36735-26-9

Upstream product

• 117439-99-3 2-phenyl-3-phthalimido-quinoline-4-carboxylic acid 
• 91-56-5 indole-2,3-dione 
• 613-89-8 2-Aminoacetophenone 
• 70-11-1 α-bromoacetophenone 
• 1032-67-3 N-benzoylmethylphthalimide 

Downstream Products

• 107621-29-4 3-acetylamino-2-phenyl-quinoline-4-carboxylic acid 
• 100954-62-9 4-chloro-2-phenyl-[3]quinolylamine 
• 485-89-2 oxycinchophen 
• 57464-25-2 2-phenyl-3-bromoquinoline-4-carboxylic acid 
• 174636-90-9 3-chloro-2-phenylquinoline-4-carboxylic acid 
• 5855-52-7 2-phenylquinolin-4-amine 
• 114946-98-4 1-phenoxy-5-phenyl-pyrimido[4,5-c]quinoline 
• 102241-29-2 4-phenoxy-2-phenyl-[3]quinolylamine 
• 109566-43-0 1-methoxy-5-phenyl-pyrimido[4,5-c]quinoline 
• 108982-16-7 N-(4-chloro-2-phenyl-[3]quinolyl)-acetamide 
• 109964-80-9 1-chloro-5-phenyl-pyrimido[4,5-c]quinoline 
• 109367-35-3 5-phenyl-pyrimido[4,5-c]quinolin-1-ylamine 
• 108619-00-7 3-amino-2-phenyl-quinolin-4-ol 

Relevant academic research and scientific papers

NOVEL COMPOUND, AGENT AND NK3 RECEPTOR ANTAGONIST

PROBLEM TO BE SOLVED: To provide a NK3 receptor antagonist that inhibits the propagation of animals without adverse effect on an ecological system. SOLUTION: The present invention provides a compound represented by formula (I') (R1 is H, a hydroxy group or the like; R2 is a hydroxy group, a mercapto group or the like; R3 is a phenyl group or naphthyl group). SELECTED DRAWING: None COPYRIGHT: (C)2017,JPOandINPIT

Development of novel NK3 receptor antagonists with reduced environmental impact

The neurokinin B (NKB)–neurokinin-3 receptor (NK3R) signaling positively regulates the release of gonadotropin-releasing hormone (GnRH) from the hypothalamus. The NK3R-selective antagonists may suppress the reproductive functions of mammals. For developme

QUINOLINE DERIVATIVES AS NEUROKININ RECEPTOR ANTAGONISTS

The present invention relates to compounds of Formula (I) and their pharmaceutically acceptable salts, pharmaceutical compositions comprising them and their use in treating diseases mediated by neurokinin-2 and/or neurokinin-3 (NK-3) receptors, such as sc

Discovery of a novel class of selective non-peptide antagonists for the human neurokinin-3 receptor. 2. Identification of (S)-N-(1-phenylpropyl)-3- hydroxy-2-phenylquinoline-4-carboxamide (SB 223412)

Optimization of the previously reported 2-phenyl-4-quinolinecarboxamide NK-3 receptor antagonist 14, with regard to potential metabolic instability of the ester moiety and affinity and selectivity for the human neurokinin-3 (hNK-3) receptor, is described. The ester functionality could be successfully replaced by the ketone (31) or by lower alkyl groups (Et, 21, or n-Pr, 24). Investigation of the substitution pattern of the quinoline ring resulted in the identification of position 3 as a key position to enhance hNK-3 binding affinity and selectivity for the hNK-3 versus the hNK-2 receptor. All of the chemical groups introduced at this position, with the exception of halogens, increased the hNK-3 binding affinity, and compounds 53 (3-OH, SB 223412, hNK- 3-CHO binding K(i) = 1.4 nM) and 55 (3-NH2, hNK-3-CHO binding K(i) = 1.2 nM) were the most potent compounds of this series. Selectivity studies versus the other neurokinin receptors (hNK-2-CHO and hNK-1-CHO) revealed that 53 is about 100-fold selective for the hNK-3 versus hNK-2 receptor, with no affinity for the hNK-1 at concentrations up to 100 μM. In vitro studies demonstrated that 53 is a potent functional antagonist of the hNK-3 receptor (reversal of senktide-induced contractions in rabbit isolated iris sphincter muscles and reversal of NKB-induced Ca2+ mobilization in CHO cells stably expressing the hNK-3 receptor), while in vive this compound showed oral and intravenous activity in NK-3 receptor-driven models (senktide-induced behavioral responses in mice and senktide-induced miosis in rabbits). Overall, the biological data indicate that (S)-N-(1-phenylpropyl)-3-hydroxy- 2-phenylquinoline-4-carboxamide (53, SB 223412) may serve as a pharmacological tool in animal models of disease to assess the functional and pathophysiological role of the NK-3 receptor and to establish therapeutic indications for non-peptide NK-3 receptor antagonists.