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3). Next, we determined the IC50 cell killing activity (and/or growth inhibition) of CPT-11 and SN-38 against MDA-MB-231 breast cancer cells. The IC50 values of CPT-11 and SN-38 were 25,000 http://www.selleckchem.com/products/forskolin.html and 100 nM, respectively (Fig. 6A). These data demonstrate that MDA-MB-231 breast cancer cells are approximately 250-fold more sensitive to SN-38 than CPT-11. To determine the cancer cell killing activity of conditioned media from NSC.rCE cells compared to media from NSCs alone or NSC.null cells, we cultured the MDA-MB-231 cells in such conditioned media in the presence of various concentrations of CPT-11 (0-100 ��M). The IC50 cell killing activities of the media from NSC.rCE, NSC alone, NSC.null cells were 0.5, 50, and 100 ��M CPT-11, respectively. These data demonstrate that the rCE secreted by NSC.rCE cells resulted in a 200-fold increase in breast cancer cell killing when compared to the NSC.null control (Fig. 6B). The data also suggest that the NSC.rCE/CPT-11 enzyme/prodrug system may be effective in killing breast cancer cells in vivo. To investigate the in vivo therapeutic efficacy of the NSC.rCE/CPT-11 system, we used our established mammary http://www.selleck.cn/products/AZD0530.html fat pad human breast cancer xenograft model. Treatment groups were as follows: (1) NSC.rCE + CPT-11; (2) NSC.rCE only; (3) CPT-11 only; (4) tumor only, no treatment. Mice received the above treatments weekly for four consecutive weeks, a regimen similar to that used in clinical trials of breast cancer patients treated with CPT-11 http://www.selleckchem.com/products/cx-5461.html [15]. A CPT-11 dose of 1.5 mg/kg body weight of mice was chosen based on the pharmacokinetics of CPT-11 and endogenous carboxylesterase activity in nu/nu mice. Organs were harvested 30�C40 days post-tumor implantation. Mice treated with NSC.rCE cells in combination with CPT-11 resulted in reduce size of tumor metastases in lung and lymph nodes compared to the control NSC.rCE only and tumor only groups (p