I'm sure that problems cropping up and patent expirations are totally unrelated and I'm just a grumpy old cynic....

Clioquinol's use as an antiprotozoal drug has been restricted or discontinued in some countries due to an event in Japan where over 10,000 people developed SMON (subacute myelo-optic neuropathy) between 1957 and 1970. The drug was used widely in many countries before and after the SMON event without similar reports.[6] As yet, no explanation exists as to why it produced this reaction, and some researchers have questioned whether clioquinol was the causative agent in the disease, noting that the drug had been used for 20 years prior to the epidemic without incident, and that the SMON cases began to reduce in number prior to the discontinuation of the drug.[7] Theories suggested have included improper dosing, the permitted use of the drug for extended periods of time, [8] and dosing which did not consider the smaller average stature of Japanese; however a dose dependant relationship between SMON development and clioquinol use was never found, suggesting the interaction of another compound. Researchers have also suggested the SMON epidemic could have been due to a viral infection with a Inoue-Melnick virus.[9]

1: Mol Nutr Food Res. 2006 Feb;50(2):229-34.

Green tea catechins as brain-permeable, natural iron chelators-antioxidants for
the treatment of neurodegenerative disorders.

Mandel S, Amit T, Reznichenko L, Weinreb O, Youdim MB.

Eve Topf, Haifa, Israel. mandel@tx.technion.ac.il

Neurodegeneration in Parkinson's, Alzheimer's, or other neurodegenerative
diseases appears to be multifactorial, where a complex set of toxic reactions,
including oxidative stress (OS), inflammation, reduced expression of trophic
factors, and accumulation of protein aggregates, lead to the demise of neurons.
One of the prominent pathological features is the abnormal accumulation of iron
on top of the dying neurons and in the surrounding microglia. The capacity of
free iron to enhance and promote the generation of toxic reactive oxygen
radicals has been discussed numerous times. The observations that iron induces
aggregation of inert alpha-synuclein and beta-amyloid peptides to toxic
aggregates have reinforced the critical role of iron in OS-induced pathogenesis
of neurodegeneration, supporting the notion that a combination of iron chelation
and antioxidant therapy may be one significant approach for neuroprotection. Tea
flavonoids (catechins) have been reported to possess divalent metal chelating,
antioxidant, and anti-inflammatory activities, to penetrate the brain barrier
and to protect neuronal death in a wide array of cellular and animal models of
neurological diseases. This review aims to shed light on the
multipharmacological neuroprotective activities of green tea catechins with
special emphasis on their brain-permeable, nontoxic, transitional metal (iron
and copper)-chelatable/radical scavenger properties.

Publication Types:
Review

PMID: 16470637 [PubMed - indexed for MEDLINE]