Human Anti-CCL2 Recombinant Antibody (clone CNTO 888) (CAT#: PABL-421)

Figure 1 CNTO888 inhibits PC-3ᴸᵘᶜ cell proliferation and migration in vitro.

PC-3ᴸᵘᶜ cells were stimulated with CCL2 (10 or 100 ng/mL) for 72 h in the presence or absence of CNTO888 (30 μg/mL), C1142 (30 μg/mL), or CNTO888 + C1142 (30 μg/mL each). The control antibody (Ab) for CNTO888 is anti-huIgG and the control antibody for C1142 is C1322 (a rat/mouse chimeric nonspecific antibody). Cell viability was measured by WST-1. Columns, mean percentage of serum-free medium control; bars, SD (*, P < 0.05; **, P < 0.01). SFM, serum-free medium.

Loberg, R. D., Ying, C., Craig, M., Day, L. L., Sargent, E., Neeley, C., ... & Pienta, K. J. (2007). Targeting CCL2 with systemic delivery of neutralizing antibodies induces prostate cancer tumor regression in vivo. Cancer research, 67(19), 9417-9424.

Figure 2 immunoblot analysis of Akt, p70S6 kinase, and mitogen-activated protein kinase p44/p42 activation.

Representative immunoblots from four independent experiments. 1, control; 2,CCL2 (100 ng/mL, 24 h); 3, CCL2(100 ng/mL) + CNTO888 (30 μg/mL); 4, CNTO888(30 μg/mL).

Loberg, R. D., Ying, C., Craig, M., Day, L. L., Sargent, E., Neeley, C., ... & Pienta, K. J. (2007). Targeting CCL2 with systemic delivery of neutralizing antibodies induces prostate cancer tumor regression in vivo. Cancer research, 67(19), 9417-9424.

Figure 3 Efficacy of single-agent anti-CCL2 antibodies compared with single-agent docetaxel in vivo.

Inhibition of CCL2 was compared with docetaxel (MTD 40 mg/kg) by bioluminescent imaging and quantification of total tumor burden. Mice received PC-3ᴸᵘᶜ cells by intracardiac injection (n = 10 per group). Beginning on day 14, mice received PBS (□), (CNTO888 (●), C1142),CNTO888 + C1142 (*), or docetaxel ( △ ) by i.p. injection (arrow, when treatment began). Solid lines, human antibodies; dashed lines, mouse antibodies.

Loberg, R. D., Ying, C., Craig, M., Day, L. L., Sargent, E., Neeley, C., ... & Pienta, K. J. (2007). Targeting CCL2 with systemic delivery of neutralizing antibodies induces prostate cancer tumor regression in vivo. Cancer research, 67(19), 9417-9424.

Figure 4 Anti-CCL2 antibodies in combination with docetaxel induce tumor regression in vivo.

Inhibition of CCL2 in combination with docetaxel (MTD 40 mg/kg)was assessed by bioluminescent imaging and quantification of total tumor burden and compared with docetaxel alone. Mice received PC-3Luccells by intracardiacinjection. Beginning on day 14, mice received PBS (□), docetaxel + CNTO888 (●), docetaxel + C1142 (□), docetaxel + CNTO888 + C1142 (*), or docetaxel ( w ) by i.p.injection. Docetaxel was administered every week for 3 wks (weeks 2–4), whereas antibodies were delivered twice per week for 6 wks (weeks 2–8). On week 8, allantibody treatments were stopped and tumor progression was monitored to week 12. [arrow (1), initiation of treatment; arrow (2), cessation of docetaxel; arrow (3),cessation of antibody therapy].

Loberg, R. D., Ying, C., Craig, M., Day, L. L., Sargent, E., Neeley, C., ... & Pienta, K. J. (2007). Targeting CCL2 with systemic delivery of neutralizing antibodies induces prostate cancer tumor regression in vivo. Cancer research, 67(19), 9417-9424.