Table 2.

TH-302 exhibits broad antitumor activity in a panel of xenograft tumors

Cell lineCancer typeDoseDrug exposureTGD500TGD1,000TGI% (day “x”)P value vs. vehicleMaximal BW loss% (day “x”)HF% (n)
H460NSCLC50500181989 (22)<0.0012.9 (4)16.3 (8)
Calu-6NSCLC50500111251 (33)<0.011.2 (11)10.2 (6)
H82SCLC505004550 (15)<0.010.1 (4)6.9 (7)
Stew2Melanoma5050014NA31 (39)<0.0506.4 (6)
A375Melanoma505005749 (18)<0.0505.0 (5)
PLC/PRF/5HCC505005NA29 (39)>0.055.6 (22)4.7 (7)
PC-3Prostate50500131147 (36)<0.011.2 (11)4.2 (8)
786-ORCC5050010NA10 (64)>0.050.1 (8)1.4 (8)
Hs766t*Pancreas7537516.5>2575 (11)<0.013.4 (11)14.8 (9)
BxPC-3*Pancreas753751640 (15)<0.011 (8)7.2 (11)
SU.86.86*Pancreas7537513.528 (18)>0.0504.8 (8)

NOTE: TH-302 was administered intraperitoneally. and the regimens were QD × 5/wk × 2 wks except *, Q3Dx5 in Hs766t, BxPc3, and SU.86.86; Drug exposure (in mg/kg) = dose (in mg/kg) × number of doses. TGI was obtained from 10 animals per group. Data are presented as mean value for each group. P value of tumor growth between TH-302–treated and vehicle-treated groups was analyzed by t test when TGI was calculated. The hypoxic fraction (HF) was evaluated in the viable tumor tissue with necrotic area excluded. day “x”, time points at which TGI and weight loss was determined. n, number of tumors samples analyzed; NA, not available before the study was terminated.