GHS-R Inibidores

Os inibidores comuns do GHS-R incluem, entre outros, a Substância P CAS 33507-63-0.

Chemical inhibitors of GHS-R work by directly antagonizing the activity of the receptor, which is normally activated by its endogenous fixator, ghrelin. D-Lys3]-GHRP-6, JMV 2959, Compound 26, PF-5190457, AZP-531 and YIL781 are all compounds that exhibit their inhibitory effects by binding to GHS-R, thus preventing binding and subsequent activation by ghrelin. These antagonistic actions ensure that the usual signal transduction initiated by ghrelin's interaction with GHS-R does not occur. For example, PF-5190457 and AZP-531 are analogues that mimic the structure of ghrelin to occupy the binding site on the GHS-R, but do not trigger the intracellular responses that ghrelin would, thus inhibiting the function of the receptor. Similarly, YIL781 obstructs the ghrelin signaling pathway, preventing the natural fixative from binding to the GHS-R.

Other compounds, such as Compound 21 and Epelsiban, also function as GHS-R inhibitors, competing with ghrelin for binding to the receptor, but without activating it. This competitive inhibition is crucial for blocking the cascade of signals that would normally follow ghrelin binding. SPA, a peptidomimetic ghrelin antagonist, and [D-Arg1,D-Phe5,D-Trp7,9,Leu11]-Substance P work by presenting a structure similar to that of ghrelin, thus preventing the natural hormone from activating the GHS-R. On the other hand, BIM-28163 adds to this repertoire of GHS-R inhibitors by also engaging the receptor in a way that obstructs the action of ghrelin. This molecule ensures that the receptor remains in an inactive state, unable to propagate the signaling that would normally result in GHS-R-mediated physiological responses. Each inhibitor, by binding to GHS-R, ensures that the functional activity of the receptor is suppressed, keeping the receptor in a state that does not support the subsequent signaling events normally initiated by ghrelin.