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Snake venom toxins from medically relevant Chinese snake species are a heterogeneous group of bioactive proteins and peptides that constitute the primary virulence factors in snakebite envenomation. These toxins are secreted by various species, most notably the Chinese cobra (Naja atra), the many-banded krait (Bungarus multicinctus), and the five-pacer viper (Deinagkistrodon acutus) (Ji et al., 2014). The molecular composition of these venoms includes diverse families such as phospholipase A2s, three-finger toxins, snake venom metalloproteinases, and serine proteases, which target the nervous system, blood coagulation cascade, and vascular integrity (Tasoulis & Isbister, 2017). Clinically, these toxins cause a range of pathologies including neuromuscular paralysis, systemic hemorrhage, and severe local tissue necrosis. While traditional treatment relies on the administration of specific or polyvalent antivenoms to neutralize these toxins, modern drug discovery is exploring small-molecule inhibitors to provide more stable and accessible field treatments (Kasturiratne et al., 2008). These toxins are considered therapeutic targets in the sense that their neutralization or inhibition is the primary goal of treating envenomation.
Antivenoms contain antibodies that bind to venom toxins, neutralizing their biological activity and facilitating their clearance (Gutiérrez et al., 2017). Varespladib is a potent inhibitor of secreted phospholipase A2 (sPLA2), preventing the hydrolysis of phospholipids and subsequent membrane damage (Lewin et al., 2016). Metalloproteinase inhibitors like marimastat and prinomastat inhibit snake venom metalloproteinases (SVMPs) by chelating the essential zinc cofactor, thereby preventing hemorrhage and tissue degradation (Albulescu et al., 2020).
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