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The discovery that efficient olefin metathesis reactions involving previously challenging terminal olefin substrates are possible using novel and readily available catalyst systems in non-distilled, non-degassed protic media in air is reported.

We report the use of efficient visible-light sensitive allyl (QA) and epoxidized (QE) quinizarin derivatives as photoinitiating systems when combined with an appropriate electron donor (methyldiethanol amine, MDEA), an electron acceptor (iodonium salt, Iod), or a H donor (thiol derivative), for free-radical photopolymerization (FRP), cationic photopolymerization (CP), and a thiol–ene process. These systems have demonstrated excellent initiating properties under air or in laminated conditions under visible-light irradiation (LEDs@405, 455, and 470 nm or Xe lamp) for FRP, CP, or the thiol–ene process and appear more efficient than the well-known camphorquinone-based photoinitiating systems. As highlighted by electron paramagnetic resonance (EPR) and laser flash photolysis experiments, QA (or QE) acts either as an electron donor via a photoinduced electron transfer pathway with Iod or as a proton/proton-coupled electron transfer promoter with MDEA or a thiol derivative. Two types of interpenetrated polymer networks have been synthesized either by CP and the thiol–ene process with di­(ethylene glycol) divinyl ether/trithiol or by a concomitant free-radical and cationic photopolymerization with an epoxide/acrylate blend mixture upon LED@455 or 470 nm exposure. Interestingly, the resulting quinizarin-derived materials showed antiadherence properties under visible-light exposure even after two cycles of antibacterial experiments. Quinizarin derivatives can not only initiate photopolymerization but also generate singlet oxygen on the surface of the materials for preventing the adhesion and proliferation of bacteria under visible-light activation.

The transcription factor Nrf2 and its downstream target heme oxygenase-1 (HO-1) are essential protective systems against oxidative stress and inflammation. The products of HO-1 enzymatic activity, biliverdin and carbon monoxide (CO), actively contribute to this protection, suggesting that exploitation of these cellular systems may offer new therapeutic avenues in a variety of diseases. Starting from a CO-releasing compound and a chemical scaffold exhibiting electrophilic characteristics (esters of fumaric acid), we report the synthesis of hybrid molecules that simultaneously activate Nrf2 and liberate CO. These hybrid compounds, which we termed "HYCOs", release CO to myoglobin and activate the CO-sensitive fluorescent probe COP-1, while also potently inducing nuclear accumulation of Nrf2 and HO-1 expression and activity in different cell types. Thus, we provide here the first example of a new class of pharmacologically active molecules that target the HO-1 pathway by combining an Nrf2 activator coordinated to a CO-releasing group.

The efficient selective cross‐metathesis (CM) of acrylonitrile using unmodified precatalyst 2 is reported. The use of copper(I) chloride as an additive and phosphane scavenger is described and significant turnover enhancement upon addition of a metallic salt in selective CM is observed for the first time. The influence of catalyst decomposition and other experimental parameters (concentration, amount of acrylonitrile used) on conversion is also demonstrated. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2003)

The Nrf2/heme oxygenase-1 (HO-1) axis affords significant protection against oxidative stress and cellular damage. We synthesized a series of cobalt-based hybrid molecules (HYCOs) that combine an Nrf2 inducer with a releaser of carbon monoxide (CO), an anti-inflammatory product of HO-1. Two HYCOs markedly increased Nrf2/HO-1 expression, liberated CO and exerted anti-inflammatory activity in vitro. HYCOs also up-regulated tissue HO-1 and delivered CO in blood after administration in vivo, supporting their potential use against inflammatory conditions.

Oxidative stress and inflammation are predominant features of several chronic diseases. The nuclear factor erythroid 2-related factor 2 (Nrf2) is a major arbiter in counteracting these insults via up-regulation of several defensive proteins, including heme oxygenase-1 (HO-1). HO-1-derived carbon monoxide (CO) exhibits anti-inflammatory actions and can be delivered to tissues by CO-releasing agents. In this study we assessed the pharmacological and anti-inflammatory properties of HYCO-3, a dual activity compound obtained by conjugating analogues of the CO-releasing molecule CORM-401 and dimethyl fumarate (DMF), an immunomodulatory drug known to activate Nrf2. HYCO-3 induced Nrf2-dependent genes and delivered CO to cells in vitro and tissues in vivo, confirming that the two expected pharmacological properties of this agent are achieved. In mice challenged with lipopolysaccharide, orally administered HYCO-3 reduced the mRNA levels of pro-inflammatory markers (TNF-α, IL-1β and IL-6) while increasing the expression of the anti-inflammatory genes ARG1 and IL-10 in brain, liver, lung and heart. In contrast, DMF or CORM-401 alone or their combination decreased the expression of pro-inflammatory genes but had limited influence on anti-inflammatory markers. Furthermore, HYCO-3 diminished TNF-α and IL-1β in brain and liver but not in lung and heart of Nrf2-/- mice, indicating that the CO-releasing part of this hybrid contributes to reduction of pro-inflammation and that this effect is organ-specific. These data demonstrate that the dual activity of HYCO-3 results in enhanced efficacy compared to the parent compounds indicating the potential exploitation of hybrid compounds in the development of effective anti-inflammatory therapies.