Pralidoxime iodide
(Synonyms: 碘解磷定) 目录号 : GC39656
Pralidoxime Iodide (2-PAM) is an antidote approved for reactivation of inhibited acetylcholinesterase (AChE) in organophosphate poisoning.
Cas No.:94-63-3
Sample solution is provided at 25 µL, 10mM.
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Pralidoxime Iodide (2-PAM) is an antidote approved for reactivation of inhibited acetylcholinesterase (AChE) in organophosphate poisoning.
[1] Sakurada K, et al. Neurochem Res. 2003, 28(9):1401-7.
Cas No. | 94-63-3 | SDF | |
别名 | 碘解磷定 | ||
Canonical SMILES | C[N+]1=CC=CC=C1/C=N/O.[I-] | ||
分子式 | C7H9IN2O | 分子量 | 264.06 |
溶解度 | DMSO: 250 mg/mL (946.75 mM) | 储存条件 | Store at -20°C, protect from light |
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1 mg | 5 mg | 10 mg |
1 mM | 3.787 mL | 18.9351 mL | 37.8702 mL |
5 mM | 0.7574 mL | 3.787 mL | 7.574 mL |
10 mM | 0.3787 mL | 1.8935 mL | 3.787 mL |
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Pralidoxime iodide (2-pAM) penetrates across the blood-brain barrier
Neurochem Res 2003 Sep;28(9):1401-7.PMID:12938863DOI:10.1023/a:1024960819430.
The in vivo rat brain microdialysis technique with HPLC/UV was used to determine the blood-brain barrier (BBB) penetration of Pralidoxime iodide (2-PAM), which is a component of the current nerve agent antidote therapy. After intravenous dosage of 2-PAM (10, 50, 100 mg/kg), 2-PAM appeared dose-dependently in the dialysate; the striatal extracellular/blood concentration ratio at 1 h after 50 mg/kg dosage was 0.093 +/- 0.053 (mean +/- SEM). This finding offered conclusive evidence of the BBB penetration of 2-PAM. We also examined whether the BBB penetration of 2-PAM was mediated by a certain specific transporter, such as a neutral or basic amino acid transport system. Although it was unclear, the neural uptake of 2-PAM was Na+ dependent. The mean BBB penetration by 2-PAM was approximately 10%, indicating the intravenous administration of 2-PAM might be to a degree effective to reactivation of the blocked cholinesterase in the brain.
Hydrolysis of an acetylthiocholine by Pralidoxime iodide (2-PAM)
Toxicol Lett 2006 Oct 25;166(3):255-60.PMID:16971069DOI:10.1016/j.toxlet.2006.07.339.
Pralidoxime iodide (2-PAM), an antidote approved for the reactivation of inhibited acetylcholinesterase (AChE) in organophosphate poisoning, dose-dependently hydrolyzed an acetylthiocholine iodide (ASCh). The AChE (0.3 U) activity inhibited by VX analog (ENMP, 0.1 microM) increased to approximately 200% of normal levels after a dosage of 5 mM 2-PAM (control 0.132+/-0.012 U/ml, 5 mM 0.253+/-0.026 U/ml). This result indicates that 2-PAM produced a thiocholine from the ASCh by hydrolysis. High-performance liquid chromatography (HPLC) analysis was then performed to further clarify the hydrolysis of ASCh with 2-PAM. It was clear that 2-PAM was converted to acetylated 2-PAM with acetic acid produced from ASCh by hydrolysis. Next, we tried to compare this esterase-like activity of 2-PAM with that of obidoxime, which is known as a strong reactivator of inhibited AChE, and with diacetylmonoxime, known as a weak reactivator. All of these oximes showed esterase-like activity, and their strengths were consistent with those of known reactivators of inhibited AChE. These results indicate that a great deal of the data obtained previously with ASCh relating to the effects of oximes must be rechecked. It is clear that oximes easily hydrolyze ASCh. We therefore strongly caution that the method of determining AChE activity with ASCh is not suitable for examining the effects of oximes.