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Catalog No. BCC6590
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Quality Control of (1S,3R)-ACPD

Chemical structure


Biological Activity of (1S,3R)-ACPD

Active isomer of (±)-trans-ACPD. Agonist at both group I and II mGlu receptors (EC50 values are 5, 15, 42 and 60 μM at mGluR2, mGluR5, mGluR1 and mGluR6 respectively). NPEC-caged-(1S,3R)-ACPD also available (Cat. No. 3331). (±)-trans-ACPD and cis-ACPD also available.

(1S,3R)-ACPD Dilution Calculator

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(1S,3R)-ACPD Molarity Calculator



Chemical Properties of (1S,3R)-ACPD

Cas No. 111900-32-4 SDF Download SDF
Chemical Name (1S,3R)-1-Aminocyclopentane-1,3-dicarboxylic acid
SMILES N[C@]1(CC[C@H](C1)C(O)=O)C(O)=O
Standard InChI InChI=1S/C7H11NO4/c8-7(6(11)12)2-1-4(3-7)5(9)10/h4H,1-3,8H2,(H,9,10)(H,11,12)/t4-,7+/m1/s1
Formula C7H11NO4 M.Wt 173.17
Solubility Soluble to 30 mM in water
Storage Store at RT
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other courier with RT , or blue ice upon request.

Preparing Stock Solutions of (1S,3R)-ACPD

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 5.7747 mL 28.8734 mL 57.7467 mL 115.4934 mL 144.3668 mL
5 mM 1.1549 mL 5.7747 mL 11.5493 mL 23.0987 mL 28.8734 mL
10 mM 0.5775 mL 2.8873 mL 5.7747 mL 11.5493 mL 14.4367 mL
50 mM 0.1155 mL 0.5775 mL 1.1549 mL 2.3099 mL 2.8873 mL
100 mM 0.0577 mL 0.2887 mL 0.5775 mL 1.1549 mL 1.4437 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

References on (1S,3R)-ACPD

The metabotropic glutamate receptor agonist 1S,3R-ACPD stimulates and modulates NMDA receptor mediated excitotoxicity in organotypic hippocampal slice cultures.[Pubmed: 11292452]

The potential toxic effects of the metabotropic glutamate receptor agonist (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid (ACPD) and its interactions with the N-methyl-D-aspartate (NMDA) receptor were studied in hippocampal brain slice cultures, using densitometric measurements of the cellular uptake of propidium iodide (PI) to quantify neuronal degeneration. Cultures exposed to ACPD, showed a concentration (2-5 mM) and time (1-4 days) dependent increase in PI uptake in CA1, CA3 and dentate subfields after 24 h and 48 h of exposure, with CA1 pyramidal cells being most sensitive. The neurodegeneration induced by 2 mM ACPD was completely abolished by addition of 10 microM of the NMDA receptor antagonist (5R,10S)-(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine (MK-801), while 20 microM of the 2-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA)/kainic acid receptor antagonist 2,3-dioxo-6-nitro-1,2,3,4-tetrahydrobenzo[f]quinoxaline-7-sulfonamide (NBQX) had no effect. Co-exposing cultures to a subtoxic dose of 300 microM ACPD together with 10 microM NMDA, which at this dose is known to induce a fairly selective degeneration of CA1 pyramidal cells, significantly increased the PI uptake in both CA1 and CA3, compared to cultures exposed to 10 microM NMDA only. Adding the 300 microM ACPD as pretreatment for 30 min followed by a 30 min wash in normal medium before the ACPD/NMDA co-exposure, eliminated the potentiation of NMDA toxicity. The potentiation was also blocked by addition of 10 or 100 microM 2-methyl-6-(phenylethynyl)pyridine (MPEP) (mGluR5 antagonist) during the co-exposure, while a corresponding addition of 10 or 100 microM 7-(hydroxyimino)cyclopropa[b]chromen-1a-carboxylate ethyl ester (CPCCOEt) (mGluR1 antagonist) had no effect. We conclude that, stimulation of metabotropic glutamate receptors with ACPD at concentrations of 2 mM or higher induces a distinct subfield-related and time and concentration dependent pattern of hippocampal degeneration, and that ACPD at subtoxic concentrations modulates NMDA-induced excitotoxicity through the mGluR5 receptor in a time dependent way.

Group II metabotropic glutamate receptors are a common target of N-anisoyl-GABA and 1S,3R-ACPD in enhancing ACh release in the prefrontal cortex of freely moving SHRSP.[Pubmed: 10699452]

Aniracetam is a therapeutically useful cognition enhancer for treating various neuropsychiatric symptoms occurring after cerebral infarction. We recently reported that local perfusion of its major metabolites N-anisoyl-GABA and p-anisic acid, but not aniracetam itself, enhanced acetylcholine (ACh) release with a delayed onset in cerebral regions of stroke-prone spontaneously hypertensive rats (SHRSP). In this study, we examined the possible involvement of metabotropic and ionotropic glutamate (mGlu and AMPA) receptors in the N-anisoyl-GABA-induced ACh release using brain in vivo microdialysis. Basal ACh release in SHRSP was commonly lower in the nucleus reticularis thalami, dorsal hippocampus and prefrontal cortex than that in age-matched Wistar Kyoto rats. The delayed ACh release in the prefrontal cortex of SHRSP was completely blocked by MCPG, a group I and II mGlu receptor antagonist, and MCCG, a group II-selective mGlu receptor antagonist. In contrast, it was largely unaffected by AIDA, a group I-selective mGlu receptor antagonist, or by YM90K, an AMPA receptor antagonist. 1S,3R-ACPD, a preferential group II mGlu receptor agonist, enhanced ACh release with a similar latency and the effect was antagonized by MCCG, whereas AMPA induced a prompt ACh release. These results indicate that N-anisoyl-GABA and 1S,3R-ACPD share a common mechanism mediated by group II mGlu receptors in enhancing ACh release. The findings suggest a possible mechanism for aniracetam's clinical efficacy in stroke patients with cholinergic deficits.

(1S,3R)-ACPD, a metabotropic glutamate receptor agonist, enhances damage after global ischaemia.[Pubmed: 9988123]

There are opposing results in the literature concerning the influence of (1S,3R)-ACPD [(1S,3R)-1-aminocyclopentane-1,3-dicarboxylate: group I/II metabotropic glutamate receptor agonist) on neurodegeneration, showing both enhancement and reduction of damage. We examined the effects of (1S,3R)-ACPD, given in various application schedules, on global ischaemia in gerbils. The most pronounced effect was a significant increase of hippocampal damage when the drug was applied at 20 mg/kg i.p. pre ischaemia. All other experiments with lower concentrations (0.02-2 mg/kg), other time schedules (post-ischaemic application) or co-application of a selective group I metabotropic glutamate receptor antagonist (4-CPG: (S)-4-carboxyphenylglycine), had no influence on neuronal density.

Metabotropic glutamate receptor agonist (1S,3R-ACPD) increased frontal cortex dopamine release in aged but not in young rats.[Pubmed: 9832384]

The effects of the metabotropic glutamate (mGlu) receptor agonist (1S,3R)-1-Amino cyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD) infusion on frontal cortex dopamine extracellular levels were studied by microdialysis in young (3 months) and aged (24 months) rats. Basal dopamine levels were significantly higher in young than in aged rats. (1S,3R)-ACPD (1 mM) significantly increased dopamine efflux in aged rats, an effect which was antagonized by the mGlu receptor antagonist, (S)-alpha-methyl-4-carboxypheniylglycine (MCPG) (2 mM). On the contrary, (IS,3R)-ACPD up to the concentration of 2 mM failed to influence dopamine extracellular levels in young rats. These results suggest that the agonist of mGlu receptor group I and/or II can improve dopamine release under conditions of deficiency of extracellular dopamine concentration as observed in aging.


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