Dinotefuran is an insecticide. Its structure is derived from the neurotransmitter acetylcholine and it acts on nicotinic acetylcholine receptors of the insect nerve synapse. Once bound to these receptors, the full agonist action of repeated excitatory impulses kills the insect. Insects do not have to ingest dinotefuran, it kills by contact. Dinotefuran has a low affinity for mammalian acetylcholine receptor sites. Fleas are killed by dinotefuran within 2 hours after treatment or infestation.

Pyriproxyfen is a photostable insect growth regulator (IGR). It acts through contact, by mimicking the juvenile hormone which regulates the moulting of insects from one life stage to the next. Pyriproxyfen stops the flea life cycle by both inducing premature oviposition and also suppressing yolk deposition in flea eggs, leading to the production of infertile eggs. Pyriproxyfen also blocks the development of juvenile stages (larvae and early (pharate) pupae) into adult emergence. This prevents infestation within the environment of the treated animal.

Following topical application, the two actives rapidly distribute over the body surface of the animal within the first day and were still measurable in different zones of the hair coat one month after treatment.

Dinotefuran and pyriproxyfen are partially absorbed by the cat skin (30% and 12% respectively), but this systemic absorption is not relevant for the clinical efficacy of the product.

In laboratory species, after intra-peritoneal administration, dinotefuran is rapidly eliminated as the unchanged parent molecule mainly via the urine. After oral administration, pyriproxyfen is rapidly metabolized, principally by hydroxylation, and eliminated mainly in the faeces, and to a lesser extent in the urine.

Vectra Felis should not enter water courses as this may be dangerous for fish and other aquatic organisms. Do not contaminate ponds, waterways or ditches with the veterinary medicinal product or with used containers.