Bromoxynil是一種萌前或萌後施用的除草劑，主要防治闊葉性雜草，其作用係與光合作用中光系統II之D1蛋白中的QB位置結合，使粒昆(plastoquinone)無法結合至QB位置，因而造成電子傳遞中斷。此藥劑具高度選擇性，常造成葉面接觸性傷害。近年由於基因轉殖技術進步，已使某些雙子葉作物對於bromoxynil具有抗性，此抗性機制之了解也有助於提高除草劑之使用範圍。一般而言，植物對於bromoxynil之抗性機制，包括減少bromoxynil之吸收量、減少除草劑轉運至其他部位、形成不可溶性物質、或是利用nitrilase代謝bromoxynil，其抗性基因bxn之遺傳行為，係由一至二個基因座所控制。

Bromoxynil is a pre- or post-emergence herbicide used for broad- leaf weed control. The mode of action of this herbicide is to occupy the QB site of D1 rotein for photosystem II, thus the plastoquinone fails to react with QB site and causes blocking of electron transport in photosystem . Bromoxynil frequently caused phytotoxicity on leaf or shoot surface of susceptible plants while it was sprayed directly on shoot. For the past decade, bromoxynil-resistant gene has been transferred to some dicots successfully. In general, the mechanism of resistance to bromoxynil in plants includes a decrease of herbicide absorption, retardation of bromoxynil translocation, formation of insoluble materials, or promotion of bromoxynil metabolism by nitrilase encoded by bxn gene. The inheritance of resistant gene is controlled by 1 to 2 genetic loci.