Electrochemically Controlled Cationic Polymerization of Vinyl Ethers

Control of polymer initiation, propagation and termination is important in the development of complex polymer structures and advanced materials. Typically, this has been achieved chemically, electrochemically, photochemically or mechanochemically. Electrochemical control has been demonstrated in radical polymerizations; however, regulation of a cationic polymerization has yet to be achieved. Through the reversible oxidation of a polymer chain end with an electrochemical mediator, temporal control over polymer chain growth in cationic polymerizations was realized. By subjecting a stable organic nitroxyl radical mediator and chain transfer agent to an oxidizing current, control over polymer molecular weight and dispersity is demonstrated and excellent chain end fidelity allows for the synthesis of block copolymers

Diastereo- and Enantioselective Formal [3 + 2] Cycloaddition of Cyclopropyl Ketones and Alkenes via Ti-Catalyzed Radical Redox Relay

We report a stereoselective formal [3 + 2] cycloaddition of cyclopropyl ketones and radical-acceptor alkenes to form polysubstituted cyclopentane derivatives. Catalyzed by a chiral Ti­(salen) complex, the cycloaddition occurs via a radical redox-relay mechanism and constructs two C–C bonds and two contiguous stereogenic centers with generally excellent diastereo- and enantioselectivity

Diastereo- and Enantioselective Formal [3 + 2] Cycloaddition of Cyclopropyl Ketones and Alkenes via Ti-Catalyzed Radical Redox Relay

We report a stereoselective formal [3 + 2] cycloaddition of cyclopropyl ketones and radical-acceptor alkenes to form polysubstituted cyclopentane derivatives. Catalyzed by a chiral Ti­(salen) complex, the cycloaddition occurs via a radical redox-relay mechanism and constructs two C–C bonds and two contiguous stereogenic centers with generally excellent diastereo- and enantioselectivity

Three-Component Cross-Electrophile Coupling: Regioselective Electrochemical Dialkylation of Alkenes

The cross-electrophile dialkylation of alkenes enables the formation of two C­(sp3)–C­(sp3) bonds from readily available starting materials in a single transformation, thereby providing a modular and expedient approach to building structural complexity in organic synthesis. Herein, we exploit the disparate electronic and steric properties of alkyl halides with varying degrees of substitution to accomplish their selective activation and addition to alkenes under electrochemical conditions. This method enables regioselective dialkylation of alkenes without the use of a transition-metal catalyst and provides access to a diverse range of synthetically useful compounds

Diastereo- and Enantioselective Formal [3 + 2] Cycloaddition of Cyclopropyl Ketones and Alkenes via Ti-Catalyzed Radical Redox Relay

We report a stereoselective formal [3 + 2] cycloaddition of cyclopropyl ketones and radical-acceptor alkenes to form polysubstituted cyclopentane derivatives. Catalyzed by a chiral Ti­(salen) complex, the cycloaddition occurs via a radical redox-relay mechanism and constructs two C–C bonds and two contiguous stereogenic centers with generally excellent diastereo- and enantioselectivity

Anodically Coupled Electrolysis for the Heterodifunctionalization of Alkenes

The emergence of new catalytic strategies that cleverly adopt concepts and techniques frequently used in areas such as photochemistry and electrochemistry has yielded a myriad of new organic reactions that would be challenging to achieve using orthodox methods. Herein, we discuss the strategic use of anodically coupled electrolysis, an electrochemical process that combines two parallel oxidative events, as a complementary approach to existing methods for redox organic transformations. Specifically, we demonstrate anodically coupled electrolysis in the regio- and chemoselective chlorotrifluoromethylation of alkenes

Radical Redox-Relay Catalysis: Formal [3+2] Cycloaddition of <i>N</i>‑Acylaziridines and Alkenes

We report Ti-catalyzed radical formal [3+2] cycloadditions of <i>N</i>-acylaziridines and alkenes. This method provides an efficient approach to the synthesis of pyrrolidines, structural units prevalent in bioactive compounds and organocatalysts, from readily available starting materials. The overall redox-neutral reaction was achieved via a redox-relay mechanism, which harnesses radical intermediates for selective CN bond cleavage and formation

Radical Redox-Relay Catalysis: Formal [3+2] Cycloaddition of <i>N</i>‑Acylaziridines and Alkenes

We report Ti-catalyzed radical formal [3+2] cycloadditions of <i>N</i>-acylaziridines and alkenes. This method provides an efficient approach to the synthesis of pyrrolidines, structural units prevalent in bioactive compounds and organocatalysts, from readily available starting materials. The overall redox-neutral reaction was achieved via a redox-relay mechanism, which harnesses radical intermediates for selective CN bond cleavage and formation

Celastrol increases the protein level of HIF-1α.

<p>1a. Celastrol dose-dependently enhanced HIF-1α expression under hypoxia. HepG2 cells were cultured in either normoxia or 3% hypoxia and treated with the indicated doses of Celastrol for 6 h. Western blotting was used to detect the expression of HIF-1α and HIF-1β, and β-actin was used as a loading control; an arrow shows the position of HIF-1α. The histogram results are representative of the mean ± SD of three independent experiments. 1b. Celastrol time-dependently enhanced HIF-1α expression under hypoxia. HepG2 cells were cultured with 4 µM Celastrol for the indicated time in hypoxia. 1c. Celastrol enhanced HIF-1α expression in HepG2 cells under mimetic hypoxia induced by 100 µM CoCl₂ and treated for 6 h. 1d. Celastrol dose-dependently enhanced HIF-1α expression under normoxia. HepG2 cells were treated with the indicated doses of Celastrol under normoxia for 6 h, and 100 µg of total protein was used for western blotting to detect HIF-1 proteins with a long exposure. 1e. Celastrol enhanced HIF-1α expression in multiple cell lines. MCF-7, HeLa, PC-3 and H1299 cells were treated with the indicated doses of Celastrol for 12 h under 3% hypoxia, and western blotting was used to detect the HIF-1 proteins. 1f. Celastrol decreased the levels of other Hsp90 client proteins but increased that of HIF-1α. HepG2 cells were treated with normal medium, 4 µM Celastrol for 6 h, 5 µM MG132 for 6 h or pretreated with MG132 for 1 h then treated with Celastrol for 6 h. Protein expression was determined by western blotting with the corresponding antibodies.</p

Celastrol promotes the hypoxia-induced accumulation of the HIF-1α protein in the nucleus, which increases the transcriptional activity of HIF-1α target genes.

<p>3a. Celastrol enhances HIF-1α protein expression, which was localized in the nucleus. HepG2 cells were cultured in medium with or without 4 µM Celastrol for 6 h under normoxia or hypoxia. The subcellular localization of HIF-1α was determined by immunofluorescent staining using the anti-HIF-1α antibody,and the nucleus was immunolabeled with Hoechst 33258. 3b. HepG2 cells were treated with the indicated dose of Celastrol for 6 h, protein was extracted from the nucleus and cytosol, and the protein expression levels were revealed by western blot analysis. PARP served as the nuclear protein loading control. 3c. Celastrol promotes HIF-1α transcriptional activation activity. After transient transfection with the HRE-luciferase reporter plasmids for 24 h, HepG2 cells were challenged with the indicated doses of Celastrol in normoxia or hypoxia for another 6 h. Then, the HIF-1α transcriptional activation activity was analyzed by luciferase assay. The values are presented as the means ± SD of three independent experiments. 3d. Celastrol promotes the transcription of the HIF-1α target genes VEGF and Glut-1. The VEGF and Glut-1 mRNA levels were evaluated by real-time PCR. The values are presented as the means±SD of three independent experiments.</p