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A2NTX is a novel low-molecular-weight (150 kDa) neurotoxin derived from the subtype A2 of botulinum neurotoxin, produced by a unique strain of Clostridium botulinum (Chiba-H) originally isolated from cases of infant botulism in Japan. Unlike the widely used onabotulinumtoxinA (subtype A1), all current clinical preparations are based on subtype A1. Preclinical studies have shown that subtype A2 toxins enter neuronal cells more rapidly and exhibit less diffusion to contralateral muscles compared to subtype A1. Clinically, one unit of mouse LD50 for A2NTX is approximately 1.54 times as potent as an equivalent unit of onabotulinumtoxinA in reducing compound muscle action potentials, with similar duration but less spread to distant muscles. A2NTX has been evaluated primarily for the treatment of spasticity and dystonia—including post-stroke lower limb spasticity—where it demonstrated good safety and tolerability up to doses of 500 units over long-term use. In head-to-head pilot studies against onabotulinumtoxinA (BOTOX), patients receiving A2NTX showed greater improvement in functional measures at day 30 and reported fewer adverse effects related to unwanted muscle weakness or spread beyond the injection site[1][2][8]. The majority of patients preferred continuing with A2NTX over traditional preparations[1].
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