BMS-561392  (Synonyms: DPC 333)

BMS-561392 (BMS-561392) is a selective ADAM17(TACE) inhibitor. BMS-561392 inhibits TNF-α secretion by regulating signaling pathways such as p44 MAPK and NF-κB. BMS-561392 also affects the survival of central nervous system-related cells including oligodendrocytes and microglia. BMS-561392 promotes microglial apoptosis, enlarges the injury area and exacerbates astrogliosis in a mouse spinal cord injury model. BMS-561392 can be used in research related to spinal cord injury and inflammatory diseases^[1][2].

BMS-561392 (10 nM; 1-2.5 h) potently inhibits recombinant human TACE (ADAM17) enzymatic activity by ~80%^[1].
BMS-561392 (10 μM; 1 h pre-incubation followed by 4 h LPS stimulation) effectively suppresses LPS-induced TNF-α secretion in RAW264.7 macrophage cells^[1].
BMS-561392 (1-100 μM; 1 h pre-incubation followed by 4 h LPS stimulation) dose-dependently inhibits LPS-induced p-IκB expression, and thus NFκB pathway activation, in RAW264.7 macrophage cells^[1].
BMS-561392 (1-100 μM; 1 h pre-incubation followed by 1 h LPS stimulation) inhibits LPS-induced p-NFκB expression in RAW264.7 macrophage cells^[1].
BMS-561392 (0.3-2.7 mM; 48 h) reduces viability of undifferentiated HOG cells in a concentration-dependent manner, with the greatest reduction (89.5-93.5%) observed at 2.7 mM after 48 h incubation^[2].
BMS-561392 (0.3-2.7 mM; 48 h) modulates viability of BV-2 microglial cells in a concentration-dependent manner after 48 h incubation, with a slight increase at 0.3 mM, 50% reduction at 1.3 mM, and 94% reduction at 2.7 mM^[2].
BMS-561392 (1.3-2.7 mM) induces apoptosis in BV-2 microglial cells, as shown by increased activated caspase-3-positive cells^[2].
BMS-561392 (2.7 mM; 3 h) increases membrane TNFR-1 expression in BV-2 microglial cells by >50% after 3 h incubation^[2].
BMS-561392 (0.3-2.7 mM; 3 h) modulates phosphorylated p44 MAPK levels in BV-2 microglial cells in a concentration-dependent manner after 3 h incubation, increasing levels at 0.3 mM and eliminating detectable levels at 2.7 mM, with no effect on phosphorylated p42 MAPK^[2].

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

BMS-561392 (2.2 mM; s.c.; daily; 15 days) significantly impairs locomotor recovery, increases lesion size and astrogliosis, reduces microglial/macrophage infiltration, and promotes microglial apoptosis in 10-week-old C57BL/6 mice post SCI^[2].

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

476.57

C₂₇H₃₂N₄O₄

611227-74-8

N[C@]1(C2=CC=C(C=C2)OCC3=CC(C)=NC4=C3C=CC=C4)C(N(CC1)[C@H](CC(C)C)C(NO)=O)=O

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• [1]. Park J, et al. Mechanistic Insights into Vorinostat as a Repositioned Modulator of TACE-Mediated TNF-α Signaling via MAPK and NFκB Pathways. Curr Issues Mol Biol. 2025 Sep 4;47(9):720.  [Content Brief]

  [2]. Vidal PM, et al. ADAM17 is a survival factor for microglial cells in vitro and in vivo after spinal cord injury in mice. Cell Death Dis. 2013;4(12):e954. Published 2013 Dec 12.  [Content Brief]