Efficacy of certain quinolines as pharmacological antagonists in botulinum neurotoxin poisoning
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Lipid and cationic polymer based transduction of botulinum holotoxin, or toxin protease alone, extends the target cell range and improves the efficiency of intoxication
2010, ToxiconCitation Excerpt :The translocation of the Lc to the cytosol occurs following a conformational change that is induced by acidification of the endosome (Cai et al., 2006b; Hoch et al., 1985). Drugs that inhibit endosome acidification, such as bafilomycin A1, are antagonists of BoNT intoxication (Deshpande et al., 1997; Simpson, 1983; Simpson et al., 1994). Once in the cytosol, the different BoNT Lcs cleave and inactivate their SNARE protein substrates leading to intoxication.
Galantamine is a novel post-exposure therapeutic against lethal VX challenge
2009, Toxicology and Applied PharmacologyNovel small molecule inhibitors of botulinum neurotoxin A metalloprotease activity
2003, Biochemical and Biophysical Research CommunicationsCitation Excerpt :In the earlier work, it was hypothesized that these compounds delayed paralysis by interfering with toxin translocation into the nerve cytoplasm and therefore they were not tested for specific inhibition of BoNT/A LC protease activity. The percent inhibition of BoNT/A LC that we observed for these drugs was not equivalent to the level of protection that they afforded against muscle paralysis in the previous studies [17,18]. For example, quinacrine, which we report to inhibit BoNT/A LC protease activity by 30% at 50 μM (0.2 mM substrate), was found, in an earlier study [17], to delay the time to 50% muscle paralysis by at least 30% (over control) at 3.3 μM [17].
Catch and Anchor Approach to Combat Both Toxicity and Longevity of Botulinum Toxin A
2020, Journal of Medicinal Chemistry