Imidacloprid is an ectoparasiticide belonging to a group of chloronicotinyl compounds. Chemically, it is more accurately described as a chloronicotinyl nitroguanidine.

Imidacloprid has a high affinity for the nicotinergic acetylcholine receptors in the post-synaptic region of the central nervous system (CNS). The ensuing inhibition of cholinergic transmission in insects results in paralysis and death. Due to the weak nature of the interaction with mammalian nicotinergic receptor sites and the postulated poor penetration through the blood/brain barrier in mammals, it has virtually no effect on the mammalian CNS. The minimal pharmacological activity in mammals is supported by safety studies involving systemic administration of sub-lethal doses to rabbits, mice and rats.

Oral studies in the rat show imidacloprid to be absorbed rapidly from the gastro-intestinal tract. Almost complete absorption (95%) occurs within 48 hours. Peak plasma concentrations are observed within 2.5 hours following administration. Tissue distribution is also rapid with the lowest levels recorded in the brain. The active ingredient undergoes extensive metabolism with only 10-16% remaining as parent compound. Almost complete (96%) elimination occurs within 48 hours, approximately 75% being removed by the kidneys and 21% with the faeces.

The solution is indicated for cutaneous administration. Following topical application, the product is quickly distributed over the animal. Acute dermal studies in the rat and target animal overdose and serum kinetic studies have established that systemic absorption is very low, transient and not relevant for clinical efficacy. This has been further demonstrated by a study in which fleas were not killed after having fed on previously treated animals once the animal's skin and fur had been cleaned of all active material.

No incompatibility has been observed between this product at twice the recommended dose and the following commonly used veterinary products: fenthion, lufenuron, milbemycin, febantel, pyrantel and praziquantel (dogs) and lufenuron, pyrantel and praziquantel (cats). The compatibility of the product was also demonstrated with a range of routine treatments including vaccination.

In cats, no adverse clinical signs were produced using doses of five times the therapeutic level for eight consecutive weeks.

In dogs, no adverse clinical signs were produced by either individual doses of up to 200 mg/kg bodyweight (five to eight times the therapeutic dose), daily treatments at 100 mg/kg bodyweight for five consecutive days or weekly treatments at five times the maximum dose rate for eight consecutive weeks.

In rabbits, no adverse clinical signs were seen using doses of up to 45 mg/kg bodyweight (4 times the therapeutic level) weekly for 4 consecutive weeks.

Poisoning following inadvertent oral uptake in either man or animals is unlikely. In this event, treatment should be symptomatic. There is no known specific antidote but administration of activated charcoal may be beneficial.

The solvent in Advantage may mark certain materials including leather, fabrics, plastics and finished surfaces. Allow application site to dry before permitting contact with such materials.