There is quite a bit being published, particularly around its role as a chelator. I wonder if it is available through off-shore pharmacies?


1. CNS Neurosci Ther. 2010 Dec 27. doi: 10.1111/j.1755-5949.2010.00231.x. [Epub
ahead of print]

Clioquinol: Review of its Mechanisms of Action and Clinical Uses in
Neurodegenerative Disorders.

Bareggi SR, Cornelli U.

Department of Pharmacology, Chemotherapy and Medical Toxicology, School of
Medicine, University of Milan, Italy Loyola University Medical School, Chicago,
IL, USA.

Clioquinol was produced as a topical antiseptic and marketed as an oral
intestinal amebicide in 1934, being used to treat a wide range of intestinal
diseases. In the early 1970s, it was withdrawn from the market as an oral agent
because of its association with subacute myelo-optic neuropathy (SMON), a
syndrome that involves sensory and motor disturbances in the lower limbs and
visual changes. The first methods for determining plasma and tissue clioquinol
(5-chloro-7-iodo-8-quinolinol) levels were set up in the 1970s and involved HPLC
separation with UV detection, these were followed by a more sensitive GC method
with electron capture detection and a gaschromatographic-massspectrometric
(GC-MS) method. Finally, an HPLC method using electrochemical detection has
proved to be as highly sensitive and specific as the GC-MS. In rats, mice,
rabbits, and hamsters, clioquinol is rapidily absorbed and undergoes first-pass
metabolization to glucuronate and sulfate conjugates; the concentrations of the
metabolites are higher than those of free clioquinol. Bioavailabilty versus
intraperitoneal dosingis about 12%. Dogs and monkeys form fewer conjugates. In
man, single-dose concentrations are dose related, and the drug's half-life is
11-14 h. There is no accumulation, and the drug is much less metabolized to
conjugates. Clioquinol acts as a zinc and copper chelator. Metal chelation is a
potential therapeutic strategy for Alzheimer's disease (AD) because zinc and
copper are involved in the deposition and stabilization of amyloid plaques, and
chelating agents can dissolve amyloid deposits in vitro and in vivo. In general,
the ability of clioquinol to chelate and redistribute metals plays an important
role in diseases characterised by Zn, Cu, Fe dyshomeostasis, such as AD and
Parkinson's disease, as it reduces oxidation and the amyloid burden. Zinc
chelators may also act as anticancer agents. Animal toxicity studies have
revealed species-specific differences in neurotoxic responses that are related to
the serum levels of clioquinol and metabolites. This is also true in humans, who
form fewer conjugates. The results of studies of Alzheimer patients are
conflicting and need further confirmation. The potential therapeutic role of the
two main effects of MPACs (the regulation of the distribution of metals and
antioxidants) has not yet been fully explored.


PMID: 21199452 [PubMed - as supplied by publisher]