Sarolaner is a member of the isoxazoline class of parasiticides. It is sold under the brand name Simparica, indicated for the treatment of tick infestations (Dermacentor reticulatus, Ixodes hexagonus, Ixodes ricinus and Rhipicephalus sanguineus), as well as of flea infestations (Ctenocephalides felis and Ctenocephalides canis) in dogs. The primary target of action of sarolaner in insects and acarines is functional blockade of ligand-gated chloride channels (GABA-receptors and glutamate-receptors). Sarolaner blocks GABA- and glutamate-gated chloride channels in the central nervous system of insects and acarines. Disruption of these receptors by sarolaner prevents the uptake of chloride ions by GABA and glutamate gated ion channels, thus resulting in increased nerve stimulation and death of the target parasite. Sarolaner exhibits higher functional potency to block insect/acarine receptors compared to mammalian receptors.

Sulfaquinoxaline is a veterinary drug, which can be given to animals to treat coccidiosis and Acute Fowl cholera. It has often used in combinations with others drugs. It had its origins in the chemical synthetic program that sprang from the introduction of sulfonamide drugs into human medicine in the 1930s. The program was sustained through the years of World War II despite declining clinical use of that chemical class. Several sulfa drugs were known to be active against the sporozoan parasite (Plasmodium spp.) that causes malaria, but were not satisfactory in clinical practice. A sulfonamide that had a long plasma half-life would ipso facto be considered promising as an antimalarial drug. Sulfaquinoxaline, synthesized during the war, was such a compound. It proved too toxic to be used in human malaria, but was found to be a superior agent against another sporozoan parasite, Eimeria spp., the causative agent of coccidiosis in domestic chickens. In 1948 sulfaquinoxaline was introduced commercially as a poultry coccidiostat. The action mechanism of sulfaquinoxaline is to inhibit the dihydrofolate synthetase to encumber the nucleate synthesis of bacterium and coccidian its active peak to coccidian is at the second schizont stage (the fourth day of coccidial life cycle), so it will not affect the anti-coccidial immunity in chicken.

Ponazuril, sold by the Bayer Corporation under the trade name Marquis, was the first FDA-approved treatment for equine protozoal myeloencephalitis (EPM) in horse, caused by Sarcocystis neurona. Also this drug was used in animals such as cats, dogs against coccidia, an intestinal parasite. Coccidia treatment is far shorter than treatment for EPM.

Pradofloxacin (trade name Veraflox) is a 3rd generation enhanced spectrum veterinary antibiotic of the fluoroquinolone class. It was developed by Bayer HealthCare AG, Animal Health GmbH, and received approval from the European Commission in April 2011 for prescription-only use in veterinary medicine for the treatment of bacterial infections in dogs and cats. The primary mode of action of fluoroquinolones involves interaction with enzymes essential for major DNA functions such as replication, transcription, and recombination. The primary targets for Pradofloxacin are the bacterial DNA gyrase and topoisomerase IV enzymes. Reversible association between Pradofloxacin and DNA gyrase or DNA topoisomerase IV in the target bacteria results in inhibition of these enzymes and rapid death of the bacterial cell. The rapidity and extent of bacterial killing are directly proportional to the drug concentration.

Chlorphenesin is a preservative and cosmetic biocide that helps prevent the growth of microorganisms. In cosmetics and personal care products, Chlorphenesin is used in the formulation of aftershave lotions, bath products, cleansing products, deodorants, hair conditioners, makeup, skin care products, personal cleanliness products, and shampoos. Chlorphenesin has been reported to cause irritation and contact dermatitis in some people, particularly those with sensitive and dry skin. The Cosmetic Ingredient Review (CIR) expert panel released a safety assessment in October 2012, however, that stated chlorphenesin at 0.3 percent (as it exists in personal care products) was classified as having “negligible dermal irritation potential.”

Fusidic acid is a anti-bacterial agent, initially isolated from Fusidium coccineum by Godtfredsen et al (Leo Pharma) in 1960. It is discussed that fusidic acid exerts its anti-microbial effect by inhibiting bacterial elongation factor G, thus suppressing the protein synthesis. Fusidic acid is widely used in Europe under the names Fucidin H(fusidic acid / hydrocortisone acetate), Fucidin (fusidic acid / sodium fusidate) and Fucicort (fusidic acid / betamethasone valerate) for the treatment of primary/secondary skin infections and inflammatory dermatoses.

Tildipirosin is a semisynthetic derivative of the naturally occurring 16-membered macrolide tylosin. Tildipirosin is intended for parenteral treatment of respiratory disease in cattle and swine. Tildipirosin will be administered as a single-dose injection: subcutaneously in cattle and intramuscularly in swine. The anticipated optimal clinical dose is 4 mg/kg bw. Tildipirosin is not used in human medicine. It is marketed under the brand name Zuprevo. As for other macrolides, the antimicrobial activity of tildipirosin is due to its binding to the ribosomal 50S subunit of bacterial cells thereby inhibiting bacterial protein synthesis. The in vitro antimicrobial activity against Gram-negative and Gram-positive pathogens indicates that tildipirosin is effective against a range of bacterial pathogens frequently associated with bovine and swine respiratory disease. Comparison of minimum inhibitory versus bactericidal concentrations shows that generally the antimicrobial action of tildipirosin is bacteriostatic.

Monensin is an antibiotic produced as a byproduct of fermentation by Streptomyces cinnamonensis and belongs to a family of drugs known as polyether antibiotics or ionophores. The drug was approved by FDA for the prevention of coccidiosis in turkeys, chickens, quail, cattle, goats, calves (Coban, Rumensin). The exact mechanism of monesin action is unknown, however there are several hypotesis, which includes the inhibition of K+ transport, the inhibition of the transport of carbohydrates across the host cell membrane, the interruption host cell invasion by sporozoites, etc.