Levalbuterol, also known as (R)-Albuterol or (R)-Salbutamol, is the active (R)-enantiomer of Salbutamol and serves as a short-acting β2-adrenergic receptor agonist. It is a more potent bronchodilator than Salbutamol and holds promise for the treatment of Chronic Obstructive Pulmonary Disease (COPD).

Levalbuterol (10 μM; 24 hours) induces 11β-HSD1 mRNA expression, however, it does not influence 11β-HSD2 expression in airway epithelial cells[1].Levalbuterol (10 μM; 24 hours) significantly reduces both LPS- and TNF-α-induced NF-κB activity while increasing GRE activation in an 11β-HSD1 dependent manner in a transformed mouse airway epithelial cell line[1]. RT-PCR[1]Cell Line: Murine Club (MTCC) cells Concentration: 10 μM Incubation Time: 24 hours Result: Increased 11β-HSD1 mRNA expression selectively.

Levalbuterol (subcutaneous injection; 1 mg/kg; 14 days) significantly decreases pulmonary inflammation in OVA mice, demonstrated a decrease in eosinophilia and IgE[3]. Animal Model: C57BL/6 female mice?with a pulmonary allergic model[3]Dosage: 1 mg/kg Administration: Subcutaneous injection; 1 mg/kg; 14 days Result: Decreased pulmonary inflammation after OVA sensitization.