Phosmet is a phthalimide-derived, non-systemic, organophosphate insecticide used on plants and animals. It is mainly used on apple trees for control of codling moth, though it is also used on a wide range of fruit crops, ornamentals, and vines for the control of aphids, suckers,^{[clarification needed]} mites, and fruit flies.

The first registered use of phosmet was in the United States in 1966, where it was used on a variety of crops including fruit trees (apple, pear, peach) and nut trees (almonds, walnuts) as a treatment for various pests such as the codling moth, leafrollers, and others. It has also been registered for use on cattle, swine, and dogs for treatment of lice, fleas, and ticks. It can also be used domestically for trees, bushes, and shrubs by homeowners. Phosmet is being used all over the world.

Phosmet is an organophosphate, consisting of a phthalimide and a dithiophosphate ester, with two methyl groups. The structure is a benzene ring connected to an imide, which is connected to the dithiophosphate.

Phosmet is produced by reaction of N-chloromethylphthalimide with dimethyldithiophosphoric acid. The former, in turn, can be prepared by the reaction of phthalimide with formaldehyde and hydrogen chloride. Phosmet can also be obtained through the condensation of phthalimide with formaldehyde and conversion of the product to chloride which is reacted with sodium dimethylphosphorodithioate.

As an organophosphate, phosmet competitively inhibits pseudocholinesterase and acetylcholinesterase (AChE), preventing hydrolysis and inactivation of acetylcholine. Its inhibitory effects on the AChE enzyme leads to a pathological excess of acetylcholine in the body. Acetylcholine accumulates at nerve junctions, causing malfunction of the sympathetic, parasympathetic, and peripheral nervous systems and some of the central nervous system. Clinical signs of cholinergic excess can develop. The mechanism of inhibition consists of phosmet blocking the active site of the enzyme that binds the ester portion of acetylcholine.

If signs of cholinesterase inhibition are present, atropine and pralidoxime are antidotal and may be coadministered.

The absorption of phosmet in the body is rapid, based on live rat studies, with almost complete absorption (84.4%) within 24 hours of administering dose. At 0.5 hours after dosing, it was observed that the peak concentration of blood and plasma concentrations are observed. The elimination of phosmet takes place in two phases. The first phase corresponds with the distribution of the compound to tissues and has an observed half life of 0.2 to 6 hours. The second phase corresponds with the direct elimination of the compound and has a significantly longer half life of 41 to 1543 hours.

The distribution of the compound can be observed and analyzed at every dosage in a variety of tissues. The areas that display the highest level of activity can be found in the liver and the whole blood as this is where the major metabolic process takes place. The lowest level of activity for the compound can be observed in the bone and fat of the individual.