For anyone curious about the proposed mechanism of action, care of the Wikipedia page https://en.wikipedia.org/wiki/Viloxazine https://en.wikipedia.org/wiki/Vil

For anyone curious about the proposed mechanism of action, care of the Wikipedia page https://en.wikipedia.org/wiki/Viloxazine https://en.wikipedia.org/wiki/Viloxazine > Viloxazine, like imipramine, inhibited norepinephrine reuptake in the hearts of rats and mice; unlike imipramine, it did not block reuptake of norepinephrine in either the medullae or the hypothalami of rats. As for serotonin, while its reuptake inhibition was comparable to that of desipramine (i.e., very weak), viloxazine did potentiate serotonin-mediated brain functions in a manner similar to amitriptyline and imipramine, which are relatively potent inhibitors of serotonin reuptake.[11] Unlike any of the other drugs tested, it did not exhibit any anticholinergic effects.[11] > More recent research has found that the mechanism of action of viloxazine may be more complex than previously assumed.[12] It appears to act as a potent antagonist of 5-HT2B receptors and as a potent agonist of 5-HT2C receptors.[12] These actions may be involved in its effectiveness for ADHD.[12] > It has also been found to up-regulate GABAB receptors in the frontal cortex of rats.[13] As always, a drug's effects cannot be interpreted simply by looking at binding affinities. It's important to focus on the actually human clinical trials. The binding affinities are interesting in the context of neuroscience and drug research, but less so for treatment decisions.