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Insect Growth Regulators

by James L. Krysan and John Dunley, originally published 1993

Several features of insect growth regulators (IGRs) make them attractive as alternatives to broad-spectrum insecticides. Because they are more selective, they are less harmful to the environment and more compatible with pest management systems that include biological control.

Insects have demonstrated a propensity to develop resistance to insecticides. Broad-spectrum insecticides that are used routinely will eventually be lost because of resistance. Intelligent use of IGRs should reduce the likelihood of resistance developing.

IGRs show good potential on pears because their selectivity preserves the natural enemies that can help control pear psylla. Because of its ability to rapidly develop resistance to insecticides, it is important that psylla be controlled by an integrated system, incorporating several control factors, The selectivity of IGRs is due to the different way they act on insects, compared with most conventional insecticides.

Virtually all chemicals used to control insects fall into one of three categories: neurotoxins, growth regulators and behavior modifiers.


Most chemicals used to control insects are neurotoxins which interfere with normal nerve function. Organophosphate insecticides were derived from nerve gases that were first exploited for military purposes. Other insecticides were discovered by testing chemicals to find those that killed pests quickly. About the only thing that kills quickly is a neurotoxin so chemicals that acted on neurotransmissions were sought and developed as insecticides. In the early discovery and development of insecticides, efforts were focused on chemistry rather than biology. Because all animals share basically the same neurochemical systems, neurotoxins are toxic to all animals.

Insect growth regulators

The origin of IGRs was entirely different. Their discovery was based on knowledge of how insects grow, develop, function and behave. They have been discovered in two ways. One way was to expose an insect to IGRs and observe abnormalities in how it develops, functions or behaves. Chemicals that produce desired effects were developed. Another was to find out what processes in the insects’ development involve hormones and to use those hormones as models to synthesize chemical analogs that will interfere with normal insect growth and development. Because IGRs act on systems unique to insects, or shared with close relatives, they are less likely to affect other organisms.

Behavior modifiers

Behavior-affecting chemicals, such as pheromones, are discovered in the same way as IGRs but tend to be even more specific. Pheromones aid the sexes of a single species to find each other so that effort is not wasted chasing mates of a different species.

How insect growth regulators work

Insects wear their skeletons on the outside. The skeletons are called exoskeletons. As the insect grows, a new exoskeleton must be formed inside the old exoskeleton and the old one shed. The new one then swells to a larger size and hardens. The process is called molting. The changes from larval to adult form, a process called metamorphosis, also take place during molting. Hormones control the phases of molting by acting on the epidermis, which is part of the exoskeleton.

There are three types of IGRs, each of which has a different mode of action:

Chitin synthesis inhibitors

These prevent the formation of chitin, a carbohydrate that is an important structural component of the insect’s exoskeleton. When treated with one of these compounds, the insect grows normally until the time to molt. When the insect molts, the exoskeleton is not properly formed and it dies. Death may be quick, but in some insects it may take several days. As well as disrupting molting, chitin synthesis inhibitors can kill eggs by disrupting the normal development of the embryo.

Juvenile hormone analogs and mimics

When applied to an insect, these abnormal sources of juvenilizing agent can have striking consequences. For example, if the normal course of events calls for a molt to the pupal stage, an abnormally high level of juvenilizing agent will produce another larval stage or produce larval-pupal intermediates. Juvenoid IGRs can also act on eggs. They can cause sterilization, disrupt behavior and disrupt diapause, the process that triggers dormancy before the onset of winter. In theory, all insect systems influenced by juvenile hormone are potential targets for a juvenoid IGR.

The early juvenoid IGRs were true analogs of juvenile hormone and were unstable when exposed to ultraviolet light. This seriously limited their use in plant protection. Another group of juvenoid IGRs, called juvenile mimics, was discovered. Entomologist found that extracts of many plant tissues have juvenilizing effects, but they have different chemical structures from juvenile hormones and are much more stable. They have been used as models to synthesize some highly effective and stable juvenile hormone mimics which have potential to control tree fruit pests.

Anti-juvenile hormone agents

Anti-juvenile hormone agents cancel the effect of juvenile hormone by blocking juvenile hormone production. For example, an early instar treated with an anti-juvenile hormone agent molts prematurely into a nonfunctional adult. A disadvantage of these chemicals is that they are so selective that they may not be economic for a manufacturer to develop.

Washington State University