Viloxazine is currently being developed as a treatment for attention deficit/hyperactivity disorder (ADHD). The aim of these studies is to update the understanding of the rat and human metabolism and the in vitro drug–drug interaction profile of viloxazine to a degree where it meets current regulatory standards for such investigations.

In vivo absorption-distribution-metabolism-excretion (ADME) studies demonstrated that in humans 5-hydroxylation followed by glucuronidation is the major metabolic route. This route was also seen as a minor route in rats where the major route is O-deethylation with subsequent sulfation.

In humans, the 5-hydoxylation pathway is mediated by CYP2D6. An estimate for the fraction of the metabolism via this pathway suggests a PM/EM difference of <2-fold, making it highly unlikely that this will be an issue of clinical significance.

Viloxazine forms a unique N-carbamoyl glucuronide in humans. The chemical reactivity characteristics of this metabolite are similar to stable glucuronide conjugates and dissimilar from acyl glucuronides; therefore, it is regarded as a stable Phase II conjugate.

In vitro drug–drug interaction (DDI) testing indicates that viloxazine is not a significant inhibitor or inducer of CYPs and transporters with the exception of CYP1A2.

目前正在开发Viloxazine作为注意力缺陷/多动障碍（ADHD）的治疗方法。这些研究的目的是在一定程度上更新维洛沙嗪对大鼠和人类代谢以及体外药物相互作用的了解，使其达到目前此类研究的监管标准。

体内吸收-分布-代谢-排泄（ADME）研究表明，在人体中，5-羟基化继之以葡萄糖醛酸化是主要的代谢途径。在大鼠中，该途径也被认为是次要途径，其中主要途径是O-脱乙基化和随后的硫酸化。

在人类中，5-羟基氧化途径是由​​CYP2D6介导的。通过该途径进行的代谢比例的估计表明PM / EM差异小于2倍，这极有可能不会成为具有临床意义的问题。

Viloxazine在人体内形成独特的N-氨基甲酰基葡萄糖醛酸。这种代谢物的化学反应特性类似于稳定的葡糖醛酸苷结合物，与酰基葡糖醛酸苷不同。因此，它被认为是稳定的II期共轭物。

体外药物-药物相互作用（DDI）测试表明，除CYP1A2外，viloxazine并不是CYP和转运蛋白的重要抑制剂或诱导剂。