Leukotriene B4 (LTB4) is a compound derived from arachidonic acid via the 5-lipoxygenase pathway that mediates certain inflammatory and immune responses. Leukotriene B4 induces neutrophil extracellular traps that impede the clearance of Pneumocystis japonicus.

PROTACs contain two different ligands connected by a linker; one is a ligand for an E3 ubiquitin ligase and the other is for the target protein. PROTACs exploit the intracellular ubiquitin-proteasome system to selectively degrade target proteins[1].
Nerve damage in rheumatoid arthritis (RA) can promote the production of Leukotriene B4 (LTB4), which acts on its receptor, leading to increased release of proinflammatory cytokines and ROS, thereby reducing neuronal viability and pain thresholds; LTB4-BLT1 activation can also increase intracellular calcium concentration and neuronal excitability as well as NF-κB pathway activation, further promoting the production of MMP-9 and CXC3R-1; the mutual promotion between LTB4 and neutrophil accumulation accelerates the release of TNF-α and IL-β, thereby enhancing the sensitization of the peripheral and central nervous systems; LTB4 is also involved in the regulation of TrpV1 channel activation and P2X3 receptor activation. [2]