D-myo-Inositol 1,4,5-trisphosphate hexapotassium salt is promotes endoplasmic The second messenger of net calcium ions.

BHPI is a potent ERα inhibitor that blocks nuclear estrogen–ERα-regulated gene expression effectively. It triggers sustained ERα-dependent activation of the endoplasmic reticulum (EnR) stress sensor, notably the unfolded protein response (UPR), and consistently inhibits protein synthesis. With an IC50 value targeting ERα, BHPI's mechanism involves the rapid hyperactivation of PLCγ on the plasma membrane in ERα(+) cancer cells, which produces inositol 1,4,5-triphosphate (IP3). This, in turn, opens EnR IP3R calcium channels, leading to a rapid depletion of EnR Ca(2+) stores. SIGNIFICANTLY, BHPI alters estrogen-ERα's usual effect of causing mild and transient UPR activation by inducing a severe and prolonged UPR activation, transforming the UPR from a protective to a toxic response.

ARN 11391 enhances the function of the IP3-gated calcium channel ITPR1 (Inositol 1,4,5-trisphosphate (IP3) receptor type 1), boosting intracellular calcium ion signaling by directly targeting ITPR1. Furthermore, ARN 11391 amplifies calcium signaling in cells with mutant ITPR1 linked to SCA29, a variant of spinocerebellar ataxia.

Xestospongins and araguspongins, marine natural products originally isolated from sponges in the Pacific basin, exhibit vasodilatory effects. Inositol phosphates (IP) serve as crucial signal transduction messengers, activating IP3 receptors to facilitate Ca2+ release from intracellular stores. Araguspongin B specifically hinders the calcium-releasing function of inositol 1,4,5-trisphosphate at the receptor level within cerebral microsomes, demonstrating an inhibition concentration (IC50) of 0.6 µM. This potency places it nearly on par with xestospongin C in obstructing the IP3 receptor's activity.