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Tesofensine

Tesofensine (NS-2330) is an oral pharmaceutical compound originally developed by NeuroSearch, a Danish biotechnology company, for the treatment of neurodegenerative conditions including Alzheimer’s disease and Parkinson’s disease. During early clinical trials for these indications, researchers consistently observed a striking and unexpected side effect: significant reductions in body weight, particularly among overweight and obese participants. Although the drug demonstrated limited efficacy for its original neurological targets, its robust weight-loss effects prompted a strategic shift in development toward obesity. Tesofensine is classified as a triple monoamine reuptake inhibitor, meaning it simultaneously increases the synaptic availability of three critical neurotransmitters: dopamine, norepinephrine, and serotonin. This multi-pathway mechanism enables it to address appetite regulation, reward- based eating behavior, and energy expenditure at the neurological level, making it fundamentally different from hormonal or peptide-based weight-loss agents such as GLP-1 receptor agonists. Phase II clinical trial results published in The Lancet (2008) demonstrated that tesofensine produced dose-dependent weight loss that significantly exceeded placebo and outperformed several legacy anti-obesity drugs available at the time. Patients receiving the 0.5 mg dose achieved an average of approximately 11.3 kg of weight loss over 24 weeks, representing nearly double the efficacy of medications like sibutramine and rimonabant. Tesofensine is currently in Phase III clinical trials for obesity and is progressing toward potential regulatory approval in Mexico through a partnership between Saniona and Productos Medix.

Quick Reference

Classification Detail Chemical Name (1R,2R,3S,5S)-3-(3,4-Dichlorophenyl)-2-(ethoxymethyl)-8- methyl-8-azabicyclo[3.2.1]octane Drug Class Triple monoamine reuptake inhibitor (SNRI/DRI) Molecular Formula C₁₇H₂₃Cl₂NO Molecular Weight 328.3 g/mol CAS Number 195875-84-4 Half-Life Approximately 220 hours (~9 days); active metabolite M1 (NS2360): ~374 hours (~16 days) Route of Administration Oral (capsule/tablet) Primary Targets Norepinephrine transporter (NET), serotonin transporter (SERT), dopamine transporter (DAT)

Metabolism Primarily hepatic via CYP3A4; renal clearance accounts for approximately 15–20% Development Status Phase III clinical trials for obesity (Saniona/Medix); not yet

FDA-approved

How It Works

Triple Monoamine Reuptake Inhibition

Tesofensine’s primary mechanism involves blocking the presynaptic reuptake of three key neurotransmitters. By inhibiting the norepinephrine transporter (NET), serotonin transporter (SERT), and dopamine transporter (DAT), tesofensine increases the concentration and duration of action of these monoamines in the synaptic cleft. In vitro studies using rat brain synaptosomes demonstrated IC₅₀ values of 1.7 nM for NET, 11 nM for SERT, and 65 nM for DAT, indicating the strongest affinity for norepinephrine reuptake inhibition followed by serotonin and dopamine. This triple-action profile distinguishes tesofensine from single-mechanism agents. Rather than targeting only one neurotransmitter pathway, tesofensine simultaneously modulates hunger signaling, reward-based eating behavior, and energy expenditure, producing a more comprehensive effect on body-weight regulation.

Serotonin-Mediated Appetite Suppression

By increasing serotonin availability in the hypothalamus and other brain regions involved in appetite regulation, tesofensine enhances satiety signaling. Elevated serotonin activates receptors (particularly 5-HT2C) that reduce hunger and decrease the drive to eat. This mechanism is similar in principle to selective serotonin reuptake inhibitors (SSRIs), but tesofensine’s additional effects on dopamine and norepinephrine provide broader metabolic benefits beyond simple appetite reduction.

Dopamine and Reward Pathway Modulation

Dopamine plays a central role in the brain’s reward system, particularly in the nucleus accumbens and prefrontal cortex. By inhibiting dopamine reuptake, tesofensine reduces the reinforcing properties of food consumption, particularly cravings for high-fat and high-sugar foods. This modulation of reward-based eating behavior helps users gain greater control over food choices and reduces compulsive or hedonic eating patterns.

Norepinephrine and Energy Expenditure

Increased norepinephrine signaling through NET inhibition supports thermogenesis and lipolysis. Norepinephrine activates adrenergic receptors that mobilize stored fat and increase metabolic rate. Preclinical studies comparing tesofensine to pair-fed controls (animals receiving the same reduced caloric intake without the drug) found that pair-fed animals regained weight while

tesofensine-treated animals maintained weight loss, suggesting that tesofensine stimulates energy expenditure beyond the effects of reduced food intake alone.

GABAergic Neuron Modulation in the Lateral Hypothalamus

A 2024 study published in PLOS ONE (Perez et al.) provided the first direct evidence that tesofensine silences a subset of GABAergic neurons in the lateral hypothalamus, a brain region critical for feeding behavior. Using optogenetic and chemogenetic techniques in transgenic mice, the researchers demonstrated that tesofensine inhibited GABAergic neurons that normally promote food-seeking and consumption. Chemogenetically silencing these neurons further enhanced tesofensine’s appetite-suppressing effects, confirming a specific neural circuit mechanism underlying the drug’s weight-loss properties.

Cholinergic Potentiation and BDNF Upregulation

Tesofensine also indirectly potentiates cholinergic neurotransmission, which has demonstrated beneficial effects on cognition, particularly learning and memory. Preclinical studies have shown that sustained tesofensine treatment upregulates brain-derived neurotrophic factor (BDNF), a protein critical for neuronal survival, synaptic plasticity, and cognitive resilience. This may contribute to the improved focus and mental clarity reported by some users during caloric restriction.

Active Metabolite (M1/NS2360) Tesofensine is metabolized primarily by CYP3A4 in the liver to its desalkyl metabolite M1 (NS2360), the only metabolite detectable in human plasma. M1 has a longer half-life than the parent compound (approximately 374 hours versus 220 hours) and reaches 31–34% of the parent compound’s plasma exposure at steady state. In vivo data indicate that M1 is responsible for approximately 6% of tesofensine’s overall pharmacological activity, contributing to the drug’s prolonged duration of action.

Benefits

1. Powerful Appetite Suppression

Tesofensine significantly reduces hunger, food preoccupation, and caloric intake. Clinical trials consistently demonstrate lower caloric intake without the nausea, jitteriness, or crash commonly associated with stimulant-based weight-loss drugs. Users frequently report reduced meal size, fewer cravings for high-fat and high-sugar foods, and improved control over eating behavior. This effect is driven by the synergistic action of serotonin-mediated satiety enhancement and dopamine-mediated reduction in reward-based eating.

2. Clinically Significant Weight Loss

In the Phase IIB clinical trial (TIPO-1), tesofensine produced dose-dependent weight loss that significantly exceeded placebo and outperformed several legacy anti-obesity drugs. Key findings include:

over 24 weeks

over 24 weeks

over 24 weeks

The 48-week open-label extension trial (TIPO-4) demonstrated sustained effects, with patients previously on the 0.5 mg dose achieving a total mean weight loss of 13–14 kg. Weight loss occurred even without aggressive lifestyle changes, highlighting the drug’s central mechanism rather than reliance on willpower alone.

3. Improved Metabolic Efficiency

Tesofensine modestly increases energy expenditure and fat oxidation, particularly during rest and overnight periods. This effect is tied to norepinephrine signaling, which supports thermogenesis and lipolysis. Preclinical pair-feeding studies confirmed that tesofensine stimulates energy expenditure beyond what can be attributed to reduced food intake alone, as pair-fed control animals regained weight while tesofensine-treated animals maintained their weight loss.

4. Favorable Effects on Metabolic Markers

Beyond weight loss, tesofensine has demonstrated improvements in several obesity-related biomarkers:

In the Hansen et al. (2010) preclinical study, tesofensine significantly suppressed the plasma insulin response during a glucose tolerance test below the level achievable by caloric restriction alone, indicating direct metabolic benefits independent of weight loss.

5. Cognitive and Mood-Related Effects

Because tesofensine enhances dopamine and serotonin signaling, users may experience secondary benefits including improved focus, elevated mood, and better mental clarity during caloric deficits. Preclinical research shows upregulation of BDNF, which supports cognitive

resilience during weight-loss phases. Tesofensine’s indirect potentiation of cholinergic neurotransmission may also contribute to improvements in learning and memory.

6. Prevention of Weight Rebound

The 2024 PLOS ONE study by Perez et al. demonstrated that tesofensine prolonged the weight loss induced by 5-HTP (a serotonin precursor) and blocked the body-weight rebound that often occurs after initial weight loss. This finding suggests that tesofensine may help maintain weight- loss results when used strategically, addressing one of the most significant challenges in obesity management.

What the Science Shows

Study 1: Phase IIB Clinical Trial (TIPO-1) – Astrup et al., The Lancet (2008) Design: Randomized, double-blind, placebo-controlled trial conducted at five Danish obesity management centers. 203 obese patients (BMI 30–40 kg/m²) were prescribed an energy- restricted diet (300 kcal deficit) and randomly assigned to tesofensine 0.25 mg, 0.5 mg, 1.0 mg, or placebo once daily for 24 weeks. Results: 161 participants (79%) completed the study. Placebo-subtracted mean weight losses were 4.5%, 9.2%, and 10.6% for the 0.25 mg, 0.5 mg, and 1.0 mg groups, respectively (p<0.0001 for all doses versus placebo). Weight loss was accompanied by reductions in body fat and waist circumference, along with modest improvements in plasma lipids. Safety: The most common adverse events were dry mouth, nausea, constipation, hard stools, diarrhea, and insomnia. The 0.25 mg and 0.5 mg doses showed no significant increases in systolic or diastolic blood pressure compared with placebo. Heart rate increased by 7.4 beats per minute in the 0.5 mg group (p=0.0001). Significance: The authors concluded that tesofensine 0.5 mg has the potential to produce weight loss approximately twice that of anti-obesity drugs approved at the time of the study.

Study 2: Open-Label Extension Trial (TIPO-4) – NeuroSearch/Saniona Design: 48-week, open-label extension trial in which 140 patients who completed the TIPO-1 trial were re-enrolled after an average 3-month washout period. All participants initially received 0.5 mg tesofensine once daily, with up-titration to 1.0 mg permitted during the first 24 weeks, followed by 0.5 mg for the final 24 weeks. Results: Patients previously on tesofensine 0.5 mg in TIPO-1 achieved a total mean weight loss of 13–14 kg over 48 weeks of treatment. Patients previously on placebo lost approximately 9 kg in the first 24 weeks of TIPO-4, confirming the TIPO-1 efficacy results. Significance: Demonstrated sustained weight-loss efficacy with continued treatment and confirmed that the weight-loss effect is reproducible in previously untreated patients.

Study 3: Preclinical Comparison – Hansen et al., European Journal of Pharmacology (2010) Design: Preclinical study in diet-induced obese rats comparing tesofensine (1.0 and 2.5 mg/kg) to sibutramine (7.5 mg/kg) and rimonabant (10 mg/kg) over 28 days. Pair-fed controls were included to distinguish between reduced food intake and metabolic effects. Results: Tesofensine produced dose-dependent, sustained weight loss of 5.7% and 9.9% at the two doses, respectively. Sibutramine produced 7.6% weight loss, while rimonabant’s effect was transient. Tesofensine’s appetite-suppressing effect lasted longer than both comparators. Pair-fed animals regained weight by the end of the study, while tesofensine-treated animals maintained their weight loss, indicating stimulation of energy expenditure. Tesofensine also significantly reduced the plasma insulin response during glucose tolerance testing beyond what caloric restriction alone achieved. Significance: Established that tesofensine’s weight-loss mechanism involves both appetite suppression and increased energy expenditure, and demonstrated superior glycemic control compared to caloric restriction alone.

Study 4: GABAergic Neuron Mechanism – Perez et al., PLOS ONE (2024) Design: Preclinical study using electrophysiological ensemble recordings, optogenetic activation, and chemogenetic silencing of GABAergic neurons in the lateral hypothalamus (LH) of mice and rats. Both lean and diet-induced obese animals were evaluated. Results: Tesofensine induced greater weight loss in obese rats than lean rats while differentially modulating neuronal ensembles in the LH. For the first time, the study demonstrated that tesofensine inhibited a subset of LH GABAergic neurons, reducing their ability to promote feeding behavior. Chemogenetically silencing these neurons enhanced tesofensine’s food- suppressing effects. Unlike phentermine, tesofensine caused few if any stereotypic behaviors at therapeutic doses. Tesofensine also prolonged weight loss induced by 5-HTP and blocked body- weight rebound. Significance: Provided the first direct evidence of tesofensine’s specific neural circuit mechanism, identifying GABAergic neurons in the lateral hypothalamus as a key target. Also demonstrated tesofensine’s potential to prevent post-weight-loss rebound.

Study 5: Dopamine Transporter Occupancy – Appel et al., European Neuropsychopharmacology (2014) Design: PET imaging study using [¹¹C]βCIT-FE to measure dopamine transporter (DAT) occupancy in healthy volunteers receiving multiple oral doses of tesofensine (0.125–1.0 mg) over 8–12 days. Results: Tesofensine induced dose-dependent blockade of DAT at anticipated steady-state conditions. The study established clear relationships between DAT occupancy, plasma concentrations, and administered doses. Significance: Confirmed that tesofensine produces measurable, dose-dependent inhibition of dopamine reuptake in the human brain, supporting the mechanistic basis for its effects on reward-based eating behavior and providing pharmacokinetic data for dose optimization in subsequent clinical trials.

Study 6: Neurological Trial Meta-Analysis – Astrup et al., Obesity (2008) Design: Meta-analysis of results from clinical trials originally conducted in patients with Parkinson’s disease and Alzheimer’s disease, examining weight-loss data as a secondary endpoint. Doses ranged from 0.125 to 1.0 mg once daily. Results: Tesofensine produced dose-dependent weight loss across the combined patient population. Approximately 32% of obese subjects receiving the highest dose achieved at least 5% weight reduction after 14 weeks of treatment. Weight loss was accompanied by reduced food intake, suggesting an appetite-suppressant mechanism. Significance: This meta-analysis provided the foundational evidence that prompted the strategic shift in tesofensine’s development from neurodegenerative diseases to obesity, ultimately leading to the Phase IIB TIPO-1 trial.

Dosing Protocol

Important: Tesofensine is not yet FDA-approved and is currently available primarily through research suppliers and select compounding pharmacies. The following dosing information is based on published clinical trial data and should not be construed as medical advice. Any use should be under the supervision of a qualified healthcare provider.

Standard Dosing (Based on Clinical Trial Data) Phase Dose Notes Starting Dose 0.25 mg/day Taken once daily, orally. Assess tolerability over 2–4 weeks before dose escalation. Therapeutic Dose 0.5 mg/day The dose most commonly studied for optimal risk-benefit ratio. Produced ~9.2% placebo- subtracted weight loss in Phase IIB. Maximum Studied 1.0 mg/day Produced marginally greater weight loss Dose (10.6%) but with increased side effects including elevated heart rate and higher incidence of mood changes.

Dosing Considerations

life (~9 days), steady-state plasma levels are achieved gradually, and once-daily dosing provides consistent 24-hour coverage.

bioavailability. Tesofensine can be taken with or without food.

approximately 4–6 weeks to reach new steady-state levels. Patience is required when titrating doses.

recommend strategic, time-limited use with a clear exit plan once fat-loss goals are achieved.

inhibitors (ketoconazole, itraconazole, ritonavir, grapefruit juice) may increase tesofensine levels, while CYP3A4 inducers (rifampicin, carbamazepine, St. John’s wort) may reduce efficacy. Discuss all medications and supplements with a healthcare provider.

Side Effects

Common Side Effects (Reported in Clinical Trials) Side Effect Frequency Notes Dry mouth Common (dose-dependent) Most frequently reported; usually mild to moderate Nausea Common Typically transient; may resolve with continued use Constipation/hard stools Common Adequate hydration and fiber intake recommended Insomnia Common (dose-dependent) Morning dosing may help minimize sleep disruption Headache Common Usually mild and self- limiting Diarrhea Common May alternate with constipation in some individuals Increased heart rate Dose-dependent 0.5 mg: +7.4 bpm (p=0.0001); 1–3 mmHg BP at 0.25–0.5 mg

Depressed mood Uncommon (6.1% at 1.0 mg) Reported primarily at the highest dose; 0% in placebo group

The overall withdrawal rate due to adverse events in clinical trials was 13% with tesofensine and 6% with placebo. The safety profile at therapeutically relevant doses (0.25–0.5 mg) is generally comparable to other approved anti-obesity medications.

Cardiovascular Considerations

Blood pressure and heart rate increases at the therapeutically relevant doses of 0.25 mg and 0.5 mg were 1–3 mmHg and up to 8 bpm, respectively. At the conclusion of Phase II clinical trials, Saniona reported that tesofensine was well tolerated with low incidence of adverse events, low increase in heart rate, and no significant effect on blood pressure. However, given the historical context of sibutramine (a related monoamine reuptake inhibitor withdrawn for cardiovascular safety concerns), ongoing Phase III trials are carefully monitoring cardiovascular endpoints.

Contraindications and Precautions

disease, heart failure, arrhythmias, or a history of stroke should not use tesofensine without thorough cardiovascular evaluation and close medical supervision.

disorders. Given that 6.1% of participants on the 1.0 mg dose reported depressed mood, individuals with a history of depression, bipolar disorder, or other psychiatric conditions should exercise extreme caution.

inhibitors due to the risk of serotonin syndrome, a potentially life-threatening condition characterized by agitation, hyperthermia, tachycardia, and neuromuscular abnormalities.

other serotonergic agents increases the risk of serotonin syndrome and should be avoided or closely monitored.

plasma levels. Dose adjustments or alternative medications should be considered.

women. Tesofensine should be avoided during pregnancy and breastfeeding.

with narrow-angle glaucoma should use tesofensine with caution.

Patients with epilepsy or a history of seizures should be closely monitored.

Tesofensine vs. Other Weight-Loss Compounds

Feature Tesofensine GLP-1 Phentermine Sibutramine Agonists (e.g., (withdrawn) Semaglutide) Mechanism Triple GLP-1 receptor Sympathomimetic Dual NE/5-HT monoamine agonist (gut amine (NE, DA reuptake reuptake hormone) release) inhibitor inhibitor (DA, NE, 5-HT) Route Oral (once Subcutaneous Oral (once daily) Oral (once daily) injection daily) (weekly) Weight Loss ~9–11% (0.5 ~12–16% ~5–7% ~4–5% (24 wks) mg) (varies by dose/agent) Key Side Dry mouth, Nausea, Insomnia, CV events Effects insomnia, mild vomiting, GI elevated HR/BP, (withdrawn) HR increase distress stimulant effects Muscle Not directly Concerns about Not specifically Not specifically Preservation studied; central lean mass loss studied studied mechanism may be more favorable FDA Status Not approved; FDA-approved FDA-approved Withdrawn Phase III (short-term) (2010)

Tesofensine occupies a unique position in the weight-loss landscape as a non-hormonal, orally administered compound that works upstream at the level of neurotransmitter regulation. Unlike GLP-1 agonists, which require weekly injections and commonly cause gastrointestinal side effects, tesofensine offers a convenient oral dosing format with a different side-effect profile. Unlike stimulant-based agents such as phentermine, tesofensine produces few if any stereotypic behaviors at therapeutic doses and addresses multiple neurotransmitter pathways simultaneously.

Success Tips

2–4 weeks before considering dose escalation to 0.5 mg. Given the long half-life, patience is essential during dose adjustments.

that includes a structured, nutrient-dense diet. A moderate caloric deficit (300–500 kcal) enhances results without extreme restriction.

weight loss, improves metabolic rate, and complements tesofensine’s effects on energy expenditure and body composition.

pressure, especially during the first 4–8 weeks and after dose changes. Report any sustained elevations to your healthcare provider.

most common dose-dependent side effects.

intake and sugar-free gum or lozenges can help manage this symptom.

clear fat-loss goals and a timeline for discontinuation. The long half-life means effects will taper gradually over several weeks after stopping.

products to your healthcare provider. Pay particular attention to MAO inhibitors, serotonergic drugs, and CYP3A4 inhibitors.

While many users report improved mood and focus, some individuals may experience depressed mood, particularly at higher doses.

Storage and Handling

temperature (20–25°C / 68–77°F). Protect from light, heat, and moisture.

other containers unless specifically instructed.

use expired product.

pharmaceutical compound and should be handled accordingly.

Legal Status

Tesofensine is not currently approved by the US Food and Drug Administration (FDA) for any indication. It is classified as an investigational drug and is in Phase III clinical trials for obesity. Tesofensine is available in some jurisdictions through research chemical suppliers and select compounding pharmacies for research purposes. As of 2024, Saniona (the company that acquired tesofensine rights from NeuroSearch in 2014) is pursuing regulatory approval for tesofensine in Mexico through a partnership with Productos Medix, S.A. de C.V. If approved, this would represent the first market authorization for tesofensine globally. Tesofensine is not a controlled substance in the United States. However, regulations vary by jurisdiction, and users should verify the legal status in their region before purchasing or using this compound. The World Anti-Doping Agency (WADA) has not specifically listed tesofensine, though athletes should verify current prohibited substance lists before use.

Product Source

When sourcing research-grade tesofensine, ensure the supplier provides third-party testing, certificates of analysis (COA), and proper documentation of purity (typically ≥98% by HPLC/MS). Always verify the legitimacy and quality standards of any research compound supplier.

Frequently Asked Questions

How quickly does tesofensine start working? Due to its long half-life (~9 days), tesofensine reaches steady-state plasma levels gradually over approximately 4–6 weeks of daily dosing. Some users report reduced appetite within the first week, but the full effects on weight loss typically become apparent after several weeks of consistent use. Is tesofensine a stimulant? No. Although tesofensine increases norepinephrine and dopamine signaling, it is not classified as a stimulant and does not produce the jitteriness, crash, or stereotypic behaviors (such as head- weaving) associated with stimulant-based weight-loss drugs like phentermine or amphetamines. Its mechanism is more accurately described as monoamine reuptake inhibition. Can tesofensine be combined with GLP-1 agonists? There is limited published research on combining tesofensine with GLP-1 receptor agonists. Because these compounds work through entirely different mechanisms (central neurotransmitter modulation versus gut hormone signaling), there is theoretical rationale for combination therapy. However, any combination should only be undertaken under direct medical supervision, as the safety profile of such combinations has not been established in clinical trials. How long can tesofensine be used? Clinical trials have evaluated tesofensine for up to 48 weeks. There is no established maximum duration, but most practitioners recommend time-limited use with clear goals and an exit strategy. The long half-life means that effects will taper gradually over several weeks after discontinuation, allowing for a smooth transition off the medication. Does tesofensine cause muscle loss? The clinical trials primarily measured total body weight and body fat rather than lean mass specifically. However, because tesofensine’s weight-loss mechanism is primarily driven by central appetite suppression and modest increases in energy expenditure rather than hormonal alterations that affect muscle metabolism, it may be more favorable for muscle preservation than some alternatives. Combining tesofensine with resistance training and adequate protein intake is strongly recommended to preserve lean mass. What happens when you stop taking tesofensine? Due to the long half-life, tesofensine’s effects diminish gradually over several weeks after the last dose. The 2024 Perez et al. study demonstrated that tesofensine blocked body-weight rebound in preclinical models, which is an encouraging finding. However, as with any weight- loss intervention, maintaining results long-term depends on sustained lifestyle changes including proper nutrition and regular physical activity. Is tesofensine safe for people with diabetes? Preclinical studies showed that tesofensine improved glycemic control and reduced insulin levels. However, individuals with diabetes may be taking multiple medications that could interact with tesofensine, and changes in appetite and caloric intake may affect blood sugar management. People with diabetes should only use tesofensine under close medical supervision with regular monitoring of blood glucose levels.

References

1. Astrup A, Madsbad S, Breum L, Jensen TJ, Kroustrup JP, Larsen TM. Effect of tesofensine on bodyweight loss, body composition, and quality of life in obese patients: a randomised, double- blind, placebo-controlled trial. Lancet. 2008;372(9653):1906–1913. 2. Astrup A, Meier DH, Mikkelsen BO, et al. Weight loss produced by tesofensine in patients with Parkinson’s or Alzheimer’s disease. Obesity. 2008;16(6):1363–1369. 3. Hansen HH, Hansen G, Tang-Christensen M, et al. The novel triple monoamine reuptake inhibitor tesofensine induces sustained weight loss and improves glycemic control in the diet- induced obese rat: comparison to sibutramine and rimonabant. Eur J Pharmacol. 2010;636(1– 3):88–95. https://pubmed.ncbi.nlm.nih.gov/20385127/ 4. Perez CI, Luis-Islas J, Lopez A, et al. Tesofensine, a novel antiobesity drug, silences GABAergic hypothalamic neurons. PLOS ONE. 2024;19(4):e0300544.

5. Appel L, Bergström M, Buus Lassen J, Långström B. Tesofensine, a novel triple monoamine re-uptake inhibitor with anti-obesity effects: dopamine transporter occupancy as measured by PET. Eur Neuropsychopharmacol. 2014;24(2):251–261. 6. Axel AM, Mikkelsen JD, Hansen HH. 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. 2010;35(7):1464–1476. https://pubmed.ncbi.nlm.nih.gov/20200507/ 7. Eisenstein SA, Bogdan R, Love-Gregory L, et al. Prediction of striatal D2 receptor binding by DRD2/ANKK1 TaqIA allele status. J Pharmacol Exp Ther. 2015;352(1):129–138.

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