Category: 617-52-7

Zhang, Xin published the artcileReverse atom transfer radical polymerization of dimethyl itaconate initiated by new azo initiator AIBME, Name: Dimethyl itaconate, the publication is RSC Advances (2022), 12(21), 13347-13351, database is CAplus and MEDLINE.

Reverse atom transfer radical polymerization (RATRP) was used to synthesize poly(di-Me itaconate) (PDMI) using an AIBME/CuBr₂/dNbpy system. The number average mol. weight (Mn) of PDMI was as high as Mn = 15 000 g mol^-1, the monomer conversion rate reached up to 70%, and the dispersity remained low (D = 1.06-1.38). The first-order kinetics of PDMI are discussed in detail. The AIBME initiator had a higher initiation efficiency than the AIBN initiator. As the ratio of initiator (AIBME) to catalyst (CuBr₂) decreased, the Mn and D of PDMI decreased. At 60°C and 80°C, the Mn of PDMI was much higher than the theor. number average (M_n,th), and the D of PDMI broadened with the conversion rate. At 100°C, the D of PDMI remained low, and the Mn of PDMI was closer to the Mn,th. As the ratio of monomer (DMI) to initiator (AIBME) increased, the Mn of PDMI changed little over time. These phenomena could be explained by the influence of the initiator and catalyst on polymerization kinetics.

RSC Advances published new progress about 617-52-7. 617-52-7 belongs to esters-buliding-blocks, auxiliary class Alkenyl,Aliphatic hydrocarbon chain,Ester, name is Dimethyl itaconate, and the molecular formula is C7H13BrSi, Name: Dimethyl itaconate.

Referemce:
https://en.wikipedia.org/wiki/Ester,
Ester – an overview | ScienceDirect Topics

Homerin, Germain published the artcilePyroglutamide-Based P2X7 Receptor Antagonists Targeting Inflammatory Bowel Disease, Synthetic Route of 617-52-7, the publication is Journal of Medicinal Chemistry (2020), 63(5), 2074-2094, database is CAplus and MEDLINE.

This report deals with the design, the synthesis, and the pharmacol. evaluation of pyroglutamide-based P2X7 antagonists. A dozen were shown to possess improved properties, among which inhibition of YO-PRO-1/TO-PRO-3 uptake and IL1β release upon BzATP activation of the receptor and dampening signs of DSS-induced colitis on mice, in comparison with reference antagonist GSK1370319A. Docking study and biol. evaluation of synthesized compounds has highlighted new SAR, and low toxicity profiles of pyroglutamides herein described are clues for the finding of a usable h-P2X7 antagonist drug. Such a drug would raise the hope for a cure to many P2X7-dependent pathologies, including inflammatory, neurol., and immune diseases.

Journal of Medicinal Chemistry published new progress about 617-52-7. 617-52-7 belongs to esters-buliding-blocks, auxiliary class Alkenyl,Aliphatic hydrocarbon chain,Ester, name is Dimethyl itaconate, and the molecular formula is C7H10O4, Synthetic Route of 617-52-7.

Referemce:
https://en.wikipedia.org/wiki/Ester,
Ester – an overview | ScienceDirect Topics

Sohail, Aaqib published the artcileItaconate and derivatives reduce interferon responses and inflammation in influenza A virus infection, Quality Control of 617-52-7, the publication is PLoS Pathogens (2022), 18(1), e1010219, database is CAplus and MEDLINE.

Excessive inflammation is a major cause of morbidity and mortality in many viral infections including influenza. Therefore, there is a need for therapeutic interventions that dampen and redirect inflammatory responses and, ideally, exert antiviral effects. Itaconate is an immunomodulatory metabolite which also reprograms cell metabolism and inflammatory responses when applied exogenously. We evaluated effects of endogenous itaconate and exogenous application of itaconate and its variants dimethyl- and 4-octyl-itaconate (DI, 4OI) on host responses to influenza A virus (IAV). Infection induced expression of ACOD1, the enzyme catalyzing itaconate synthesis, in monocytes and macrophages, which correlated with viral replication and was abrogated by DI and 4OI treatment. In IAV-infected mice, pulmonary inflammation and weight loss were greater in Acod1-/- than in wild-type mice, and DI treatment reduced pulmonary inflammation and mortality. The compounds reversed infection-triggered interferon responses and modulated inflammation in human cells supporting non-productive and productive infection, in peripheral blood mononuclear cells, and in human lung tissue. All three itaconates reduced ROS levels and STAT1 phosphorylation, whereas AKT phosphorylation was reduced by 4OI and DI but increased by itaconate. Single-cell RNA sequencing identified monocytes as the main target of infection and the exclusive source of ACOD1 mRNA in peripheral blood. DI treatment silenced IFN-responses predominantly in monocytes, but also in lymphocytes and natural killer cells. Ectopic synthesis of itaconate in A549 cells, which do not physiol. express ACOD1, reduced infection-driven inflammation, and DI reduced IAV- and IFNγ-induced CXCL10 expression in murine macrophages independent of the presence of endogenous ACOD1. The compounds differed greatly in their effects on cellular gene homeostasis and released cytokines/chemokines, but all three markedly reduced release of the pro-inflammatory chemokines CXCL10 (IP-10) and CCL2 (MCP-1). Viral replication did not increase under treatment despite the dramatically repressed IFN responses. In fact, 4OI strongly inhibited viral transcription in peripheral blood mononuclear cells, and the compounds reduced viral titers (4OI>Ita>DI) in A549 cells whereas viral transcription was unaffected. Taken together, these results reveal itaconates as immunomodulatory and antiviral interventions for influenza virus infection.

PLoS Pathogens published new progress about 617-52-7. 617-52-7 belongs to esters-buliding-blocks, auxiliary class Alkenyl,Aliphatic hydrocarbon chain,Ester, name is Dimethyl itaconate, and the molecular formula is C12H15NO, Quality Control of 617-52-7.

Referemce:
https://en.wikipedia.org/wiki/Ester,
Ester – an overview | ScienceDirect Topics

Oh, Tae Seok published the artcileItaconate and its derivatives repress early myogenesis in vitro and in vivo, Related Products of esters-buliding-blocks, the publication is Frontiers in Immunology (2022), 748375, database is CAplus and MEDLINE.

A Krebs cycle intermediate metabolite, itaconate, has gained attention as a potential antimicrobial and autoimmune disease treatment due to its anti-inflammatory effects. While itaconate and its derivatives pose an attractive therapeutic option for the treatment of inflammatory diseases, the effects outside the immune system still remain limited, particularly in the muscle. Therefore, we endeavored to determine if itaconate signaling impacts muscle differentiation. Utilizing the well-established C2C12 model of in vitro myogenesis, we evaluated the effects of itaconate and its derivatives on transcriptional and protein markers of muscle differentiation as well as mitochondrial function. We found itaconate and the derivatives di-Me itaconate and 4-octyl itaconate disrupt differentiation media-induced myogenesis. A primary biol. effect of itaconate is a succinate dehydrogenase (SDH) inhibitor. We find the SDH inhibitors di-Me malonate and harzianopyridone phenocopie the anti-myogenic effects of itaconate. Furthermore, we find treatment with exogenous succinate results in blunted myogenesis. Together our data indicate itaconate and its derivatives interfere with in vitro myogenesis, potentially through inhibition of SDH and subsequent succinate accumulation. We also show 4-octyl itaconate suppresses injury-induced MYOG expression in vivo. More importantly, our findings suggest the therapeutic potential of itaconate, and its derivatives could be limited due to deleterious effects on myogenesis.

Frontiers in Immunology published new progress about 617-52-7. 617-52-7 belongs to esters-buliding-blocks, auxiliary class Alkenyl,Aliphatic hydrocarbon chain,Ester, name is Dimethyl itaconate, and the molecular formula is C7H10O4, Related Products of esters-buliding-blocks.

Referemce:
https://en.wikipedia.org/wiki/Ester,
Ester – an overview | ScienceDirect Topics

Abbas, Zaheer published the artcileChiral ferrocene/indole-based diphosphine ligands for Rh-catalyzed asymmetric hydrogenation of functionalized olefins, HPLC of Formula: 617-52-7, the publication is Tetrahedron Letters (2020), 61(20), 151860, database is CAplus.

Convenient synthesis of a new family of chiral ferrocene/indole-based diphosphine ligands, (Rc,Rp)-IndoFerroPhos (L), from (Sc,Rp)-PPFA and 2-(diphenylphosphino)indole has been described. These new ligands exhibited high efficiency in the Rh-catalyzed asym. hydrogenation of functionalized olefins including α-dehydroamino acid esters, α-enamides and di-Me itaconate, in which up to >99% yield and 98% ee were achieved.

Tetrahedron Letters published new progress about 617-52-7. 617-52-7 belongs to esters-buliding-blocks, auxiliary class Alkenyl,Aliphatic hydrocarbon chain,Ester, name is Dimethyl itaconate, and the molecular formula is C7H10O4, HPLC of Formula: 617-52-7.

Referemce:
https://en.wikipedia.org/wiki/Ester,
Ester – an overview | ScienceDirect Topics

Brannigan, Ruairi P. published the artcileSynthesis of mechanically robust renewable poly(ester-amide)s through co-polymerisation of unsaturated polyesters and synthetic polypeptides, Safety of Dimethyl itaconate, the publication is European Polymer Journal (2020), 109417, database is CAplus.

As an alternative to polyester-based materials, synthetic polypeptides have received a great deal of attention as bio-derived polymers for various applications. Polypeptide-based materials offer numerous advantages over traditional polyesters such as efficient and complete bio- and ecol. absorption, however, poor mech. robustness and low processability has prevented the com. application of polypeptides. Conversely, copolymers of polyesters and polypeptides have the potential to combine the mech. versatility of aliphatic polyesters while retaining the enhanced bio-absorption of polypeptides. Itaconic acid-based polyesters were crosslinked with modified telechelic poly(L-aspartic acid β-benzyl ester) and the amino acid-derived 2-vinyl-4,4-dimethylazlactone in order to assess their effect on their bulk materials properties. It was found that through variance of the polymer composition that the mech. properties and the hydrolytic degradation of the materials could be modulated. We believe that these crosslinked polymers offer a unique platform for the development of sustainable degradable materials.

European Polymer Journal published new progress about 617-52-7. 617-52-7 belongs to esters-buliding-blocks, auxiliary class Alkenyl,Aliphatic hydrocarbon chain,Ester, name is Dimethyl itaconate, and the molecular formula is C7H10O4, Safety of Dimethyl itaconate.

Referemce:
https://en.wikipedia.org/wiki/Ester,
Ester – an overview | ScienceDirect Topics

Feng, Liyan published the artcileVisible-Light-Induced Palladium-Catalyzed Intermolecular Narasaka-Heck Reaction at Room Temperature, Synthetic Route of 617-52-7, the publication is Organic Letters (2020), 22(10), 3964-3968, database is CAplus and MEDLINE.

A palladium-catalyzed Narasaka-Heck reaction by a domino cross-coupling reaction with aromatic alkenes under blue LED irradiation at room temperature was developed. The undesired β-hydride elimination of the hybrid alkyl palladium radical species was prohibited, enabling a broad range of oxime esters to undergo 5-exo cyclization and subsequent coupling with olefins. The practicality of the method was well illustrated by the construction of a nitrogen bridgehead tricycle as a core skeleton of alkaloids.

Organic Letters published new progress about 617-52-7. 617-52-7 belongs to esters-buliding-blocks, auxiliary class Alkenyl,Aliphatic hydrocarbon chain,Ester, name is Dimethyl itaconate, and the molecular formula is C7H10O4, Synthetic Route of 617-52-7.

Referemce:
https://en.wikipedia.org/wiki/Ester,
Ester – an overview | ScienceDirect Topics

Huang, Shan-Shan published the artcileDimethyl itaconate alleviates the pyroptosis of macrophages through oxidative stress, Computed Properties of 617-52-7, the publication is BMC Immunology (2021), 22(1), 72, database is CAplus and MEDLINE.

Macrophages are involved in the pathophysiol. of many diseases as critical cells of the innate immune system. Pyroptosis is a form of macrophage death that induces cytokinesis of phagocytic substances in the macrophages, thereby defending against infection. Di-Me itaconate (DI) is an analog of itaconic acid with anti-inflammatory effects. However, the effect of di-Me itaconate on macrophage pyroptosis has not been elucidated clearly. Thus, the present study aimed to analyze the effect of DI treatment on a macrophage pyroptosis model (Lipopolysaccharide, LPS + ATP, ATP). The results showed that 0.25 mM DI ameliorated macrophage pyroptosis and downregulated interleukin (IL)-1β expression. Then, real-time quant. polymerase chain reaction (RT-qPCR) was used to confirm the result of RNA-sequencing of the upregulated oxidative stress-related genes (Gclc and Gss) and downregulated inflammation-related genes (IL-12β and IL-1β). In addition, Gene Ontol. (GO) enrichment anal. showed that differential genes were associated with transcript levels and DNA replication. Kyoto encyclopedia of genes and genomes (KEGG) enrichment showed that signaling pathways, such as tumor necrosis factor (TNF), Jak, Toll-like receptor and IL-17, were altered after DI treatment. N-acetyl-L-cysteine (NAC) reversed the DI effect on the LPS + ATP-induced macrophage pyroptosis and upregulated the IL-1β expression. Oxidative stress-related protein Nrf2 is involved in the DI regulation of macrophage pyroptosis. Taken together, these findings suggested that DI alleviates the pyroptosis of macrophages through oxidative stress.

BMC Immunology published new progress about 617-52-7. 617-52-7 belongs to esters-buliding-blocks, auxiliary class Alkenyl,Aliphatic hydrocarbon chain,Ester, name is Dimethyl itaconate, and the molecular formula is C7H10O4, Computed Properties of 617-52-7.

Referemce:
https://en.wikipedia.org/wiki/Ester,
Ester – an overview | ScienceDirect Topics

Il’in, Anton published the artcilePhosphine catalyzed addition of long-chain dialkyl phosphites to electron-deficient alkenes, SDS of cas: 617-52-7, the publication is Synthetic Communications (2020), 50(21), 3287-3297, database is CAplus.

Conjugate addition of the long chain dialkyl phosphites to electron-deficient alkenes under PBu₃ catalysis afforded the corresponding phosphonates in good yields in a short reaction time. Long chain alkyl groups in the phosphites were well tolerated in this transformation. The products of this reaction are of particular interest as components of lubrication oil composition

Synthetic Communications published new progress about 617-52-7. 617-52-7 belongs to esters-buliding-blocks, auxiliary class Alkenyl,Aliphatic hydrocarbon chain,Ester, name is Dimethyl itaconate, and the molecular formula is C7H10O4, SDS of cas: 617-52-7.

Referemce:
https://en.wikipedia.org/wiki/Ester,
Ester – an overview | ScienceDirect Topics

Han, Yong-Yue published the artcileProtective effect of dimethyl itaconate against fibroblast-myofibroblast differentiation during pulmonary fibrosis by inhibiting TXNIP, Safety of Dimethyl itaconate, the publication is Journal of Cellular Physiology (2021), 236(11), 7734-7744, database is CAplus and MEDLINE.

Fibroblast-myofibroblast differentiation (FMD) is a critical cellular phenotype during the occurrence and deterioration of pulmonary fibrosis (PF). FMD can increase with an elevated level of reactive oxygen species (ROS) on fibroblasts under oxidative stress. Thioredoxin-interacting protein (TXNIP) is an α-arrestin family protein that regulates the level of intracellular ROS. Nuclear factor erythroid 2-related factor 2 (Nrf2) can protect against FMD in PF. However, the relationship between Nrf2 and TXNIP in FMD remains elusive. Therefore, we established TGF-β1-induced FMD in vitro and bleomycin (BLM)-induced mouse PF model in vivo to explore whether the activation of Nrf2 can inhibit TXNIP-mediated FMD in PF. Di-Me itaconate (DMI) was selected to activate Nrf2. Our results showed that TXNIP was elevated and FMD was aggravated in mice lung tissues after BLM administration compared with the saline group. Inversely, Nrf2 decreased TXNIP expression and alleviated FMD in PF. In vitro, TXNIP overexpression enhanced FMD and increased the level of ROS. In contrast, TXNIP deficiency by small interfering RNA (siRNA) attenuated TGF-β1-induced FMD and reduced ROS. An increase in ROS by H₂O₂ can upregulate TXNIP expression. Moreover, Nrf2 also inhibited TGF-β1-induced FMD and the increase of ROS, with reducing expression of TXNIP, and the inhibitory effect was better than TXNIP siRNA. These results suggest that activation of Nrf2 by DMI can protect against PF via inhibiting TXNIP expression. Our study may provide new therapeutic targets and treatment approaches for PF.

Journal of Cellular Physiology published new progress about 617-52-7. 617-52-7 belongs to esters-buliding-blocks, auxiliary class Alkenyl,Aliphatic hydrocarbon chain,Ester, name is Dimethyl itaconate, and the molecular formula is C7H10O4, Safety of Dimethyl itaconate.

Referemce:
https://en.wikipedia.org/wiki/Ester,
Ester – an overview | ScienceDirect Topics