Table 1

Inhibition of IGF-I-stimulated proliferation and survival of human cancer cells by EM164 antibody

Cancer cell typeFold increase in MTT signal upon IGF-I stimulationaPercentage inhibition of IGF-I-stimulated MTT signal increase by EM164
MCF-7 (breast)∼3100%
T-47D1.695%
NCI-H838 (lung)3100%
Calu-61.785%
NCI-H12991.595%
NCI-H4601.680%
NCI-H231.685%
NCI-H5961.7100%
NCI-H4411.760%
HT-3 (cervical)385%
Colo 205 (colon)2.260%
HT-291.560%
BxPC-3 (pancreatic)2.180%
MiaPaCa-22.670%
ASPC-12.375%
A-375 (melanoma)1.470%
M141.570%
RD (rhabdomyosarcoma)1.895%
SaOS-2 (osteosarcoma)2.5100%
Ovcar-5 (ovarian)1.765%
A 431 (epidermoid)2.285%
PC-3 (prostate)1.370%
SK-N-SH (neuroblastoma)285%
  • a MTT assay was performed after 3 days of growth of cancer cells under four conditions: (a) no IGF-I, no EM164; (b) no IGF-I, + EM164; (c) + IGF-I, no EM164; and (d) + IGF-I, + EM164. To account for the inhibition of autocrine signaling by EM164, the percentage of inhibition by EM164 was calculated from the MTT assay signals as: 100 × [((c)–(d))/((c)–(b))]. Concentrations used were [IGF-I] = 10–20 ng/ml (1.2–2.4 nm) and [EM164 antibody] = 10–20 μg/ml (60–120 nm).