Gambogic amide 

Gambogic amide is a potent and selective agonist of TrkA and also induces its tyrosine phosphorylation and activation of downstream signaling, including Akt and MAPK. Gambogic amide specifically interacts with the cytoplasmic juxtamembrane domain of the TrkA receptor and triggers its dimerization, leading to activation. Gambogic amide has neuroprotective activity preventing glutamate-induced neuronal cell death. Gambogic amide has improved efficacy in a transient middle cerebral artery occlusion model of stroke and could be used to study neurodegenerative diseases and stroke^[1].

Gambogic amide (0.5 μM; 30 min) elicits TrkA tyrosine phosphorylation in hippocampal neurons^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Gambogic amide (2 mg/kg; sc; single dose) prevents neuronal cell death and decreases infarct volume in MCAO animal model^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

627.77

C₃₈H₄₅NO₇

286935-60-2

Solid

Light yellow to yellow

NC(/C(C)=C\C[C@@]12[C@]34C(C(C5=C(O)C(C=C[C@](CC/C=C(C)/C)(C)O6)=C6C(C/C=C(C)\C)=C5O3)=O)=C[C@H](C[C@H]4C(C)(C)O2)C1=O)=O

Room temperature in continental US; may vary elsewhere.

• [1]. Jang SW, et al. Gambogic amide, a selective agonist for TrkA receptor that possesses robust neurotrophic activity, prevents neuronal cell death. Proc Natl Acad Sci U S A. 2007 Oct 9;104(41):16329-34.  [Content Brief]