1753-19-1

Upstream product

• 1575-37-7 4-Bromo-benzene-1,2-diamine 
• 5228-61-5 5-bromo-2-nitroaniline 

Downstream Products

• 1753-20-4 5-bromo-4-nitrobenzo-2,1,3-selenadiazole 
• 147021-82-7 4-nitro-2,1,3-benzoselenadiazol-5-ol 
• 147021-89-4 4-bromo-3-nitro-1,2-phenylenediamine 

Relevant academic research and scientific papers

The investigation and bioorthogonal anticancer activity enhancement of a triphenylphosphine-labile prodrug of seleno-combretastatin-4

Here, a triphenylphosphine (TPP)-labile prodrug of seleno-combretastatin-4 (CSeD) was designed and synthesized. A detailed investigation revealed that CSeD, which was shown to be very safe in circulating blood, could react with TPP to release CA-4 and a selenodiazole derivative, with accompanying powerful anticancer and antiangiogenesis effects, as well as radiosensitization properties.

Synthesis and in vitro anticancer activities of some selenadiazole derivatives

A novel series of fourteen substituted selenadiazoles has been synthesized and the compounds tested for their in vitro antiproliferative and cytotoxic activities. The tests were carried out against leukemia (CCRF-CEM), colon (HT-29), lung (HTB-54), and breast (MCF-7) cancer cells. In order to assess the selectivity of the compounds under investigation the assays were also carried out on two non-tumoral lines - one mammary (184B5) and one bronchial epithelium (BEAS-2B) cell line. Assay-based antiproliferative activity studies revealed that seven derivatives (2a, 2c, 2e, 2f, 2g, 3a, and 3b) exhibited good activity against MCF-7 cells: for instance, 2c and 2f inhibited cell growth with nanomolar GI50 values. Compound 2f had a better antitumoral profile than vinorelbine and paclitaxel, two drugs that are used as first-line treatments in advanced, recurrent, and/or metastatic cancer. In the other cell lines the compounds showed moderate activity or were inactive - with the exception of 2a, which was also found to have antiproliferative activity. Modulation of the cell cycle and apoptotic effects of active compounds were further evaluated in MCF-7 cells. Of these, 6-bromo[1,2,5]selenadiazolo[3,4-b] pyridine (2a) was the most active, with an apoptogenic effect 3.9 times higher than that of camptothecin, which was used as a positive control. Compound 2a also provoked cell cycle arrest with a significant decrease in the G 0/G1 phase cell population and an increase in S and G 2/M cells, thus suggesting mitotic arrest prior to metaphase. A novel series of fourteen substituted selenadiazoles has been synthesized and the compounds tested for their in vitro antiproliferative and cytotoxic activities against several cancer cells and in order to assess the selectivity of the compounds on two non-tumoral lines. Modulation of cell cycle and apoptotic effects of active compounds were further evaluated. Copyright

Synthesis and structure-activity relationships of substituted 1,4- dihydroquinoxaline-2,3-diones: Antagonists of N-methyl-D-aspartate (NMDA) receptor glycine sites and non-NMDA glutamate receptors

A series of mono-, di-, tri-, and tetrasubstituted 1,4- dihydroquinoxaline-2,3-diones (QXs) were synthesized and evaluated as antagonists at N-methyl-D-aspartate (NMDA)/glycine sites and α-amino-3- hydroxy-5-methylisoxazole-4-propionic acid-preferring non-NMDA receptors. Antagonist potencies were measured by electrical assays in Xenopus oocytes expressing rat whole brain poly(A)+ RNA. Trisubstituted QXs 17a (ACEA 1021), 17b (ACEA 1031), 24a, and 27, containing a nitro group in the 5 position and halogen in the 6 and 7 positions, displayed high potency (K(b) ~ 6-8 nM) at the glycine site, moderate potency at non-NMDA receptors (K(b) = 0.9-1.5 μM), and the highest (120-250-fold) selectivity in favor of glycine site antagonism over non-NMDA receptors. Tetrasubstituted QXs 17d,e were more than 100-fold weaker glycine site antagonists than the corresponding trisubstituted QXs with F being better tolerated than Cl as a substituent at the 8 position. Di- and monosubstituted QXs showed progressively weaker antagonism compared to trisubstituted analogues. For example, removal of the 5-nitro group of 17a results in a ~100-fold decrease in potency (10a,b,z), while removal of both halogens from 17a results in a ~3000-fold decrease in potency (10v). In terms of steady-state inhibition, most QX substitution patterns favor antagonism at NMDA/glycine sites over antagonism at non-NMDA receptors. Among the QXs tested, only 17i was slightly selective for non- NMDA receptors.