| abstract |
In accordance with the present invention, it is described for the first time that CS2 is capable of directly inhibiting the activity of NFλB, without the need for any other active agents to be present. It is assumed, therefor, that the inhibitory effect of, for example, pyrrolidine dithiocarbamate and other dithiocarbamates on NFλB may simply be attributed to CS2 released upon in vivo hydrolysis of dithiocarbamates rather than as a result of the action of the parental compound per se. Dithiocarbamates may therefore be considered as pro-drugs for CS2 for the treatment of inflammatory conditions mediated via NFλB pathways. Thus, in accordance with the present invention, there are provided methods for the treatment of inflammatory conditions mediated by NFλB pathways, as well as novel compositions useful for such methods. |