181223-80-3

DEL-22379 is an ERK dimerization Inhibitor. DEL-22379 readily binds to ERK2 with a Kd estimated in the low micromolar range, though binding is detectable even at low nanomolar concentrations. ERK2 dimerization is progressively inhibited with an IC50 of ~0.5 μM.

ChEBI: DEL-22379 is an oxindole that is 5-amino-oxindole in which the 5-amino group has undergone formal condensation with the carboxy group of 3-(piperidin-1-yl)propanoic acid to give the corresponding carboxamide and in which the hydrogens at position 3 have been replaced by a (5-methoxy-1H-indol-3-yl)methylene group (Z configuration). It is an inhibitor of extracellular signal-regulated kinase (ERK) dimerisation. It has a role as an ERK dimerisation inhibitor and an antineoplastic agent. It is a member of piperidines, a member of oxindoles, an enamide and a secondary carboxamide.

del-22379 is an inhibitor of the dimerization of erk with ic50 values ranging from 150-400 nm regardless of genotypes in oncogenic cells [1].as an spatial regulator of erk signals, erk dimerization is essential. impeding erk dimerization can result in the impeding of erk signals’ extranuclear component and hence result in curtailing tumor development and cellular transformation [1].in hek293 cells, del-22379 abolished egf-stimulated erk dimerization. in these cells, the egf-induced co-immunoprecipitation of hemagglutinin- or flag epitopes- tagged ectopic erk2 molecules, was abolished by del-22379 with an ic50 value of ~0.5 μm. in both assays, the inhibition of del-22379 to erk dimerization was not associated with erk phosphorylation. in the cytoplasm of egf-stimulated hela cells, erk dimerization was prominent, but previous treatment with del-22379 also resulted in no detected erk dimmers [1].in nude mice with some of the aforementioned tumor cell lines, del-22379 at a dose of 15 mg/kg inhibited erk dimerization evidently in xenografted tumors and in liver extracts. del-22379 inhibited the tumor progression of a375 cells (braf mutant) markedly. activated-ras-driven tumors were very sensitive to del-22379. data indicated that tumorigenesis had greater requirements for erk dimerization than for proliferation. in tumors, treatment with del-22379 resulted in extensive mucinous differentiation and cell death [1].

ERK2: 0.5 μM (IC₅₀)

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[1]. herrero a, pinto a, colón-bolea p, et al. small molecule inhibition of erk dimerization prevents tumorigenesis by ras-erk pathway oncogenes. cancer cell, 2015, 28(2): 170-182.