New treatments of obesity

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madman

Super Moderator
ABSTRACT

Several pharmacological approaches to controlling body weight have been developed over the last decades, albeit with limited success. Currently, available agents include centrally-acting appetite suppressants and peripherally acting compounds. The efficacy and safety of these agents in the clinical setting require a difficult balance. Further strategies including multiagonists able to simultaneously target multiple actors involved in obesity initiation and expansion such as the glucagon receptor family are under investigation. The results of recent clinical trials are encouraging and highlight emerging compounds as potential game-changers. In view of the rising prevalence of obesity and the associated burden of comorbidities worldwide, and compared with other areas of pharmacological intervention, we feel that the field of obesity has been affected by therapeutic inertia. Of note, obesity may also affect the response to concomitant medications such as low-dose aspirin. Lessons from withdrawn agents such as the cannabinoid receptor antagonist rimonabant include developing compounds with a more targeted action profile (i.e., central vs peripheral, or antagonist versus inverse agonist) as well as careful selection of patients based on individual risk factors. We anticipate that the expanding knowledge base and clinical testing will result in improved outcomes for patients with obesity in the near future.




1. Introduction

Obesity is a chronic disease affecting millions of people worldwide and is often associated with numerous co-morbidities, including type 2 diabetes, liver disease, and cardiovascular disease. As the prevalence of obesity continues to sharply increase at a global level, it is crucial to develop strategies to prevent this chronic condition at a population level and at the individual level. Emerging research on the gut/brain axis including the microbiota has made transformational steps in our understanding of obesity etiology, as well as in treatment. There is strong evidence that the gut/brain axis is important not just for appetitive behavior but also energy homeostasis, blood glucose and even emotional state [1,2]. Connecting scientists in basic, transitional, clinical and pharmaceutical research will be crucial to moving the field forward.




2. Pharmacological Approaches to Obesity

3. Agents approved for use in the United States and/or European Union

3.1. Centrally acting appetite suppressants

3.1.1. Phentermine / topiramate
3.1.2. Naltrexone / bupropion
3.1.3. Setmelanotide


3.2. Agents with mixed central and peripheral action: liraglutide

3.3. Peripherally acting agents: orlistat

4. The rise and fall of the selective serotonin (5-HT)2C receptor agonist lorcaserin

5. Investigational anti-obesity agents: spotlight on the pipeline

5.1. Tesofensine
5.2. Semaglutide
5.3. Dual GLP-1/GIP receptor agonist
5.4. Dual GLP-1/glucagon receptor agonists


6. Obesity as a risk factor for drug toxicity or impaired responsiveness




7. Conclusions


There is a considerable scientific and financial interest in developing pharmacologic therapy for obesity. Despite improved understanding of the neurochemical signals that regulate food intake, translation of this research into effective and safe pharmacological agents in clinical practice has been limited. Pharmacological research has been successful in identifying specific ligands that modulate signaling systems in the brain involved in food intake, satiety, and energy homeostasis. Delivering these agents specifically to the brain regions, specific cells, and subcellular structures where such signaling events take place, however, remains challenging. This is why the benefits of current anti-obesity medications do not necessarily outweigh the risks. Peripherally acting agents appear to be safer, but limited efficacy with orlistat and lack of long-term safety data with GLP-1R agonists are to be considered.

At variance with type 2 diabetes and hypertension, we feel that the field of obesity pharmacotherapy has been affected by therapeutic inertia. Careful selection of patients for pharmacological treatment appears to be a priority and may result in improved outcomes with acceptable safety. A blend of nonpharmacological and pharmacological approaches may provide incremental benefit over current strategies. Of note, recent trials of investigational agents have yielded encouraging results. Thus, exciting developments are poised to expand the therapeutic armamentarium for obesity.
 

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madman

Super Moderator
Currently approved medicines for obesity treatment.
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nodoctor

Active Member
Will report back here, and I mentioned this on another thread, but it seems like more than a few people with some knowledge are touting that Semaglutide could be a game changer, so I'm going to do a run carefully first hand. Would love to hear more anecdotes though.
 

captain

Active Member
I been on Semaglutide for 6 months. It hasn't been a game changer, but I am only using 1mg. a week. Nausea and headache lasted for 3-4 months. Nausea still comes goes at times. There is change in taste where everything doesn't taste good. Weight loss comes but you still have to work for it.
 

modest13

New Member
Hi Nelson,
Have you heard anything about the peptide version of Liraglutide instead of getting it as the name brand Saxenda or Victoza etc? There are several peptide vendors who sell Liraglutide 3mg vials, but I am not sure how you would dose that? Do you know how many doses one would get out of 1 of the vials labeled 3mg? it would not be one whole vial per shot/per day, right? I super appreciate the assistance.
 

nodoctor

Active Member
update: Semaglutide/Ozempic still absolutely rocks. I've hovered around 10-14% bodyfat for a decade plus (with 7-8% for brief very painful periods) and would rather get more cut. I dislike the feeling of fat burners. For me, this had no change in taste, definite satiety feeling, and no real downside, dizziness, sides. Will update again at some point, but thrilled for now. I suspect I'll get back to 8% but without the severe pain it took me to get there before.

Also considering Tesofensine mentioned above in Nelson's post partially because I try not to stay on things I don't understand for very long. Haha.

I catch myself wondering if Semaglutide will lead to desensitized leptin receptors (so I'll gorge when I come off) or something similar. Would love to hear from someone that came off of it and still kept the lower fat %, or switched to something else they liked.
 
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