Silver-Catalyzed Decarboxylative Fluorination of Aliphatic Carboxylic Acids in Aqueous Solution

Although fluorinated compounds have found widespread applications in the chemical and materials industries, general and site-specific C­(sp³)–F bond formations are still a challenging task. We report here that with the catalysis of AgNO₃, various aliphatic carboxylic acids undergo efficient decarboxylative fluorination with SELECTFLUOR^® reagent in aqueous solution, leading to the synthesis of the corresponding alkyl fluorides in satisfactory yields under mild conditions. This radical fluorination method is not only efficient and general but also chemoselective and functional-group-compatible, thus making it highly practical in the synthesis of fluorinated molecules. A mechanism involvinig Ag­(III)-mediated single electron transfer followed by fluorine atom transfer is proposed for this catalytic fluorodecarboxylation

Silver-Catalyzed Decarboxylative Chlorination of Aliphatic Carboxylic Acids

Decarboxylative halogenation of carboxylic acids, the Hunsdiecker reaction, is one of the fundamental functional group transformations in organic chemistry. As the initial method requires the preparations of strictly anhydrous silver carboxylates, several modifications have been developed to simplify the procedures. However, these methods suffer from the use of highly toxic reagents, harsh reaction conditions, or limited scope of application. In addition, none is catalytic for aliphatic carboxylic acids. In this Article, we report the first catalytic Hunsdiecker reaction of aliphatic carboxylic acids. Thus, with the catalysis of Ag­(Phen)₂OTf, the reactions of carboxylic acids with <i>t</i>-butyl hypochlorite afforded the corresponding chlorodecarboxylation products in high yields under mild conditions. This method is not only efficient and general, but also chemoselective. Moreover, it exhibits remarkable functional group compatibility, making it of more practical value in organic synthesis. The mechanism of single electron transfer followed by chlorine atom transfer is proposed for the catalytic chlorodecarboxylation

4‑Iodine <i>N</i>‑Methylpyridinium-Mediated Peptide Synthesis

Through systematic optimization of halopyridinium compounds, we established a peptide coupling protocol utilizing 4-iodine N-methylpyridinium (4IMP) for solid-phase peptide synthesis (SPPS). The 4IMP coupling reagent is easily prepared, bench stable, and cost-effective. Employing 4IMP in the SPPS process has showcased remarkable chemoselectivity and efficiency, effectively eliminating racemization and epimerization. This achievement has been substantiated through the successful synthesis of a range of peptides via the direct utilization of commercially available amino acid substrates for SPPS

Additional file 1 of Single-domain antibodies against SARS-CoV-2 RBD from a two-stage phage screening of universal and focused synthetic libraries

Supplementary Material

Visible Light-Mediated C–H Difluoromethylation of Electron-Rich Heteroarenes

A novel method for visible-light photoredox-catalyzed difluoromethylation of electron-rich <i>N</i>-, <i>O</i>-, and <i>S</i>-containingheteroarenes under mild reaction conditions is developed. Mechanistic investigation indicates that the net C–H difluoromethylation proceeds through an electrophilic radical-type pathway

Reintroduction of miR125a-3p suppresses glioma tumorigenesis and invasiveness <i>in vivo</i>.

<p>A) The tumor mass raised from glioblastoma cells that were transfected with miR-125a-3p mimics was significant smaller than those transfected with control vectors. B) H&E staining analysis showed that transfection of miR-125a-3p mimics could significantly inhibit the invasion of intracranial glioblastoma, and that this effect of inhibition on invasion could be blocked by Nrg1 overexpression. The immunohischemical (IHC) analysis showed that miR-125a-3p mimics effectively inhibited the expression of Nrg1, and down-regulated the expression of Ki67. A TUNEL assay in xenograft tumor sections revealed that miR-125a-3p induced apoptosis of intracranial glioblastomas. Furthermore, overexpression of Nrg1 could block above expressional changes in intracranial glioblastomas.</p

MiR125a-3p directly targets the Nrg1 3’UTR in U87 glioblastoma cell line.

<p>A) Western blotting for Nrg1 at 48 hrs. after transfection of miR125a-3p mimics in U87 cells. B) Double luciferase reporter assays confirmed that Nrg1 is the direct target of miR125a-3p in U87 cells. *P<0.05.</p

miR125a-3p induces apoptosis and inhibits proliferation of glioblastom cells.

<p>A) An Annexin V assay was performed 48 hrs. after transfection of U251 and U87 cells with miR125a-3p mimics, scrambled and further infected with Nrg1 expression plasmid (left). A statistical analysis of the numbers of apoptosis cells of above groups (right), B) The ability of glioblastoma cells to proliferate was detected by CCK8 assay. All experiments were performed in triplicate in three independent sets. The values are shown as mean ± SD. * represents a significant difference (p<0.05) by student’s t test.</p

The expressions of miR-125a-3p and Nrg1 in glioma development and the relationship between their expressions and the survival time of glioma patients.

<p>A) Using qRT-PCR method, the expressions of miR125a-3p and Nrg1 in glioma tissues of different grades and normal brain tissues derived from epilepsy patients (left), as well as their expressions in normal astrocytes and glioblastoma cell lines (right), were analyzed. B) Kaplan-Meier overall survival curves of glioma patients according to the levels of miR125a-3p expression (left) and Nrg1 expression (right). The high miR-125a-3p expression group (n = 8) and the low miR-125a-3p expression group (n = 12); the high Nrg1 expression group (n = 10) and the low Nrg1 expression group (n = 10).</p

Effects of miR125a-3p on the migratory ability of glioblastoma cell lines.

<p>A) Wound scraping assay results showed that the distance of migration in U251 and U87 cells were significantly decreased after transfection of miR-125a-3p mimics, and that Nrg1 overexpression could increase the migration distances of glioblastoma cells transfected with miR-125a-3p. B) A Transwell assay showed that the numbers of U251 and U87 cells that migrated through a microporos membrane were significantly decreased after transfection of miR-125a-3p mimics, and that Nrg1 overexpression could eradicate the effect of miR-125a-3p in inhibiting invasion. All experiments were performed in triplicate in three independent sets. The values are shown as mean ± SD.</p