Investigations of Thiosemicarbazides as Botulinum Toxin Active-Site Inhibitors: Enzyme, Cellular, and Rodent Intoxication Studies - PubMed
- ️Sat Nov 08 2025
. 2024 Nov 8;10(11):3744-3750.
doi: 10.1021/acsinfecdis.4c00750. Epub 2024 Oct 28.
Affiliations
- PMID: 39467164
- PMCID: PMC11584025 (available on 2025-11-08)
- DOI: 10.1021/acsinfecdis.4c00750
Investigations of Thiosemicarbazides as Botulinum Toxin Active-Site Inhibitors: Enzyme, Cellular, and Rodent Intoxication Studies
Ealin N Patel et al. ACS Infect Dis. 2024.
Abstract
Botulinum neurotoxin type A (BoNT/A) is an exceptionally potent neurotoxin of great therapeutic value; however, it is also considered a weapon of mass destruction, as it is one of the most poisonous biological substances known to man. The etiology behind BoNT/A is its action as a zinc-dependent protease, which can cause extended paralysis through the cleavage of SNARE proteins. Thiosemicarbazones, known zinc chelators, provide a privileged scaffold that can be leveraged for the development of BoNT/A LC inhibitors. Through a combination of biochemical and kinetic assays, it was demonstrated that the thiosemicarbazone ZMC1, an antitumor agent, is an effective competitive inhibitor of the BoNT/A LC. Based on these results, a series of thiosemicarbazones were designed/synthesized using structure-based analysis and examined in enzyme activity and cell-based assays. From this screen, two analogues presented noteworthy cellular activity. The most potent inhibitors were then tested in a BoNT/A mouse lethality assay, providing statistically significant prolonged survival.
Keywords: Botulinum Neurotoxin; Cellular Assays; Competitive Inhibition; Lethality Rodent Model.
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