Passion for People Development
The approach
We target resistant bacteria and fungi at new binding sites.
Conventional antibiotics bind at a single site. A single mutation can be enough to cause resistance.
Selmod's compounds are built around a different logic: dual binding at a large, essential structural site that resistance cannot mutate without destroying the enzyme itself. The observed resistance rate is approximately 10-10 - 1000 times lower than many conventional antibiotics.
Albicidin is the lead structure of our SLM500 asset. It blocks bacterial DNA Gyrase and Topoisomerase IV through a two-pronged binding strategy: one end of the molecule inserts into the essential Gyrase dimer interface, while the other wedges between the broken DNA strands of the cleaved substrate. By simultaneously occupying these critical sites, Albicidin irreversibly locks the enzyme, halting DNA replication and triggering bacterial cell death.
Comparison of conventional single-site binding and Selmod's dual binding at a new dimer interface.
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