DL-AP5CAS# 76326-31-3 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 76326-31-3 | SDF | Download SDF |
| PubChem ID | 1216 | Appearance | Powder |
| Formula | C5H12NO5P | M.Wt | 197.13 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Synonyms | DL-APV | ||
| Solubility | Soluble to 10 mM in water and to 100 mM in 1eq. NaOH | ||
| Chemical Name | 2-amino-5-phosphonopentanoic acid | ||
| SMILES | C(CC(C(=O)O)N)CP(=O)(O)O | ||
| Standard InChIKey | VOROEQBFPPIACJ-UHFFFAOYSA-N | ||
| Standard InChI | InChI=1S/C5H12NO5P/c6-4(5(7)8)2-1-3-12(9,10)11/h4H,1-3,6H2,(H,7,8)(H2,9,10,11) | ||
| 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. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
| Description | Potent NMDA antagonist. Separate isomers D-AP5, L-AP5 and sodium salt DL-AP5 Sodium salt also available. |
DL-AP5 Dilution Calculator
DL-AP5 Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 5.0728 mL | 25.364 mL | 50.7279 mL | 101.4559 mL | 126.8199 mL |
| 5 mM | 1.0146 mL | 5.0728 mL | 10.1456 mL | 20.2912 mL | 25.364 mL |
| 10 mM | 0.5073 mL | 2.5364 mL | 5.0728 mL | 10.1456 mL | 12.682 mL |
| 50 mM | 0.1015 mL | 0.5073 mL | 1.0146 mL | 2.0291 mL | 2.5364 mL |
| 100 mM | 0.0507 mL | 0.2536 mL | 0.5073 mL | 1.0146 mL | 1.2682 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. | |||||
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The effects of DL-AP5 and glutamate on ghrelin-induced feeding behavior in 3-h food-deprived broiler cockerels.[Pubmed:21203879]
J Physiol Biochem. 2011 Jun;67(2):217-23.
This study was designed to examine the effects of intracerebroventricular injection of DL-AP5 (N-methyl-D-aspartate (NMDA) receptor antagonist) and glutamate on ghrelin-induced feeding behavior in 3-h food-deprived (FD3) broiler cockerels. At first, guide cannula was surgically implanted in the right lateral ventricle of chickens. In experiment 1, birds were intracerebroventricularly injected with 0, 2.5, 5, and 10 nmol of DL-AP5. In experiment 2, chickens received 5 nmol DL-AP5 prior to the injection of 0.6 nmol ghrelin. In experiment 3, birds were administered with 0.6 nmol ghrelin after 300 nmol glutamate, and the cumulative feed intake was determined at 3-h postinjection. The results of this study showed that the intracerebroventricular injection of DL-AP5 increased food consumption in FD3 broiler cockerels (P DL-AP5 administration(P
Actions of D and L forms of 2-amino-5-phosphonovalerate and 2-amino-4-phosphonobutyrate in the cat spinal cord.[Pubmed:6145492]
Brain Res. 1982 Mar 11;235(2):378-86.
The separate optical enantiomers of 2-amino-5-phosphonovalerate (APV) and 2-amino-4-phosphonobutyrate (APB) have been tested for their ability to modify amino acid-induced and synaptic excitation of cat spinal neurones. D-(-)-APV was a highly potent and selective antagonist of amino acid-induced and synaptic excitation. Polysynaptic excitation was more susceptible to antagonism by D-APV than was monosynaptic excitation. It was considered likely that the depression of synaptic excitation by D-APV was due to the blockade of an excitatory amino acid transmitter acting at N-methyl-D-aspartate (NMDA) receptors. L-(+)-APV showed a relatively weak amino acid and synaptic blocking activity, which was similar in character to that of D-APV, and which may have been due to a slight residuum of the D isomer in the sample of the L form used. D-(-)-APB was a weak and relatively non-selective antagonist of amino acid-induced responses. In contrast, L-(+)-APB either had no effect or, at higher concentrations, enhanced these responses. Both isomers depressed synaptic responses in a proportion of the cells tested, the L form being the more potent isomer in producing this effect. Monosynaptic and polysynaptic excitations were both susceptible to this type of action. The depression of synaptic excitation by D-APB may have been due in some cases to the blockade of an excitatory amino acid transmitter. However, it is unlikely that the synaptic depressant action of L-APB is due to this mechanism.
The effects of a series of omega-phosphonic alpha-carboxylic amino acids on electrically evoked and excitant amino acid-induced responses in isolated spinal cord preparations.[Pubmed:7042024]
Br J Pharmacol. 1982 Jan;75(1):65-75.
1 The depressant actions on evoked electrical activity and the excitant amino acid antagonist properties of a range of omega-phosphonic alpha-carboxylic amino acids have been investigated in the isolated spinal cord preparations of the frog or immature rat. 2 When tested on dorsal root-evoked ventral root potentials, members of the homologous series from 2- amino-5-phosphonovaleric acid to 2-amino-8-phosphonooctanoic acid showed depressant actions which correlated with the ability of the substances to antagonize selectivity motoneuronal depolarizations induced by N-methyl-D-aspartate. 3 2-Amino-5-phosphonovalerate was the most potent substance of the series giving an apparent KD of 1.4 microM for the antagonism of responses to N-methyl-D-aspartate. 4 A comparison of the (+)- and (-)-forms of 2-amino-5-phosphonovalerate indicated that the N-methyl-D-aspartate antagonist activity and the neuronal depressant action of this substance were both due mainly to the (-)-isomer. 5 The (-)- and (+)-forms of 2-amino-4-phosphonobutyrate had different actions. The (-)-forms of this substance had a relatively weak and non-selective antagonist action on depolarizations induced by N-methyl-D-aspartate, quisqualate and kainate and a similarly weak depressant effect when tested on evoked electrical activity. The (+)-form was more potent than he (-)-form in depressing electrically evoked activity but did not antagonize responses to amino acid excitants. At concentrations higher than those required to depress electrically evoked activity, the (+)-form produced depolarization. This action was blocked by 2-amino-5-phosphonovalerate.
