Selective ADAM10 metalloprotease inhibitor; displays over 100-fold higher potency at ADAM10 compared to ADAM17. Blocks constitutive release of IL-6R, CX3CL1 and CXCL16 in cell-based cleavage experiments. Inhibits calcium ionophore-induced betacellulin shedding in IMPE cells. Prevents E-cadherin cleavage in A549 cells.
21H 33N 3O 4
Soluble to 20 mM in DMSO
Store at -20°C
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All Tocris products are intended for laboratory research use only.
Sold for research purposes under agreement from GlaxoSmithKline.
The ADAM10 prodomain is a specific inhibitor of ADAM10 proteolytic activity and inhibits cellular shedding events.
Moss ML, Bomar M, Liu Q, Sage H, Dempsey P, Lenhart PM, Gillispie PA, Stoeck A, Wildeboer D, Bartsch JW, Palmisano R, Zhou P
J. Biol. Chem., 2007;282(49):35712-21.
Metalloprotease inhibitors for the disintegrin-like metalloproteinases ADAM10 and ADAM17 that differentially block constitutive and phorbol ester-inducible shedding of cell surface molecules.
Ludwig et al.
Comb.Chem.High Throughput Screen., 2005;8:161
The disintegrin-like metalloproteinase ADAM10 is involved in constitutive cleavage of CX3CL1 (fractalkine) and regulates CX3CL1-mediates cell-cell adhesion.
Hundhausen et al.
A Staphylococcus aureus pore-forming toxin subverts the activity of ADAM10 to cause lethal infection in mice.
Inoshima et al.
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