Typically, agonists generate maximal biological response by binding only some of the total available receptors. The unoccupied ones are called spare receptors. Spare receptors can result from two mechanisms. In some pathways, one agonist-receptor complex interacts with many intermediary protein molecules to activate multiple effector molecules. So, the number of receptors exceeds the available effector molecules, leaving many receptors spare. In other cases, even after the agonist-receptor complex disassembles, the activated intermediary proteins keep interacting with the effector proteins. As a result, only a few activated receptors are enough to evoke a maximal response, leaving the rest unused. Such mechanisms allow the cell to use a low concentration of endogenous agonists, such as hormones and neurotransmitters, to produce the full response. For example, 99% of insulin receptors are spare. The remaining are activated at low insulin concentration, maintaining blood glucose levels around the clock. Spare receptors also increase the cell's sensitivity to agonist drugs as the chances of drug-receptor interaction increase in a large receptor pool.