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Topic

Dithiocarbamate

About: Dithiocarbamate is a(n) research topic. Over the lifetime, 2996 publication(s) have been published within this topic receiving 41318 citation(s). The topic is also known as: dithiocarbamates.


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Journal ArticleDOI
Abstract: Compounds with general formulas R3Sn(SSCNR′2 (REt, Ph, R′) or R2Sn(SSCNR′2)2 (Rhalogen, Et, Ph; R′Et, Ph) were prepared and their physical data are reported and discussed. In X2SN(SSCNEt2)2 an octahedral cis coordination of the tin atom is shown to be present with a chelated dithiocarbamato moiety. A similar labile type of coordination seems to exist in solution for the corresponding organotin derivatives. In the case R3Sn(SSCNR′2), no sure evidence was found for or against the chelation of the dithiocarbamate moiety. A discussion as to what physical measurements actually serve as convincing criteria of structure and chelation in dithiocarbamates is presented.

455 citations

Book ChapterDOI
27 Jan 2005

393 citations

Journal ArticleDOI
TL;DR: A series of 4(3H)-quinazolinone derivatives with dithiocarbamate side chains were synthesized and tested for their in vitro antitumor activity against human myelogenous leukemia K562 cells, and Piperazine-1-carbodithioate 8q exhibited significant inhibitory activity.
Abstract: A series of 4(3H)-quinazolinone derivatives with dithiocarbamate side chains were synthesized and tested for their in vitro antitumor activity against human myelogenous leukemia K562 cells. Among them, (3,4-dihydro-2-methyl-4-oxoquinazolin-6-yl)methyl 4-(4-fluorophenyl)piperazine-1-carbodithioate 8q exhibited significant inhibitory activity against K562 cells with IC(50) value of 0.5 microM.

306 citations

Journal ArticleDOI
TL;DR: These gold(III) complexes show high reactivity toward some biologically important isolated macromolecules, resulting in a dramatic inhibition of both DNA and RNA synthesis and inducing DNA lesions with a faster kinetics than cisplatin, suggesting that intracellular DNA might not represent their primary or exclusive biological target.
Abstract: Gold(III) compounds are emerging as a new class of metal complexes with outstanding cytotoxic properties and are presently being evaluated as potential antitumor agents. We report here on the solution and electrochemical properties, and the biological behavior of some gold(III) dithiocarbamate derivatives which have been recently proved to be one to 4 orders of magnitude more cytotoxic in vitro than the reference drug (cisplatin) and to be able to overcome to a large extent both intrinsic and acquired resistance to cisplatin itself. Their solution properties have been monitored in order to study their stability under physiological conditions; remarkably, they have shown to undergo complete hydrolysis within 1 h, the metal center remaining in the +3 oxidation state. Their DNA binding properties and ability in hemolyzing red blood cells have been also evaluated. These gold(III) complexes show high reactivity toward some biologically important isolated macromolecules, resulting in a dramatic inhibition of both DNA and RNA synthesis and inducing DNA lesions with a faster kinetics than cisplatin. Nevertheless, they also induce a strong and fast hemolytic effect (compared to cisplatin), suggesting that intracellular DNA might not represent their primary or exclusive biological target.

263 citations

Journal ArticleDOI
TL;DR: The adsorbed dithiocarbamates are robust under a wide pH range and can resist displacement by other chemisorptive surfactants, providing an attractive method for conjugating sensitive molecules onto metal surfaces.
Abstract: Au surfaces are functionalized by stable dithiocarbamate ligands when exposed to carbon disulfide and secondary amines. The adsorbed dithiocarbamates are robust under a wide pH range and can resist displacement by other chemisorptive surfactants, providing an attractive method for conjugating sensitive molecules onto metal surfaces.

244 citations

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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
20221
202173
202088
2019100
201891
201795