Fluormetholone + Neomycin Sulphate

The exact mechanism by which ocular corticosteroids work is not fully agreed upon. However, they are thought to act by inducing phospholipase A2-inhibitory proteins known collectively as lipocortins. These proteins are believed to regulate the production of potent inflammatory mediators such as prostaglandins and leukotrienes, by blocking the release of their shared precursor, arachidonic acid, which is otherwise released from membrane phospholipids by phospholipase A2. Corticosteroids act mainly on the cytosolic glucocorticoid receptor; once bound, the resulting receptor-ligand complex moves into the cell nucleus, where it attaches to glucocorticoid response elements (GRE) in the promoter region of target genes. The DNA-bound receptor then interacts with basic transcription factors, increasing the expression of specific target genes.

Neomycin, like other aminoglycoside antibiotics, works by binding to the 30S ribosomal subunit of susceptible bacteria, disrupting the machinery responsible for bacterial protein synthesis. Normally, bacterial translation begins with mRNA binding to the 30S subunit, followed by binding of the 50S subunit for elongation.