trpm4

TRPM4 inhibitor 8 is an inhibitor of Transient receptor potential melastatin 4(TRPM4) which contributes to viability, migration, cell cycle shift, and adhesion.

TRPM4-IN-2 (NBA), also known as NBA, is a highly effective inhibitor of transient receptor potential melastatin 4 (TRPM4). Its inhibitory potency is represented by an IC 50 value of 0.16 μM. This compound serves as a valuable tool in the investigation of prostate cancer and colorectal cancer [1] [2].

NMDAR/TRPM4-IN-2 is a potent interfacial inhibitor of NMDAR/TRPM4 interaction.NMDAR/TRPM4-IN-2 protects against MCAO-induced brain damage and NMDA-induced retinal ganglion cell loss in mice.NMDAR/TRPM4-IN-2 has neuroprotective activity against NMDA-induced hippocampal neuronal cell death and mitochondrial dysfunction. NMDAR/TRPM4-IN-2 showed neuroprotective activity against NMDA-induced cell death and mitochondrial dysfunction in hippocampal neurons with an IC50 value of 2.1 μM.

TRPM4-IN-1 (4-chloro-2-(2-(2-chlorophenoxy)acetamido)benzoic acid) is a potent and selective inhibitor of TRPM4 with an IC50 of 1.5 μM.

9-Phenanthrol is inhibitor of the transient receptor potential melastatin 4 (TRPM) channel, a Ca2+ -activated non-selective cation channel.

CMP233 is a potent antagonist of TRPM4, with an IC50 of 0.15 μM. It plays a significant role in the research of neurodegenerative diseases.

ErSO-TFPy activates the sodium ion channel TRPM4, resulting in an imbalance of intracellular calcium and sodium ions. It exhibits low nanomolar-level cytotoxicity (IC50 = 5-25 nM) by inducing necrosis in ERα+ breast cancer cell lines. Additionally, ErSO-TFPy shows antitumor activity in mouse models.

HZS60 is a brain-penetrant NMDAR/TRPM4 inhibitor that shows promise in ameliorating cerebral ischemia. It provides significant neuroprotection against ischemic injury in primary neurons caused by NMDA and oxygen-glucose deprivation/reoxygenation. HZS60 demonstrates favorable pharmacokinetic properties and can inhibit cerebral ischemia-reperfusion injury, positioning it as a potential inhibitor for ischemic stroke.

FP802 is a potent oral TwinF interface inhibitor capable of disrupting and neutralizing the toxicity of the NMDAR/TRPM4 death complex. Within the 5xFAD Alzheimer's disease (AD) mouse model, FP802 demonstrates significant neuroprotective effects, preventing cognitive decline, preserving neuronal structural integrity, reducing β-amyloid plaque formation, and mitigating mitochondrial damage. In the amyotrophic lateral sclerosis (ALS) mouse model, FP802 prevents motor neuron loss, lowers serum neurofilament light chain (NfL) levels, improves motor performance, and extends the lifespan of mice. FP802 can be utilized for research related to Alzheimer's disease and amyotrophic lateral sclerosis [1][2].

TRPM5 agonist-1 is an orally active TRPM5 agonist with a pEC50 value of 8.1. It displays excellent selectivity for related cation channels (TRPM8, TRPV1, TRPV4, TRPA1, TRPM4) with selectivity greater than 100-fold. TRPM5 agonist-1 induces local stimulation of gastrointestinal transit in mice and is useful for studying the promotion of gastric motility.

CIM0216 is a synthetic TRPM3 activator whose potency and apparent affinity greatly exceeds that of the canonical TRPM3 agonist.

FP802 2HCl is an orally active TwinF interface inhibitor with neuroprotective effects. It disrupts the toxicity of the NMDAR/TRPM4 death complex to selectively eliminate eNMDAR-mediated toxicity, suitable for studying Alzheimer's disease (AD) and amyotrophic lateral sclerosis (ALS).