Tesofensine 500mcg (30 Capsules)

What is Tesofensine?

Tesofensine represents a synthetic small-molecule compound with unique research potential. This compound functions as a triple monoamine reuptake inhibitor. Researchers designate Tesofensine as NS-2330 in scientific literature. The compound targets three major neurotransmitter systems simultaneously.

The phenyltropane-derived structure distinguishes Tesofensine from other compounds. This structural classification influences its binding properties and effects. Unlike peptides, Tesofensine functions as a synthetic organic molecule. The molecular weight of 328.3 g/mol allows for efficient distribution in research models.

Tesofensine operates through comprehensive inhibition of monoamine transporters. The compound blocks dopamine, norepinephrine, and serotonin reuptake. This triple action creates extensive modulation of monoaminergic pathways. Researchers value this comprehensive approach for investigating neurotransmitter dynamics.

The 500mcg capsule format provides precise dosing control for researchers. Each bottle contains 30 capsules, allowing for various study durations. The low dosage strength enables titration and dose-response studies. Researchers can easily adjust dosing based on experimental requirements.

Understanding Triple Monoamine Reuptake Inhibition

Monoamine transporters regulate neurotransmitter levels in the brain. These transporters remove dopamine, norepinephrine, and serotonin from synapses. Inhibition of these transporters increases neurotransmitter availability. Tesofensine targets all three major monoamine transporters simultaneously.

Dopamine transporter inhibition increases synaptic dopamine levels. Dopamine influences reward, motivation, and movement. Enhanced dopamine signaling affects numerous behavioral and physiological processes. Researchers study these effects in various experimental models.

Norepinephrine transporter inhibition elevates norepinephrine concentrations. This neurotransmitter regulates attention, arousal, and energy expenditure. Increased norepinephrine activation influences metabolic processes and cardiovascular function. Tesofensine’s effects on norepinephrine contribute to its metabolic research applications.

Serotonin transporter inhibition raises serotonin levels in synapses. Serotonin modulates mood, appetite, and various other functions. Enhanced serotonin signaling affects feeding behavior and emotional regulation. Tesofensine’s comprehensive inhibition addresses multiple aspects of monoaminergic signaling.

Triple reuptake inhibitors represent an advanced pharmacological approach. Single transporter inhibitors like SSRIs target only serotonin. Dual inhibitors address two neurotransmitter systems. Tesofensine’s triple action provides more comprehensive modulation. Visit the Research Hub to learn more about monoamine transporters.

Tesofensine’s Mechanism in Energy Metabolism

Tesofensine demonstrates significant effects on energy metabolism in preclinical studies. The compound influences multiple metabolic pathways simultaneously. Energy expenditure increases through norepinephrine-mediated mechanisms. This effect contributes to the compound’s weight loss research potential.

Appetite regulation represents another key metabolic effect. Tesofensine suppresses appetite through indirect receptor stimulation. Alpha1 adrenoceptors and dopamine D1 receptors mediate these effects. The combined monoamine elevation creates powerful appetite suppression. Researchers study these mechanisms for obesity treatment research.

Glycemic control improves with Tesofensine administration in experimental models. The compound enhances insulin sensitivity and glucose regulation. These effects extend beyond simple appetite suppression. Metabolic research investigates Tesofensine’s comprehensive effects on glucose homeostasis.

Fat oxidation increases with Tesofensine treatment in animal studies. The compound promotes utilization of stored fat for energy. This effect contributes to weight loss and body composition changes. Researchers study fat metabolism pathways to understand Tesofensine’s metabolic actions.

Energy balance regulation involves both intake and expenditure. Tesofensine addresses both sides of this equation. Appetite suppression reduces caloric intake. Increased energy expenditure burns stored energy. This dual approach creates comprehensive metabolic effects in research models.

Research Applications in Weight Loss Studies

Tesofensine shows exceptional promise in weight loss research applications. Preclinical studies demonstrate substantial weight reduction effects. The compound produces weight loss approximately 2-3 times greater than sibutramine. This impressive potency makes Tesofensine a subject of intense investigation.

Obesity research incorporates Tesofensine in various experimental models. Diet-induced obese rats show significant weight reduction with treatment. The compound reduces both fat mass and overall body weight. These effects persist throughout treatment periods in research studies.

Body composition research reveals preferential fat loss effects. Tesofensine reduces adipose tissue while preserving lean mass. This selective fat loss improves body composition in experimental models. Researchers study the mechanisms underlying this selective fat reduction.

Phase 3 clinical trials have investigated Tesofensine in obese patients. These trials demonstrated significant weight loss with treatment. The compound met primary and secondary efficacy endpoints. Research continues to optimize dosing and safety profiles for potential therapeutic applications.

Parkinson’s and Alzheimer’s disease patients showed unexpected weight loss in early studies. This serendipitous discovery led to focused obesity research. The weight loss effects proved substantial in patient populations. These findings prompted comprehensive investigation of Tesofensine’s metabolic properties.

Neurotrophic Effects and BDNF Expression

Tesofensine demonstrates significant neurotrophic effects in preclinical studies. The compound enhances expression of brain-derived neurotrophic factor (BDNF). BDNF plays crucial roles in neuronal survival, growth, and plasticity. Researchers study Tesofensine’s effects on BDNF for neuroprotection research.

Hippocampal neurogenesis increases with Tesofensine treatment. Adult rats show enhanced neurogenesis after chronic administration. New neuron formation in the hippocampus supports cognitive function. Researchers investigate these effects for depression and cognitive disorder research.

Activity-regulated cytoskeleton protein expression responds to Tesofensine. This protein supports synaptic plasticity and neuronal adaptation. Enhanced expression indicates improved neuronal function and adaptability. These neurotrophic effects complement Tesofensine’s monoaminergic actions.

Antiapoptotic effects have been observed in research studies. Tesofensine may protect neurons from programmed cell death. This neuroprotective property extends beyond monoaminergic enhancement. Researchers study these effects for neurodegenerative disease applications.

Transcriptomic analyses reveal differential gene expression patterns. Tesofensine treatment alters expression of neurotrophic and metabolic genes. These changes support the compound’s observed biological effects. Molecular research continues to investigate gene expression patterns.

Dopaminergic Pathway Modulation

Tesofensine’s effects on dopaminergic pathways represent a key research area. Dopamine transporter inhibition increases synaptic dopamine availability. Enhanced dopamine signaling affects reward, motivation, and movement pathways. Researchers study these effects in various behavioral and cognitive models.

Dopamine D1 receptor stimulation mediates some Tesofensine effects. The compound indirectly activates these receptors through increased dopamine. D1 receptor activation influences appetite regulation and reward processing. Appetite suppression effects partly depend on this dopaminergic pathway.

Behavioral research investigates Tesofensine’s effects on motivation and reward. Increased dopamine availability may enhance motivation and goal-directed behavior. These effects have implications for depression and addiction research. Studies examine how Tesofensine influences reward-related behaviors.

Motor function research also incorporates dopaminergic effects. Dopamine plays crucial roles in movement coordination and control. Tesofensine’s dopaminergic enhancement may affect motor performance. Researchers study these effects in Parkinson’s disease models and other movement disorders.

Comparative studies examine Tesofensine versus other dopaminergic compounds. The triple reuptake inhibition provides unique advantages over dopamine-specific agents. Researchers compare efficacy, safety, and side effect profiles. These comparisons inform potential therapeutic applications.

Noradrenergic and Serotonergic Effects

Tesofensine’s noradrenergic effects contribute significantly to its profile. Norepinephrine transporter inhibition elevates synaptic norepinephrine levels. Increased norepinephrine activation affects attention, arousal, and energy metabolism. These effects support Tesofensine’s metabolic and weight loss research applications.

Energy expenditure increases through norepinephrine-mediated mechanisms. Norepinephrine stimulates thermogenesis and lipolysis in adipose tissue. This metabolic effect contributes to weight loss observed in studies. Researchers investigate the specific pathways involved in norepinephrine-induced energy expenditure.

Attention and cognitive function benefit from noradrenergic enhancement. Norepinephrine improves focus, alertness, and cognitive performance. Tesofensine’s noradrenergic effects may enhance cognitive function in research models. Studies examine potential applications for attention disorders and cognitive enhancement.

Serotonergic effects complement Tesofensine’s dopaminergic and noradrenergic actions. Serotonin transporter inhibition increases synaptic serotonin levels. Enhanced serotonin signaling affects mood, appetite, and emotional regulation. The combination of three monoamines creates comprehensive neurotransmitter modulation.

Mood-related research investigates Tesofensine’s serotonergic effects. Increased serotonin availability may alleviate depressive symptoms. Triple reuptake inhibition offers advantages for depression treatment research. Studies compare Tesofensine to traditional antidepressants targeting single transporters.

Dosage Protocols and Administration

Tesofensine dosing requires careful consideration based on research objectives. The 500mcg capsule strength provides flexibility in protocol design. Research protocols typically utilize dosages ranging from 500mcg to 1mg daily. The 30-capsule bottle supports various dosing strategies for studies of different durations.

Frequency of administration depends on specific research goals. Most protocols utilize once-daily dosing due to the compound’s prolonged half-life. The sustained effects allow convenient single daily administration in research studies. This dosing frequency supports compliance in longer-term protocols.

Timing of administration may influence research outcomes. Morning administration often aligns with circadian patterns of monoamine activity. Some studies prefer administration before meals to maximize appetite suppression effects. Optimal timing depends on the specific research endpoints under investigation.

Capsule administration offers convenient oral delivery of Tesofensine. The 500mcg strength provides precise dose control for research protocols. Oral bioavailability allows systemic administration without injection requirements. Researchers can easily track compliance with capsule-based administration.

Dose titration protocols may be appropriate for certain research designs. Starting with lower doses and gradually increasing allows assessment of individual responses. The 500mcg capsule strength facilitates precise titration steps. Researchers establish clear titration schedules and monitoring protocols.

Use our Peptide Calculator to determine optimal dosing for your research protocol. Note that while designed for peptides, the calculator principles apply to dosing calculations for Tesofensine as well.

Tesofensine Safety Profile and Side Effects

Research on Tesofensine reveals important safety considerations. Clinical trials demonstrated significant weight loss effects but also identified side effects. Understanding the safety profile is crucial for research design and interpretation.

Cardiovascular effects represent a primary safety consideration. Increased norepinephrine can elevate heart rate and blood pressure. Clinical trials reported dose-dependent increases in these parameters. Researchers monitor cardiovascular endpoints closely in Tesofensine studies.

Central nervous system effects include various symptoms. Insomnia, dry mouth, and headache have been reported in clinical studies. These effects relate to the compound’s monoaminergic enhancement properties. Most CNS side effects appear dose-dependent and may diminish over time.

Gastrointestinal effects occur in some research subjects. Nausea, constipation, and other digestive symptoms have been observed. These effects typically remain mild to moderate in severity. Research protocols track gastrointestinal symptoms as part of safety monitoring.

Safety data from Parkinson’s and Alzheimer’s studies provided initial insights. Weight loss emerged as an unexpected effect in these early studies. Researchers noted side effects that informed subsequent obesity trial designs. These early safety observations guided dosing and monitoring protocols.

Adverse event reporting requires careful consideration in research. Some studies reported under-reporting of side effects initially. Comprehensive safety monitoring is essential for accurate adverse event capture. Researchers implement systematic tracking of all potential side effects.

Comparative Research to Other Compounds

Tesofensine shows unique properties compared to other weight loss compounds. Comparisons to sibutramine reveal approximately 2-3 times greater potency. This enhanced efficacy makes Tesofensine an important compound for obesity research.

Sibutramine functions primarily as a serotonin-norepinephrine reuptake inhibitor. Tesofensine adds dopamine reuptake inhibition to create triple action. This additional dopaminergic component may contribute to enhanced efficacy. Researchers study how triple inhibition differs from dual inhibition approaches.

Rimonabant comparisons focus on different mechanisms of action. Rimonabant targets cannabinoid receptors rather than monoamine transporters. Tesofensine’s monoaminergic approach provides distinct advantages and disadvantages. Comparative studies examine efficacy and safety profiles of both compounds.

Traditional antidepressants offer important comparison points. SSRIs target only serotonin reuptake. SNRIs inhibit serotonin and norepinephrine. Tesofensine’s triple reuptake inhibition provides more comprehensive modulation. Researchers study potential applications for depression treatment research.

Tricyclic antidepressants share some properties with Tesofensine. These older compounds affect multiple neurotransmitter systems but with less selectivity. Tesofensine’s more targeted triple reuptake inhibition may offer improved safety profiles. Comparative pharmacology studies examine these differences in detail.

Combination Protocols with Metabolic Compounds

Tesofensine may be combined with other metabolic research compounds. Combination approaches can target multiple pathways simultaneously. This strategy may provide synergistic benefits beyond single-compound administration in research models.

Metabolic peptides like MOTS-C 40mg complement Tesofensine’s actions. MOTS-C improves mitochondrial function and glucose metabolism. Enhanced cellular energy production supports metabolic processes. The combination addresses both neurotransmitter signaling and cellular energy metabolism.

NAD+ boosters like NAD+ 1000mg support cellular repair processes. NAD+ participates in numerous metabolic reactions including energy production. Enhanced NAD+ levels may support metabolic enhancement alongside Tesofensine’s effects. This combination addresses cellular metabolism and neurotransmitter modulation.

5-Amino-1MQ works through different metabolic pathways. This compound inhibits NNMT to boost NAD+ levels and enhance metabolism. Combining with Tesofensine may provide complementary effects on weight regulation. The combination addresses neurotransmitter signaling and NAD+-dependent metabolic pathways.

Appetite suppression compounds may offer additional research insights. Peptides or other compounds affecting hunger pathways could complement Tesofensine’s effects. Research examines whether combination approaches enhance weight loss beyond monotherapy. These combinations require careful evaluation of potential interactions.

Combination protocols require careful consideration of dosing and timing. Researchers must evaluate potential interactions between compounds. Separate administration times may optimize absorption and minimize potential competition. The 500mcg capsule format facilitates precise combination dosing protocols.

Preclinical Research Summary and Future Directions

Preclinical investigations reveal extensive Tesofensine research findings. Rodent models demonstrate significant effects on neurotransmitter dynamics. Behavioral studies show changes in activity, feeding, and metabolic parameters. These preclinical results support continued investigation of Tesofensine’s potential.

Transcriptomic and proteomic analyses provide molecular insights. Differential expression patterns emerge in neurotrophic and metabolic genes. These molecular changes correlate with observed physiological effects. Research continues to map comprehensive gene expression profiles following Tesofensine treatment.

Phase 3 clinical trials represent advanced investigation stages. Tesofensine met primary and secondary endpoints in obesity registration trials. These trials demonstrated significant weight loss with acceptable safety profiles. Research continues to optimize therapeutic windows and dosing strategies.

Neurodegenerative disease research incorporates Tesofensine’s neurotrophic effects. BDNF enhancement and hippocampal neurogenesis suggest potential applications. Studies investigate Tesofensine for depression, cognitive impairment, and neurodegenerative conditions. These applications extend beyond metabolic research.

Personalized medicine approaches may benefit from Tesofensine research. Major depression presents with varying symptoms and treatment responses. Tesofensine’s triple reuptake inhibition may address multiple symptom domains. Research examines individual differences in response to comprehensive monoaminergic modulation.

Future research directions include mechanism refinement and safety optimization. Understanding precise pathways involved in Tesofensine’s effects remains ongoing. Researchers investigate receptor subtypes, signaling cascades, and downstream effects. This knowledge will inform potential therapeutic applications and safety profiles.

Frequently Asked Questions

1. What is Tesofensine and how does it work as a triple reuptake inhibitor?

Tesofensine (NS-2330) is a synthetic phenyltropane-derived compound that functions as a novel triple monoamine reuptake inhibitor. The compound simultaneously inhibits dopamine transporter (DAT), norepinephrine transporter (NET), and serotonin transporter (SERT). This comprehensive inhibition increases synaptic availability of all three major monoamines. Tesofensine’s effects extend beyond simple neurotransmitter elevation to include appetite suppression through alpha1 adrenoceptor and dopamine D1 receptor pathways, enhanced BDNF expression, and increased hippocampal neurogenesis. The triple action provides more comprehensive modulation than single or dual reuptake inhibitors.

2. What are the primary research applications of Tesofensine?

Tesofensine demonstrates significant research potential across multiple domains including weight loss and obesity research, energy metabolism studies, appetite regulation investigation, and neurotrophic factor expression studies. Preclinical studies show approximately 2-3 times greater weight loss efficacy compared to sibutramine. Additional applications include glycemic control research, fat metabolism studies, depression investigation due to neurotrophic effects, and cognitive function research. The compound’s comprehensive monoaminergic modulation makes it valuable for studying integrated neurotransmitter systems and their effects on metabolism and behavior.

3. What is the recommended Tesofensine dosage for research studies?

Most research protocols utilize Tesofensine dosages ranging from 500mcg to 1mg daily. The 500mcg capsule strength provides flexibility for protocol design and dose titration. Due to the compound’s prolonged half-life, most protocols recommend once-daily administration. The 30-capsule bottle provides sufficient supply for various study durations depending on dosing frequency. Morning administration typically aligns with circadian patterns of monoamine activity, though optimal timing depends on specific research endpoints. Always consult established research protocols and use our Peptide Calculator to determine optimal dosing for your specific study design.

4. How does Tesofensine compare to other weight loss compounds like sibutramine or rimonabant?

Tesofensine demonstrates approximately 2-3 times greater potency than sibutramine in inducing weight loss. While sibutramine functions as a serotonin-norepinephrine reuptake inhibitor, Tesofensine adds dopamine inhibition to create triple action. This additional dopaminergic component may contribute to enhanced efficacy. Compared to rimonabant which targets cannabinoid receptors, Tesofensine uses monoaminergic pathways with distinct mechanisms and side effect profiles. Preclinical studies show Tesofensine produces sustained weight loss and improves glycemic control more effectively than both sibutramine and rimonabant in diet-induced obese rat models.

5. What are the potential side effects of Tesofensine in research studies?

Clinical trials identified several side effects requiring careful monitoring. Cardiovascular effects include dose-dependent increases in heart rate and blood pressure due to norepinephrine elevation. Central nervous system effects include insomnia, dry mouth, and headache related to monoaminergic enhancement. Gastrointestinal effects such as nausea and constipation have been reported in some subjects. Researchers implement comprehensive safety monitoring including cardiovascular assessment, CNS symptom tracking, and adverse event reporting. Some studies noted initial under-reporting of side effects, emphasizing the need for systematic safety monitoring protocols.

6. What neurotrophic effects does Tesofensine demonstrate in preclinical studies?

Tesofensine exhibits significant neurotrophic effects beyond its monoaminergic actions. The compound enhances expression of brain-derived neurotrophic factor (BDNF), which plays crucial roles in neuronal survival, growth, and plasticity. Studies show enhanced adult hippocampal neurogenesis following sub-chronic and chronic Tesofensine treatment. Activity-regulated cytoskeleton protein expression increases, supporting synaptic plasticity and neuronal adaptation. Antiapoptotic effects protect neurons from programmed cell death. Transcriptomic analyses reveal differential expression patterns in neurotrophic and metabolic genes, supporting the compound’s comprehensive biological effects.

7. How does Tesofensine influence appetite regulation and energy metabolism?

Tesofensine suppresses appetite through indirect stimulation of alpha1 adrenoceptors and dopamine D1 receptors. The combined elevation of dopamine, norepinephrine, and serotonin creates powerful appetite suppression effects. Energy metabolism increases through norepinephrine-mediated thermogenesis and lipolysis in adipose tissue. Glycemic control improves with enhanced insulin sensitivity and glucose regulation. The compound promotes fat oxidation and preferential fat loss while preserving lean mass. This dual approach of reducing intake through appetite suppression and increasing expenditure through enhanced metabolism creates comprehensive metabolic effects.

8. Can Tesofensine be combined with other metabolic research compounds?

Yes, Tesofensine may be combined with other metabolic research compounds to target multiple pathways simultaneously. Combining with MOTS-C 40mg addresses both neurotransmitter signaling and cellular energy metabolism through mitochondrial enhancement. NAD+ 1000mg supports cellular repair processes alongside Tesofensine’s metabolic effects. 5-Amino-1MQ provides complementary NNMT inhibition and NAD+ boosting for comprehensive metabolic modulation. Combination protocols require careful consideration of dosing, timing, and potential interactions. The 500mcg capsule format facilitates precise combination dosing for research studies.

9. What distinguishes Tesofensine from traditional antidepressants?

Tesofensine differs from traditional antidepressants through its comprehensive triple reuptake inhibition. SSRIs target only serotonin reuptake, while SNRIs inhibit serotonin and norepinephrine. Tesofensine adds dopamine reuptake inhibition to create complete monoaminergic modulation. This triple action may address multiple symptom domains in depression and other conditions. Additionally, Tesofensine’s significant metabolic effects and weight loss properties distinguish it from traditional antidepressants, which often cause weight gain. The compound’s neurotrophic effects including BDNF enhancement and hippocampal neurogenesis provide additional benefits beyond simple neurotransmitter elevation.

10. What are the storage requirements for Tesofensine 500mcg capsules?

Tesofensine capsules should be stored in a cool, dry location away from direct sunlight to maintain potency and stability. Room temperature storage (15-25°C or 59-77°F) is typically adequate for short-term use during active research protocols. For longer storage periods, refrigeration (2-8°C or 36-46°F) may help extend shelf life and preserve compound stability. Always keep capsules in their original container with the lid tightly closed to protect from moisture and humidity. Avoid storing in bathrooms or other humid environments. Do not freeze the capsules. Check expiration dates and discard capsules showing signs of degradation or discoloration.

11. How long does it take to see Tesofensine effects in research subjects?

Research suggests Tesofensine’s effects on appetite and metabolism may emerge within the first week of administration. Weight loss effects typically become measurable within 2-4 weeks of consistent treatment in preclinical models. Neurotrophic effects including BDNF expression and hippocampal neurogenesis may require 4-8 weeks of chronic treatment to manifest fully. The compound’s prolonged half-life supports sustained effects with once-daily dosing. Research protocols should account for these different timelines when designing study schedules and outcome measurements. Behavioral and metabolic effects appear more rapidly than neurotrophic and gene expression changes.

12. What makes Tesofensine unique among triple reuptake inhibitors?

Tesofensine’s uniqueness stems from its phenyltropane-derived structure and exceptional potency. The compound demonstrates approximately 2-3 times greater weight loss efficacy than other monoamine reuptake inhibitors like sibutramine. Unlike many other triple reuptake inhibitors, Tesofensine has progressed through Phase 3 clinical trials for obesity, demonstrating significant efficacy in human studies. The compound’s comprehensive effects on metabolism, appetite, neurotrophic factors, and glycemic control create a unique research profile. The serendipitous discovery of weight loss effects in Parkinson’s and Alzheimer’s disease patients led to focused investigation not seen with other compounds in this class.