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29241-62-1

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29241-62-1 Usage

Chemical Properties

White solid

Check Digit Verification of cas no

The CAS Registry Mumber 29241-62-1 includes 8 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 5 digits, 2,9,2,4 and 1 respectively; the second part has 2 digits, 6 and 2 respectively.
Calculate Digit Verification of CAS Registry Number 29241-62:
(7*2)+(6*9)+(5*2)+(4*4)+(3*1)+(2*6)+(1*2)=111
111 % 10 = 1
So 29241-62-1 is a valid CAS Registry Number.
InChI:InChI=1/C6H3BrClNO2/c7-4-1-3(6(10)11)2-9-5(4)8/h1-2H,(H,10,11)/p-1

29241-62-1 Well-known Company Product Price

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  • Alfa Aesar

  • (H32384)  5-Bromo-6-chloronicotinic acid, 97%   

  • 29241-62-1

  • 1g

  • 1039.0CNY

  • Detail
  • Alfa Aesar

  • (H32384)  5-Bromo-6-chloronicotinic acid, 97%   

  • 29241-62-1

  • 5g

  • 3469.0CNY

  • Detail

29241-62-1SDS

SAFETY DATA SHEETS

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

Version: 1.0

Creation Date: Aug 11, 2017

Revision Date: Aug 11, 2017

1.Identification

1.1 GHS Product identifier

Product name 5-bromo-6-chloropyridine-3-carboxylic acid

1.2 Other means of identification

Product number -
Other names 5-bromo-6-chloro-3-pyridinecarboxylic acid

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:29241-62-1 SDS

29241-62-1Relevant articles and documents

SUBSTITUTED HETEROCYCLIC AMIDE COMPOUND AND PREPARATION METHOD THEREFOR AND PHARMACEUTICAL USE THEREOF

-

Paragraph 0175-0176; 0247-0248, (2022/02/02)

Provided are a substituted heterocyclic amide compound having a selective inhibitory effect on RIPK1, and a pharmaceutically acceptable salt, a stereoisomer, a solvate or a prodrug thereof, and a pharmaceutical composition containing the compound, and the

Iron-Catalyzed Amination of Strong Aliphatic C(sp3)-H Bonds

Das, Sandip Kumar,Roy, Satyajit,Khatua, Hillol,Chattopadhyay, Buddhadeb

supporting information, p. 16211 - 16217 (2020/10/26)

A concept for intramolecular denitrogenative C(sp3)-H amination of 1,2,3,4-tetrazoles bearing unactivated primary, secondary, and tertiary C-H bonds is discovered. This catalytic amination follows an unprecedented metalloradical activation mechanism. The utility of the method is showcased with the short synthesis of a bioactive molecule. Moreover, an initial effort has been embarked on for the enantioselective C(sp3)-H amination through the catalyst design. Collectively, this study underlines the development of C(sp3)-H bond functionalization chemistry that should find wide application in the context of drug discovery and natural product synthesis.

6-alkoxy-5-aryl-3-pyridinecarboxamides, a new series of bioavailable cannabinoid receptor type 1 (CB1) antagonists including peripherally selective compounds

R?ver, Stephan,Andjelkovic, Mirjana,Bénardeau, Agnès,Chaput, Evelyne,Guba, Wolfgang,Hebeisen, Paul,Mohr, Susanne,Nettekoven, Matthias,Obst, Ulrike,Richter, Wolfgang F.,Ullmer, Christoph,Waldmeier, Pius,Wright, Matthew B.

, p. 9874 - 9896 (2014/01/17)

We identified 6-alkoxy-5-aryl-3-pyridinecarboxamides as potent CB1 receptor antagonists with high selectivity over CB2 receptors. The series was optimized to reduce lipophilicity compared to rimonabant to achieve peripherally active molecules with minimal central effects. Several compounds that showed high plasma exposures in rats were evaluated in vivo to probe the contribution of central vs peripheral CB1 agonism to metabolic improvement. Both rimonabant and 14g, a potent brain penetrant CB1 receptor antagonist, significantly reduced the rate of body weight gain. However, 14h, a molecule with markedly reduced brain exposure, had no significant effect on body weight. PK studies confirmed similarly high exposure of both 14h and 14g in the periphery but 10-fold lower exposure in the brain for 14h. On the basis of these data, which are consistent with reported effects in tissue-specific CB1 receptor KO mice, we conclude that the metabolic benefits of CB1 receptor antagonists are primarily centrally mediated as originally believed.

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