trans-ACPD ((±)-trans-ACPD) is an equimolecular mixture of (1S, 3R)- and (1R, 3S)-ACPD. trans-ACPD is a selective agonist of the mGluR (metabotropic glutamate receptor); active at the group I/II mGlu receptors (EC50: 2/15/23/800 μM, mGluR2/1/5/4).

mGluR2:2μM(EC50), mGluR1:15μM(EC50), mGluR5:23μM(EC50), mGluR4:800 μM(EC50)

Excitatory amino acid (EAA) analogues activate receptors linked to increased hydrolysis of phosphoinositides (PIs). In these studies, hippocampal slices from neonatal rats (6-11 days old) characterize the effects of EAA analogues on these receptors. The EC50 value of trans-ACPD is 51 μM, and DL-2-Amino-3-phosphonopropionate (DL-AP3) serves as an equally potent inhibitor of PI hydrolysis induced by ibotenate, quisqualate, and trans-ACPD, with IC50 values ranging from 480 to 850 μM [2].

Intrathecal administration of NMDA, kainate, and trans-ACPD, along with the pro-inflammatory cytokines TNF-α or IL-1β, markedly increases biting behavior in mice, a paradigm shift from the control group receiving saline. Pre-systemic intervention with GM at a dosage of 100 mg/kg intraperitoneally notably decreases biting behavior in comparison to saline treatment (10 mL/kg, i.p.), with statistical significance (p<0.001). The efficacy of GM is particularly pronounced against pro-inflammatory cytokines and NMDA, exhibiting inhibition rates of TNF-α (92±7%), IL-1β (91±5%), NMDA (69±1%), and trans-ACPD (71±12%). Conversely, kainate-induced biting responses remain unaffected by GM at the same concentration.