Mixed
Selective, long-acting NK2R agonists (e.g., EB1002) reduce body weight and improve insulin sensitivity in obese mice and diabetic macaques by simultaneously increasing energy expenditure and suppressing appetite without causing aversive side effects.
This research identifies a new drug target (NK2R) that could lead to medications for obesity and type 2 diabetes. These drugs work by making your body burn more energy and reducing your appetite, without causing the unpleasant side effects often associated with other weight loss treatments. While promising in animals, this is not yet a human treatment.
In mice, these agonists elicit weight loss by inducing energy expenditure and non-aversive appetite suppression that circumvents canonical leptin signalling. Additionally, a hyperinsulinaemic–euglycaemic clamp reveals that NK2R agonism acutely enhances insulin sensitization. In diabetic, obese macaques, NK2R activation significantly decreases body weight, blood glucose, triglycerides and cholesterol, and ameliorates insulin resistance.
Why this rating
High-quality preclinical data in mice and non-human primates; no human clinical trial data provided.
Source
NK2R control of energy expenditure and feeding to treat metabolic diseases
Frederike Sass et al. · Nature · 2024
DOI 10.1038/s41586-024-08207-0
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