ip3

RO2959 Hydrochloride (RO2959 HCl) is a potent and selective inhibitor of CRAC channel(IC50: 402 nM). It is also a potent inhibitor of human IL-2.

CI-IP3 /PM is a cell-permeable caged inositol triphosphate that promotes the release of Ca2+ from internal storage under UV photolysis.

SMIP34 is an inhibitor of PELP1, binding to this target with a dissociation constant (Kd) of 37.4 μM. It demonstrates efficacy in inhibiting the proliferation of cancer cells and tumor progression. Specifically, SMIP34 is effective in breast cancer research, showing activity against wild-type (WT), mutant (MT) estrogen receptor-positive (ER+), and treatment-resistant (TR)-ER+ breast cancers.

RIP3 Activator 1 (compound C8) is an effective RIP3 activator that inhibits cell growth and induces necroptotic cell death (necroptosis) and autophagy through the RIP3 p62 Keap1 signaling pathway. Additionally, this compound enhances the expression of p-MLKL and promotes the accumulation of LC3-II and p62 proteins.

iP300v is a negative control for iP300w

OSIP339391 is a A2BAR antagonist.

TIP39, a neuropeptide and an agonist for the parathyroid hormone receptor type 2 (PTH2R), effectively increases cAMP levels in COS-7 cells featuring recombinant PTH2R from humans or rats (EC50s = 0.5 and 0.8 nM, respectively), as well as in F-11 cells that naturally express PTH2R (EC50 = 1.15 nM). Furthermore, TIP39 at 1 nM halts the cell cycle at the G0/G1 phase and reduces Sox9 expression, a crucial regulator of cartilage differentiation, in CFK2 rat chondrocytes. Additionally, administering 100 pmol/animal of TIP39 reduces the immobility period in the forced swim test in mice, indicating a potential antidepressant effect.

SMIP34 is an inhibitor of PELP1 that demonstrates the capability to reduce cell viability and colony formation. Additionally, SMIP34 induces cell apoptosis (apoptosis) and causes cell cycle arrest in the S phase. It reduces the expression of PELP1 and exhibits anti-tumor activity. SMIP34 also has potential for research in triple-negative breast cancer (TNBC).

IP3RPEP6 serves as a competitive inhibitor of IP3R. Its IC50 values for IP3R1, IP3R2, and IP3R3 are 9.0 μM, 3.9 μM, and 4.3 μM, respectively. This compound does not affect ryanodine receptors and Cx43 hemichannels, and it is capable of modulating intracellular calcium signaling.

IP3RCYT is an inhibitory peptide of IP3R that can prevent cytochrome C from binding with IP3R, with an IC50 of approximately 100 nM. It regulates intracellular calcium signaling. Additionally, IP3RCYT inhibits apoptosis in HeLa and Jurkat cells treated with staurosporine or membrane-bound Fas ligand (FasL).

(E)-GABAB receptor antagonist 1 is a trans-GABAB receptor antagonist that decreases GABA-induced IP3 (inositol trisphosphate) production with an IC50 of 37.9 μM. It is a selective and negative allosteric modulator of GABAB (γ-Aminobutyric acid) receptors.

2-Aminoethyl diphenylborinate (2-APB) is a chemical compound that inhibits IP3 receptors and TRP channels, though it activates TRPV1, TRPV2, and TRPV3 at higher concentrations.

(E)-GABAB receptor antagonist 1 decreases GABA-induced IP3 (inositol trisphosphate) production with IC50 of 37.9 μM.GABAB receptor antagonist 1 is a selective and negative allosteric modulator of GABAB (γ-Aminobutyric acid) receptors.

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.

D-myo-Inositol 1,4,5-trisphosphate hexapotassium salt is a second messenger that promotes the release of calcium ions from the endoplasmic reticulum.

Adenophostin A is a potent agonist of inositol trisphosphate (IP3) receptors, binding with high affinity to these receptors and effectively stimulating the release of calcium ions (Ca2+).

The phosphatidylinositol (PtdIns) phosphates represent a small percentage of total membrane phospholipids. However, they play a critical role in the generation and transmission of cellular signals. PtdIns-(1,2-dioctanoyl) is a synthetic analog of natural phosphatidylinositol (PtdIns) containing C8:0 fatty acids at the sn-1 and sn-2 positions. The compound features the same inositol and diacyl glycerol (DAG) stereochemistry as that of the natural compound. The short fatty acid chains of this analog, compared to naturally-occurring PtdIns, gives it different physical properties including high solubility in aqueous media. PtdIns are phosphorylated to mono- (PtdIns-P; PIP), di- (PtdIns-P2; PIP2), and triphosphates (PtdIns-P3; PIP3). Hydrolysis of PtdIns-(4,5)-P2 by phosphoinositide (PI)-specific phospholipase C generates inositol triphosphate (IP3) and DAG which are key second messengers in an intricate biochemical signal transduction cascade.

The phosphatidylinositol (PtdIns) phosphates represent a small percentage of total membrane phospholipids. However, they play a critical role in the generation and transmission of cellular signals. PtdIns-(4)-P1 (1,2-dioctanoyl) is a synthetic analog of natural phosphatidylinositol (PtdIns) featuring C8:0 fatty acids at the sn-1 and sn-2 positions. The compound contains the same inositol and diacylglycerol (DAG) stereochemistry as the natural compound. PtdIns-(4)-P1 can be phosphorylated to di- (PtdIns-P2; PIP2) and triphosphates (PtdIns-P3; PIP3). Hydrolysis of PtdIns-(4,5)-P2 by phosphoinositide (PI)-specific phospholipase C generates inositol triphosphate (IP3) and DAG which are key second messengers in an intricate biochemical signal transduction cascade.

Actein has a stimulatory effect on osteoblastic bone formation or has potential activity against osteoporosis, it also can prevent oxidative damage to osteoblasts in osteoporotic patients. Actein's ability to pathways involved in lipid disorders and carci

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.

Phosphatidylinositol-(4,5)-P2(1,2-dipalmitoyl), a synthetic analog of natural phosphatidylinositol (PtdIns) with C16:0 fatty acids at the sn-1 and sn-2 positions, maintains the inositol and diacylglycerol (DAG) stereochemistry of its natural counterpart. Although phosphatidylinositol phosphates constitute a minor fraction of total membrane phospholipids, they are pivotal in initiating and propagating cellular signals. This compound mirrors the activity of the natural phosphatidylinositol produced by PtdIns-4-phosphate 5-kinase's action on PtdIns-(4)-P1. Its hydrolysis by phosphoinositide (PI)-specific phospholipase C yields inositol triphosphate (IP3) and DAG, crucial secondary messengers in a complex signal transduction pathway.

MCU-i4 is a novel negative modulator of the MCU, binding MICU1 and impairing muscle cell growth.

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.

Calmodulin Binding Peptide 1, a potent CaM-binding peptide with picomolar (pM) affinity, originates from smooth muscle myosin light-chain kinase (MLCK peptide). It effectively blocks inositol trisphosphate (IP3)-induced calcium (Ca2+) release [1].