Vilanterol (GW642444) is a potent, orally active and long-acting β₂-AR  (β₂-adrenergic receptor) agonist with inherent 24-hour activity. The pEC₅₀s for β₂-AR, β₁-AR and β₃-AR are 10.37, 6.98 and 7.36, respectively.

β₂-AR is a member of the 7-transmembrane family of receptors. And, β₂-AR is a subtype of β-adrenergic receptors, distributing in the respiratory tract. In addition, β₂-AR plays an important role in the regulation of heart functionand. First, β₂-AR can modify in vitro cytokine release upon stimulation. Second, β₂-AR can cause the response including bronchiectasis, vasodilation and so on. Third, β₂-AR can activate the intracellular signaling, which is largely affected through cyclic adenosine monophosphate and protein kinase A. Therefore, The β₂-AR agonist has potential to treat respiratory disease, such as asthma and chronic obstructive pulmonary disease (COPD).

Vilanterol is a potent, orally active, selective and long-acting β₂-AR agonist with a long duration of action.

Vilanterol shows highly selective for the β₂-AR with at least a 1000-fold selectivity over both β₁– and β₃-AR subtypes. In addition, Vilanterol shows reassertion activity in both cell and tissue systems. And, the activity was comparable with salmeterol and indacaterol but longer than formoterol.  Vilanterol  has a faster onset and longer duration of action than salmeterol. In human airways, Vilanterol exhibits a significant level of bronchodilation 22 h after treatment. Vilanterol has potential to treat asthma and COPD. Vilanterol can improve lung function in COPD. And, this compound is well tolerated in subjects with COPD at a single dose (25-100 μg). In addition, Vilanterol also can treat asthma by activating the β₂ AR to dilate obstructed airways.

In summary, Vilanterol is a potent, orally active, selective and long-acting β₂-AR agonist, and has potential to treat asthma and COPD.

Reference:

[1] Slack RJ, et al. J Pharmacol Exp Ther. 2013 Jan;344(1):218-30.

[2] McGraw DW, Liggett SB. Proc Am Thorac Soc. 2005;2(4):292-6; discussion 311-2.

[3] Hervé J, et al. J Immunol. 2013 Apr 1;190(7):3163-71.