872514-65-3

872514-65-3 structure
872514-65-3 structure
  • Name: Rilotumumab
  • Chemical Name: Rilotumumab
  • CAS Number: 872514-65-3
  • Molecular Formula:
  • Molecular Weight:
  • Catalog: Signaling Pathways Protein Tyrosine Kinase/RTK c-Met/HGFR
  • Create Date: 2022-10-13 07:00:09
  • Modify Date: 2024-01-11 11:46:02
  • Rilotumumab (AMG 102) is an anti-HGF (anti-hepatocyte growth factor) monoclonal antibody, inhibits HGF/MET-driven signaling. Rilotumumab shows anti-tumor activity, and can be used in castration-resistant prostate cancer (CRPC) and solid tumor research[1][2].

Name Rilotumumab
Description Rilotumumab (AMG 102) is an anti-HGF (anti-hepatocyte growth factor) monoclonal antibody, inhibits HGF/MET-driven signaling. Rilotumumab shows anti-tumor activity, and can be used in castration-resistant prostate cancer (CRPC) and solid tumor research[1][2].
Related Catalog
In Vitro Rilotumumab (10 μg/mL; overnight) shows the decrease of MET phosphorylation at Y1234 and Y1235, and an increase in total MET[2]. Western Blot Analysis[2] Cell Line: U87MG.vIII cells Concentration: 10 μg/mL Incubation Time: Overnight Result: Showed MET phosphorylation at tyrosine residue 1234 (Y1234) and Y1235 ~50% lower in U87MG.vIII cells than in untreated cells. Showed an increase in total MET compared with untreated cells.
In Vivo Rilotumumab (intraperitoneal injection; 1.5 mg/kg; once two days; 11 d) treatment inhibits glioma cell growth in vivo[2]. Animal Model: 6-8-week-old BALB/c nu/nu female mice subcutaneous injected with U87MG.vIII cells[2] Dosage: 1.5 mg/kg Administration: Intraperitoneal injection; 1.5 mg/kg; once two days; 11 days Result: Reduced U87MG.vIII xenograft growth (P=0.0002) compared with vehicle-treated xenografts (P=0.0001).
References

[1]. Ryan CJ, et al. Targeted MET inhibition in castration-resistant prostate cancer: a randomized phase II study and biomarker analysis with rilotumumab plus mitoxantrone and prednisone. Clin Cancer Res. 2013 Jan 1;19(1):215-24.

[2]. Greenall SA, et al. EGFRvIII-mediated transactivation of receptor tyrosine kinases in glioma: mechanism and therapeutic implications. Oncogene. 2015 Oct 8;34(41):5277-87.

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