39905-48-1

Basic information

• Product Name: 4-(cyclohexyloxy)aniline
• Synonyms: 4-(cyclohexyloxy)aniline;AKOS DM0070;4-(Cyclohexyloxy)benzenamine;4-(Cyclohexyloxy)phenylamine;p-(Cyclohexyloxy)aniline
• CAS NO: 39905-48-1
• Molecular Formula: C₁₂H₁₇NO
• Molecular Weight: 191.272
• Mol File: 39905-48-1.mol

Chemical Properties

• Boiling Point: 101-102℃ (0.05 Torr)
• Flash Point: 158.1°C
• Appearance: /
• Density: 1.073g/cm³
• Vapor Pressure: 0.000175mmHg at 25°C
• Refractive Index: 1.566
• Storage Temp.: Keep in dark place,Inert atmosphere,Room temperature
• CAS DataBase Reference: 4-(cyclohexyloxy)aniline(CAS DataBase Reference)
• NIST Chemistry Reference: 4-(cyclohexyloxy)aniline(39905-48-1)
• EPA Substance Registry System: 4-(cyclohexyloxy)aniline(39905-48-1)

Safety Data

• Hazardous Substances Data: 39905-48-1(Hazardous Substances Data)

Usage

Synthesis Reference(s)

Journal of Medicinal Chemistry, 45, p. 2260, 2002 DOI: 10.1021/jm010261z

InChI:InChI=1/C12H17NO/c13-10-6-8-12(9-7-10)14-11-4-2-1-3-5-11/h6-9,11H,1-5,13H2

Upstream product

• 108-85-0 1-bromocyclohexane 
• 5493-73-2 1-(cyclohexyloxy)-4-nitrobenzene 
• 103-90-2 4-acetaminophenol 
• 108-93-0 cyclohexanol 
• 350-46-9 4-Fluoronitrobenzene 
• 824-78-2 4-nitrophenol sodium salt 
• 123-30-8 4-amino-phenol 
• 72056-57-6 p-Cyclohexyloxy-acetanilid 

Downstream Products

• 85010-69-1 5-(4-Cyclohexyloxy-benzyl)-2-imino-thiazolidin-4-one 
• 85002-28-4 5-(4-Cyclohexyloxy-benzyl)-thiazolidine-2,4-dione 
• 1067239-49-9 C₁₅H₁₉ClN₂O₃ 
• 1067239-62-6 C₁₅H₂₂N₂O₂ 
• 1221879-36-2 (S)-2-(2-(1H-imidazol-5-yl)acetamido)-3-(benzyloxy)-N-(4-(cyclohexyloxy)phenyl)propanamide 
• 1222196-43-1 (S)-2-amino-3-benzyloxy-N-(4-(cyclohexyloxy)phenyl)propanamide 
• 1043931-98-1 1-(2-chloroethyl)-3-(4-(cyclohexyloxy)phenyl)urea 
• 438590-19-3 dimethyl 6-cyclohexyloxyquinoline-2,4-dicarboxylate 
• 85003-35-6 2-Chloro-3-(4-cyclohexyloxy-phenyl)-propionic acid methyl ester 
• 76198-54-4 chloro-acetic acid-(4-cyclohexyloxy-anilide) 

Relevant articles and documents

AGRICULTURAL CHEMICALS

The present invention relates to picolinic acid derivatives that are useful in treating fungal diseases ofplants.

5-SULFAMOYL-2-HYDROXYBENZAMIDE DERIVATIVES

The invention is directed to substituted salicylamide derivatives. Specifically, the invention is directed to compounds according to Formula (I): wherein R, R1 and R2 are as defined herein, or a pharmaceutically acceptable salt thereof. The compounds of the invention are inhibitors of CD73 and can be useful in the treatment of cancer, pre-cancerous syndromes and diseases associated with CD73 inhibition, such as AIDS, the treatment of HIV, autoimmune diseases, infections, atherosclerosis, and ischemia–reperfusion injury. Accordingly, the invention is further directed to pharmaceutical compositions comprising a compound of the invention. The invention is still further directed to methods of inhibiting CD73 activity and treatment of disorders associated therewith using a compound of the invention or a pharmaceutical composition comprising a compound of the invention.

PIPERIDINE DERIVATIVES AS HUMAN PAPILLOMA VIRUS INHIBITORS

HPV inhibitors with formula (I) where G1 represents a hydrocarbonated bond or chain possibly substituted by one or two alkyl groups, G2 represents a group (see formula Ia+Ib) or R represents a hydrogen, an alkyl, halogenoalkyl, or a prodrug radical such as carbamate, acetyl or dialkylaminomethyl, G represents a bond or a hydrocarbonated chain possibly substituted by one or two alkyls, W represents an oxygen or sulphur, R1 and R2 each represent a group chosen from among hydrogen, halogen, hydroxyl, thio, alkoxy, halogenoalkoxy, alkylthio, halogenoalkylthio, amino, monoalkylamino, dialkylamino, cycloalkyl, alkyl or halogenoalkyl, R3 represents an acid or a prodrug radical of the acid function or a bioisostere of the acid function, A represents an aryl, cycloalkyl, cycloalkenyl or a heterocycle, each possibly substituted, and B represents an aryl or a heterocycle with 6 chains, each possibly substituted, and pharmaceutically acceptable salts.

Cycloalkyl-substituted aryl chloroethylureas inhibiting cell cycle progression in G0/G1 phase and thioredoxin-1 nuclear translocation

1-(2-Chloroethyl)-3-(4-cyclohexylphenyl)urea (cHCEU) has been shown to abrogate the presence of thioredoxin-1 into the nucleus through its selective covalent alkylation. In the present letter we have evaluated the structure-activity relationships of the s

Synthesis of glutamic acid analogs as potent inhibitors of leukotriene A4 hydrolase

Leukotriene B4 (LTB4) is a potent pro-inflammatory mediator that has been implicated in the pathogenesis of multiple diseases, including psoriasis, inflammatory bowel disease, multiple sclerosis and asthma. As a method to decrease the level of LTB4 and possibly identify novel treatments, inhibitors of the LTB4 biosynthetic enzyme, leukotriene A4 hydrolase (LTA4-h), have been explored. Here we describe the discovery of a potent inhibitor of LTA4-h, arylamide of glutamic acid 4f, starting from the corresponding glycinamide 2. Analogs of 4f are then described, focusing on compounds that are both active and stable in whole blood. This effort culminated in the identification of amino alcohol 12a and amino ester 6b which meet these criteria.

Structure-activity relationships in the binding of chemically derivatized CD4 to gp120 from human immunodeficiency virus

The first step in HIV infection is the binding of the envelope glycoprotein gp120 to the host cell receptor CD4. An interfacial "Phe43 cavity" in gp120, adjacent to residue Phe43 of gp120-bound CD4, has been suggested as a potential target for therapeutic intervention. We designed a CD4 mutant (D1D2F43C) for site-specific coupling of compounds for screening against the cavity. Altogether, 81 cysteine-reactive compounds were designed, synthesized, and tested. Eight derivatives exceeded the affinity of native D1D2 for gp120. Structure-activity relationships (SAR) for derivatized CD4 binding to gp120 revealed significant plasticity of the Phe43 cavity and a narrow entrance. The primary contacts for compound recognition inside the cavity were found to be van der Waals interactions, whereas hydrophilic interactions were detected in the entrance. This first SAR on ligand binding to an interior cavity of gp120 may provide a starting point for structure-based assembly of small molecules targeting gp120-CD4 interaction.

Synthesis and in vitro pharmacology of substituted quinoline-2,4-dicarboxylic acids as inhibitors of vesicular glutamate transport

The vesicular glutamate transport (VGLUT) system selectively mediates the uptake of L-glutamate into synaptic vesicles. Uptake is linked to an H+-ATPase that provides coupling among ATP hydrolysis, an electrochemical proton gradient, and glutamate transport. Substituted quinoline-2,4-dicarboxylic acids (QDCs), prepared by condensation of dimethyl ketoglutaconate (DKG) with substituted anilines and subsequent hydrolysis, were investigated as potential VGLUT inhibitors in synaptic vesicles. A brief panel of substituted QDCs was previously reported (Carrigan et al. Bioorg. Med. Chem. Lett. 1999, 9, 2607-2612)1 and showed that certain substituents led to more potent competitive inhibitors of VGLUT. Using these compounds as leads, an expanded series of QDC analogues were prepared either by condensation of DKG with novel anilines or via aryl-coupling (Suzuki or Heck) to dimethyl 6-bromoquinolinedicarboxylate. From the panel of almost 50 substituted QDCs tested as inhibitors of the VGLUT system, the 6-PhCH=CH-QDC (Ki = 167 μM), 6-PhCH2CH2-QDC (Ki = 143 μM), 6-(4′-phenylstyryl)-QDC (Ki = 64 μM), and 6-biphenyl-4-yl-QDC (Ki=41 μM) were found to be the most potent blockers. A preliminary assessment of the key elements needed for binding to the VGLUT protein based on the structure-activity relationships for the panel of substituted QDCs is discussed herein. The substituted QDCs represent the first synthetically derived VGLUT inhibitors and are promising templates for the development of selective transporter inhibitors.