19353-86-7

Usage

Physical form

Yellow-orange crystalline solid

Uses

Manufacturing of dyes, pharmaceuticals, and as a synthetic intermediate for the production of other organic compounds

Hazardous nature

Potentially hazardous to human health and the environment

Handling and disposal

Proper handling and disposal procedures are recommended, and safety protocols and regulations should be followed to minimize the risk of exposure and adverse effects.

InChI:InChI=1/C10H11NO2/c12-11(13)10-6-5-8-3-1-2-4-9(8)7-10/h5-7H,1-4H2

Upstream product

• 119-64-2 tetralin 
• 2217-43-8 6-amino-1,2,3,4-tetrahydronaphthalene 
• 50537-00-3 2-amino-3-nitro-5,6,7,8-tetrahydronaphthalene 
• 90-15-3 α-naphthol 

Downstream Products

• 2217-43-8 6-amino-1,2,3,4-tetrahydronaphthalene 
• 22246-26-0 6-nitrotetralone 
• 101734-39-8 N-(5,6,7,8-tetrahydro-[2]naphthyl)-phthalamic acid 
• 40300-80-9 5,6-diamino-1,2,3,4-tetrahydronaphthalene 
• 342043-42-9 2-amino-1-nitro-5,6,7,8-tetrahydronaphthalene 
• 56163-17-8 5,6,7,8-tetrahydronaphthalene-2,3-diamine 
• 50878-03-0 N-(5,6,7,8-tetrahydronaphth-2-yl)acetamide 
• 67878-75-5 1-bromo-6-nitro-naphthalene 
• 581-89-5 2-nitronaphthalene 
• 610-27-5 4-nitrophthalic acid 
• 2217-41-6 1-amino-5,6,7,8-tetrahydronaphthalene 

Relevant academic research and scientific papers

N-(1-HYDROXY-3-(PYRROLIDINYL)PROPAN-2-YL)PYRROLIDINE-3-CARBOXAMIDE DERIVATIVES AS GLUCOSYLCERAMIDE SYNTHASE INHIBITORS

Described herein are compounds of Formula I, methods of making such compounds, pharmaceutical compositions and medicaments containing such compounds, and compounds I for use to treat or prevent diseases or conditions associated with the enzyme glucosylceramide synthase (GCS).

HETEROARYL COMPOUNDS AND METHODS OF USE THEREOF

Provided herein are heteroaryl compounds, methods of their synthesis, pharmaceutical compositions comprising the compounds, and methods of their use. In one embodiment, the compounds provided herein are useful for the treatment, prevention, and/or management of various disorders, such as CNS disorders and metabolic disorders, including, but not limited to, e.g., neurological disorders, psychosis, schizophrenia, obesity, and diabetes.

Novel sulfamoyl benzamides as selective CB2 agonists with improved in vitro metabolic stability

A lead optimization campaign in our previously reported sulfamoyl benzamide class of CB2 agonists was conducted to improve the in vitro metabolic stability profile in this series while retaining high potency and selectivity for the CB2 receptor. From this study, compound 14, N-(3,4-dimethyl-5-(morpholinosulfonyl)phenyl)-2,2-dimethylbutanamide, was identified as a potent and selective CB2 agonist exhibiting moderate in vitro metabolic stability and oral bioavailability. Compound 14 demonstrated in vivo efficacy in a rat model of post-surgical pain.

Conformationally constrained analogues of N′-(4-tert-butylbenzyl)-N-(4-methylsulfonylaminobenzyl)thiourea as TRPV1 antagonists

A series of bicyclic analogues having indan and tetrahydronaphthalene templates in the A-region were designed as conformationally constrained analogues of our previously reported potent TRPV1 antagonists (1, 3). The activities for rat TRPV1 of the conformationally restricted analogues were moderately or markedly diminished, particularly in the case of the tetrahydronaphthalene analogues. The analysis indicated that steric constraints at the benzylic position in the bicyclic analogues may be an important factor for their unfavorable interaction with the receptor.

Selective alkylation of βII-tubulin and thioredoxin-1 by structurally related subsets of aryl chloroethylureas leading to either anti-microtubules or redox modulating agents

Aryl chloroethylureas (CEUs) are potent anti-neoplastic agents alkylating specific intracellular proteins such as βII-tubulin. Recently we have identified a new subset of CEU derived from compound 36 that alkylates thioredoxin isoform 1 (Trx-1), inhibits the nuclear translocation of Trx-1, and favors the accumulation of cells in G0/G1 phase. We have evaluated the effects of various substituents and their position on the aromatic ring of a series of derivatives of 36 on (i) the anti-proliferative activity, (ii) the cell cycle progression, (iii) the nuclear translocation of Trx-1, and (iv) their covalent binding to β-tubulin. The same experiments were performed on representative CEU derivatives where the 2-chloroethyl amino moiety is replaced by either an ethyl, a 2-aminooxazolinyl or a 2-chloroacetyl group. On one hand, our results suggest that CEUs substituted on the phenyl ring at position 3 or 4 by cycloalkyl and substituted cycloalkyl or cycloalkoxy groups inhibit the nuclear translocation of Trx-1 and arrest the cell cycle progression in G0/G1. On the other hand, CEUs substituted by a fused aromatic ring, an aliphatic chain, or a fused aliphatic ring are alkylating βII-tubulin but not Trx-1. Beside the expected inactivity of the ethylurea derivatives, none of the modification to the electrophilic moiety led to cross-selectivity of the drugs toward β-tubulin but increased the anti-proliferative activity and resulted in mitigated effects on Trx-1 translocation.

COMPOUNDS AND METHODS FOR TREATING DYSLIPIDEMIA

Compounds of Formula (I): wherein n, m, p, q, Y, R1 R2, R3a, R3b, R4, R5, and R6 are as defined herein and their pharmaceutical compositions and methods of use are disclosed.

Tricyclic indole-2-carboxylic acid derivatives

A tricyclic indole-2-carboxylic acid derivative represented by the formula 1: STR1 wherein X represents alkyl, halogen or cyano;R 1 represents hydrogen, or a protecting group of carboxyl group;W represents hydrogen, --CO 2 R 3i, --CONR 3i R 4i, --A--CO 2 R 3i or --A--CONR 3i R 4i, wherein --A-- represents alkylene and R 3i and R 4i independently represent hydrogen, alkyl, aryl or substituted aryl,or a pharmaceutically acceptable salt thereof, these compounds are selective antagonists of glycine binding site of the NMDA receptor.