Gambogic amide acts as a potent and selective agonist for TrkA, promoting tyrosine phosphorylation and activating downstream signaling pathways such as Akt and MAPK. It specifically binds to the cytoplasmic juxtamembrane domain of the TrkA receptor, stimulating dimerization and activation. The compound demonstrates neuroprotective properties by preventing neuronal cell death caused by glutamate. Additionally, gambogic amide shows enhanced efficacy in a transient middle cerebral artery occlusion model of stroke and may be useful for investigating neurodegenerative diseases and stroke [1].