OnCo
technologiesTechnologyPhase 2

Hypoxia-activated prodrugs

A harmless molecule that turns into a poison only where there is no oxygen, which in the body means inside a tumour.

Tumour cores are hypoxic in a way normal tissue is not, so a prodrug reduced only under low oxygen should be tumour-selective. Evofosfamide failed two phase 3 trials in 2015; the field has since focused on better patient selection using hypoxia imaging or gene signatures, and on newer scaffolds. It remains a clean idea with a poor clinical record.

Generic schematic · not to scale · placeholder for the chemotherapy front
Chromosomes at spindle · Drug blocks division / damages DNA

How it works

One-electron reduction of a nitroaromatic or quinone trigger is reversed by oxygen; where oxygen is absent, fragmentation releases an active cytotoxin.

Strengths
  • Exploits a difference no normal tissue shares
  • Kills the hypoxic cells radiotherapy misses
  • Combines with radiation and antiangiogenics
Limitations
  • Two phase 3 failures without hypoxia selection
  • Needs a validated hypoxia biomarker
  • The prodrug must diffuse into a poorly perfused region

Latest papers

top
Latest papers · live from Europe PMC
Open in Europe PMC

Query for this technology: (TITLE:"Hypoxia-activated prodrugs" OR ABSTRACT:"Hypoxia-activated prodrugs") AND (cancer OR tumor OR tumour OR oncology OR carcinoma OR lymphoma OR leukemia OR leukaemia OR myeloma OR sarcoma OR melanoma OR glioma). Results are unfiltered search hits about Hypoxia-activated prodrugs, not a curated reading list.

Connected

12top