🔬 A New Hope Against TB: SuFEx-Based Molecule CMX410 Irreversibly Disarms M. tuberculosis
Tuberculosis (TB), caused by Mycobacterium tuberculosis (Mtb), remains one of the deadliest infectious diseases globally—especially due to rising multi-drug-resistant (MDR) and extensively drug-resistant (XDR) strains. Current treatments are outdated, often toxic, and require long durations. But a new compound might just change that narrative.
🌟 Introducing CMX410: A First-in-Class Antitubercular Candidate
Published in Nature (July 2025), researchers present CMX410, a preclinical molecule with a novel SuFEx (Sulfur(VI) Fluoride Exchange) warhead. This compound:
✅ Irreversibly inhibits Pks13, an essential enzyme in Mtb’s cell-wall biosynthesis
✅ Shows equal potency against drug-sensitive and drug-resistant TB strains
✅ Demonstrates oral bioavailability and favorable combination synergy
✅ Exhibits no observed toxicity even at high doses in preclinical models
🧪 Mechanism of Action
CMX410 targets the acyltransferase (AT) domain of Pks13 and binds irreversibly through an innovative mechanism:
It forms a β-lactam by reacting with the catalytic serine of Pks13—effectively disabling the enzyme’s active site. This covalent mode of action has not been previously described in TB drug development.
🧫 Preclinical Promise
In multiple mouse models of infection, CMX410 proved efficacious. Importantly, it maintained potency across clinical Mtb isolates, including MDR and XDR strains. The compound’s selectivity also supports excellent safety profiles, with no toxicity in 14-day rat studies up to 1,000 mg/kg/day.
🧩 Why This Matters
CMX410 could become a game-changer in TB therapy. Its novel target (Pks13) and distinct mechanism make it a strong candidate to replace old drugs like isoniazid and ethambutol in future TB regimens.
📄 Read the full study here: Nature Article
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