Name | Brontictuzumab |
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Description | Brontictuzumab (OMP 52M51) is a monoclonal antibody (MAb) that inhibits Notch1 signal. Brontictuzumab selectively binds the negative regulatory region of the Notch1. Brontictuzumab inhibits tumor cell proliferation. Brontictuzumab can be used in the research of leukemia and lymphoma[1][2][3]. |
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Related Catalog | |
In Vitro | Brontictuzumab (0-100 μg/mL) inhibits Notch1 signaling, including DLL4, JAG1/2 activity[1]. Brontictuzumab (25 μg/mL, 4 days) reduces the levels of Notch1 intracellular domain in the HPB-ALL cell line[1]. Brontictuzumab (25 μg/mL, 48 h) inhibits DLL4-mediated cleaved-Notch1 overexpression in MCL cells[2]. Brontictuzumab (25 μg/mL, 48 h) blocks the increased phosphorylation of both, MEK and ERK by DLL4 stimulation in Mino cells[2]. Western Blot Analysis[2] Cell Line: DLL4 (4 μg/mL)-stimulated MCL cells Concentration: 25 μg/mL Incubation Time: 24 or 48 h Result: Inhibited DLL4-dependent activation of Notch1. |
In Vivo | Brontictuzumab (15 mg/kg, i.p.) reduces tumor burden in T-ALL xenograft[3]. Brontictuzumab (20 mg/kg, i.p., every 4 days) inhibits DLL4 induced activation of Notch1 in MCL model[2]. Animal Model: T-ALL xenograft[3] Dosage: 15 mg/kg Administration: Intraperitoneal injection (i.p.), twice weekly. Result: Inhibited tumor growth and reduced the size of the spleen. Showed massive infiltration and replacement of normal hematopoiesis by leukemia cells. Animal Model: NSG mice injected with DLL4-stimulated NOTCH1-mutated mino cells ex vivo[2] Dosage: 20 mg/kg Administration: Intraperitoneal injection (i.p.) Result: Inhibited cleaved Notch1 but was not enough to cause a significant efficacy in tumor growth. |
References |
No Any Chemical & Physical Properties |