1383718-29-3

1383718-29-3 structure

Name: Necrox-5 methanesulfonate
Chemical Name: NecroX-5
CAS Number: 1383718-29-3
Molecular Formula: C₂₇H₃₉N₃O₉S₃
Molecular Weight: 645.808
Catalog: Signaling Pathways Membrane Transporter/Ion Channel Calcium Channel
Create Date: 2018-08-23 13:25:45
Modify Date: 2024-01-09 16:54:28
NecroX-5 is a derivative of the NecroX, reduces intracellular calcium concentration, and possesses anti-inflammatory and anti-cancer activity.

Name	NecroX-5
Synonyms	1H-Indol-7-amine, 5-[(1,1-dioxido-4-thiomorpholinyl)methyl]-2-phenyl-N-[(tetrahydro-2H-pyran-4-yl)methyl]-, methanesulfonate (1:2) 5-[(1,1-Dioxido-4-thiomorpholinyl)methyl]-2-phenyl-N-(tetrahydro-2H-pyran-4-ylmethyl)-1H-indol-7-amine methanesulfonate (1:2)

Description	NecroX-5 is a derivative of the NecroX, reduces intracellular calcium concentration, and possesses anti-inflammatory and anti-cancer activity.
Related Catalog	Signaling Pathways >> Membrane Transporter/Ion Channel >> Calcium Channel Research Areas >> Cancer Research Areas >> Inflammation/Immunology
Target	Calcium channel[1]
In Vitro	NecroX-5 (10 or 40 μM) inhibits breast cancer cell migration, which is correlated with mitoROS reduction, and mediated by AKT inhibition. NecroX-5 (10 μM) decreases intracellular calcium concentration in 4T1 cells by blocking Ca2+ influx, which mediated the inhibition of cell migration, AKT downregulation and the reduction of mitochondrial ROS levels[1]. NecroX-5 (10 µM) treatment for 24 h, effectively decreases the increased TNFα, TGFβ1, pSmad2 and the expression of Dcn in LPS-stimulated H9C2 cells[2].
In Vivo	NecroX-5 (2.5 mg/kg, everyday other day) inhibits breast cancer cell metastasis in TUBO-P2J tumour-bearing mice[1].
References	[1]. Park JH, et al. NecroX-5 prevents breast cancer metastasis by AKT inhibition via reducing intracellular calcium levels. Int J Oncol. 2017 Jan;50(1):185-192. [2]. Thu VT, et al. NecroX-5 exerts anti-inflammatory and anti-fibrotic effects via modulation of the TNFα/Dcn/TGFβ1/Smad2 pathway in hypoxia/reoxygenation-treated rat hearts. Korean J Physiol Pharmacol. 2016 May;20(3):305-14.