88537-45-5

Upstream product

• 52244-70-9 4-(4-methoxyphenyl)butan-1-ol 
• 98-59-9 p-toluenesulfonyl chloride 

Downstream Products

• 35191-43-6 1-(4-bromo-butyl)-4-methoxy-benzene 
• 705266-31-5 N,N-bis-(4-(4-methoxyphenyl)butyl)-p-toluenesulfonamide 
• 18272-84-9 4-n-butylanisole 
• 20574-98-5 4-(p-methoxyphenyl)but-1-ene 
• 391202-16-7 1-(4-(4-methoxyphenyl)butyl)-1H-1,2,3-triazole 
• 366016-82-2 4-[4-(1H-1,2,3-triazole-1-yl)butyl]phenol 
• 72457-26-2 4-(4-Methoxyphenyl)butylamine 
• 7508-04-5 5-(4-methoxyphenyl)pentanoic acid 
• 583825-27-8 1-(4-azidobutyl)-4-methoxybezene 
• 74185-15-2 1,7-bis(4-methoxyphenyl)heptan-3-ol 
• 88537-41-1 1,7-bis(3-iodo-4-methoxyphenyl)heptan-3-yl acetate 
• 88537-48-8 3-(3-iodo-4-methoxyphenyl)propyl 4-(3-iodo-4-methoxyphenyl)butyl sulphone 
• 88537-40-0 Acetic acid 5-(4-methoxy-phenyl)-1-[2-(4-methoxy-phenyl)-ethyl]-pentyl ester 
• 88537-47-7 3-(4-methoxyphenyl)propyl 4-(4-methoxyphenyl)butyl sulphone 

Relevant academic research and scientific papers

Synthesis of 11C-labelled bis(phenylalkyl)amines and their in vitro and in vivo binding properties in rodent and monkey brains

Two new 11C-labelled ligands, N-(3-(4-hydroxyphenyl)propyl)-3- (4-methoxyphenyl)propylamine ([11C]2) and N-(3-(4-hydroxyphenyl) butyl)-3-(4-methoxyphenyl)butylamine ([11C]3) were designed based on bis(phenylalkyl)-amines (1) which have been reported as polyamine site antagonists with high-selectivity for NR1A/2B NMDA receptors, and radiolabelling of the corresponding phenol precursors with [11C]methyl iodide was readily accomplished. The in vitro inhibition experiments using rat brain slices showed that [11C]2 and [11C]3 share the binding sites with spermine and/or ifenprodil but not with CP-101,606, a highly potent NR2B-selective NMDA antagonist, and that divalent cations such as Zn 2+ produced significant inhibition of both [11C]2 and [11C]3 bindings. Intravenous injection of [11C]3 in mice showed almost homogenous distribution throughout the brain. Attempts to block the tracer uptake of [11C]3 by pre-injection with the unlabelled 3 or spermine in rats were unsuccessful, but a small decrease in the cerebral uptake of [11C]3 by co-treatment with the unlabelled 3 was observed in a monkey PET study. The present findings indicate that none of these 11C-labelled analogues have potential for PET study of binding sites on the N-methly-D-aspartate (NMDA) receptors.

Identification of a novel toxicophore in anti-cancer chemotherapeutics that targets mitochondrial respiratory complex i

Disruption of mitochondrial function selectively targets tumour cells that are dependent on oxidative phosphorylation. However, due to their high energy demands, cardiac cells are disproportionately targeted by mitochondrial toxins resulting in a loss of cardiac function. An analysis of the effects of mubritinib on cardiac cells showed that this drug did not inhibit HER2 as reported, but directly inhibits mitochondrial respiratory complex I, reducing cardiac-cell beat rate, with prolonged exposure resulting in cell death. We used a library of chemical variants of mubritinib and showed that modifying the 1H-1,2,3-triazole altered complex I inhibition, identifying the heterocyclic 1,3-nitrogen motif as the toxicophore. The same toxicophore is present in a second anti-cancer therapeutic carboxyamidotriazole (CAI) and we demonstrate that CAI also functions through complex I inhibition, mediated by the toxicophore. Complex I inhibition is directly linked to anti-cancer cell activity, with toxicophore modification ablating the desired effects of these compounds on cancer cell proliferation and apoptosis.

SODIUM CHANNEL BLOCKERS

The present invention relates to sodium channel blockers. The present invention also includes a variety of methods of treatment using these inventive sodium channel blockers.

Ni-catalyzed carboxylation of unactivated primary alkyl bromides and sulfonates with CO2

A Ni-catalyzed carboxylation of unactivated primary alkyl bromides and sulfonates with CO2 at atmospheric pressure is described. The method is characterized by its mild conditions and remarkably wide scope without the need for air- or moisture-sensitive reagents, which make it a user-friendly and operationally simple protocol en route to carboxylic acids.

Sodium channel blockers

The present invention relates to sodium channel blockers. The present invention also relates to a variety of methods of treatment using the sodium channel blockers.

Sodium channel blockers

The present invention relates to sodium channel blockers. The present invention also relates to a variety of methods of treatment using these sodium channel blockers.

Development of a new class of nonimidazole histamine H3 receptor ligands with combined inhibitory histamine N-methyltransferase activity

In search of novel ways to enhance histaminergic neurotransmission in the central nervous system, a new class of nonimidazole histamine H3 receptor ligands were developed that simultaneously possess strong inhibitory activity on the main histamine metabolizing enzyme, histamine N-methyltransferase (HMT). The novel compounds contain an aminoquinoline moiety, which is an important structural feature for HMT inhibitory activity, connected by different spacers to a piperidino group (for H3 receptor antagonism). Variation of the spacer structure provides two different series of compounds. One series, having only an alkylene spacer between the basic centers, led to highly potent HMT inhibitors with moderate to high affinity at human histamine H3 receptors. The second series possesses a p-phenoxypropyl spacer, which may be extended by another alkylene chain. This latter series also showed strong inhibitory activity on HMT, and in most cases, the H3 receptor affinity even surpassed that of the first series. One of the most potent compounds with this dual mode of action is 4-(4-(3-piperidinopropoxy)phenylamino)quinoline (34) (hH3, Ki = 0.09 nM; HMT, IC50 = 51 nM). This class of compounds showed high antagonist potency and good H3 receptor selectivity in functional assays in guinea pig on H1, H2, and H3 receptors. Because of low or missing in vivo activity of two selected compounds, the proof of concept of these valuable pharmacological tools for the supposed superior overall enhancing effect on histaminergic neurotransmission failed to appear hitherto.

Synthesis of meta,meta-Bridged Biaryls (-Metacyclophanes) via Aryl-Aryl Coupling: Factors affecting the Cyclisation

Two bis(iodoaryl)heptanoids (28) and (33), the iodoarylbutyl iodoarylpropyl sulphide (39), and the corresponding sulphone (40) have been prepared, and each treated with tetrakis(triphenylphosphine)nikel(0).Two new m,m-bridged biaryls (29) (31percent) and (34) (49percent) were obtained; the sulphur compounds were deiodinated in preference to coupling.These reactions are compared with those used previously in myricanol synthesis and the factors affecting ring closure are discussed.Steric effects at the coupling sites appear more important in determining product yield than torsional strain in the products.