A new naturally occurring N 1 , N 6-dihydrocinnamyl putrescine bisamide, JBIR-94, along with nine structural analogs and a series of substituted phenyl and alkyl putrescine bisamides have been synthesized from putrescine and appropriately substituted carboxylic acids, through carboxylic acid chlorides. Antimicrobial, 5-Lipooxygenase enzyme inhibitory and antioxidant studies were performed for all synthesized compounds. Dihydrocinnamyl series of putrescine bisamides (4a-4i) showed good bioactivities compared to substituted phenyl (6a-6g) and diakyl (6h-6j) series of compounds. Among all compounds, 4h (methylenedioxy analog) and 4a (JBIR-94) showed good antimicrobial, antiinflammatory and antioxidant activities.

A new series of phenolic glycoside esters, saccharumoside-B and its analogs (9b-9n, 10) have been synthesized by the Koenigs-Knorr reaction. Antiproliferative activities of the compounds (9b-9n, 10) were evaluated on various cancer cell lines including, MCF-7 breast, HL-60 leukemia, MIA PaCa-2 pancreatic, DU145 prostate, HeLa cervical and CaCo-2 colon, as well as normal human MCF10A mammary epithelial and human peripheral blood mononuclear cells (PBMC) by MTT assay. Compounds (9b-9n, 10) exhibited considerable antiproliferative effects against cancer cells with IC50 range of 4.43 ± 0.35 to 49.63 ± 3.59 µM, but they are less cytotoxic on normal cells (IC50 > 100 µM). Among all the compounds, 9f showed substantial antiproliferative activity against MCF-7 and HL-60 cells with IC50 of 6.13 ± 0.64 and 4.43 ± 0.35, respectively. Further mechanistic studies of 9f were carried out on MCF-7 and HL-60 cell lines. 9f caused arrest of cell cycle of MCF-7 and HL-60 cells at G0/G1 phase. Apoptotic population elevation, mitochondrial membrane potential loss, increase of cytosolic cytochrome c and Bax levels, decrease of Bcl-2 levels and enhanced caspases-9 and -3 activities were observed in 9f-treated MCF-7 and HL-60 cells. These results demonstrate anticancer and apoptosis-inducing potentials of 9f in MCF-7 and HL-60 cells via intrinsic pathway.

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