Names | |
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Preferred IUPAC name
2-Amino-7-phosphonoheptanoic acid | |
Identifiers | |
3D model (JSmol)
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ChEMBL | |
ChemSpider | |
PubChem CID
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UNII | |
CompTox Dashboard (EPA)
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Properties | |
C7H16NO5P | |
Molar mass | 225.179 g/mol |
Density | 1.39 g/mL |
Boiling point | 480.1 °C (896.2 °F; 753.2 K) |
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
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AP-7 is a selective NMDA receptor (NMDAR) antagonist that competitively inhibits the glutamate binding site and thus activation of NMDAR. It has anticonvulsant effects.[1]
AP-7 functions specifically as a NMDA recognition site blocker, in contrast with 7-chlorokynurenate, which acts as a glycine site modulation blocker.[2]
AP-7 injected directly into the dorsal periaqueductal grey (DPAG) of rats produced an anxiolytic effect, whereas direct injection outside of the DPAG did not elicit anxiolytic effects. This suggests that a portion of systemically taken NMDA antagonist's anxiolytic effects comes from the DPAG region of the brain, at least in rats.[3]
The DPAG of the brain is thought to deal with fear-like defensive behavior via NMDA and glycine B receptors.[4] These excitatory glutamate receptors work with the inhibitory GABA receptors to achieve equilibrium in the DPAG of the brain.[5]
AP-7 has been known to cause muscle rigidity and catalepsy in rats following bilateral microinjections (0.02-0.5 nmol) into the globus pallidus and ventral-posterior portions of the caudate-putamen.[6]
The optically pure D-(−)-2-amino-7-phosphonoheptanoic acid [D-AP7], has also been examined. In groups of hypoxia-treated rats, D-AP7 enhanced motility, exhibited anxiogenic-like effect and impaired consolidation in passive avoidance. Both AP-7 and D-AP7 function as potent, specific antagonists of the NMDA receptor.[7]