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209223-86-9

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209223-86-9 Usage

Check Digit Verification of cas no

The CAS Registry Mumber 209223-86-9 includes 9 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 6 digits, 2,0,9,2,2 and 3 respectively; the second part has 2 digits, 8 and 6 respectively.
Calculate Digit Verification of CAS Registry Number 209223-86:
(8*2)+(7*0)+(6*9)+(5*2)+(4*2)+(3*3)+(2*8)+(1*6)=119
119 % 10 = 9
So 209223-86-9 is a valid CAS Registry Number.

209223-86-9SDS

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 N-(1-Benzyl-4-piperidinyl)-2-bromoacetamide

1.2 Other means of identification

Product number -
Other names -

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:209223-86-9 SDS

209223-86-9Downstream Products

209223-86-9Relevant articles and documents

Novel Multitarget-Directed Ligands Aiming at Symptoms and Causes of Alzheimer's Disease

Wi?ckowska, Anna,Wichur, Tomasz,Godyń, Justyna,Bucki, Adam,Marcinkowska, Monika,Siwek, Agata,Wi?ckowski, Krzysztof,Zar?ba, Paula,Knez, Damijan,G?uch-Lutwin, Monika,Kazek, Grzegorz,Latacz, Gniewomir,Mika, Kamil,Ko?aczkowski, Marcin,Korabecny, Jan,Soukup, Ondrej,Benkova, Marketa,Kie?-Kononowicz, Katarzyna,Gobec, Stanislav,Malawska, Barbara

, p. 1195 - 1214 (2018/05/25)

Alzheimer's disease (AD) is a major public health problem, which is due to its increasing prevalence and lack of effective therapy or diagnostics. The complexity of the AD pathomechanism requires complex treatment, e.g. multifunctional ligands targeting both the causes and symptoms of the disease. Here, we present new multitarget-directed ligands combining pharmacophore fragments that provide a blockade of serotonin 5-HT6 receptors, acetyl/butyrylcholinesterase inhibition, and amyloid β antiaggregation activity. Compound 12 has displayed balanced activity as an antagonist of 5-HT6 receptors (Ki = 18 nM) and noncompetitive inhibitor of cholinesterases (IC50hAChE = 14 nM, IC50eqBuChE = 22 nM). In further in vitro studies, compound 12 has shown amyloid β antiaggregation activity (IC50 = 1.27 μM) and ability to permeate through the blood-brain barrier. The presented findings may provide an excellent starting point for further studies and facilitate efforts to develop new effective anti-AD therapy.

Targeting mycobacterium protein tyrosine phosphatase B for antituberculosis agents

Zhou, Bo,He, Yantao,Zhang, Xian,Xu, Jie,Luo, Yong,Wang, Yuehong,Franzblau, Scott G.,Yang, Zhenyun,Chan, Rebecca J.,Liu, Yan,Zheng, Jianyu,Zhang, Zhong-Yin

scheme or table, p. 4573 - 4578 (2010/10/03)

Protein tyrosine phosphatases are often exploited and subverted by pathogenic bacteria to cause human diseases. The tyrosine phosphatase mPTPB from Mycobacterium tuberculosis is an essential virulence factor that is secreted by the bacterium into the cytoplasm of macrophages, where it mediates mycobacterial survival in the host. Consequently, there is considerable interest in understanding the mechanism by which mPTPB evades the host immune responses, and in developing potent and selective mPTPB inhibitors as unique antituberculosis (antiTB) agents. We uncovered that mPTPB subverts the innate immune responses by blocking the ERK1/2 and p38 mediated IL-6 production and promoting host cell survival by activating the Akt pathway. We identified a potent and selective mPTPB inhibitor I-A09 with highly efficacious cellular activity, from a combinatorial library of bidentate benzofuran salicylic acid derivatives assembled by click chemistry. We demonstrated that inhibition of mPTPB with I-A09 in macrophages reverses the altered host immune responses induced by the bacterial phosphatase and prevents TB growth in host cells. The results provide the necessary proof-of-principle data to support the notion that specific inhibitors of the mPTPB may serve as effective antiTB therapeutics.

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