Terbinafine (brand name Lamisil, Terbisil, Terboderm and others) is an antifungal medication used to treat ringworm and fungal nail infections. Terbinafine inhibits ergosterol synthesis by inhibiting squalene epoxidase, an enzyme that is part of the fungal cell membrane synthesis pathway. Because terbinafine prevents the conversion of squalene to lanosterol, ergosterol cannot be synthesized. This is thought to change cell membrane permeability, causing fungal cell lysis. Many side effects and adverse drug reactions have been reported with oral terbinafine hydrochloride possibly due to its extensive biodistribution and the often extended durations involved in antifungal treatment (longer than two months).

Rufinamide is an anti-epileptic drug that is FDA approved for the treatment of lennox-gastaut syndrome (LGS). The principal mechanism of action of rufinamide is modulation of the activity of sodium channels and, in particular, prolongation of the inactive state of the channel. Hormonal contraceptives may be less effective with rufinamide. Patients on valproate should begin at a rufinamide dose lower than 10 mg/kg per day (pediatric patients) or 400 mg per day (adults). Common adverse reactions include headache, dizziness, fatigue, somnolence, and nausea.

Mometasone is a medium-potency synthetic corticosteroid with antiinflammatory, antipruritic, and vasoconstrictive properties. Studies in asthmatic patients have demonstrated that mometasone provides a favorable ratio of topical to systemic activity due to its primary local effect along with the extensive hepatic metabolism and the lack of active metabolites. Though effective for the treatment of asthma, glucocorticoids do not affect asthma symptoms immediately. Maximum improvement in symptoms following inhaled administration of mometasone furoate may not be achieved for 1 to 2 weeks or longer after starting treatment. When glucocorticoids are discontinued, asthma stability may persist for several days or longer. Mometasone has been shown in vitro to exhibit a binding affinity for the human glucocorticoid receptor which is approximately 12 times that of dexamethasone, 7 times that of triamcinolone acetonide, 5 times that of budesonide, and 1.5 times that of fluticasone. Mometasone inhaler is indicated for the maintenance treatment of asthma as prophylactic therapy. The nasal spray is indicated for the treatment of the nasal symptoms of seasonal allergic and perennial allergic rhinitis. ELOCON Lotion (Mometasone) is indicated for the relief of the inflammatory and pruritic manifestations of corticosteroid-responsive dermatoses.

Florfenicol (Nuflor) is a fluorinated synthetic analog of thiamphenicol. Florfenicol is indicated for the treatment of bovine respiratory disease (BRD) associated with Mannheimia (Pasteurella) haemolytica, Pasteurella multocida, and Haemophilus somnus, for treatment of bovine interdigital phlegmon (foot rot, acute interdigital necrobacillosis, infectious pododermatitis) associated with Fusobacterium necrophorum and Bacteroides melaninogenicus. Florfenicol is a broad-spectrum, primarily bacteriostatic, antibiotic with a range of activity similar to that of chloramphenicol, including many gram-negative and gram-positive organisms; however, florfenicol does not carry the risk of inducing human aplastic anemia that is associated with chloramphenicol. It also has activity against some chloramphenicol resistant strains of bacteria, possibly because it is less affected by the major enzyme produced in plasmid-mediated bacterial resistance against chloramphenicol and thiamphenicol. Although the activity of florfenicol against obligate anaerobes is not addressed in the literature, it is likely to be quite effective. Antibiotic principle of Florfenicol is similar to that of chloramphenicol and Thiamphenicol. Florfenicol inhibits protein synthesis by binding to 70S ribosomal 50S subunits of susceptible bacteria, leading to the inhibition of peptidyl transferase and thereby preventing the transfer of amino acids to extending peptide chains and subsequent protein formation. The bacterial receptor that is the site of action for florfenicol is also considered to be the same as that for chloramphenicol and thiamphenicol. Florfenicol has a fluorine atom instead of the hydroxyl group located at C-3 in the structure of chloramphenicol and thiamphenicol. This prevents the acetylation of bacterial acetyltransferase in this site as to allow florfenicol to be less susceptible to deactivation by bacteria with plasmid-transmissible resistance that involves acetylation of the C-3 hydroxyl group in chloramphenicol and thiamphenicol, and prevents their interaction with bacterial ribosomes.