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25296-66-6

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25296-66-6 Usage

Check Digit Verification of cas no

The CAS Registry Mumber 25296-66-6 includes 8 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 5 digits, 2,5,2,9 and 6 respectively; the second part has 2 digits, 6 and 6 respectively.
Calculate Digit Verification of CAS Registry Number 25296-66:
(7*2)+(6*5)+(5*2)+(4*9)+(3*6)+(2*6)+(1*6)=126
126 % 10 = 6
So 25296-66-6 is a valid CAS Registry Number.
InChI:InChI=1/C5H12O2P/c1-5(2)4-7-8(3)6/h5H,4H2,1-3H3/q+1

25296-66-6SDS

SAFETY DATA SHEETS

According to Globally Harmonized System of Classification and Labelling of Chemicals (GHS) - Sixth revised edition

Version: 1.0

Creation Date: Aug 13, 2017

Revision Date: Aug 13, 2017

1.Identification

1.1 GHS Product identifier

Product name methyl-(2-methylpropoxy)-oxophosphanium

1.2 Other means of identification

Product number -
Other names isobutyl methylphosphonate

1.3 Recommended use of the chemical and restrictions on use

Identified uses For industry use only.
Uses advised against no data available

1.4 Supplier's details

1.5 Emergency phone number

Emergency phone number -
Service hours Monday to Friday, 9am-5pm (Standard time zone: UTC/GMT +8 hours).

More Details:25296-66-6 SDS

25296-66-6Relevant articles and documents

A kind of preparation method for treating keratoconjunctival

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Paragraph 0037; 0038, (2017/01/12)

The invention belongs to the field of chemical synthesis, and in particular relates to a novel method for preparing herbicide, namely glufosinate-ammonium. The method comprises the following steps: conducting addition reaction on methyl phosphonic acid ester compounds and DL-2-hydroxy-3-crotonic acid ester compounds to obtain hydroxybutyric acid ester derivatives, and conducting acidification and ammonification reaction on the hydroxybutyric acid ester derivatives to obtain a glufosinate-ammonium compound. The method can avoid using high-toxic cyanide and obviously shortens a reaction route, so that the reaction steps of a process for preparing glufosinate-ammonium are reduced, the operation is simpler and more convenient, and many times of recrystallization is not needed for removing ammonium salt. The cost is reduced, and the method is completely suitable for large-scale production.

Phosphinic acid analogues of GABA. 2. Selective, orally active GABA(B) antagonists

Froestl,Mickel,Von Sprecher,Diel,Hall,Maier,Strub,Melillo,Baumann,Bernasconi,Gentsch,Hauser,Jaekel,Karlsson,Klebs,Maitre,Marescaux,Pozza,Schmutz,et al.

, p. 3313 - 3331 (2007/10/02)

In 1987, 25 years after the synthesis of the potent and selective GABA(B) agonist baclofen (1), Kerr et al. described the first GABA(B) antagonist phaclofen 2. However, phaclofen and structurally similar derivatives 3-5 did not cross the blood-brain barrier and hence were inactive in vivo as central nervous system agents. As a consequence, the therapeutic potential of GABA(B) antagonists remained unclear. In exploring GABA and baclofen derivatives by replacing the carboxylic acid residue with various phosphinic acid groups, we discovered more potent and water soluble GABA(B) antagonists. Electrophysiological experiments in vivo demonstrated that some of the new compounds were capable of penetrating the blood-brain barrier after oral administration. Neurotransmitter release experiments showed that they interacted with several presynaptic GABA(B) receptor subtypes, enhancing the release of GABA, glutamate, aspartate, and somatostatin. The new GABA(B) antagonists interacted also with postsynaptic GABA(B) receptors, as they blocked late inhibitory postsynaptic potentials. They facilitated the induction of long-term potentiation in vitro and in vivo, suggesting potential cognition enhancing effects. Fifteen compounds were investigated in various memory and learning paradigms in rodents. Although several compounds were found to be active, only 10 reversed the age-related deficits of old rats in a multiple-trial one-way active avoidance test after chronic treatment. The cognition facilitating effects of 10 were confirmed in learning experiments in Rhesus monkeys. The novel GABA(B) antagonists showed also protective effects in various animal models of absence epilepsy.

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