tetrathiomolybdate / SOD1 Cancer Research Results

TM, tetrathiomolybdate: Click to Expand ⟱

Features:

Tetrathiomolybdate, often abbreviated TM, is a copper-chelating / copper-depleting agent. In cancer, it is mainly studied as an anti-angiogenic, anti-metastatic, tumor-microenvironment-modifying compound rather than as a conventional cytotoxic chemotherapy.
TM → copper depletion ↓ → angiogenesis ↓ / endothelial progenitor cells ↓ / LOX-family activity ↓ / SOD1 activity ↓ → metastasis support ↓
Tetrathiomolybdate binds copper and reduces biologically available copper.

Pathway / target	Effect of tetrathiomolybdate	Cancer relevance	Notes
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.

SOD1, superoxide dismutase 1: Click to Expand ⟱

Source:

Type:

SOD1 (superoxide dismutase 1) is a key antioxidant enzyme that catalyzes the dismutation of superoxide radicals into oxygen and hydrogen peroxide.

In several cancers including breast, lung, HCC, and others, alterations in SOD1 expression have been observed, reflecting its role in managing oxidative stress.
• Elevated SOD1 levels are sometimes associated with aggressive tumor behavior, therapy resistance, or decreased apoptosis due to enhanced ROS detoxification.
• Conversely, the protective role of antioxidants can also mitigate oxidative mutation loads, leading to context-dependent and occasionally favorable outcomes.

In non-small cell lung cancer (NSCLC), increased SOD1 levels have been reported in some cohorts, potentially as a mechanism to cope with high reactive oxygen species (ROS) levels.

Scientific Papers found: Click to Expand⟱

6175-

TM,

Copper binding by tetrathiomolybdate attenuates angiogenesis and tumor cell proliferation through the inhibition of superoxide dismutase 1

vitro+vivo,

Var,

SOD1↓, TumCP↓, angioG↓,

Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

SOD1↓, 1,

Migration ⓘ

TumCP↓, 1,

Angiogenesis & Vasculature ⓘ

angioG↓, 1,
Total Targets: 3

Pathway results for Effect on Normal Cells:

Total Targets: 0

Scientific Paper Hit Count for: SOD1, superoxide dismutase 1

Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells