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The system that switches off the cell's metabolic meter.
ThsA/B cooperate to deplete the cell of NAD+ after phage detection. TIR domain is homologous to human SARM1. This is the first testable oncological target.
NAD+ is the rechargeable battery of every one of our cells — it powers the redox reactions that produce ATP. Wipe it out and you switch off metabolism. Thoeris does exactly that upon phage infection. The sensor ThsB detects infection and produces a second messenger (3'-cADPR). The effector ThsA, an NADase, is activated by cADPR and degrades all available NAD+. Abortive cell death, aborted phage. The striking parallel: this is exactly the mechanism human SARM1 uses in injured axons — stress detection, cADPR production, NAD+ degradation, axonal death. Same grammar, but 2 billion years of evolution apart.
The Thoeris/SARM1 parallel is our best entry point for targeting human SARM1 in peripheral neuropathies (chemo-induced, diabetic, post-surgical). The recent ThsA small-molecule inhibitors provide scaffolds. The inhibition kinetics observed in the bacterium (fast, reversible effect) are exactly what we want in humans in acute post-injury settings.
In 2026 (Zhang et al., bioRxiv) researchers identified the first small-molecule chemical inhibitors of ThsA via screening. The central finding: Thoeris immunity must be maintained continuously — briefly inhibiting ThsA is enough to let phages come back. And it is enough for 10% of the bacterial population to be inhibited for the whole population to be lysed. Cooperative immunity is fragile.
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