Homologation of alpha-amino acids to beta-amino acids using Fmoc-amino acid pentafluorophenyl esters

The homologation of alpha-amino acids to beta-amino acids by the two-step Arndt-Eister method is achieved by using Fmoc-alpha-amino acid pentafluorophenyl esters for the acylation of diazomethane, synthesizing the key intermediates Fmoc-aminoacyldiazomethanes as crystalline solids in good yields and purity

ChemInform Abstract: Coupling in the Absence of a Tertiary Base: A Method for the Deprotection of Hydrochloride Salts of Peptide Esters to Free Amino Peptide Esters.

ChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 100 leading journals. To access a ChemInform Abstract of an article which was published elsewhere, please select a “Full Text” option. The original article is trackable via the “References” option

ChemInform Abstract: Synthesis of Boc‐ and Z‐Protected Amino Acid Fluorides Employing DAST as a Fluorinating Agent.

ChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 100 leading journals. To access a ChemInform Abstract of an article which was published elsewhere, please select a “Full Text” option. The original article is trackable via the “References” option

Diethyl 3,4-bis­(2,5-dimethoxy­benz­yl)thieno[2,3-b]thio­phene-2,5-di­car­boxylate

In the title compound, C30H32O8S2, the dihedral angle between the two benzene rings is 18.8 (1)°. The mol­ecular structure is stabilized by weak intra­molecular C—H⋯O hydrogen bonds. In the crystal structure, the mol­ecules are linked via weak inter­molecular C—H⋯O hydrogen bonds and π–π inter­actions between two benzene rings [centroid–centroid distance = 3.672 (1) Å]

Ethyl 2-acetoxy­methyl-1-phenyl­sulfonyl-1H-indole-3-carboxyl­ate

In the title compound, C20H19NO6S, the phenyl ring of the phenyl­sulfonyl group makes a dihedral angle of 83.35 (5)° with the indole ring system. The mol­ecular structure exhibits a number of short intramolecular C—H⋯O contacts

Diethyl 3,4-bis(acetoxy­meth­yl)thieno[2,3-b]thio­phene-2,5-dicarboxyl­ate

In the title compound, C18H20O8S2, the dihedral angle between the two thio­phene rings is 2.33 (7)°. The methyl C atoms of the ester groups are disordered over two positions; the site-occupancy factors of the terminal methyl C atoms are 0.632 (18):0.368 (18) and 0.623 (17):0.377 (17). The mol­ecular structure is stabilized by weak intra­molecular C—H⋯O inter­actions and the crystal structure is stabilized through weak inter­molecular C—H⋯O inter­actions

Ethyl 2-[N-(2-formyl­phen­yl)benzene­sulfonamido]acetate

In the mol­ecule of the title compound, C17H17NO5S, the two aromatic rings are oriented at an angle of 30.13 (10)°. The ethyl acetate group assumes an extended conformation. Mol­ecules are linked into C(7) chains running along the a axis by inter­molecular C—H⋯O hydrogen bonds, and the chains are crosslinked via C—H⋯π inter­actions, with the sulfonyl-bound phenyl ring acting as an acceptor

Fmoc-amino acid azides in peptide synthesis

Fmoc-amino acid azides can be prepared from the corresponding acid chlorides and sodium azide. All the compounds made have been obtained as solids in good yield and purity. They are found to be shelf stable at room temperature for longer periods. Their storage at room temperature does not lead to the formation of isocyanates. Employing them as coupling agents, the synthesis of a few dipeptides is described

Ethyl 2-(bromo­meth­yl)-5-meth­oxy-1-phenyl­sulfonyl-1H-indole-3-carboxyl­ate

In the title compound, C19H18BrNO5S, the plane of the phenyl ring forms a dihedral angle of 76.99 (6)° with the indole ring system. The Br atom is disordered over two positions, with site-occupancy factors of 0.833 (14) and 0.167 (14). The mol­ecular structure is stabilized by weak intra­molecular C—H⋯O inter­actions and the crystal packing is stabilized by weak inter­molecular C—H⋯O inter­actions

A potential role of the JNK pathway in hyperoxia-induced cell death, myofibroblast transdifferentiation and TGF-β1-mediated injury in the developing murine lung

<p>Abstract</p> <p>Background</p> <p>Transforming growth factor-beta 1 (TGF-β1) has been implicated in hyperoxia-induced cell death and impaired alveolarization in the developing lung. In addition, the c-JunNH2-terminal kinase (JNK) pathway has been shown to have a role for TGF-β1-mediated effects. We hypothesized that the JNK pathway is an important regulator of hyperoxia-induced pulmonary responses in the developing murine lung.</p> <p>Results</p> <p>We used cultured human lung epithelial cells, fetal rat lung fibroblasts and a neonatal TGF-β1 transgenic mouse model. We demonstrate that hyperoxia inhibits cell proliferation, activates cell death mediators and causes cell death, and promotes myofibroblast transdifferentiation, in a dose-dependent manner. Except for fibroblast proliferation, the effects were mediated via the JNK pathway. In addition, since we observed increased expression of TGF-β1 by epithelial cells on exposure to hyperoxia, we used a TGF-β1 transgenic mouse model to determine the role of JNK activation in TGF-β1 induced effects on lung development and on exposure to hyperoxia. We noted that, in this model, inhibition of JNK signaling significantly improved the spontaneously impaired alveolarization in room air and decreased mortality on exposure to hyperoxia.</p> <p>Conclusions</p> <p>When viewed in combination, these studies demonstrate that hyperoxia-induced cell death, myofibroblast transdifferentiation, TGF-β1- and hyperoxia-mediated pulmonary responses are mediated, at least in part, via signaling through the JNK pathway.</p