tThe catalytic oxidation of CO into CO2on mesoporous Fe–Co mixed oxide nanocatalystsat low temperature was carried out. The catalysts with different ratios of Co3O4(1–30 wt.%)were prepared by a simple co-precipitation method. The original and calcined catalysts werecharacterized by TG, DTA, XRD, TEM, VSM, N2sorption analysis, surface chemisorbed oxy-gen and dc electrical conductivity measurements. The results revealed that the addition ofCo3O4to Fe2O3monotonically increases the amount of surface chemisorbed oxygen, elec-trical conductivity and catalytic activity of the nanocatalysts. The role of the active redoxsites established in these nanocatalysts such as, Co3+/Co2+, Fe3+/Fe2+and Co3+/Fe2+whichare responsible for such modification was discussed. The magnetic studies indicated thatthe Fe–Co mixed oxide nanocatalysts exhibited ferromagnetic nature and the catalyst con-taining 30 wt.% Co3O4calcined at 600◦C possessed the highest saturation magnetization(Ms= 51.5 emu g−1). In addition the kinetic data illustrated that, the activation energy val-ues of CO oxidation gradually decreased with increasing of Co3O4content. Moreover, thecatalytic behavior under different atmospheres during calcination was also studied.

tThe catalytic oxidation of CO into CO2on mesoporous Fe–Co mixed oxide nanocatalystsat low temperature was carried out. The catalysts with different ratios of Co3O4(1–30 wt.%)were prepared by a simple co-precipitation method. The original and calcined catalysts werecharacterized by TG, DTA, XRD, TEM, VSM, N2sorption analysis, surface chemisorbed oxy-gen and dc electrical conductivity measurements. The results revealed that the addition ofCo3O4to Fe2O3monotonically increases the amount of surface chemisorbed oxygen, elec-trical conductivity and catalytic activity of the nanocatalysts. The role of the active redoxsites established in these nanocatalysts such as, Co3+/Co2+, Fe3+/Fe2+and Co3+/Fe2+whichare responsible for such modification was discussed. The magnetic studies indicated thatthe Fe–Co mixed oxide nanocatalysts exhibited ferromagnetic nature and the catalyst con-taining 30 wt.% Co3O4calcined at 600◦C possessed the highest saturation magnetization(Ms= 51.5 emu g−1). In addition the kinetic data illustrated that, the activation energy val-ues of CO oxidation gradually decreased with increasing of Co3O4content. Moreover, thecatalytic behavior under different atmospheres during calcination was also studied.

tThe catalytic oxidation of CO into CO2on mesoporous Fe–Co mixed oxide nanocatalystsat low temperature was carried out. The catalysts with different ratios of Co3O4(1–30 wt.%)were prepared by a simple co-precipitation method. The original and calcined catalysts werecharacterized by TG, DTA, XRD, TEM, VSM, N2sorption analysis, surface chemisorbed oxy-gen and dc electrical conductivity measurements. The results revealed that the addition ofCo3O4to Fe2O3monotonically increases the amount of surface chemisorbed oxygen, elec-trical conductivity and catalytic activity of the nanocatalysts. The role of the active redoxsites established in these nanocatalysts such as, Co3+/Co2+, Fe3+/Fe2+and Co3+/Fe2+whichare responsible for such modification was discussed. The magnetic studies indicated thatthe Fe–Co mixed oxide nanocatalysts exhibited ferromagnetic nature and the catalyst con-taining 30 wt.% Co3O4calcined at 600◦C possessed the highest saturation magnetization(Ms= 51.5 emu g−1). In addition the kinetic data illustrated that, the activation energy val-ues of CO oxidation gradually decreased with increasing of Co3O4content. Moreover, thecatalytic behavior under different atmospheres during calcination was also studied.

Four series of 5-amino-2-ethylmercapto-4-phenyl-6-subistitutedthieno[2,3-d]pyrimidine (8a-d), 4-chloro-7-ethylmercapto-9-phenylpyrimido[5',4':4,5]thieno[3,2-d]triazine (9) and 2-ethylmercapto-8-oxo-4-phenyl-7-(4-chlorophenyl)pyrimido [4',5':4,5]thieno[2,3-d]pyrimidine (10) were synthesized and their structures were confirmed by 1H NMR, 13C NMR and MS spectrum. All compounds were evaluated for the IC50 values against three cancer cell lines (MCF-7, HUH-7 and BHK) and WISH cell. The IC50 of compound (8d) was calculated for each cell line. Interestingly, the IC50 for the normal human amnion WISH cell line was much higher (723 μg/ml) than those found for tumor cell lines; for BHK (17 μg/ml), for HUH-7 (5.8μg/ml), and for MCF-7 (8.3 μg/ml). The proliferation inhibition of normal (WISH) and tumor (BHK, HUH-7, and MCF-7) cells by compound (8d) was investigated using MTT assay and IC50 was calculated after 48 hrs of treatment for each cell line.

Four series of 5-amino-2-ethylmercapto-4-phenyl-6-subistitutedthieno[2,3-d]pyrimidine (8a-d), 4-chloro-7-ethylmercapto-9-phenylpyrimido[5',4':4,5]thieno[3,2-d]triazine (9) and 2-ethylmercapto-8-oxo-4-phenyl-7-(4-chlorophenyl)pyrimido [4',5':4,5]thieno[2,3-d]pyrimidine (10) were synthesized and their structures were confirmed by 1H NMR, 13C NMR and MS spectrum. All compounds were evaluated for the IC50 values against three cancer cell lines (MCF-7, HUH-7 and BHK) and WISH cell. The IC50 of compound (8d) was calculated for each cell line. Interestingly, the IC50 for the normal human amnion WISH cell line was much higher (723 μg/ml) than those found for tumor cell lines; for BHK (17 μg/ml), for HUH-7 (5.8μg/ml), and for MCF-7 (8.3 μg/ml). The proliferation inhibition of normal (WISH) and tumor (BHK, HUH-7, and MCF-7) cells by compound (8d) was investigated using MTT assay and IC50 was calculated after 48 hrs of treatment for each cell line.

Four series of 5-amino-2-ethylmercapto-4-phenyl-6-subistitutedthieno[2,3-d]pyrimidine (8a-d), 4-chloro-7-ethylmercapto-9-phenylpyrimido[5',4':4,5]thieno[3,2-d]triazine (9) and 2-ethylmercapto-8-oxo-4-phenyl-7-(4-chlorophenyl)pyrimido [4',5':4,5]thieno[2,3-d]pyrimidine (10) were synthesized and their structures were confirmed by 1H NMR, 13C NMR and MS spectrum. All compounds were evaluated for the IC50 values against three cancer cell lines (MCF-7, HUH-7 and BHK) and WISH cell. The IC50 of compound (8d) was calculated for each cell line. Interestingly, the IC50 for the normal human amnion WISH cell line was much higher (723 μg/ml) than those found for tumor cell lines; for BHK (17 μg/ml), for HUH-7 (5.8μg/ml), and for MCF-7 (8.3 μg/ml). The proliferation inhibition of normal (WISH) and tumor (BHK, HUH-7, and MCF-7) cells by compound (8d) was investigated using MTT assay and IC50 was calculated after 48 hrs of treatment for each cell line.

Four series of 5-amino-2-ethylmercapto-4-phenyl-6-subistitutedthieno[2,3-d]pyrimidine (8a-d), 4-chloro-7-ethylmercapto-9-phenylpyrimido[5',4':4,5]thieno[3,2-d]triazine (9) and 2-ethylmercapto-8-oxo-4-phenyl-7-(4-chlorophenyl)pyrimido [4',5':4,5]thieno[2,3-d]pyrimidine (10) were synthesized and their structures were confirmed by 1H NMR, 13C NMR and MS spectrum. All compounds were evaluated for the IC50 values against three cancer cell lines (MCF-7, HUH-7 and BHK) and WISH cell. The IC50 of compound (8d) was calculated for each cell line. Interestingly, the IC50 for the normal human amnion WISH cell line was much higher (723 μg/ml) than those found for tumor cell lines; for BHK (17 μg/ml), for HUH-7 (5.8μg/ml), and for MCF-7 (8.3 μg/ml). The proliferation inhibition of normal (WISH) and tumor (BHK, HUH-7, and MCF-7) cells by compound (8d) was investigated using MTT assay and IC50 was calculated after 48 hrs of treatment for each cell line.

Four series of 5-amino-2-ethylmercapto-4-phenyl-6-subistitutedthieno[2,3-d]pyrimidine (8a-d), 4-chloro-7-ethylmercapto-9-phenylpyrimido[5',4':4,5]thieno[3,2-d]triazine (9) and 2-ethylmercapto-8-oxo-4-phenyl-7-(4-chlorophenyl)pyrimido [4',5':4,5]thieno[2,3-d]pyrimidine (10) were synthesized and their structures were confirmed by 1H NMR, 13C NMR and MS spectrum. All compounds were evaluated for the IC50 values against three cancer cell lines (MCF-7, HUH-7 and BHK) and WISH cell. The IC50 of compound (8d) was calculated for each cell line. Interestingly, the IC50 for the normal human amnion WISH cell line was much higher (723 μg/ml) than those found for tumor cell lines; for BHK (17 μg/ml), for HUH-7 (5.8μg/ml), and for MCF-7 (8.3 μg/ml). The proliferation inhibition of normal (WISH) and tumor (BHK, HUH-7, and MCF-7) cells by compound (8d) was investigated using MTT assay and IC50 was calculated after 48 hrs of treatment for each cell line.

Four series of 5-amino-2-ethylmercapto-4-phenyl-6-subistitutedthieno[2,3-d]pyrimidine (8a-d), 4-chloro-7-ethylmercapto-9-phenylpyrimido[5',4':4,5]thieno[3,2-d]triazine (9) and 2-ethylmercapto-8-oxo-4-phenyl-7-(4-chlorophenyl)pyrimido [4',5':4,5]thieno[2,3-d]pyrimidine (10) were synthesized and their structures were confirmed by 1H NMR, 13C NMR and MS spectrum. All compounds were evaluated for the IC50 values against three cancer cell lines (MCF-7, HUH-7 and BHK) and WISH cell. The IC50 of compound (8d) was calculated for each cell line. Interestingly, the IC50 for the normal human amnion WISH cell line was much higher (723 μg/ml) than those found for tumor cell lines; for BHK (17 μg/ml), for HUH-7 (5.8μg/ml), and for MCF-7 (8.3 μg/ml). The proliferation inhibition of normal (WISH) and tumor (BHK, HUH-7, and MCF-7) cells by compound (8d) was investigated using MTT assay and IC50 was calculated after 48 hrs of treatment for each cell line.

Four series of 5-amino-2-ethylmercapto-4-phenyl-6-subistitutedthieno[2,3-d]pyrimidine (8a-d), 4-chloro-7-ethylmercapto-9-phenylpyrimido[5',4':4,5]thieno[3,2-d]triazine (9) and 2-ethylmercapto-8-oxo-4-phenyl-7-(4-chlorophenyl)pyrimido [4',5':4,5]thieno[2,3-d]pyrimidine (10) were synthesized and their structures were confirmed by 1H NMR, 13C NMR and MS spectrum. All compounds were evaluated for the IC50 values against three cancer cell lines (MCF-7, HUH-7 and BHK) and WISH cell. The IC50 of compound (8d) was calculated for each cell line. Interestingly, the IC50 for the normal human amnion WISH cell line was much higher (723 μg/ml) than those found for tumor cell lines; for BHK (17 μg/ml), for HUH-7 (5.8μg/ml), and for MCF-7 (8.3 μg/ml). The proliferation inhibition of normal (WISH) and tumor (BHK, HUH-7, and MCF-7) cells by compound (8d) was investigated using MTT assay and IC50 was calculated after 48 hrs of treatment for each cell line.