An anti-cancer agent is provided comprising a tumour homing peptide having, or having been modified to present, two cysteine residues, with an arsenic atom between, such that the tumour homing peptide cyclises to give an arsenic-containing anti-cancer agent. This allows for selection of an appropriate tumour homing peptide for treatment of a given cancer whereby the subsequent agent provides for a more targeted delivery of arsenic to the tumour microenvironment.

A composite anti-restenosis drug for use with a coronary drug-eluting stent, and a controlled release system for the drug. The composite drug comprises arsenic trioxide and rapamycin, which may be used in combination to prevent in-stent restenosis and reduce the incidence of intravascular thrombosis. The controlled release system for the composite drug may control the release of the composite drug so as to achieve the therapeutic effect of controlling restenosis and preventing the formation of thromboses.

A composite anti-restenosis drug for use with a coronary drug-eluting stent, and a controlled release system for the drug. The composite drug comprises arsenic trioxide and rapamycin, which may be used in combination to prevent in-stent restenosis and reduce the incidence of intravascular thrombosis. The controlled release system for the composite drug may control the release of the composite drug so as to achieve the therapeutic effect of controlling restenosis and preventing the formation of thromboses.

A method for treating a lymphoma selected from non-Hodgkin's and Hodgkin's lymphoma comprising administering an organoarsenic compound having a structure of the formula (I) wherein X is S or Se and R.sub.1 and R.sub.2 are independently C.sub.1-30alkyl (R.sub.3, R.sub.3, R.sub.4, R.sub.5, W and n are as defined in claim 1) in particular where the compound is S-dimethylarsinoglutathione, N-(2-S-dimethylarsinothiopropionyl)glycine, 2-amino-3-(dimethylarsino)thio-3-methylbutanoic acid, S-dimethylarsino-thiosuccinic acid or S-dipropylarsino-1-thioglycerol. ##STR00001##

A method for treating a lymphoma selected from non-Hodgkin's and Hodgkin's lymphoma comprising administering an organoarsenic compound having a structure of the formula (I) wherein X is S or Se and R.sub.1 and R.sub.2 are independently C.sub.1-30alkyl (R.sub.3, R.sub.3, R.sub.4, R.sub.5, W and n are as defined in claim 1) in particular where the compound is S-dimethylarsinoglutathione, N-(2-S-dimethylarsinothiopropionyl)glycine, 2-amino-3-(dimethylarsino)thio-3-methylbutanoic acid, S-dimethylarsino-thiosuccinic acid or S-dipropylarsino-1-thioglycerol. ##STR00001##

The present invention relates to synergistic pharmaceutical combinations comprising organic arsenoxide compounds and mTOR inhibitors. Further, the present invention relates to the use of these pharmaceutical combinations in therapy, in particular, treatment of proliferative diseases.

The present invention relates to synergistic pharmaceutical combinations comprising organic arsenoxide compounds and mTOR inhibitors. Further, the present invention relates to the use of these pharmaceutical combinations in therapy, in particular, treatment of proliferative diseases.

The present invention relates to synergistic pharmaceutical combinations comprising organic arsenoxide compounds and mTOR inhibitors. Further, the present invention relates to the use of these pharmaceutical combinations in therapy, in particular, treatment of proliferative diseases.

Presently provided are indoximod prodrug and salt compounds and pharmaceutical compositions comprising salts and prodrugs of indoximod, that produce enhanced plasma concentration and exposure to indoximod compared to direct administration of indoximod, in patients in need of treatment of immunosuppression mediated by the indoleamine-2,3-dioxygenase pathway, such as patients with cancer or chronic infectious diseases.

Presently provided are indoximod prodrug and salt compounds and pharmaceutical compositions comprising salts and prodrugs of indoximod, that produce enhanced plasma concentration and exposure to indoximod compared to direct administration of indoximod, in patients in need of treatment of immunosuppression mediated by the indoleamine-2,3-dioxygenase pathway, such as patients with cancer or chronic infectious diseases.