Rilotumumab
Rilotumumab Basic information
- Product Name:
- Rilotumumab
- Synonyms:
-
- Rilotumumab
- Research Grade Rilotumumab(DHD03702)
- Rilotumumab (anti-HGF)
- AMG 102
- Research Grade Rilotumumab
- CAS:
- 872514-65-3
- MW:
- 0
- Mol File:
- Mol File
Rilotumumab Chemical Properties
- form
- Liquid
- color
- Colorless to light yellow
Rilotumumab Usage And Synthesis
Description
Rilotumumab is an anti-HGF antibody that prevents ligand binding to MET and its activation.
Uses
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].
Clinical Use
A phase I/II trial of rilotumumab in combination with erlotinib was evaluated in previously treated NSCLC patients with metastatic disease. The results indicated a favorable safety profile and success in terms of disease control rate. A phase Ib/II trial of rilotumumab or ganitumab in combination with etoposide and carboplatin or cisplatin was evaluated in extensive-stage SCLC patients.
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. DOI:10.1158/1078-0432.CCR-12-2605
[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. DOI:10.1038/onc.2014.448
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