Pharmacological inhibition of ADAM10 and ADAM17 improves functional recovery after spinal cord injury (SCI)[3]. Animal Model: C57BL/6 mice[3] Dosage: 100 µg/kg Administration: I.p. injected; every day for one week starting 4 h post-surgery Result: Showed significantly improved functional recovery compared to the control group.
In Vitro
The proliferation of GS-7 cells was significantly reduced upon treatment with GW280264X or ADAM10/17 co-knockdown[2]. Cell Viability Assay[2] Cell Line: Glioblastoma-initiating cells (GIC) GS-7 cells Concentration: 0.1, 1, and 3 µM Incubation Time: 48 hours Result: Proliferation of GIC is inhibited through inhibition of ADAM10 and ADAM17.
Kinase Assay
Cell Assay
Animal Administration
References
[1]. Christian Hundhausen, et al. The disintegrin-like metalloproteinase ADAM10 is involved in constitutive cleavage of CX3CL1 (fractalkine) and regulates CX3CL1-mediated cell-cell adhesion. Blood. 2003 Aug 15;102(4):1186-95.
[2]. Fabian Wolpert, et al. A disintegrin and metalloproteinases 10 and 17 modulate the immunogenicity of glioblastoma-initiating cells. Neuro Oncol. 2014 Mar;16(3):382-91.
[3]. Daniela Sommer, et al. ADAM17-deficiency on microglia but not on macrophages promotes phagocytosis and functional recovery after spinal cord injury. Brain Behav Immun. 2019 Aug;80:129-145.
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