Indacaterol acetate

This work represents different spectrophotometric techniques for concurrent quantification of Indacaterol (IND) and Mometasone furoate (MOM); co-formulated inhalation capsules to control asthma symptoms. Direct spectrophotometric (D⁰) approach was applied for IND assay. While, absorption factor (AF), ratio difference (RD), mean centering of the ratio spectra (MC), and continuous wavelet transform (CW) techniques were utilized for MOM quantification. The applied methods' validation was accomplished relative to the ICH guidelines. Within the linearity range of (4-20 μg/mL), these approaches provided accurate and precise assessment of IND and MOM in laboratory-synthetic mixtures and pharmaceutical formulation with determination coefficients higher than 0.9997. Moreover, the proposed methods demonstrated good detection and quantification levels. The respective LOD and LOQ for IND were (0.33 μg/mL) and (1.01 μg/mL). While, the LOD and LOQ for MOM were ranging from (0.16-0.30 μg/mL) and (0.47-0.91 μg/mL), respectively. Statistical comparison revealed no significant differences between the findings derived from the proposed methods and the reported one. The applied methods' environmental effect was cheeked using Analytical Greenness Calculator (AGREE), Blue Applicability Grade Index (BAGI), and Red-Green-Blue 12 (RGB12). All the utilized metrics showed reliable scores, approving that the proposed methods were adhered to the sustainability principles.

Adrenergic receptors (ARs) are preferentially expressed by innate lymphocytes such as natural killer (NK) cells. Here, we study the effect of epinephrine‐mediated stimulation of the β2‐adrenergic receptor (β2AR) on the function of human NK cells. Epinephrine stimulation inhibited early NK cell signaling events and blocked the function of the integrin LFA‐1. This reduced the adhesion of NK cells to ICAM‐1, explaining how NK cells are mobilized into the peripheral blood upon epinephrine release during acute stress or exercise. Additionally, epinephrine stimulation transiently reduced NK cell degranulation, serial killing, and cytokine production and affected metabolic changes upon NK cell activation via the cAMP‐protein kinase A (PKA) pathway. Repeated exposure to β2AR agonists resulted in the desensitization of the β2AR via a PKA feedback loop‐initiated G‐protein switch. Therefore, acute epinephrine stimulation of chronically β2AR stimulated NK cells no longer resulted in inhibited signaling and reduced LFA‐1 activity. Sustained stimulation by long‐acting β2‐agonists (LABA) not only inhibited NK cell functions but also resulted in desensitization of the β2AR. However, peripheral NK cells from LABA‐treated asthma patients still reacted unchanged to epinephrine stimulation, demonstrating that local LABA administration does not result in detectable systemic effects on NK cells.