| 包装 | 价格(元) |
| 1mg | 电议 |
| 5mg | 电议 |
Cell lines | SCC1 and UM-SCC-22B cells |
Preparation Method | The toxicity of cetuximab to SCC1 and UM-SCC-22B cells was determined by MTT assay. At 72 h or 120 h after treatment with different doses of cetuximab (ranging from 0.1 nM to 0.5 μM), the culture medium was replaced and 50 μl of 1.0 mg/ml sterile filtered 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide (MTT; Sigma) was added to each well. |
Reaction Conditions | 0.1 nM to 0.5 μM at 72 h or 120 h |
Applications | Treatment with cetuximab produced only modest inhibition of cell proliferation on SCC1 cells in vitro as determined by MMT assay. |
Animal models | BALB/c (nu/nu) female nude mice |
Preparation Method | Xenografts were established in female nude mice (BALB c[nu/nu]) by subcutaneous injection of head and neck squamous cell carcinoma cell lines a UT-SCC-14 and b UT-SCC-2. Cetuximab (1 mg/injection) was administered by intraperitoneal injection at day 10, 13 and 16. The tumour size was recorded at an interval of 2–3 days, n = 10-14. |
Dosage form | 1 mg, i.p. |
Applications | Cetuximab treatment showed reduction in the nuclear accumulation of HIF-1α, while the overall HIF-1α expression was not significantly altered. And after cetuximab treatment a downregulation of CAIX was only found in UT-SCC-14 xenografts. Cetuximab treatment affects the tumour growth and the tumour partial oxygen pressure as measured by LiPc EPR oximetry. |
| 产品描述 | Cetuximab is a chimeric monoclonal antibody generated from fusion of the variable region of the murine anti-EGFR monoclonal antibody M225 and the human IgG1 constant region. It produced antibody retains high affinity and specificity to EGFR and reduces immunogenicity.[1]Cetuximab bound with high affinity to FcγRI (EC50 = 0.13 nM) and FcγRIIIa (EC50 = 6 nM). It effectively induced ADCC across multiple tumor cell lines.[4]Treatment with 100 μg/ml cetuximab for 24h enhances the cytotoxicity effect of RSL3 treatment on KRAS mutant CRC cells.[2] In vitro experiment indicated it that radiation enhances cetuximab (0.5 μg/ml)-mediated ADCC and activation of NK cells.[3]Treatment with 20 μg/mL cetuximab inhibited the proliferation of the parental UMSCC1 cell line (UMSCC1-P) ,while the three HNSCC cetuximab-resistant clones (C2, C5, and C11) were completely refractory to cetuximab.[6] In vivo experiment it shown that cetuximab (13 mg/kg, s.c.) enhances the inhibitory effects of RSL3 and RSL3-induced ferroptosis.[2]In vivo, after i.v. injection of 4 doses of 10 mg/kg body-weight demonstrated that cetuximab markly inhibited tumor growth in SCC1 tumor bearing mice.[5]In vivo experiment it illustrated that cetuximab-treated (50 mg/kg, i.p.) tumors showed delayed growth, when mice were inoculated with the NSCLC H226 cell line individually with 2x106 tumor cells in the dorsal flank.[6] References: |
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