CPA inhibitorPotent carboxypeptidase A (CPA) inhibitor CAS# 223532-02-3 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 223532-02-3 | SDF | Download SDF |
| PubChem ID | 44374998 | Appearance | Powder |
| Formula | C18H19NO4 | M.Wt | 313.36 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Synonyms | carboxypeptidase inhibitor | ||
| Solubility | DMSO : 100 mg/mL (319.13 mM; Need ultrasonic) | ||
| Chemical Name | 2-benzyl-3-[hydroxy-(2-phenylacetyl)amino]propanoic acid | ||
| SMILES | C1=CC=C(C=C1)CC(CN(C(=O)CC2=CC=CC=C2)O)C(=O)O | ||
| Standard InChIKey | PONANXDRJJIGPG-UHFFFAOYSA-N | ||
| Standard InChI | InChI=1S/C18H19NO4/c20-17(12-15-9-5-2-6-10-15)19(23)13-16(18(21)22)11-14-7-3-1-4-8-14/h1-10,16,23H,11-13H2,(H,21,22) | ||
| 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 | CPA inhibitor is a potent inhibitor for carboxypeptidase A (CPA) | |||||
| Targets | CPA | |||||
CPA inhibitor Dilution Calculator
CPA inhibitor Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 3.1912 mL | 15.9561 mL | 31.9122 mL | 63.8244 mL | 79.7804 mL |
| 5 mM | 0.6382 mL | 3.1912 mL | 6.3824 mL | 12.7649 mL | 15.9561 mL |
| 10 mM | 0.3191 mL | 1.5956 mL | 3.1912 mL | 6.3824 mL | 7.978 mL |
| 50 mM | 0.0638 mL | 0.3191 mL | 0.6382 mL | 1.2765 mL | 1.5956 mL |
| 100 mM | 0.0319 mL | 0.1596 mL | 0.3191 mL | 0.6382 mL | 0.7978 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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CPA inhibitor (carboxypeptidase inhibitor) is a potent inhibitor of EGFR [1].
EGFR (epidermal growth factor receptor) is a member of ErbB family of receptors and binds to the members of EGF-family. It has been reported that EGFR aberrant expression is correlated with cancer, inflammatory disease, monogenic disease and so on [1, 2].
When tested with human pancreatic adenocarcinoma cell lines Capan-1, CPA inhibitor treatment significantly inhibited cells growth at the concentration more than 10 μg/ml and pre-treatment markedly inhibited cell proliferation rate [1]. In A431 and MDA-MB-453 cell lines, pre-treated with CPA inhibitor markedly suppressed EGFR expression level [2].
In nude mouse model with Capan-1 cells subcutaneous xenograft, administration of CPA inhibitor significantly reduced solid tumor growth without side effects [1].
References:
[1].Blanco-Aparicio, C., et al., Potato carboxypeptidase inhibitor, a T-knot protein, is an epidermal growth factor antagonist that inhibits tumor cell growth. J Biol Chem, 1998. 273(20): p. 12370-7.
[2].Sitja-Arnau, M., et al., Mechanism of action of potato carboxypeptidase inhibitor (PCI) as an EGF blocker. Cancer Lett, 2005. 226(2): p. 169-84.
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Cartilage protective agent (CPA) Ro 32-3555, a new matrix metalloproteinase inhibitor for the treatment of rheumatoid arthritis.[Pubmed:9426828]
Agents Actions Suppl. 1998;49:49-55.
CPA was well tolerated at all dose levels (10-150 mg) following single oral dose administration to healthy male volunteers. There was no relationship between the intensity, duration and number of adverse events reported and the dose of CPA. There was a dose-related increase in exposure as measured by AUC0-infinity and Cmax. Administration of 10 mg CPA following food resulted in a delayed tmax, and a significant decrease in Cmax but not AUC0-infinity.
Spinal cord injury induced c-fos expression is reduced by p-CPA, a serotonin synthesis inhibitor. An experimental study using immunohistochemistry in the rat.[Pubmed:11450029]
Acta Neurochir Suppl. 2000;76:297-301.
Influence of serotonin on upregulation of cellular-fos (c-fos) following a focal spinal cord injury was examined using immunohistochemistry in a rat model. Spinal cord injury was produced by making a unilateral longitudinal incision of the dorsal horn of the T10-11 segments. A focal lesion to the cord markedly upregulated c-fos immunohistochemistry at 5 h which was mainly located in the edematous regions of the cord in the injured as well as in the perifocal T9 and T12 segments. Pretreatment with p-CPA, a serotonin synthesis inhibitor, significantly attenuated the c-fos upregulation along with the edematous expansion of the cord. These results for the first time suggest that trauma induced release of serotonin and edema formation are important biological signals inducing c-fos expression.
Effects of the serotonin synthesis inhibitor p-CPA on the expression of the crossed phrenic phenomenon 4 h following C2 spinal cord hemisection.[Pubmed:10619565]
Exp Neurol. 1999 Dec;160(2):479-88.
The present study assesses the effects of para-chlorophenylalanine (p-CPA), a serotonin-depleting drug, on the recovery of respiratory-related activity in the phrenic nerve induced by asphyxia 4 h following ipsilateral C2 hemisection in young adult rats. HPLC analysis was used to quantify levels of serotonin (5-HT), dopamine (DA), norepinephrine, and the 5-HT metabolite, 5-hydroxyindoleacetic acid, in the C4 segment of the spinal cord, all of which were significantly lower in p-CPA-treated hemisected rats compared to hemisected controls receiving saline. Hemisection alone was found to significantly increase 5-HT levels and significantly decrease DA levels compared to normal controls. Eight of eight saline-injected rats expressed recovery of respiratory-related activity in the ipsilateral phrenic nerve during asphyxia 4 h following hemisection, while only 4/8 rats in the p-CPA-treated group expressed recovery in the ipsilateral nerve. Quantification of integrated phrenic nerve wave-forms indicated that the mean amplitude of respiratory-related activity in the ipsilateral phrenic nerve was significantly lower in p-CPA-treated rats than in saline controls. In addition, saline controls demonstrated significant increases in mean respiratory frequency and mean amplitude of contralateral phrenic nerve activity during asphyxia, compared to normocapnia. However, p-CPA-treated rats did not express significant differences in either mean respiratory frequency or mean amplitude of integrated respiratory wave-forms during asphyxia, compared to normocapnia. The results suggest that p-CPA treatment attenuates the recovery of respiratory-related activity in the phrenic nerve 4 h following ipsilateral C2 hemisection and attenuates asphyxia-induced increases in respiratory frequency and respiratory burst amplitude recorded from the contralateral phrenic nerve.
