NecroX-5NecroX-5
MedChemExpress (MCE)
HY-104015
1383718-29-3
98.16%
4°C, stored under nitrogen *In solvent : -80°C, 6 months
-20°C, 1 month (stored under nitrogen)
Room temperature in continental US
may vary elsewhere.
NecroX-5 is a derivative of the NecroX, reduces intracellular calcium concentration, and possesses anti-inflammatory and anti-cancer activity.
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].
NecroX-5 (2.5 mg/kg, everyday other day) inhibits breast cancer cell metastasis in TUBO-P2J tumour-bearing mice[1].
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]. MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. 0 --> NecroX-5 Related Antibodies
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[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. [Content Brief]
[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. [Content Brief]