Rifaximin or Saccharomyces boulardii in heart failure with reduced ejection fraction: Results from the randomized GutHeart trial was written by Awoyemi, Ayodeji;Mayerhofer, Cristiane;Felix, Alex S.;Hov, Johannes R.;Moscavitch, Samuel D.;Lappegaard, Knut Tore;Hovland, Anders;Halvorsen, Sigrun;Halvorsen, Bente;Gregersen, Ida;Svardal, Asbjoern;Berge, Rolf K.;Hansen, Simen H.;Gotz, Alexandra;Holm, Kristian;Aukrust, Paal;Aakra, Sissel;Seljeflot, Ingebjoerg;Solheim, Svein;Lorenzo, Andrea;Gullestad, Lars;Troeseid, Marius;Broch, Kaspar. And the article was included in EBioMedicine in 2021.Computed Properties of C43H51N3O11 This article mentions the following:
The gut microbiota represents a potential treatment target in heart failure (HF) through microbial metabolites such as trimethylamine N-oxide (TMAO) and systemic inflammation. Treatment with the probiotic yeast Saccharomyces boulardii have been suggested to improve left ventricular ejection fraction (LVEF). In a multicentre, prospective randomized open label, blinded end-point trial, we randomized patients with LVEF <40% and New York Heart Association functional class II or III, despite optimal medical therapy, to treatment (1:1:1) with the probiotic yeast Saccharomyces boulardii, the antibiotic rifaximin, or standard of care (SoC) only. The primary endpoint, the baseline-adjusted LVEF at three months, was assessed in an intention-to-treat anal. We enrolled a total of 151 patients. After three months treatment, the LVEF did not differ significantly between the SoC arm and the rifaximin arm (mean difference was -1•2 percentage points; 95% CI -3•2 – 0•7; p=0•22) or between the SoC arm and the Saccharomyces boulardii arm (mean difference -0•2 percentage points; 95% CI -2•2 – 1•9; p=0•87). We observed no significant between-group differences in changes in microbiota diversity, TMAO, or C-reactive protein. Three months treatment with Saccharomyces boulardii or rifaximin on top of SoC had no significant effect on LVEF, microbiota diversity, or the measured biomarkers in our population with HF. The trial was funded by the Norwegian Association for Public Health, the Blix foundation, Stein Erik Hagens Foundation for Clin. Heart Research, Ada og Hagbart Waages humanitaere og veldedige stiftelse, Alfasigma, and Biocodex. In the experiment, the researchers used many compounds, for example, (2S,16Z,18E,20S,21S,22R,23R,24R,25S,26R,27S,28E)-25-(Acetyloxy)-5,6,21,23-tetrahydroxy-27-methoxy-2,4,11,16,20,22,24,26-octamethyl-2,7-(epoxypentadeca[1,11,13]trienimino)benzofuro[4,5-e]pyrido[1,2-a]benzimidazole-1,15(2H)-dione (cas: 80621-81-4Computed Properties of C43H51N3O11).
(2S,16Z,18E,20S,21S,22R,23R,24R,25S,26R,27S,28E)-25-(Acetyloxy)-5,6,21,23-tetrahydroxy-27-methoxy-2,4,11,16,20,22,24,26-octamethyl-2,7-(epoxypentadeca[1,11,13]trienimino)benzofuro[4,5-e]pyrido[1,2-a]benzimidazole-1,15(2H)-dione (cas: 80621-81-4) belongs to benzofurans derivatives. Benzofurans are only weakly aromatic in nature and they are cleaved by many oxidative and reductive conditions. Benzofurans are stable towards alkali and readily polymerize on treatment with sulfuric acid, due to which they are useful for the preparation of low cost chemically relatively inert resins.Computed Properties of C43H51N3O11
Referemce:
Benzofuran – Wikipedia,
Benzofuran | C8H6O – PubChem