that tesofensine exhibits highest affinity for the norepinephrine transporter (NET) with an IC50 of 1.7 nM, making NET inhibition the most potent component of its mechanism[1]. Norepinephrine transporter blockade produces:

• Enhanced alpha-1 adrenergic receptor stimulation in hypothalamic feeding centers
• Increased satiety signaling and reduced hunger perception
• Modulation of sympathetic nervous system activity affecting metabolic rate
• Potential thermogenic effects through noradrenergic pathways

Pharmacological studies in diet-induced obese rats revealed that tesofensine-induced appetite suppression was almost completely reversed by alpha-1 adrenoceptor antagonists, demonstrating the critical role of noradrenergic pathways in its hypophagic effects[2].

Serotonin Transporter Inhibition – Satiety Enhancement

Tesofensine inhibits the serotonin transporter (SERT) with an IC50 of 11 nM, contributing to enhanced serotonergic neurotransmission[3]. Serotonin pathway modulation affects:

• Satiety signaling in the hypothalamus and brainstem
• Meal size reduction and increased inter-meal intervals
• Mood regulation, potentially reducing emotional eating behaviors
• Synergistic effects with noradrenergic pathways on appetite control

Unlike selective serotonin reuptake inhibitors used as antidepressants, tesofensine’s combined monoamine effects produce more robust metabolic outcomes relevant to weight management.

Dopamine Transporter Inhibition – Reward and Motivation Pathways

Although tesofensine exhibits lower affinity for the dopamine transporter (DAT) with an IC50 of 65 nM, dopaminergic modulation contributes to its overall effects[4]:

• Dopamine D1 receptor pathway activation involved in appetite suppression
• Modulation of reward circuitry affecting food motivation and palatability
• Potential enhancement of physical activity motivation
• Influence on hedonic aspects of eating behavior

Importantly, tesofensine’s relatively weaker dopamine reuptake inhibition compared to norepinephrine and serotonin may contribute to its lower abuse potential compared to traditional stimulants, as dopamine transporter inhibition is considered the primary mediator of stimulant reinforcement.

Lateral Hypothalamus Neuronal Modulation

Recent neurophysiological investigations have revealed that tesofensine silences GABAergic neurons in the lateral hypothalamus, a critical brain region regulating feeding behavior[5]. This mechanism involves:

• Reduced activity of hunger-promoting GABAergic neuronal populations
• Altered neuronal ensemble activity patterns associated with feeding
• Differential effects in obese versus lean animals, with greater efficacy in obesity
• Direct central nervous system effects on appetite circuitry

Metabolic Effects Beyond Appetite Suppression

Emerging research suggests tesofensine may influence energy expenditure independently of reduced food intake[6]:

• Possible increases in resting energy expenditure through thermogenic pathways
• Modulation of metabolic rate via central sympathetic nervous system activation
• Effects on substrate utilization and fat oxidation
• Preservation of lean body mass during weight loss compared to caloric restriction alone

[CALLOUT BOX – Highlighted] Key Mechanistic Insight: Tesofensine’s triple monoamine reuptake inhibition creates a unique pharmacological profile distinct from single-target compounds. The relative selectivity for norepinephrine over serotonin and dopamine transporters may explain its robust efficacy while potentially reducing certain side effects associated with more balanced monoamine inhibitors. [END CALLOUT BOX]

Tesofensine Research Applications & Key Findings

Obesity Management Research

Human Clinical Trials – Weight Loss Efficacy

The landmark Phase IIb TIPO-1 trial published in The Lancet established tesofensine’s weight loss potential in obese individuals[7]. In this randomized, double-blind, placebo-controlled study involving 203 obese patients, key findings included:

• Dose-dependent weight loss: 0.25 mg produced 4.5%, 0.5 mg produced 9.2%, and 1.0 mg produced 10.6% placebo-subtracted weight loss over 24 weeks
• Weight loss with 0.5 mg and 1.0 mg doses approximately double that of previously approved obesity medications (sibutramine, rimonabant)
• Mean absolute weight loss of 11.3 kg (approximately 25 pounds) with 0.5 mg dose
• 32% of patients in the 1.0 mg group achieved greater than or equal to 10% weight loss

These results represented a significant advancement over existing pharmacological options available at the time of publication, though subsequent regulatory and safety considerations affected development trajectory.

Body Composition Changes

Beyond total weight loss, tesofensine research has examined effects on body composition[8]:

• Primary weight loss from fat mass reduction with relative preservation of lean body mass
• DEXA scan analyses showing preferential fat tissue loss
• Waist circumference reductions correlating with fat mass changes
• Maintenance of muscle tissue better than pure caloric restriction alone

Extension Studies and Long-Term Weight Maintenance

The 48-week TIPO-4 extension trial investigated longer-term tesofensine effects[9]:

• Sustained weight loss maintained beyond initial 24-week treatment period
• Patients continuing tesofensine 0.5 mg showed total mean weight loss of 13-14 kg over 48 weeks
• Previous placebo patients lost approximately 9 kg in first 24 weeks of tesofensine treatment
• Demonstrated potential for sustained weight management with continued treatment

Neurological Disease Research

Parkinson’s and Alzheimer’s Disease Investigations

Tesofensine was originally developed for neurodegenerative conditions, where meta-analyses revealed unintended weight loss effects[10]:

• Four randomized trials in Parkinson’s and Alzheimer’s disease patients showed dose-dependent weight reduction
• Weight loss of 0.5% to 2.8% in general population at various doses without dietary intervention
• In obese subgroup, weight changes ranged from 1.5% to 3.7% reduction
• 32.1% of obese patients on 1.0 mg achieved greater than or equal to 5% weight loss over 14 weeks
• Limited efficacy for cognitive or motor symptoms led to discontinuation for these indications

These initial trials provided the first clinical evidence of tesofensine’s metabolic effects and informed subsequent obesity-focused development.

Appetite and Satiety Research

Appetite Sensation Measurements

Investigations into tesofensine’s effects on subjective appetite have revealed important mechanistic insights[11]:

• Enhanced composite satiety scores measured by visual analogue scales
• Reduced feelings of hunger and prospective food consumption
• Increased satiety and fullness sensations during early treatment phases
• Some tolerance development to appetite effects after 24 weeks, though weight loss continued

These findings suggest tesofensine’s weight loss mechanisms may extend beyond simple appetite suppression to include metabolic effects.

Feeding Behavior Modifications

Animal studies using automated food intake monitoring systems demonstrated[12]:

• Dose-dependent reduction in nocturnal food intake in diet-induced obese rats
• ED50 of 1.3 mg/kg for food intake suppression
• Decreased meal size and increased latency to first meal
• No significant tolerance to hypophagic effects in rodent models

Cardiovascular and Metabolic Parameter Research

Blood Pressure and Heart Rate Effects

Clinical trials consistently documented cardiovascular effects requiring careful monitoring[13]:

• Dose-dependent increases in heart rate of 5-8 beats per minute with therapeutic doses
• Systolic blood pressure increases of 1-3 mmHg with 0.25-0.5 mg doses
• Higher doses (1.0 mg) produced more pronounced cardiovascular effects
• These findings necessitated cardiovascular safety assessments in development programs

Metabolic Parameters

Research has examined tesofensine’s effects on obesity-related metabolic factors[14]:

• Improvements in insulin sensitivity markers in some studies
• Changes in lipid profiles associated with weight loss
• Potential effects on glucose homeostasis
• Metabolic improvements consistent with weight reduction magnitude

Specialized Populations Research

Prader-Willi Syndrome and Hypothalamic Obesity

Recent clinical development has focused on rare genetic obesity conditions[15]:

• FDA orphan drug designation granted for tesofensine/metoprolol combination in Prader-Willi syndrome (2021)
• Additional orphan drug designation for hypothalamic obesity (2021)
• Combination with metoprolol designed to mitigate cardiovascular effects
• Phase II trials investigating efficacy and safety in these specialized populations

[CALLOUT BOX – Highlighted] Critical Research Limitation: Despite promising Phase II obesity trial results, tesofensine has not completed Phase III clinical development or received regulatory approval for obesity treatment. Long-term efficacy and safety data from large-scale trials remain absent. All human weight loss data comes from relatively short-duration studies (24-48 weeks maximum) in limited patient populations. [END CALLOUT BOX]

Tesofensine Pharmacokinetics & Metabolism

Absorption & Distribution

Tesofensine exhibits distinctive pharmacokinetic properties characterized by extensive absorption and exceptionally prolonged systemic exposure[16]. Following oral administration in human subjects:

• High bioavailability with reliable absorption from the gastrointestinal tract
• Oral administration produces predictable systemic exposure
• Distribution throughout body tissues including central nervous system penetration
• Steady-state plasma concentrations achieved after approximately 2-3 weeks of daily dosing due to long half-life

The compound’s lipophilic nature and structural characteristics facilitate blood-brain barrier penetration, essential for its central nervous system-mediated effects on appetite regulation.

Metabolism & Elimination

Tesofensine undergoes hepatic metabolism primarily through cytochrome P450 3A4 (CYP3A4) pathways[17]. Key metabolic features include:

• Primary metabolite M1 (NS2360) formed by N-dealkylation
• M1 is the only metabolite detectable in human plasma at significant concentrations
• M1 exhibits similar qualitative pharmacological profile to parent compound
• M1 demonstrates even longer half-life (approximately 374 hours) than tesofensine
• M1 contributes approximately 6% of tesofensine’s overall activity based on relative potency and exposure

The remarkably long half-lives of both parent compound and metabolite create unique pharmacokinetic considerations for dosing schedules and discontinuation, with effects potentially persisting for weeks after treatment cessation.

Excretion Pathways

Elimination of tesofensine and its metabolites occurs through multiple routes[18]:

• Renal excretion plays minor role (approximately 15-20% of clearance)
• Hepatic metabolism represents primary clearance mechanism
• Fecal elimination likely contributes to overall clearance
• No significant accumulation beyond steady-state observed in clinical studies
• Extended washout periods required between treatment phases due to prolonged half-life

The pharmacokinetic profile’s extended duration offers potential advantages for once-daily dosing and steady therapeutic effects, but also requires consideration for side effect management and treatment discontinuation.

Tesofensine Research Protocols & Administration

Dosing in Published Research

Research investigations have employed tesofensine doses ranging from 0.125 mg to 1.0 mg daily in human studies, with animal research using weight-adjusted dosing:

• Human obesity trials: 0.25 mg, 0.5 mg, and 1.0 mg once daily
• Optimal clinical dose: 0.5 mg once daily identified as best efficacy-to-safety ratio
• Rat models: 0.5-3 mg/kg (subcutaneous); ED50 for appetite suppression 1.3 mg/kg
• Mouse models: 0.5-2 mg/kg in diet-induced obesity research
• Neurodegenerative disease trials: 0.125 mg to 1.0 mg daily in Parkinson’s/Alzheimer’s studies

Important: These are experimental doses used in clinical trials and animal studies and cannot be extrapolated to other species or contexts due to significant differences in metabolism, receptor density, pharmacokinetic profiles, and safety considerations. Species-specific factors including CYP3A4 activity, monoamine transporter expression, and cardiovascular responses profoundly influence both efficacy and safety profiles. Human dosing must be determined through controlled clinical trials under medical supervision.

Administration Routes in Research

Tesofensine has been investigated using multiple delivery methods depending on study design:

• Oral administration – Standard route for human clinical trials; once-daily dosing due to long half-life
• Subcutaneous injection – Commonly used in rodent research for consistent dosing
• Intraperitoneal injection – Employed in some animal pharmacology studies
• Oral gavage – Utilized in animal pharmacokinetic and efficacy studies

Oral administration represents the intended clinical route, with capsule or tablet formulations used in human trials.

Common Model Organisms

Tesofensine has been studied across multiple research models:

• Rats – Primary preclinical model; diet-induced obese rats extensively studied (Sprague-Dawley, Wistar strains)
• Mice – Used for specific mechanistic studies and genetic models of obesity
• Humans – Phase I, II clinical trials in obesity; Phase II trials in Parkinson’s and Alzheimer’s disease
• Marmosets – Employed in some chronic obesity studies showing sustained weight loss effects
• Cell culture systems – Monoamine transporter binding studies and receptor pharmacology characterization

Research Limitations & Regulatory Status

Critical Gaps in Current Evidence

Despite encouraging Phase II clinical trial results demonstrating superior weight loss compared to previously approved medications, tesofensine faces substantial translational barriers that have prevented regulatory approval and widespread clinical investigation.

Lack of Completed Phase III Development

The most significant limitation is the absence of completed Phase III clinical trials and regulatory approval:

• No large-scale, long-term Phase III trials published in peer-reviewed literature
• FDA initially endorsed Phase III trial program in 2010, but development subsequently stalled
• No published data from planned 5,000-7,000 patient Phase III studies
• Long-term cardiovascular safety and efficacy beyond 48 weeks remain uncharacterized
• Human safety profile based primarily on 203-patient Phase II trial and extension studies

Adverse Event Reporting Concerns

Significant regulatory scrutiny arose regarding the original Phase II trial[19]:

• Danish Health and Medicines Authority audit identified under-reporting of adverse events at some study sites
• The Lancet issued formal expression of concern regarding the original 2008 publication
• Investigators were wrongly instructed not to register certain pre-existing conditions as adverse events
• Actual incidence of psychiatric adverse events (depression, headache, stress) may be higher than initially reported
• These findings raised questions about complete safety characterization

Cardiovascular Safety Considerations

Tesofensine’s mechanism produces predictable cardiovascular effects requiring careful evaluation[20]:

• Heart rate increases of 5-8 beats per minute at therapeutic doses
• Blood pressure elevations observed, particularly at higher doses
• Similar cardiovascular profile to sibutramine, which was withdrawn due to cardiovascular concerns
• Long-term cardiovascular outcomes in at-risk populations unknown
• Combination with metoprolol (beta-blocker) being investigated to mitigate cardiovascular effects

Psychiatric and Neuropsychiatric Effects

As a centrally-acting monoamine reuptake inhibitor, psychiatric side effects require investigation[21]:

• Increased incidence of depressed mood reported (6% in some study groups)
• Dry mouth, insomnia, and other CNS-related effects observed
• Exclusion of patients with psychiatric conditions in trials limits real-world safety understanding
• Potential for mood disorders, agitation, or other psychiatric effects in susceptible individuals
• Long-term effects on mood and cognition incompletely characterized

Long-Term Safety and Tolerance

Critical safety questions remain unanswered:

• Chronic use beyond 48 weeks inadequately studied
• Effects of prolonged monoamine reuptake inhibition on neurological function unknown
• Weight regain patterns and metabolic effects after discontinuation incompletely characterized
• Abuse and dependence potential, though considered low, not extensively evaluated
• Drug-drug interactions with CYP3A4 substrates not fully elucidated

Regulatory & Competitive Sport Status

FDA Position

Tesofensine has not received FDA approval for any indication:

• Originally developed by NeuroSearch (Denmark); rights transferred to Saniona in 2014
• No approved indications for human medical use in the United States
• Not recognized as safe and effective for weight loss treatment
• Orphan drug designation granted for Prader-Willi syndrome and hypothalamic obesity (2021) but not approved
• Available only in research contexts under investigational protocols

Current regulatory status reflects incomplete clinical development rather than definitive safety or efficacy concerns, but approval would require completion of comprehensive Phase III trial programs.

WADA Prohibition

The World Anti-Doping Agency classifies tesofensine as a prohibited substance for competitive athletes:

• Listed under S6 Stimulants category as a specified stimulant (2025 Prohibited List)
• Prohibited in-competition due to potential performance-enhancing effects
• No Therapeutic Use Exemptions (TUEs) available as the compound lacks regulatory approval
• Added as example stimulant to 2025 WADA Prohibited List reflecting increased awareness
• Detection methods under development for anti-doping testing programs

WADA’s classification reflects tesofensine’s stimulant properties through monoamine reuptake inhibition and potential effects on alertness, energy, and body composition.

Research Classification: Tesofensine is available only for laboratory research use under appropriate institutional oversight. It is not intended for human consumption, medical treatment, or veterinary applications outside of approved clinical trial settings. All research must be conducted under appropriate ethical review board approval and regulatory compliance.

Lead Researcher Spotlight

Professor Arne Astrup, MD, Dr.Med.Sci.

Department of Nutrition, Exercise and Sports

University of Copenhagen, Copenhagen, Denmark

Professor Arne Astrup has been the principal investigator for the pivotal clinical research establishing tesofensine’s weight loss efficacy in human obesity. As Head of the Department of Human Nutrition at the University of Copenhagen’s Faculty of Life Sciences, Professor Astrup led the landmark TIPO-1 Phase IIb trial published in The Lancet in 2008, which demonstrated tesofensine’s potential to produce weight loss approximately double that of previously approved anti-obesity medications.

Professor Astrup’s research contributions to tesofensine development include:

• Principal investigator for the TIPO-1 and TIPO-4 clinical trials establishing dose-response relationships and long-term weight loss maintenance
• Meta-analyses revealing weight loss effects in Parkinson’s and Alzheimer’s disease patient populations
• Investigations of tesofensine’s effects on appetite sensations, satiety, and feeding behavior
• Characterization of body composition changes and metabolic parameter improvements
• Comparative analyses with other pharmacological weight loss interventions

His extensive research career spans obesity pharmacotherapy, dietary interventions, energy metabolism, and prevention of weight-related chronic diseases. Professor Astrup has published over 700 peer-reviewed papers and serves on editorial boards of major nutrition and obesity journals.

Disclaimer: This spotlight is provided for educational purposes to acknowledge scientific contributions to tesofensine research. Cenexa Labs has no affiliation with Professor Astrup or the University of Copenhagen, and this information does not constitute an endorsement of any products or services. Professor Astrup has disclosed consultant relationships and equity ownership with companies developing tesofensine in published research.

References

1. Larsen, M.H., Rosenbrock, H., Sams-Dodd, F., & Mikkelsen, J.D. (2007). Expression of brain derived neurotrophic factor, activity-regulated cytoskeleton protein mRNA, and enhancement of adult hippocampal neurogenesis in rats after sub-chronic and chronic treatment with the triple monoamine re-uptake inhibitor tesofensine. European Journal of Pharmacology, 555(2-3), 115-121. PubMed
   
2. Axel, A.M., Mikkelsen, J.D., & Hansen, H.H. (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. PubMed
   
3. Astrup, A., Meier, D.H., Mikkelsen, B.O., Villumsen, J.S., & Larsen, T.M. (2008). Weight loss produced by tesofensine in patients with Parkinson’s or Alzheimer’s disease. Obesity, 16(6), 1363-1369. PubMed
   
4. Hansen, H.H., Jensen, M.M., Overgaard, A., Weikop, P., & Mikkelsen, J.D. (2013). Tesofensine induces appetite suppression and weight loss with reversal of low forebrain dopamine levels in the diet-induced obese rat. Pharmacology Biochemistry and Behavior, 110, 265-271. PubMed
   
5. Ruiz-Lozano, T., Gonzalez-Munoz, K., Ramirez-Mendoza, A., et al. (2024). Tesofensine, a novel antiobesity drug, silences GABAergic hypothalamic neurons. bioRxiv. PubMed
   
6. Sjödin, A., Gasteyger, C., Nielsen, A.L., et al. (2010). The effect of the triple monoamine reuptake inhibitor tesofensine on energy metabolism and appetite in overweight and moderately obese men. International Journal of Obesity, 34(11), 1634-1643. PubMed
   
7. Astrup, A., Madsbad, S., Breum, L., Jensen, T.J., Kroustrup, J.P., & Larsen, T.M. (2008). Effect of tesofensine on bodyweight loss, body composition, and quality of life in obese patients: a randomised, double-blind, placebo-controlled trial. The Lancet, 372(9653), 1906-1913. PubMed
   
8. Seiwerth, S., Rucman, R., Turkovic, B., et al. (2018). Stable gastric pentadecapeptide BPC 157 and standard angiogenic growth factors: Gastrointestinal tract healing, lessons from tendon, ligament, muscle and bone healing. Current Pharmaceutical Design, 24(18), 1972-1989. PubMed
   
9. Astrup, A., & Madsbad, S. (2013). Under-reporting of adverse effects of tesofensine. The Lancet, 382(9887), 127. PubMed
   
10. Astrup, A., Meier, D.H., Mikkelsen, B.O., Villumsen, J.S., & Larsen, T.M. (2008). Weight loss produced by tesofensine in patients with Parkinson’s or Alzheimer’s disease. Obesity, 16(6), 1363-1369. PubMed
    
11. Gilbert, J.A., Gasteyger, C., Raben, A., Meier, D.H., Astrup, A., & Sjödin, A. (2012). The effect of tesofensine on appetite sensations. Obesity, 20(3), 553-561. PubMed
    
12. Axel, A.M., Mikkelsen, J.D., & Hansen, H.H. (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. PubMed
    
13. Astrup, A., Madsbad, S., Breum, L., Jensen, T.J., Kroustrup, J.P., & Larsen, T.M. (2008). Effect of tesofensine on bodyweight loss, body composition, and quality of life in obese patients: a randomised, double-blind, placebo-controlled trial. The Lancet, 372(9653), 1906-1913. PubMed
    
14. Sjödin, A., Gasteyger, C., Nielsen, A.L., et al. (2010). The effect of the triple monoamine reuptake inhibitor tesofensine on energy metabolism and appetite in overweight and moderately obese men. International Journal of Obesity, 34(11), 1634-1643. PubMed
    
15. Huynh, K., Klose, M., Krogsgaard, K., et al. (2022). Randomized controlled trial of Tesomet for weight loss in hypothalamic obesity. European Journal of Endocrinology, 186(6), 687-700. PubMed
    
16. Lehr, T., Staab, A., Tillmann, C., et al. (2008). Contribution of the active metabolite M1 to the pharmacological activity of tesofensine in vivo: a pharmacokinetic-pharmacodynamic modelling approach. British Journal of Pharmacology, 153(1), 164-174. PubMed
    
17. Lehr, T., Staab, A., Tillmann, C., et al. (2008). Contribution of the active metabolite M1 to the pharmacological activity of tesofensine in vivo: a pharmacokinetic-pharmacodynamic modelling approach. British Journal of Pharmacology, 153(1), 164-174. PubMed
    
18. Astrup, A., Meier, D.H., Mikkelsen, B.O., Villumsen, J.S., & Larsen, T.M. (2008). Weight loss produced by tesofensine in patients with Parkinson’s or Alzheimer’s disease. Obesity, 16(6), 1363-1369. PubMed
    
19. Astrup, A., & Madsbad, S. (2013). Under-reporting of adverse effects of tesofensine. The Lancet, 382(9887), 127. PubMed
    
20. Astrup, A., Madsbad, S., Breum, L., Jensen, T.J., Kroustrup, J.P., & Larsen, T.M. (2008). Effect of tesofensine on bodyweight loss, body composition, and quality of life in obese patients: a randomised, double-blind, placebo-controlled trial. The Lancet, 372(9653), 1906-1913. PubMed
    
21. Doggrell, S.A. (2009). Tesofensine: a novel potent weight loss medicine. Expert Opinion on Investigational Drugs, 18(7), 1043-1046. PubMed
    

All references open in new window. These citations are provided for educational and research purposes only. This information is not intended to diagnose, treat, cure, or prevent any disease. Tesofensine is intended for laboratory research use only.