The loops have functional sites, including two cysteines for a disulfide bridge, Asp-Arg-Tyr, responsible for association with arrestin, and Lys/Arg-Lys/Arg-X-X-Lys/Arg, which interacts with G-proteins.

[11] The binding of SP to the NK1 receptor has been associated with the transmission of stress signals and pain, the contraction of smooth muscles, and inflammation.

[6] When NK1 receptors are stimulated, they can generate various second messengers, which can trigger a wide range of effector mechanisms that regulate cellular excitability and function.

There are three well-defined, independent second messenger systems: It has also been reported that SP elicits interleukin-1 (IL-1) production in macrophages, sensitizes neutrophils, and enhances dopamine release in the substantia nigra region in cat brain.

Likewise, SP is known to bind to N-methyl-D-aspartate (NMDA) receptors, eliciting excitation with calcium ion influx, which further releases nitric oxide.

Studies in frogs have shown that SP elicits the release of prostaglandin E2 and prostacyclin by the arachidonic acid pathway, which leads to an increase in corticosteroid output.

[14] It has been reported that centrally-acting NK1 receptor antagonists, such as CP-99994, inhibit emesis induced by apomorphine and loperimidine, which are two compounds that act through central mechanisms.

[24][25] NK-1R antagonists, such as aprepitant, have shown promise as potential anticancer treatments by inhibiting tumor growth, inducing apoptosis, and blocking metastasis.