39891-09-3

Basic information

• Product Name: 2-Chloro-5-pyridineacetonitrile
• Synonyms: 2-(6-CHLORO-3-PYRIDINYL)ACETONITRILE;2-CHLORO-5-(CYANOMETHYL)PYRIDINE;2-CHLOROPYRIDINE-5-ACETONITRILE;(6-CHLORO-PYRIDIN-3-YL)-ACETONITRILE;2-CHLORO-5-PYRIDINEACETONITRILE;2-(6-chloropyridin-3-yl)acetonitrile;2-Chloro-5-pyridinea;6-Chloro-3-(cyanomethyl)pyridine
• CAS NO: 39891-09-3
• Molecular Formula: C₇H₅ClN₂
• Molecular Weight: 152.58
• Product Categories: Pyridine;Pyridines
• Mol File: 39891-09-3.mol

Chemical Properties

• Melting Point: 49-54°C
• Boiling Point: 294.1 °C at 760 mmHg
• Flash Point: >110℃
• Appearance: /
• Density: 1.262 g/cm³
• Vapor Pressure: 0.00166mmHg at 25°C
• Refractive Index: 1.553
• Storage Temp.: under inert gas (nitrogen or Argon) at 2-8°C
• PKA: -1.02±0.10(Predicted)
• CAS DataBase Reference: 2-Chloro-5-pyridineacetonitrile(CAS DataBase Reference)
• NIST Chemistry Reference: 2-Chloro-5-pyridineacetonitrile(39891-09-3)
• EPA Substance Registry System: 2-Chloro-5-pyridineacetonitrile(39891-09-3)

Safety Data

• Hazard Codes: Xi,T,Xn
• Statements: 22-37/38-41
• Safety Statements: 26-39
• RIDADR: UN 3439 6.1 / PGIII
• WGK Germany: 3
• HazardClass: IRRITANT, TOXIC
• Hazardous Substances Data: 39891-09-3(Hazardous Substances Data)

Usage

Uses

2-Chloro-5-cyanomethylpyridine

InChI:InChI=1/C7H5ClN2/c8-7-2-1-6(3-4-9)5-10-7/h1-2,5H,3H2

Upstream product

• 6635-88-7 3-(cyanomethyl)pyridine 1-oxide 
• 10025-87-3 trichlorophosphate 
• 70258-18-3 2-chloro-5-(chloromethyl)pyridine 
• 143-33-9 sodium cyanide 
• 151-50-8 potassium cyanide 
• 6443-85-2 3-pyridinylacetonitrile 
• 6959-48-4 3-chloromethylpyridinium chloride 
• 21543-49-7 2-Chloro-5-hydroxymethylpyridine 
• 773837-37-9 sodium cyanide 
• 133457-49-5 6-chloro-α-methanesulfonyloxy-3-picoline 
• 73781-91-6 6-Chloronicotinic acid methyl ester 
• 23100-12-1 6-chloronicotinylaldehyde 

Downstream Products

• 39891-13-9 2-(6-chloropyridin-3-yl)acetic acid 
• 854267-90-6 1-(6-chloropyridin-3-yl)cyclopropanecarboxylic acid 
• 846548-86-5 (2-chloropyridin-5-yl)acetic acid hydrazide 
• 197376-47-9 ethyl (6-chloro-pyridin-3-yl)acetate 
• 854267-89-3 1-(6-chloropyridin-3-yl)cyclopropanecarbonitrile 
• 691872-18-1 tert-butyl (2-(6-chloropyridin-3-yl)ethyl)carbamate 
• 54127-64-9 2-chloro-5-aminoethylpyridine 
• 1305330-06-6 (Z)-3-(3-chloro-phenyl)-2-(6-chloro-pyridin-3-yl)-acrylonitrile 
• 1192165-36-8 [6-(4-tert-butylphenyl)pyridin-3-yl]acetonitrile 
• 1372399-14-8 4-(6-phenylpyridin-3-yl)-1H-pyrazol-5-amine 
• 1372401-72-3 tert-butyl 9-amino-3-(6-phenylpyridin-3-yl)-5,6-dihydropyrazolo[1,5-a]pyrido[4,3-d]pyrimidine-7(8H)-carboxylate 
• 1372401-65-4 3-(6-phenylpyridin-3-yl)-5,6,7,8-tetrahydropyrazolo[1,5-a]pyrido[4,3-d]pyrimidin-9-amine 
• 1372401-43-8 (R)-1-(8-amino-3-(6-phenylpyridin-3-yl)-5H-pyrazolo[1,5-a]pyrrolo[3,4-d]pyrimidin-6(7H)-yl)-2-hydroxypropan-1-one 
• 1372399-13-7 3-(dimethylamino)-2-(6-phenylpyridin-3-yl)acrylonitrile 

Relevant articles and documents

Synthesis and biological evaluation of N-difluoromethyl-1,2-dihydropyrid-2-one acetic acid regioisomers: Dual Inhibitors of cyclooxygenases and 5-lipoxygenase

A new group of acetic acid (7a-c, R1 = H), and propionic acid (7d-f, R1 = Me), regioisomers wherein a N-difluoromethyl-1,2-dihydropyrid-2-one moiety is attached via its C-3, C-4, and C-5 position was synthesized. This group of compounds exhibited a more potent inhibition, and hence selectivity, for the cyclooxygenase-2 (COX-2) relative to the COX-1 isozyme. Attachment of the N-difluoromethyl-1,2-dihydropyrid-2-one ring system to an acetic acid, or propionic acid, moiety confers potent 5-LOX inhibitory activity, that is, absent in traditional arylacetic acid NSAIDs. 2-(1-Difluoromethyl-2-oxo-1,2-dihydropyridin-5-yl)acetic acid (7c) exhibited the best combination of dual COX-2 and 5-LOX inhibitory activities. Molecular modeling (docking) studies showed that the highly electronegative CHF2 substituent present in 7c, that showed a modest selectivity for the COX-2 isozyme, is oriented within the secondary pocket (Val523) present in COX-2 similar to the sulfonamide (SO2NH2) COX-2 pharmacophore present in celecoxib, and that the N-difluoromethyl-1,2-dihydropyrid-2-one pharmacophore is oriented close to the region containing the LOX enzyme catalytic iron (His361, His366, and His545). Accordingly, the N-difluoromethyl-1,2-dihyrdopyrid-2-one moiety possesses properties suitable for the design of dual COX-2/5-LOX inhibitory drugs.

Rapid and Simple Access to α-(Hetero)arylacetonitriles from Gem-Difluoroalkenes

A scalable cyanation of gem-difluoroalkenes to (hetero)arylacetonitrile derivatives was developed. This strategy features mild reaction conditions, excellent yields, wide substrate scope, and broad functional group tolerance. Significantly, in this reacti

High-selectivity herbicide N-substitutive alkyl aryloxy phenoxyl propanamide compound and preparation and application thereof

The invention discloses novel N-substitutive alkyl aryloxy phenoxyl propanamide with herbicidal activity represented by the formula (I) and a preparation method thereof, a purpose of controlling vacious grassy weeds in a rice field and a proper weeding composition.The formula (I) is shown in the description.In the formula, R1 is selected from hydrogen or C1-C6 alkane, R3 is selected from hydrogen or C1-C6 alkyl groups or C1-C6 halogenated alkyl groups or C2-C6 alkenyl or C2-C6 alkine groups or C5-C12 aryl groups or heterocyclic aryl, Ar is selected from C6-C12 aryl and C5-C12 heterocyclic aryl, part or all of hydrogen atoms in aryl and heterocyclic aryl are replaced with identical or different substituent groups selected from halogen, cyanogroups, nitryl, C1-C6 alkyl groups, C1-C6 alkoxy, C1-C6 alkylthiol, C1-C6 alkyl amidogen, C1-C6 halogen alkyl and C1-C6 halogen alkoxy, x is selected from N and O, and chiral carbon atoms marked with * are of R or S configuration or are a mixture with R and S with different proportions.

Design, synthesis, and characterization of α-ketoheterocycles that additionally target the cytosolic port Cys269 of fatty acid amide hydrolase

A series of α-ketooxazoles incorporating electrophiles at the C5 position of the pyridyl ring of 2 (OL-135) and related compounds were prepared and examined as inhibitors of fatty acid amide hydrolase (FAAH) that additionally target the cytosolic port Cys269. From this series, a subset of the candidate inhibitors exhibited time-dependent FAAH inhibition and noncompetitive irreversible inactivation of the enzyme, consistent with the targeted Cys269 covalent alkylation or addition, and maintained or enhanced the intrinsic selectivity for FAAH versus other serine hydrolases. A preliminary in vivo assessment demonstrates that these inhibitors raise endogenous brain levels of anandamide and other FAAH substrates upon intraperitoneal (i.p.) administration to mice, with peak levels achieved within 1.5-3 h, and that the elevations of the signaling lipids were maintained >6 h, indicating that the inhibitors effectively reach and remain active in the brain, inhibiting FAAH for a sustained period.

Rational design of fatty acid amide hydrolase inhibitors that act by covalently bonding to two active site residues

The design and characterization of α-ketoheterocycle fatty acid amide hydrolase (FAAH) inhibitors are disclosed that additionally and irreversibly target a cysteine (Cys269) found in the enzyme cytosolic port while maintaining the reversible covalent Ser241 attachment responsible for their rapid and initially reversible enzyme inhibition. Two α-ketooxazoles (3 and 4) containing strategically placed electrophiles at the C5 position of the pyridyl substituent of 2 (OL-135) were prepared and examined as inhibitors of FAAH. Consistent with the observed time-dependent noncompetitive inhibition, the cocrystal X-ray structure of 3 bound to a humanized variant of rat FAAH revealed that 3 was not only covalently bound to the active site catalytic nucleophile Ser241 as a deprotonated hemiketal, but also to Cys269 through the pyridyl C5-substituent, thus providing an inhibitor with dual covalent attachment in the enzyme active site. In vivo characterization of the prototypical inhibitors in mice demonstrates that they raise endogenous brain levels of FAAH substrates to a greater extent and for a much longer duration (>6 h) than the reversible inhibitor 2, indicating that the inhibitors accumulate and persist in the brain to completely inhibit FAAH for a prolonged period. Consistent with this behavior and the targeted irreversible enzyme inhibition, 3 reversed cold allodynia in the chronic constriction injury model of neuropathic pain in mice for a sustained period (>6 h) beyond that observed with the reversible inhibitor 2, providing effects that were unchanged over the 1-6 h time course monitored.

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Substituted Heterocyclic Aza Compounds

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