(+)-Fenchone, a bicyclic monoterpene, is widely distributed in plants and found in essential oils from Foeniculum vulgare. This component has camphoraceous fragrance. (+)-Fenchone is used as a food flavour and in perfumes. Although, there are report that (+)-fenchone has toxic. P450 enzymes are shown to detoxify and/or toxify these compounds to metabolites more polar and sometimes more reactive metabolites. (+)-fenchone are oxidized to 6-endo-hydroxyfenchone, 6-exo-hydroxyfenchone and 10-hydroxyfenchone derivatives in human liver microsomes. CYP2A6 is suggested to be a principal enzyme in catalyzing (+)-fenchone 6-exo and 6-endo hydroxylation by human liver microsomes. 10-Hydroxylation of (+)-fenchone is also metabolized by CYP2B6.

Fluticasone is a medium-potency synthetic trifluorinated corticosteroid which is used in some countries to manage nasal symptoms of allergic and non-allergic rhinitis. Fluticasone binds and activates glucocorticoid receptor, resulting in the activation of lipocortin. Lipocortin, in turn, inhibits cytosolic phospholipase A2, which triggers a cascade of reactions involved in the synthesis of inflammatory mediators, such as prostaglandins and leukotrienes. Both the furoate and propanoate esters, fluticasone furoate and fluticasone propionate, are much more commonly used as topical anti-inflammatories and inhaled corticosteroids.

Vilanterol (INN, USAN) is an ultra-long-acting β2 adrenoreceptor agonist (ultra-LABA), which was approved in May 2013 in combination with fluticasone furoate for sale as Breo Ellipta by GlaxoSmithKline for the treatment of chronic obstructive pulmonary disease (COPD). Its pharmacological effect is attributable to stimulation of intracellular adenylyl cyclase which catalyzes the conversion of adenosine triphosphate (ATP) to cyclic-3’,5’-adenosine monophosphate (cAMP). Increases in cyclic AMP are associated with relaxation of bronchial smooth muscle and inhibition of release of hypersensitivity mediators from mast cells in the lungs. Vilanterol is available in following combinations: a) with inhaled corticosteroid fluticasone furoate — fluticasone furoate/vilanterol (trade names Breo Ellipta , Relvar Ellipta; b) with muscarinic antagonist umeclidinium bromide — umeclidinium bromide/vilanterol (trade name Anoro Ellipta).

Umeclidinium (used as a bromide salt) is a long-acting, antimuscarinic antagonist, often referred to as an anticholinergic, developed for the treatment of chronic obstructive pulmonary disease (COPD) (alone and in combination with Vilanterol - long-acting beta2-adrenergic agonist). Umeclidinium has similar affinity to the subtypes of muscarinic receptors M1 to M5 with Ki values of 0.16 nM, 0.15 nM, 0.06 nM, 0.05 nM and 0.13 nM for M1, M2, M3, M4 and M5, respectively. Umeclidinium is selective against mAChR over other unrelated receptors or channels such as κ and σ opiod receptors, Na+ channel and dopamine transporter. In the airways, it exhibits pharmacological effects through the inhibition of M3 receptor at the smooth muscle leading to bronchodilation. There is potential for an additive interaction with concomitantly used anticholinergic medicines.

Salmeterol is a long-acting beta2-adrenergic agonist. Although beta2-adrenoceptors are the predominant adrenergic receptors in bronchial smooth muscle and beta1-adrenoceptors are the predominant receptors in the heart, there are also beta2-adrenoceptors in the human heart comprising 10% to 50% of the total beta-adrenoceptors. The precise function of these is not yet established, but they raise the possibility that even highly selective beta2-agonists may have cardiac effects. It is FDA approved for the treatment of asthma, prevention of exercise-induced bronchospasm, maintenance treatment of chronic obstructive pulmonary disease. Common adverse reactions include musculoskeletal pain, headache, influenza, nasal/sinus congestion, pharyngitis, rhinitis, tracheitis/bronchitis, cough, throat irritation, viral respiratory infection. Salmeterol should be administered with extreme caution to patients being treated with monoamine oxidase inhibitors or tricyclic antidepressants, or within 2 weeks of discontinuation of such agents, because the action of salmeterol on the vascular system may be potentiated by these agents. Coadministration of salmeterol and ketoconazole was associated with more frequent increases in QTc duration compared with salmeterol and placebo administration.