162269-90-1

Upstream product

• 2973-78-6 3-bromo-4-hydroxybenzylaldehyde 
• 107-30-2 chloromethyl methyl ether 
• 13057-17-5 bromethyl methyl ether 
• 123-08-0 4-hydroxy-benzaldehyde 
• 542-88-1 bis(2-chloromethyl)ether 
• 123-11-5 4-methoxy-benzaldehyde 

Downstream Products

• 1020399-89-6 C₁₉H₁₇Br₃O₅ 
• 1020400-13-8 C₂₅H₂₆Br₂O₆ 
• 1020400-11-6 C₂₈H₂₄Br₂O₆ 
• 1020400-09-2 C₂₈H₂₄Br₂O₆ 
• 1020399-87-4 C₁₇H₁₅BrO₃ 
• 1020399-79-4 C₂₁H₂₀Br₂O₅ 
• 1065546-02-2 bipinnatone A 
• 1065546-06-6 bipinnatone B 
• 1333078-53-7 C₃₀H₅₀O₃Si 
• 1333078-60-6 C₂₅H₄₂O₃Si 
• 1333078-54-8 C₂₄H₃₆O₃ 
• 1333078-61-7 C₁₉H₂₈O₃ 
• 1333078-58-2 C₂₃H₂₉BrO₉ 
• 1333078-59-3 C₂₁H₂₅BrO₈ 

Relevant academic research and scientific papers

Structure-Activity-Relationship-Aided Design and Synthesis of xCT Antiporter Inhibitors

The xCT antiporter is a cell membrane protein involved in active counter-transportation of glutamate (outflux) with cystine (influx) over the human cell membrane. This feature makes the xCT antiporter a crucial element of the biosynthesis of the vital free radical scavenger glutathione. The prodrug sulfasalazine, a medication for the treatment of ulcerative colitis, was previously proven to inhibit the xCT antiporter. Starting from sulfasalazine, a molecular scaffold jumping followed by SAR-assisted design and synthesis provided a series of styryl hydroxy-benzoic acid analogues that were biologically tested in vitro for their ability to decrease intracellular glutathione levels using four different cancer cell lines: A172 (glioma), A375 (melanoma), U87 (glioma) and MCF7 (breast carcinoma). Depletion of glutathione levels varied among the compounds as well as among the cell lines. Flow cytometry using propidium iodide and the annexin V marker demonstrated minimal toxicity in normal human astrocytes for a promising candidate molecule (E)-5-(2-([1,1′-biphenyl]-4-yl)vinyl)-2-hydroxybenzoic acid.

A study of enantioselective syntheses by Sharpless asymmetric oxidation for aryl sulfoxides containing oxygen groups at the ortho position

Abstract: While ortho-alkoxy aryl sulfoxides including various substituents were synthesized by Sharpless asymmetric oxidation reaction, we optimized the reaction conditions and screened better combination of starting materials to obtain high enantioselectivity. The result suggested new information that electron-withdrawing substituents on the aromatic ring have a strong influence upon enantioselectivity of the products. Also, several chiral ligands for Sharpless asymmetric oxidation reaction were evaluated to improve the enantioselectivity. Graphic abstract: High enantioselectivity of ortho-alkoxy aryl chiral sulfoxides have been achieved by Sharpless oxidation reaction using Ti(O-i-Pr)4 and diethyl tartrate under anhydrous condition. In particular, the enantioselctivity of products was influenced by electron-withdrawing substituents on the aromatic ring, such as nitro, ester and aldehyde groups.[Figure not available: see fulltext.]

Scalable Total Synthesis of (+)- And (-)-Codonopiloneolignanin A via Ti(IV)/NHC Cooperative Control Highly Enantioselective Dimerization of Multisubstituted Cinnamaldehyde

The first gram-scale asymmetric total synthesis of (+)- and (-)-codonopiloneolignanin A has been achieved from multisubstituted cinnamaldehyde in four steps with 37% overall yield. The synthetically challenging tricyclic [5, 3, 0, 03,8] decane skeleton was efficiently constructed via a highly enantioselective dimerization of multisubstituted cinnamaldehyde, followed by a sequence of cascade reactions including Prins cyclization, cation mediated cyclization, and deprotection. Furthermore, the scope of NHC-catalyzed/Ti(IV)-mediated synergistic control multisubstituted cinnamaldehyde dimerization was investigated. Significantly, the bioactivity of codonopiloneolignanin A and its enantiomer, particularly scarce in nature, was tested and showed good anticancer activity.

STYRYLBENZOTHIAZOLE DERIVATIVES AND USES IN IMAGING

This disclosure relates to styrylbenzothiazole derivatives for use as in vivo imaging agents for the diagnosis of Parkinson's disease (PD) or other degenerative disorders or conditions of the central nervous system. Early diagnosis is particularly advantageous as neuroprotective treatment can be applied to healthy neural cells to delay or even prevent the onset of debilitating clinical symptoms.

Rhodium(II)-Catalyzed Aryl C?H Carboxylation of 2-Pyridylphenols with CO2

A protocol for C?H carboxylation of electron-deficient 2-pyridylphenols with CO2 through a Rh(II)-catalyzed C?H bond activation under redox-neutral conditions has been developed. A suitable phosphine ligand was crucial for this reaction. This m

Synthesis and biological evaluation of 6-hydroxyl C-aryl glucoside derivatives as novel sodium glucose co-transporter 2 (SGLT2) inhibitors

The sodium glucose co-transporter 2 (SGLT2) was considered as an important target for the treatment of type 2 diabetes mellitus in recent years. This report describes the design and synthesis of a series of novel SGLT2 inhibitors (11a–17a) as well as thei

IMMUNE CHECKPOINT INHIBITORS, COMPOSITIONS AND METHODS THEREOF

The present invention provides synthesis, pharmaceutically acceptable formulations and uses of compounds in accordance with Formula (I), or a stereoisomer, a tautomer or a pharmaceutically acceptable salt thereof. For Formula (I) compounds R1, R2, X1, Y1 and n are as defined in the specification. The inventive Formula (I) compounds are inhibitors of the PD-1/PD-L1 protein/protein binding or functional interaction and find utility in any number of therapeutic applications, including but not limited to treatment of proliferative disorders such as cancer and infectious diseases.

Bismuth trichloride–mediated cleavage of phenolic methoxymethyl ethers

A simple and efficient method for removal of phenolic methoxymethyl ethers in the presence of 30?mol% of bismuth trichloride in acetonitrile/water is described. Notable features of the cleavage protocol entail use of an ecofriendly bismuth reagent, ease of handling, low cost, operational simplicity, and good functional group compatibility. A number of structurally varied phenolic methoxymethyl ethers were cleaved in good to excellent yields.

Cellular protection of SNAP-25 against botulinum neurotoxin/A: Inhibition of thioredoxin reductase through a suicide substrate mechanism

Botulium neurotoxins (BoNTs) are among the most lethal toxins known to man. They are comprised of seven serotypes with BoNT/A being the most deadly; yet, there is no approved therapeutic for their intoxication or one that has even advanced to clinical trials. Botulinum neurotoxicity is ultimately governed through light chain (LC) protease SNARE protein cleavage leading to a loss of neurotransmitter release. Pharmacological attempts to ablate BoNT/A intoxication have sought to either nullify cellular toxin entry or critical biochemical junctions found within its intricate mechanism of action. In these regards, reports have surfaced of nonpeptidic small molecule inhibitors, but few have demonstrated efficacy in neutralizing cellular toxicity, a key prerequisite before rodent lethality studies can be initiated. On the basis of a lead discovered in our BoNT/A cellular assay campaign, we investigated a family of N-hydroxysuccinimide inhibitors grounded upon structure activity relationship (SAR) fundamentals. Molecules stemming from this SAR exercise were theorized to be protease inhibitors. However, this proposition was overturned on the basis of extensive kinetic analysis. Unexpectedly, inhibitor data pointed to thioredoxin reductase (TrxR), an essential component required for BoNT protease translocation. Also unforeseen was the inhibitors' mechanism of action against TrxR, which was found to be brokered through a suicide-mechanism utilizing quinone methide as the inactivating element. This new series of TrxR inhibitors provides an alternative means to negate the etiological agent responsible for BoNT intoxication, the LC protease.