Arformoterol Tartrate ((R,R)-Formoterol tartrate) is the tartrate salt of arformoterol. Arformoterol is a long-acting beta-2 adrenergic agonist with bronchodilator activity[2].

β2-adrenoceptor:2.9 nM (Kd)

Arformoterol (R,R-formoterol) 是 racemic formoterol 的活性异构体，适用于长期维护治疗COPD（包括慢性支气管炎和肺气肿）患者的支气管收缩。作为一种强效且选择性的化合物，它通过促使支气管平滑肌松弛并抑制炎症介质的释放来发挥作用。其药理效果归因于内源性腺苷酸环化酶的刺激，进而增加细胞内环磷酸腺苷（cAMP）水平。当通过雾化器吸入时，Arformoterol tartrate 可以被肺部良好吸收。在COPD患者中，每12小时吸入15 μg arformoterol 连续14天，其平均峰值血浆浓度（Cmax）和系统暴露程度（AUC0-12h）分别为4.3 pg/mL 和 34.5 pg·h/mL。中位稳态峰值血浆浓度（tmax）大约在化合物给药后半小时达到。在COPD患者中，经过14天每天两次吸入15 μg arformoterol 治疗的平均终末半衰期为26小时。Arformoterol 与人类血浆蛋白的结合率在0.25, 0.5 和 1.0 ng/mL 的放射性标记arformoterol 浓度下为52-65%。其代谢主要通过直接结合（糖醛酸化）发生，次要的代谢途径为O-脱甲基化。代谢由至少五种人类尿苷酸二磷酸葡萄糖醛酸转移酶（UGT）同工酶以及CYP2D6 和CYP2C19介导。在给予一次性口服放射性标记的arformoterol 后，48小时内通过尿液回收放射性物质的63%，通过粪便回收11%。在14天内，共回收了89%的放射性剂量，其中尿液67%，粪便22%。

Exposure of C57BL/6 mice(8 wk old) to 400 ppm Cl(2) for 30 minutes increased respiratory system resistance and airway responsiveness to aerosolized methacholine. Intranasal administration of arformoterol mitigated the Cl(2) effects on airway reactivity and AFC, presumably by increasing lung cyclic AMP level. Arformoterol did not modify the inflammatory responses, as evidenced by the number of inflammatory cells and concentrations of IL-6 and TNF-α in the bronchoalveolar lavage. NF-κB activity (assessed by p65 Western blots and electrophoretic mobility shift assay) remained at control levels up to 24 hours after Cl(2) exposure. Our results provide mechanistic insight into the effectiveness of long-term β(2)-agonists in reversing Cl(2)-induced reactive airway dysfunction syndrome and injury to distal lung epithelial cells[2].