The products were isolated by column chromatography and have been characterized by detailed spectroscopic analysis. In-vitro cytotoxic evaluation of the investigational compounds (3a–j) were carried out on Colon (COLO-205), Prostate (PC-3), Ovary (OVCAR-5), Lung (A-549) and Neuroblastoma (IMR-32) cancer cell lines following the protocol reported by Skehan et al 11 The cytotoxicity of compounds is determined in terms of IC50. 5-flourouracil was used as positive control against Colon (COLO-205) and for Prostate (PC-3) cancer cells mitomycin was used. Paclitaxel was used as standard against Ovary (OVCAR-5) and Lung (A-549) cancer

cell lines where as Adriamycin was used as positive controls for Neuroblastoma (IMR-32) cancer cell line respectively. The results of in-vitro cytotoxic studies were found to be significant and

presented in Table 1. GW3965 cost Among the compounds SB431542 (3a–j) under investigation for cytotoxic potential, compounds 3b was found to be more active than standard 5-flourouracil (IC50 21 μM) against colon (COLO-05) cancer cells as evident by the IC50 12.6 μM and 3f was found to be comparable (IC50 27.7 μM). The compounds 3h (IC50 46.9 μM) and 3i (IC5059.4 μM) were moderately potent, where as compounds 3e (IC50 87.1 μM) and 3d (IC50 95.2 μM) were less active and for compounds 3a, c, g and j colon cancer cells were found to be resistant. The results for prostate (PC-3) cancer cells revealed that compounds 3b, e, f and h were able to inhibit the growth of cancer but found to be less active than positive control mitomycin as observed

from the value of IC50 (Table 1) where as the rest of tested compounds were not active 17-DMAG (Alvespimycin) HCl toward prostate cancer cells. Similar were the results for ovary (OVCAR-5) cancer cells where only compounds 3b (IC50 76.5 μM) and 3e (IC50 85.5 μM) were shown to possess moderate cytotoxic potential and for rest of the compounds under investigation these cancer cells were resistant. For lung (A-549) cancer cells the tested compounds were able to inhibit the growth, however less potent as the value of IC50 was on higher side compared to standard drug used Paclitaxel. The potency of compound 3e against neuroblastoma (IMR-32) cancer cell was revealed from its observed IC50 10.7 μM which is close to Adriamycin used as positive control, where as compound 3b, h and d were moderately acting against neuroblastoma cancer cells (Table 1) and all other compound were found to be very less active. It is pertinent to mention here that Adriamycin is a DNA alkylating agent and topoisomerase-II inhibitor, and is known to be active on the neuroblastoma (IC50 1.7 μM). Also, recently, we reported the design, synthesis and evaluation of chromone based molecules as potential topoisomerase inhibitor anticancer agents4; plausibly presently investigated molecules may be having similar mode of action as compound 3e has comparable results for cytotoxicity against neuroblastoma cancer cells.