University of Bradford

University of London

School of Pharmacy

Mark Searcey

Laurence Hylton Patterson

Compounds of the general formula (I) or (IA) in which X is H, Y is a leaving group, Rpreferably being an aromatic DNA binding subunit are prodrug analogues of duocarmycin. The compounds are expected to be hydroxylated at the carbon atom to which C is joined, by cytochrome P450, in particular by CYP1B1, expressed at high levels in tumors. The prodrug is expected to be activated preferentially in tumor cells, which it will act as a DNA alkylating agent preventing cell division.

Benz-indole and benzo-quinoline derivatives as prodrugs for tumor treatment

Compounds of the general formula (I) or (IA) in which X is H, Y is a leaving group, Rand optionally also Rpreferably being an aromatic DNA binding subunit are prodrug analogues of duocarmycin. The compounds are expected to be hydroxylated at the carbon atom to which X is joined, by cytochrome P450, in particular by CYP1B1, expressed at high levels in tumors. The prodrug is expected to be activated preferentially in tumor cells, where it will act as a DNA alkylating agent preventing cell division. 

Pyrrolo-indole and pyrrolo-quinoline derivatives as prodrugs for tumour treatment

Compounds of the general formula (I) or (IA) in which X is H, Y is a leaving group, Rpreferably being an aromatic DNA binding subunit are prodrug analogues of duocarmycin. The compounds are expected to be hydroxylated at the carbon atom to which X is joined, by cytochrome P450, in particular by CYP1B1, expressed at high levels in tumors. The prodrug is expected to be activated preferentially in tumor cells, where it will act as a DNA alkylating agent preventing cell division 

Compounds of the general formula I or IA or a salt in which X is H, Y is a leaving group, Rpreferably being an aromatic DNA binding subunit are prodrug analogues of duocarmycin. The compounds are expected to be hydroxylated at the carbon atom to which X is joined, by cytochrome P450, in particular by CYP1B1, expressed at high levels in tumours. The prodrug is expected to be activated preferentially in tumour cells, where it will act as a DNA alkylating agent preventing cell division 

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Mark Searcey