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Table 3: Some mAbs against GFRs for treating cancer
Name of mAB Target Targeted stages Indication Mechanism of Resistance (known Status
action mechanism) (highest level)
Cetuximab (human ErbB1 Suppresses cell Metastatic Inhibition EGFR Yes (mutations in a Approved
IgG1) (use as single growth and colorectal; signaling (down number of diverse
or conjunction with metastasis head and neck regulates active genes are blamable
radiotherapy) carcinoma EGFRVII) and for intrinsic
ADCC resistance)
Panitumumab ErbB1 Suppresses cell Metastatic Prevents EGFR Approved
(human IgG2) (use as growth colorectal cancer activation
single agent)
Trastuzumab ErbB2 Suppresses cell HER2+ Inhibition ErbB2 Yes (overexpression Approved
(humanized IgG1) growth and metastatic breast signaling and of membrane
(use as single or angiogenesis, cancer ADCC associated
as adjuvant for induces cell glycoprotein MUC4;
chemotherapy) death increase IGF1R
signaling are some
of the reasons that
confer resistance)
Ganitumab (human IGF1R Inhibits cell Non-Hodgkin Blocks IGF-1 and-2 Yes (calcium Clinical
IgG1) (use as single growth, lymphoma, binding to IGF1R dependent trials (passed
or combined with delays tumor metastatic without crosslinking proliferation effects phase II)
different neoplastic progression pancreatic with IR, inhibits acquire resistance in
drugs) cancer, activation of prostate cancer cells)
metastatic Ewing IGF1R homodimer
family of tumors and IGF1R/IR
heterodimer
Cixutumumab (human IGF1R Induces cancer Solid tumors, Prevents IGF1 NA Clinical
IgG1) (use as single cell apoptosis, Ewing sarcoma binding to receptor trials (phase
or combined with decreases cell family tumors and subsequent I-II)
different neoplastic proliferation activation of
drugs) PI3K/AKT
survival pathway,
mediates receptor
internalization and
degradation
PF03446962/ TGF-βR Prevents Transitional cell Disrupts NA Clinical
Anti-Alk1 (human) angiogenesis carcinoma of co-localization of trials (phase
(dose dependent) bladder endothelial cells II)
with perivascular
cells and reduces
blood fl ow
Ramucirumab VEGFR2 Inhibits tumor Hepatocellular, Blocks VEGF Yes (VEGF-axis Clinical trials
(human IgG1): use angiogenesis and renal cell, binding to the dependent pathway (phase II)
as single or with growth and ovarian receptor and thus is involved for
neoplastic drugs carcinomas VEGF-signaling resistance)
and subsequently
angiogenesis
1B3 (used in Mouse Inhibits Pancreatic and Blocks PDGFR NA Preclinical
combination with PDGFRβ angiogenesis a nonsmall cell binding with trial
mAB against lung tumor receptor,
antitumor/ xenograft models ligand-stimulated
anti-angiogenic activation of
agent) PDGFRβ and
IMC-2C5 (human) Both Delays growth downstream NA Preclinical
mouse and (cell specifi c), signaling molecules trial
human inhibits in tumor cells
PDGFRβ angiogenesis
Clinical phase studies are checked in www.clinicaltrial.gov site. The targeted stages of mAbs in cancer progression are given based cell
line studies and preclinical trials. ADCC: Antibody-dependent cell-mediated cytotoxicity; NA: Not available data; EGFR: Epidermal
growth factor receptor; VEGF: Vascular endothelial growth factor; IGF: Insulin-like growth factor; PDGFR: Platelet-derived growth
factor receptor; mAbs: Monoclonal antibodies

Journal of Cancer Metastasis and Treatment ¦ Volume 1 ¦ Issue 3 ¦ October 15, 2015 ¦ 195