Tesofensine is sold for laboratory research use only. Terms of sale apply. Not for human consumption, nor medical, veterinary, or household uses. Please familiarize yourself with our Terms & Conditions prior to ordering.


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Tesofensine Nootropic Liquid

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CAS Number 195875-84-4
Molecular Formula C₁₇H₂₃Cl₂NO
Molecular Weight 328.28
Purity ≥99% Pure (LC-MS)
Liquid Availability adamax for sale 30mL liquid (1mg/mL, 30MG Bottle)
Powder Availability   adamax for sale 60 capsules (250mcg/capsule, 15mg (15,000mcg) total bottle)
Storage Store in a dry, cool, dark place. For best preservation, store at 4°C or colder away from bright light.
Terms All products are for laboratory developmental research USE ONLY. Products are not for human consumption.

What is Tesofensine?

Tesofensine is a peptide that derives from the phenyltropane family of drugs and acts as a serotonin-noradrenaline-dopamine reuptake inhibitor. The compound is best known for its ability to promote weight loss by suppressing appetite and increasing resting energy expenditure. Tesofensine has also shown the potential to improve cognitive functioning through its indirect potentiation of cholinergic neurotransmission, however, as of 2019 all experimental use of the peptide to enhance cognition was discontinued. All current trials being run focus on tesofensine effectively combating obesity.


Main Research Findings

1) Researchers determined that from weeks 12-24 of treatment with tesofensine, weight loss was primarily driven by enhanced satiety and reduced appetite.

2) Tesofensine was shown to drive weight loss by suppressing appetite and indirectly stimulating the alpha 1 adrenoceptor and dopamine D1 receptor pathways.


Selected Data

1) The study conducted by the research team of Gilbert et. Al divided their experiment into two parts of 24 weeks each and divided by a drug-free period of 12 +/- 3 weeks. The first part of the study included a randomized, double-blind, placebo-controlled, parallel-group design. After a two week adjustment period the test subjects were assigned to a group receiving either a placebo treatment or 0.25 mg, 0.5 mg, or 1.0 mg of tesofensine; drug treatment was in addition to a calorie-restricted diet and increased physical activity. All of the subjects that successfully completed the first portion of the study went through a drug-free period and were then invited to participate in the second part of the study. Part two maintained the same diet and exercise habits while including a reintroduction of the drug where all subjects received daily administration of 0.5 mg of tesofensine. After 4 weeks researchers were able to increase administration of tesofensine to 1.0 mg per day [1].

The subjects used in this study were obese females and males between the ages of 18 and 65. All women of childbearing age had to have a negative pregnancy test and use safe contraceptive methods. Smokers were allowed in the study as long as smoking habits had been stable for two months, however, a subject was excluded from the study if taking a medication known to significantly alter body weight. Subjects were also excluded if they were dependent on drugs or alcohol or had any number of endocrine, neurological, hepatic, renal, cardiovascular or psychiatric diseases. In terms of psychiatric diseases it is important to note that if a subject had previous experience with depression or anxiety and were completely recovered they were allowed to participate in the study [1].

During the experimental treatment period body weight of the subjects was measured while they were in light clothing and all recorded weights were rounded to the nearest 0.1 kg. Height was measured next by having the subjects stand barefoot against a wall-mounted stadiometer and all measurements were rounded to the nearest 0.5 cm. Previously validated standards were used to assess appetite sensations such as hunger, satiety, fullness, and prospective food consumption (PFC), as well as the desire to eat fatty, salty, sweet, or savory foods. The subjects were presented with a 100 mm scale with a question and two phrases on either end representing the most negative and the most positive ratings. For example, the subjects would read the question “How hungry do you feel?” and placed their answer on the scale between the most negative rating: “I am not hungry at all”, and the most positive rating: “I have never been more hungry”. Participants of the study filled this form out when they first arrived at the laboratory following an overnight fast. All appetite sensation responses were used to calculate the composite satiety score (CSS) as follows:

CSS (mm) = (Satiety + Fullness + (100 – PFC) + (100 – Hunger))/4

A higher CSS is associated with higher satiety, reduced appetite, and lower motivation to eat.

In order to compare the means between each treatment group, the research team used the one-way ANOVA method while repeated-measurements ANOVA was used to analyze changes over time within each group and within the entire sample. Next, two-way ANOVA was used to observe the effects of time in each treatment group, followed by the Tukey post-hoc analysis test used to compare treatment groups. Finally, the Sobel test was used to assess the potential mediation effect of variations in CSS on changes in body weight. Statistical analyses were performed using the JMP version 7.0 statistical software and all data was expressed as mean +/- s.d [1].

2) Researchers Axel et. Al examined the mechanism through which tesofensine induces weight loss. The study used five-week-old male Sprague-Dawley rats that were initially housed four rats per cage in a solid Plexiglass cage containing dust-free wood chippings and a cardboard tube. The rats were maintained on a strict 12-hour light/12-hour dark schedule while ambient temperature was kept at 18.0-22.0 degrees Celsius. Over the course of 10 weeks, high-fat food was provided ad libitum in order to make the rats obese. After 3-4 weeks on the high fat diet the housing situation changed and the rats were randomly matched and housed 2 rats per cage. 10 weeks on the high-fat diet resulted in a 22% increase in body weight; the subjects were then referred to as diet-induced obese (DIO) rats. The rats were then randomly assigned to experimental groups to be treated with tesofensine or a placebo [2].

After 9-10 weeks on a high-fat diet the DIO rats and their partners were re-housed to fully automated food intake monitoring cages (HM-2). The HM-2 cages were similar to those in the holding room as they were placed in a modified ventilated cabinet and maintained on a 12-hour light/12-hour dark schedule. The subjects were allowed to assimilate to the new food intake monitoring system for 5 days before treatment with tesofensine began. The feeding behavior of each test subject was strictly monitored during the habituation period in order to ensure that the animals’ food intake returned to pre-housing levels. The rats were then subcutaneously injected with a microchip in order for the HM-2 food intake monitoring system to identify and track feeding behavior of each individual animal in real time throughout the entire experiment.

Food intake was constantly monitored starting after the tagged animal entered the tag-reading food channel. After the animals left the food channel, the net food intake was calculated by the HM-2 control unit software. The calculation was then adjusted to take into consideration any food that may have been split during the feeding period. Additionally, the microstructural analysis of nocturnal food intake was performed by analyzing the different parameters of meal consumption such as, total number of meals, mean meal size, average meal duration, latency to first meal, and first meal size. The minimum meal size criterion was 0.3 g while the minimum meal duration criterion was 30 seconds and the minimum intermeal interval was 15 minutes measured from the last recorded meal intake [2].

Tesofensine and the vehicle compound were subcutaneously administered to the animals in doses of 1 ml/kg. All experiments conducted by the research team examining the tesofensine dose-response and monoamine receptor antagonist interaction were designed as between-subjects studies including 6-8 DIO rats per group. When observing drug interactions, bilateral subcutaneous injections were administered to the subjects within 1 minute between each injection, followed by drug administration 30-60 minutes before the onset of the 12-hour dark period. The home cage was removed from the HM-2 food intake monitoring system while drugs were administered to the subjects and was returned after the injection was complete. This procedure was followed by the initiation of automated monitoring of feeding behavior.

A secondary study was performed by the research team examining DIO rats that were housed in the pair environment until 1 week prior to the study when the subjects were then singly housed in cages equipped with a food hopper that utilized manual weighing in order to assess net food intake. 2.0 mg/kg of tesofensine or a saline vehicle was subcutaneously administered to the DIO test subjects once daily for 16 days, approximately 1 hour prior to the onset of the dark period. All recorded body weight data was expressed as daily body weight gain relative to the first day of drug administration; all data was then fed into a standard graphic and statistical analysis program [2].



1) The results of the study conducted by Gilbert et. Al found that dose-dependent weight loss was observed during the first 24 weeks of treatment with tesofensine. There was also a corresponding dose-dependent increase in CSS in response to tesofensine administration. The peptide-treated subjects continued to experience significant weight loss from weeks 12-24, however, CSS decreased during this period. It is important to note that CSS remained elevated above baseline levels only in the group of subjects administered 1.0 mg of tesofensine. Additionally, the desire to eat sweet, salty, and fatty foods decreased in a dose-dependent manner. At week 12, changes in CSS were found to be related to changes in body weight at both week 12 and 24. The body weight changes were also associated with changes in ratings for the desire to eat sweet, salty, and fatty food and both week 12 and 24. There was no observed association between weight change and the desire to eat savory food [1].

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Figure 1: Changes in A) CSS and B) body weight in response to treatment with varying doses of tesofensine.

After the first 24 week experimental period, all test subjects went through a drug-free period of 12 +/- 3 weeks. Over the course of the drug-free period the subject groups experienced a mean weight regain of 2.6 +/- 3.3 kg. The researchers noted a correlation between the initial weight change achieved during the first 24 weeks of treatment and the individual weight rebound during the drug-free period. All individual changes in CSS during the 12 week drug-free period were found to be independent of weight changes.

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Figure 2: Changes in A) CSS and B) body weight over the course of the project

The results of the second part of the study including a single-group intervention reported a significant reduction in body weight throughout the whole sample. The researchers noted that body weight changes differed according to the previous group attribution. That being said, it was found that the group treated with a placebo in part one experienced the highest rate of weight loss. All treatment groups also showed an increase in CSS, however, this was not related to any of the weight changes recorded during the same period of time. The increase in CSS was also shown to be independent of former group attribution as well as the initial weight loss prior to the second treatment period. It was also mentioned that the desire to eat fatty foods significantly increased while there were no observed changes in desire to eat sweet, salty, and savory foods [1].

Over the course of the entire project, the average loss of body weight was 12.8 +/- 8.9 kg, irrespective of the initial treatment the subject was administered. However, it is important to mention that individual weight change after 60 weeks was positively correlated with the weight change the subjects’ experienced during the first portion of the project. Similarly, the change from baseline in CSS was not dependent on the treatment each subject received in the first part of the study. The research team also reported significant weight loss in groups treated with the 0.5 and 1.0 mg doses of tesofensine (12.0 +/- 6.3 kg and 13.8 +/- 5.5 kg, respectively). The groups treated with these doses were then combined as an initial procedure of subsequent analysis. At the end of the study both treatment groups exhibited a similar change in CSS in comparison to baseline values. CSS was shown to increase in both treatment groups during the second part of the study; the combined group increased by 6.2 +/- 18.2 mm while the smaller placebo groups increased by 6.1 +/- 17.8 mm [1].

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Figure 3: Changes in CSS over the course of the project in subjects treated with a placebo, 0.5 mg of tesofensine, or 1.0 mg of tesofensine

2) The research team of Axel et. Al reported that tesofensine is capable of inducing hypophagic in DIO rats. When subcutaneously injected with a dose of the peptide, varying from 0.1-3 mg/kg, the subjects experienced inhibited food intake over a 12 hour nocturnal observation period. Inhibition of total food intake was shown to reach a threshold at doses of 1.0 mg/kg. Over the 12 hour observation period, the rats treated with a vehicle consumed approximately 54.1 +/- 2.1 kcal of food; the food intake of rats that received a 3.0 mg/kg dose of tesofensine decreased by 77% to approximately 12.6 +/- 3.9 kcal. When analyzing the temporal effects of tesofensine, the results indicated that doses of the peptide greater than 0.5 mg/kg tended to significantly affect cumulative food intake.

Results of the analysis also reported that the onset and duration of hypophagia induced by tesofensine, was dose-dependent. When the subjects were administered doses greater than 2.0 mg/kg, the hypophagic effects were elicited immediately after the drug was given and maintained through the nocturnal observation period. However, lower doses of tesofensine ranging from 0.5-1.5 mg/kg, showed a progressive increase in the lag-time for the onset of food intake suppression. The researchers noted that treatment with intermediate doses of tesofensine resulted in significant inhibition of cumulative food intake 2-12 hours post-injection. That being said the inhibitory effects on food intake were delayed when the peptide was administered in lower doses, only being significant at 10-12 hours post-injection [2].

Despite the changes in food intake in response to tesofensine treatment, feeding activity of the subjects was shown to have re-established to the same level as the vehicle control during the remaining 12-72 hours of the light-dark cycle period. This suggests that acute treatment with tesofensine did not lead to any compensatory feeding activity. Additionally, microstructural analysis was used to examine the effects of tesofensine on nocturnal food consumption. Treatment with the peptide significantly decreased several parameters of feeding kinetics, such as total number of meals, average meal size, and average meal duration. Tesofensine was also found to impact the latency and size of the subjects’ first meals [2].

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Figure 4: A) dose-dependent response of tesofensine on total food intake in the DIO rat during a 12 hour nocturnal period. B) time-response effect of increasing doses of tesofensine on cumulative nocturnal food intake.

After observing food intake the researchers examined how those changes affected body weight during the 12 hour observation period. The DIO rats treated with a vehicle gained 5.0 +/- 1.0 grams during the experiment; tesofensine treatment administered in doses of 1.0 and 3.0 mg/kg was found to significantly reduce weight gain by 2.0% +/- 1.0 grams and 7.3 +/- 1.8 grams, respectively. Furthermore, when assessing the effect of tesofensine on monoamine neurotransmission pathways, a 1.5 mg/kg dose of the peptide was found to inhibit food intake corresponding to approximately 50% of the basal food consumption of the DIO rats. This indicated that the 1.5 mg/kg dose can be used to study interaction with various monoamine receptor antagonists.

Finally, the researchers ran a secondary test examining how chronic tesofensine treatment affects body weight. 16 consecutive days of treatment with a moderate dose of the peptide (2.0 mg/kg), was shown to significantly reduce body weight after only four days of treatment relative to the vehicle-treated control subjects. The reduction in weight was sustained throughout the rest of the experiment, reaching a plateau at day 10. Tesofensine-treated DIO rats experienced an 8.6 +/- 1.4% average relative decrease in body weight. In comparison to the vehicle-treated control subjects , the relative weight loss induced by tesofensine was approximately 13.8 +/- 1.4%. Daily administration of tesofensine was also shown to significantly impact food intake over the 16-day experimental period, starting on the first day of treatment and lasting until day 14. Overall, treatment with testosterone suppressed daily food intake by 49.4 +/- 4.7% over the course of treatment days 1-14, in comparison to the vehicle-treated control group [2].

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Figure 5: Effects of chronic tesofensine treatment on A) body weight and B) food intake



*This information is for educational purposes only and does not constitute medical advice. THE PRODUCTS DESCRIBED HEREIN ARE FOR RESEARCH USE ONLY. All clinical research must be conducted with oversight from the appropriate Institutional Review Board (IRB). All preclinical research must be conducted with oversight from the appropriate Institutional Animal Care and Use Committee (IACUC) following the guidelines of the Animal Welfare Act (AWA).



[1] Gilbert JA, Gasteyger C, Raben A, Meier DH, Astrup A, Sjödin A. The effect of tesofensine on appetite sensations. Obesity (Silver Spring). 2012 Mar;20(3):553-61. doi: 10.1038/oby.2011.197. Epub 2011 Jun 30. PMID: 21720440.

[2] 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 Jun;35(7):1464-76. doi: 10.1038/npp.2010.16. Epub 2010 Mar 3. PMID: 20200509; PMCID: PMC3055463.


Tesofensine is sold for laboratory research use only. Terms of sale apply. Not for human consumption, nor medical, veterinary, or household uses. Please familiarize yourself with our Terms & Conditions prior to ordering.
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Additional information

Weight 1 oz
Dimensions 0.5 × 0.5 × 1 in