Treatment
- abiraterone
- anastrozole
- bicalutamide
- capecitabine
- CAPOX
- carboplatin
- cetuximab
- cisplatin
- crizotinib
- dacarbazine
- docetaxel
- doxorubicin
- epirubicin
- erlotinib
- everolimus
- exemestane
- fluorouracil
- flutamide
- FOLFOX
- FOLFIRI
- fulvestrant
- gefitinib
- gemcitabine
- goserelin
- imatinib
- irinotecan
- lapatinib
- letrozole
- leuprolide
- liposomal doxorubicin
- megestrol acetate
- nab-paclitaxel
- oxaliplatin
- paclitaxel
- panitumumab
- pemetrexed
- pertuzumab
- sorafenib
- sunitinib
- tamoxifen
- temozolomide
- temsirolimus
- topotecan
- toremifene
- trastuzumab
- vemurafenib
cetuximab
Cetuximab binds specifically to EGFR on both normal and tumor cells and
competitively inhibits the binding of epidermal growth factor (EGF) and other ligands.
Animal studies have shown that binding of cetuximab to EGFR blocks phosphorylation
and activation of receptor-associated kinases, resulting in inhibition of cell growth,
induction of apoptosis, and decreased matrix metalloproteinase and vascular
endothelial growth factor production. Signal transduction through EGFR results in
activation of wild-type KRAS protein. However, in cells with activating KRAS somatic
mutations, the mutant KRAS protein is continuously active and appears independent of
EGFR regulation.
Cetuximab is indicated* for treatment of head and neck cancer and colorectal cancer.
*Please refer to full prescribing information/package insert for precise indications.


