Inward Rectifier Potassium (Kir) Channel Inhibitors Protect Citrus from the Asian Citrus Psyllid by Inducing Toxicity and Inhibition of Feeding.

Abstract

Huanglongbing (HLB), caused by the phloem-restricted bacterium <i>Candidatus Liberibacter asiaticus</i> (<i>C. Las</i>), is vectored by the Asian citrus psyllid (ACP) and threatens global citrus production. We demonstrate that VU041 (C₁₉H₂₀F₃N₃O), a small-molecule inhibitor of inward rectifier potassium (Kir) channels, provides a dual-mechanism approach to management of Huanglongbing (HLB) disease by combining acute toxicity with antifeedant activity. Topical and tarsal contact bioassays revealed that VU041 induced rapid mortality to ACP (24 h LD₅₀ = 25 ng/insect) and reduced salivary gland secretion to suppress feeding behaviors. In semifield acquisition assays on <i>C. Las</i>-infected citrus, foliar application of VU041 significantly reduced both ACP survival (up to 96% at 365 ppb) and <i>C. Las</i> acquisition in surviving ACP. Combined, these results indicate that VU041 represents a promising chemical lead for developing insecticides that simultaneously kill ACP vectors and block pathogen acquisition at sublethal concentrations, representing a potentially transformative approach to reducing HLB-mediated losses in citrus production.