157338-47-1

Upstream product

• 31252-42-3 4-benzylpyperidine 
• 407-25-0 trifluoroacetic anhydride 
• 354-32-5 trifluoracetyl chloride 
• 431-47-0 trifluoroacetic acid-methyl ester 

Downstream Products

• 331765-80-1 1-[4-(4-bromobenzyl)piperidin-1-yl]-2,2,2-trifluoroethanone 
• 333794-97-1 4-{[1-(Trifluoroacetyl)-4-piperidinyl]methyl}benzenesulfonyl chloride 
• 835595-65-8 N,N-dimethyl-4-{[1-(trifluoroacetyl)piperidin-4-yl]methyl}benzenesulfonamide 
• 333795-01-0 4-{[4-(4-Piperidinylmethyl)phenyl]sulfonyl}morpholine 
• 333795-00-9 4-[(4-{[1-(Trifluoroacetyl)-4-piperidinyl]methyl)phenyl)-sulfonyl]morpholine 
• 203187-18-2 4-(4-bromobenzyl)piperidine 
• 203187-19-3 4-(4-bromo-benzyl)-[1,4']bipiperidinyl-1'-carboxylic acid tert-butyl ester 
• 362512-04-7 4-(4-bromo-benzyl)-[1,4']bipiperidinyl 
• 711029-84-4 N-(3-{4-[4-(morpholin-4-ylsulfonyl)benzyl]piperidin-1-yl}propyl)aniline 
• 333796-43-3 N'-(4-chlorophenyl)-N-(3-{4-[4-(morpholin-4-ylsulfonyl)benzyl]piperidin-1-yl}propyl)-N-phenylurea hydrochloride 
• 331765-50-5 Sch 211803 
• 331765-62-9 4-[4-(3-chloro-benzenesulfonyl)-benzyl]-[1,4']bipiperidinyl 
• 690269-09-1 4-[4-(4-methoxy-benzenesulfonyl)-benzyl]-[1,4']bipiperidinyl-1'-carboxylic acid tert-butyl ester 
• 331765-61-8 4-[4-(3-chloro-benzenesulfonyl)-benzyl]-[1,4']bipiperidinyl-1'-carboxylic acid tert-butyl ester 

Relevant academic research and scientific papers

MUSCARINIC M2 RECEPTOR BLOCKADE TO DELAY OR PREVENT ONSET OF PROGRESSIVE MEMORY DECLINE

Provided are methods for delaying or preventing onset of progressive memory decline by administering a muscarinic M2 receptor blocking compound to patients identified as at risk of developing a condition characterized by progressive memory decline, prior

Reactive derivatives for affinity labeling in the ifenprodil site of NMDA receptors

To prepare thiol-reactive ifenprodil derivatives designed as potential probes for cysteine-substituted NR2B containing NMDA receptors, electrophilic centers were introduced in different areas of the ifenprodil structure. Intermediates and final compounds were evaluated by binding studies and by electrophysiology to determine the structural requirements for their selectivity. The reactive compounds were further tested for their stability and for their reactivity in model reactions; some were found suitable as structural probes to investigate the binding site and the docking mode of ifenprodil in the NR2B subunit.

CCR5 antagonists as anti-HIV-1 agents. Part 3: Synthesis and biological evaluation of piperidine-4-carboxamide derivatives

Replacement of the 5-oxopyrrolidin-3-yl fragment in the previously reported lead structure with a 1-acetylpiperidin-4-yl group led to the discovery of a novel series of potent CCR5 antagonists. Introduction of small hydrophobic substituents on the central phenyl ring increased the binding affinity, providing low to sub-nanomolar CCR5 antagonists. The selected compound 11f showed excellent antiviral activity against CCR5-using HIV-1 replication in human peripheral blood mononuclear cells (EC50 = 0.59 nM) and an acceptable pharmacokinetic profile in dogs.

The synthesis of substituted bipiperidine amide compounds as CCR3 antagonists

Bipiperidine amide 1 has been identified as a CC chemokine receptor 3 (CCR3) antagonist. Optimization of its structure-activity relationship has resulted in the identification of cis (R,R)-4-[(3,4-dichlorophenyl)methyl]-3- hydroxymethyl-1′(6-quinolinylcar

CCR5 antagonists as anti-HIV-1 agents. Part 2: Synthesis and biological evaluation of N-[3-(4-benzylpiperidin-1-yl)propyl]-N,N′- diphenylureas

We have previously reported the novel lead compound 1a as a CCR5 antagonist for treatment of HIV-1 infection. SAR studies on incorporating various acyl groups as a replacement for the 5-oxopyrrolidine-3-carbonyl group of the lead structure resulted in the

Muscarinic M2 antagonists: Anthranilamide derivatives with exceptional selectivity and in vivo activity

Anthranilamide analogues such as 23 are potent and highly selective muscarinic M2 antagonists that also show good oral bioavailability and in vivo activity.

Urethanes derived from azacycloalkanes, the thio and dithio analogues thereof and their use as cholesterol biosynthesis inhibitors

The present invention relates to urethanes derived from azacycloalkanes and the thio and dithio analogues thereof of general formula wherein m, n, A, X, Y, E and R1to R8are defined as in claim 1, the enantiomers, diastereomers and the salts thereof, particularly the physiologically acceptable acid addition salts thereof which have valuable properties, particularly an inhibitory effect on cholesterol biosynthesis, pharmaceutical compositions containing these compounds, their use and processes for preparing them.

Secondary amides of (R)-3,3,3-trifluoro-2-hydroxy-2-methylpropionic acid as inhibitors of pyruvate dehydrogenase kinase

N'-Methyl-N-(4-tert-butyl-1,2,5,6-tetrahydropyridine)thiourea, SDZ048- 619 (1), is a modest inhibitor (IC50 = 180 μM) of pyruvate dehydrogenase kinase (PDHK). In an optimization of the N-methylcarbothioamide moiety of 1, it was discovered that amides with a small acyl group, in particular appropriately substituted amides of (R)-3,3,3-trifluoro-2-hydroxy-2- methylpropionic acid, are inhibitors of PDHK. Utilizing this acyl moiety, herein is reported the rationale leading to the optimization of a series of acylated piperazine derivatives. Methyl substitution of the piperazine at the 2- and 5-positions (with S and R absolute stereochemistry) markedly increased the potency of the lead compound (> 1000-fold). Oral bioavailability of the compounds in this series is good and is optimal (as measured by AUC) when the 4-position of the piperazine is substituted with an electron-poor benzoyl moiety. (+)-1-N-[2,5-(S,R)-Dimethyl-4-N-(4-cyanobenzoyl)piperazine]-(R)- 3,3,3-trifluoro-2-hydroxy-2-methylpropanamide (14e) inhibits PDHK in the primary enzymatic assay with an IC50 of 16 ± 2 nM, enhances the oxidation of [14C]lactate into 14CO2 in human fibroblasts with an EC50 of 57 ± 13 nM, diminishes lactate significantly 2.5 h post-oral-dose at doses as low as 1 μmol/kg, and increases the ex vivo activity of PDH in muscle, liver, and fat tissues in normal Sprague-Dawley rats. These PDHK inhibitors, however, do not lower glucose in diabetic animal models.