| Copper bioavailability |
Decreases |
Anti-cancer |
TM binds copper and lowers biologically available copper needed by tumor-supporting enzymes. |
| Angiogenesis |
Decreases |
Anti-cancer |
Copper depletion reduces angiogenic support and may limit tumor vascularization. |
| Endothelial progenitor cells |
Decreases |
Anti-metastatic |
Relevant to high-risk breast cancer recurrence / tumor-microenvironment studies. |
| LOX / ECM remodeling |
Likely decreases through copper depletion |
Anti-invasive / anti-metastatic |
LOX-family enzymes are copper-dependent and contribute to extracellular-matrix remodeling and metastatic niche formation. |
| SOD1 |
Decreases, especially with ATN-224 |
Can increase tumor oxidative stress vulnerability |
This makes TM redox-active rather than a simple antioxidant. |
| Tumor dormancy |
May promote / maintain |
Potential anti-recurrence effect |
Most relevant where microscopic residual disease remains after standard therapy. |
| Gross tumor shrinkage |
Usually limited as monotherapy |
Weak direct cytotoxic effect |
Clinical signal appears stronger for stabilization or recurrence prevention than for tumor regression. |