MJE3

MJE3 (20-27 μM; 12 h) potently inhibits proliferation of human breast cancer MDA-MB-231 cells, reducing proliferation by 60% after a 12 h treatment with an initial 20 μM dose followed by a second dose to reach 27 μM^[1].
MJE3 (19 μM; 12 h) inhibits proliferation of human breast cancer MDA-MB-231 cells with an IC₅₀ of 19 mM following a single 12 h treatment, while an alkene-containing analog is inactive^[1].
MJE3 (50 μM; 12 h) potently inhibits proliferation of MDA-MB-231 breast cancer cells and MUM2B melanoma cells^[2].
MJE3 (20 μM; 12 h) selectively covalently labels PGAM1, a 26-kDa glycolytic enzyme, in human breast cancer MDA-MB-231 cells after 12 h treatment with 20 μM MJE3^[1].
MJE3 (20 μM; 12 h in situ) selectively covalently labels recombinantly expressed PGAM1 in intact monkey kidney COS7 cells after 12 h treatment with 20 μM MJE3, but does not label the enzyme in cell extracts^[1].
MJE3 (20 μM; 1 h) covalently labels endogenous PGAM1 in intact human breast cancer MDA-MB-231 cells after 1 h treatment with 20 μM MJE3, but does not label the enzyme in cell extracts, while its ester-hydrolyzed product MJE51 shows no significant PGAM1 labeling^[1].
MJE3 (2 h) inhibits PGAM1 activity in human breast cancer MDA-MB-231 cells with an IC₅₀ of 33 μM following 2 h treatment, while structurally related MJE4 has no inhibitory effect at 100 μM, and in vitro treatment of cell extracts with MJE3 does not inhibit PGAM1 activity^[1].
MJE3 inhibits proliferation of MDA-MB-231 breast cancer cells by targeting PGAM1, with activity restricted to intact cells^[3].
MJE3 specifically targets PGAM1 and inhibits breast cancer cell proliferation via covalent modification of the PGAM1 active site by its in situ hydrolysis product MJE51^[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.