ATN-224 抑制内皮细胞中的 SOD1 活性，这种作用呈剂量依赖性，IC50 为 17.5±3.7 nM。 ATN-224 是一种口服 Cu2+/Zn2+-超氧化物歧化酶 1 (SOD1) 抑制剂。

ATN-224 inhibits SOD1 activity in endothelial cells, an effect that is dose dependent with an IC50 of 17.5±3.7 nM. ATN-224 is an oral Cu2+/Zn2+-superoxide dismutase 1 (SOD1) inhibitor.

ATN-224 is an orally-available inorganic small molecule that inhibits the copper/zinc-dependent enzyme, superoxide dismutase 1 (Cu/Zn-SOD1), in endothelial and tumor cells[2] amd it is able to inhibit SOD1 activity in endothelial cells, an effect that is dose dependent with an IC50 of 17.5±3.7 nM. ATN-224 inhibits FGF-2-induced ERK1/2 phosphorylation in a dose-dependent and time-dependent manner with an IC50 between 1.25 and 2.5 μM, consistent with the IC50 for the inhibition of proliferation[1], and it inhibits the proliferation of both HUVEC (IC50=1.4±0.3 μM; n=5) and it is also able to inhibit the activity of purified bovine SOD1 with an IC50 of 0.33±0.03 μM after 24 hours of incubation. ATN-224 has a specific and high affinity for copper ions (108 mol/L-1) and shows no binding to calcium, iron, magnesium, zinc, or manganese ions at concentrations up to 1 mM as determined by isothermal titration calorimetry. The SOD1 inhibition by ATN-224 is time dependent, reaching maximal inhibition at ~16 hours. ATN-224 seems to inhibit SOD1 by depleting the enzyme of copper.

Inhibition of angiogenesis when ATN-224 is given by oral gavage occurred before there is measurable depletion of copper in either plasma or copper from the Matrigel plug. ATN-224 also significantly (P<0.05) inhibits angiogenesis in the Matrigel plug model in mice either when added directly to the plug or when given by oral gavage. This result shows that ATN-224 inhibits angiogenesis independently of copper depletion[1].

649749-10-0

C5H14MoNOS4

328.37

四硫钼酸二胆碱;Bis(choline)tetrathiomolybdate

DMSO:50 mg/mL (115.59 mM),Need ultrasonic
Powder: -20°C for 3 years
In solvent: -80°C for 2 years