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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. Inhibits ADAM10 mediated neuronal outgrowth of dorsal root ganglion neurons in vitro.
Sold for research purposes under agreement from GlaxoSmithKline.
|Storage||Store at -20°C|
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
|Solvent||Max Conc. mg/mL||Max Conc. mM|
Preparing Stock Solutions
The following data is based on the product molecular weight 391.5. Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.
|Concentration / Solvent Volume / Mass||1 mg||5 mg||10 mg|
|0.2 mM||12.77 mL||63.86 mL||127.71 mL|
|1 mM||2.55 mL||12.77 mL||25.54 mL|
|2 mM||1.28 mL||6.39 mL||12.77 mL|
|10 mM||0.26 mL||1.28 mL||2.55 mL|
References are publications that support the biological activity of the product.
Ludwig et al (2005) Metalloprotease inhibitors for the disintegrin-like metalloproteinases ADAM10 and ADAM17 that differentially block constitutive and phorbol ester-inducible shedding of cell surface molecules. Comb.Chem.High Throughput Screen. 8 161 PMID: 15777180
Moss et al (2007) The ADAM10 prodomain is a specific inhibitor of ADAM10 proteolytic activity and inhibits cellular shedding events. J.Biol.Chem. 282 35712 PMID: 17895248
Hundhausen et al (2003) The disintegrin-like metalloproteinase ADAM10 is involved in constitutive cleavage of CX3CL1 (fractalkine) and regulates CX3CL1-mediates cell-cell adhesion. Blood 102 1186 PMID: 12714508
Inoshima et al (2011) A Staphylococcus aureus pore-forming toxin subverts the activity of ADAM10 to cause lethal infection in mice. Nat.Med. 17 1310 PMID: 21926978
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Keywords: GI 254023X, GI 254023X supplier, GI254023X, ADAM10, metalloproteases, MMPs, metalloproteinases, inhibits, inhibitors, adams, Matrix, Metalloprotease, ADAMs, 3995, Tocris Bioscience
8 Citations for GI 254023X
Citations are publications that use Tocris products. Selected citations for GI 254023X include:
Leoni et al (2015) Annexin A1-containing extracellular vesicles and polymeric nanoparticles promote epithelial wound repair. J Clin Invest 125 1215 PMID: 25664854
Sanz (2017) Ectodomain shedding of Limbic System-Associated Membrane Protein (LSAMP) by ADAM Metallopeptidases promotes neurite outgrowth in DRG neurons. Sci Rep 7 7961 PMID: 28801670
Gooden et al (2014) Elevated serum CXCL16 is an independent predictor of poor survival in ovarian cancer and may reflect pro-metastatic ADAM protease activity. Br J Cancer 110 1535 PMID: 24518602
Mikuličić et al (2019) ADAM17-dependent signaling is required for oncogenic human papillomavirus entry platform assembly. Elife 8 PMID: 31107240
Beerli et al (2019) Vaccinia virus hijacks EGFR signalling to enhance virus spread through rapid and directed infected cell motility. Nat Microbiol 4 216 PMID: 30420785
Wang and Pei (2018) Visualization of Alzheimer's Disease Related α-/β-/γ-Secretase Ternary Complex by Bimolecular Fluorescence Complementation Based Fluorescence Resonance Energy Transfer. Front Mol Neurosci 11 431 PMID: 30538620
O'Sullivan et al (2016) Fractalkine shedding is mediated by p38 and the ADAM10 protease under pro-inflammatory conditions inhuman astrocytes. Journal of Neuroinflammation 13 189 PMID: 27549131
Ezekwe et al (2016) ADAM10 Cell Surface Expression but Not Activity Is Critical for Staphylococcus aureus α-Hemolysin-Mediated Activation of the NLRP3 Inflammasome in Human Monocytes. J Bone Miner Res 8 PMID: 27043625
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Literature in this Area
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Alzheimer's disease (AD) is a degenerative brain disease and the most common cause of dementia, affecting approximately 47 million people worldwide. Updated in 2015, this poster summarizes the structural and functional changes observed in the progression of this neurodegenerative disease, as well as classic AD drug targets.