NK1R Antibody (YA7707)

Neurokinin-1 receptor (NK1R), encoded by TACR1, is the preferred receptor for substance P and functions as a G protein-coupled receptor that links neuronal, immune, and inflammatory signaling systems^[1][2]. Upon substance P binding, NK1R activates phospholipase C-, protein kinase C-, and MAPK-associated pathways, leading to intracellular calcium mobilization, NF-κB activation, and production of pro-inflammatory mediators^[2][3]. Mechanistically, the substance P/NK1R axis regulates neurogenic inflammation, immune cell activity, vascular permeability, cytokine production, and cellular responses relevant to pain, stress, and tissue injury^[1][2][3]. In disease models, increased NK1R signaling has been associated with neuroinflammation, inflammatory disorders, infection-related pathology, and multiple cancer types, where receptor activation contributes to cell proliferation, migration, angiogenesis, and survival signaling^[1][2][4]. Compared with related tachykinin receptors NK2R and NK3R, NK1R exhibits the highest affinity for substance P and possesses two major isoforms, a full-length receptor and a truncated receptor that differ in signaling capacity and biological function^[1][5]. The full-length isoform more effectively supports NF-κB-dependent inflammatory signaling, whereas the truncated isoform displays distinct regulatory properties and has been implicated in immune modulation and cancer-associated biology^[3][5]. For experimental applications, selective NK1R antagonists have been widely used to investigate substance P-dependent signaling pathways and have demonstrated therapeutic utility in chemotherapy-induced nausea and vomiting, while remaining valuable pharmacological tools for studying inflammation, neurobiology, and tumor-related mechanisms^[2][4].