GPR162 Inhibitoren

Gängige GPR162 Inhibitors sind unter underem SCH 23390 CAS 125941-87-9, Raclopride CAS 84225-95-6, Haloperidol CAS 52-86-8, (RS)-(±)-Sulpiride CAS 15676-16-1 und Spiperone CAS 749-02-0.

Chemical inhibitors of GPR162 can exert their inhibitory action through several mechanisms that involve interference with neurotransmitter systems, particularly the dopaminergic and serotonergic pathways. SCH-23390 serves as a selective antagonist for the D1 dopamine receptor, which when inhibited, can lead to a decrease in the signaling pathways that GPR162 is involved with. This is because GPR162 activity is modulated by the dopaminergic system, and antagonism of a receptor within this system can diminish GPR162's functional activity. Similarly, Raclopride, Sulpiride, L-741,626, and Domperidone, all dopamine D2 receptor antagonists, inhibit GPR162 by dampening the dopaminergic activity that influences the protein's function. The action of these chemicals can lead to a reduced dopaminergic signal transduction, thereby decreasing the functional activity of GPR162, which is responsive to changes in this neurotransmitter system.

In addition to the D2 receptor antagonists, chemicals like Haloperidol and Chlorpromazine are known to inhibit multiple dopamine receptors, which in turn can reduce the signaling cascade that involves GPR162. Spiperone, which acts as an antagonist of both dopamine D2 and serotonin 5-HT2 receptors, can inhibit GPR162 by attenuating the signaling of both dopamine and serotonin neurotransmitters. The complex interaction between these neurotransmitter systems and GPR162 suggests that alterations in either system can lead to a decrease in GPR162 activity. Tetrabenazine reduces vesicular monoamine transporter (VMAT) activity, leading to dopamine depletion, which in turn can inhibit GPR162 activity by reducing dopaminergic signaling. Clozapine and Olanzapine, both acting as antagonists to dopamine and serotonin receptors, also inhibit GPR162 through a similar mechanism of decreased neurotransmission, thereby reducing the signal relay that would otherwise involve GPR162's functional role in the brain. Through these various actions on neurotransmitter receptors and transporters, these chemicals can inhibit the functional activity of GPR162 by altering the neurotransmitter balance and signal transduction processes it is associated with.