I didn't even knew about tetrathiomolybdate or that is prescribed for Wilson disease, until I just read it there. Nor would I know where tetrathomolybdate would be available. That's what this articles says:
Excess dietary molybdenum has been found to result in copper deficiency in grazing animals (ruminants). In the digestive tract of ruminants, the formation of compounds containing sulfur and molybdenum, known as thiomolybdates, prevents the absorption of copper and can cause fatal copper-dependent disorders (10). Tetrathiomolybdate (TM) is a molecule that can form high-affinity complexes with copper, controlling free copper (copper that is not bound to ceruloplasmin), and inhibiting copper chaperones and copper-containing enzymes(11, 12). TM's ability to lower free copper levels is exploited in the treatment of Wilson's disease, a genetic disorder characterized by copper accumulation in tissues responsible for hepatic and neurologic disorders. Neurologic worsening has been linked with toxic levels of free copper in the serum of neurologically presenting patients. TM therapy seems able to stabilize neurologic status and prevent neurologic deterioration in these patients, as opposed to the standard initial treatment of choice (13).
Copper is also a required cofactor for enzymes involved in inflammation and angiogenesis, known to accelerate cancer progression and metastasis. Copper depletion studies employing TM have been initiated in patients with advanced malignancies with the aim of preventing disease progression or relapse. These pilot trials showed promising results in individuals with metastatic kidney cancer (14), metastatic colorectal cancer (15), and breast cancer with high risk of relapse (16). TM was relatively well-tolerated and stabilized disease or prevented relapse in correlation with copper depletion. TM's efficacy is also investigated in animal models of inflammatory and immune-related diseases (17, 18) and, at this point, clinical studies are needed to evaluate whether copper depletion could stabilize diseases and improve survival in humans, as suggested by a trial of TM therapy with patients with biliarycirrhosis(19).
High levels of molybdenum can interfere with the body's uptake of copper, producing copper deficiency. Molybdenum prevents plasma proteins from binding to copper, and it also increases the amount of copper that is excreted in urine. Ruminants that consume high levels of molybdenum suffer from diarrhea, stunted growth, anemia, and achromotrichia (loss of fur pigment). These symptoms can be alleviated by copper supplements, either dietary and injection. The effective copper deficiency can be aggravated by excess sulfur.
Copper reduction or deficiency can also be deliberately induced for therapeutic purposes by the compound ammonium tetrathiomolybdate, in which the bright red anion tetrathiomolybdate is the copper-chelating agent. Tetrathiomolybdate was first used therapeutically in the treatment of copper toxicosis in animals. It was then introduced as a treatment in Wilson's disease, a hereditary copper metabolism disorder in humans; it acts both by competing with copper absorption in the bowel and by increasing excretion. It has also been found to have an inhibitory effect on angiogenesis, potentially by inhibiting the membrane translocation process that is dependent on copper ions. This is a promising avenue for investigation of treatments for cancer, age-related macular degeneration, and other diseases that involve a pathologic proliferation of blood vessels.
Molybdenum has been indispensable to me for copper control. When I have symptoms of copper toxicity, molybdenum, zinc and chromium all provide relief within hours. You can take them all together.
Molybdenum will combine with copper in the blood and bile to facilitate excretion. I have MOCS and CBS SNPS so my molybdenum needs are very high. During copper dumps, I will take up to 6 mg per day of molybdenum.
Strangely, at other times I have copper deficiency and can't take any molybdenum without making the deficiency symptoms worse. I seem to keep cycling between deficiency and toxicity since I started doing methylation protocols. My suspicion is that this is related to oxalate dumping and general detoxification caused by increased methylation.