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  1. Article ; Online: Synthesis and characterization of carbohydrate-based biosurfactant mimetics.

    Sockett, Kaitlynn A / Loffredo, Madeline / Korunes-Miller, Jenny / Varghese, Maria / Grinstaff, Mark W

    Carbohydrate research

    2022  Volume 522, Page(s) 108697

    Abstract: Glycolipid biosurfactants are of interest for various industry sectors. We report the synthesis and characterization of enantiopure poly-amido-saccharides (PASs) containing myristoyl (C14), palmitoyl (C16), or stearoyl (C18) terminal chain lengths as ... ...

    Abstract Glycolipid biosurfactants are of interest for various industry sectors. We report the synthesis and characterization of enantiopure poly-amido-saccharides (PASs) containing myristoyl (C14), palmitoyl (C16), or stearoyl (C18) terminal chain lengths as mimetics of glycolipid biosurfactants. These amphiphilic polymers are water soluble, adopt a helical secondary structure, decompose at temperatures greater than 240 °C, are non-cytotoxic, and self-assemble into nanostructures. Polymers containing the shorter hydrophilic chain lengths and the hydrophobic C14 chain exhibit the lowest surface tension among all polymers.
    MeSH term(s) Carbohydrates/chemistry ; Hydrophobic and Hydrophilic Interactions ; Glycolipids ; Polymers/chemistry ; Surface-Active Agents/chemistry
    Chemical Substances Carbohydrates ; Glycolipids ; Polymers ; Surface-Active Agents
    Language English
    Publishing date 2022-10-07
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 1435-7
    ISSN 1873-426X ; 0008-6215
    ISSN (online) 1873-426X
    ISSN 0008-6215
    DOI 10.1016/j.carres.2022.108697
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: The in-vitro effect of famotidine on sars-cov-2 proteases and virus replication.

    Loffredo, Madeline / Lucero, Hector / Chen, Da-Yuan / O'Connell, Aoife / Bergqvist, Simon / Munawar, Ahmad / Bandara, Asanga / De Graef, Steff / Weeks, Stephen D / Douam, Florian / Saeed, Mohsan / Munawar, Ali H

    Scientific reports

    2021  Volume 11, Issue 1, Page(s) 5433

    Abstract: The lack of coronavirus-specific antiviral drugs has instigated multiple drug repurposing studies to redirect previously approved medicines for the treatment of SARS-CoV-2, the coronavirus behind the ongoing COVID-19 pandemic. A recent, large-scale, ... ...

    Abstract The lack of coronavirus-specific antiviral drugs has instigated multiple drug repurposing studies to redirect previously approved medicines for the treatment of SARS-CoV-2, the coronavirus behind the ongoing COVID-19 pandemic. A recent, large-scale, retrospective clinical study showed that famotidine, when administered at a high dose to hospitalized COVID-19 patients, reduced the rates of intubation and mortality. A separate, patient-reported study associated famotidine use with improvements in mild to moderate symptoms such as cough and shortness of breath. While a prospective, multi-center clinical study is ongoing, two parallel in silico studies have proposed one of the two SARS-CoV-2 proteases, 3CL
    MeSH term(s) A549 Cells ; Animals ; COVID-19/virology ; Chlorocebus aethiops ; Famotidine/pharmacology ; Humans ; Peptide Hydrolases/metabolism ; SARS-CoV-2/drug effects ; SARS-CoV-2/enzymology ; Vero Cells ; Virus Replication/drug effects
    Chemical Substances Famotidine (5QZO15J2Z8) ; Peptide Hydrolases (EC 3.4.-)
    Language English
    Publishing date 2021-03-08
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-021-84782-w
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: The in-vitro effect of famotidine on sars-cov-2 proteases and virus replication

    Madeline Loffredo / Hector Lucero / Da-Yuan Chen / Aoife O’Connell / Simon Bergqvist / Ahmad Munawar / Asanga Bandara / Steff De Graef / Stephen D. Weeks / Florian Douam / Mohsan Saeed / Ali H. Munawar

    Scientific Reports, Vol 11, Iss 1, Pp 1-

    2021  Volume 9

    Abstract: Abstract The lack of coronavirus-specific antiviral drugs has instigated multiple drug repurposing studies to redirect previously approved medicines for the treatment of SARS-CoV-2, the coronavirus behind the ongoing COVID-19 pandemic. A recent, large- ... ...

    Abstract Abstract The lack of coronavirus-specific antiviral drugs has instigated multiple drug repurposing studies to redirect previously approved medicines for the treatment of SARS-CoV-2, the coronavirus behind the ongoing COVID-19 pandemic. A recent, large-scale, retrospective clinical study showed that famotidine, when administered at a high dose to hospitalized COVID-19 patients, reduced the rates of intubation and mortality. A separate, patient-reported study associated famotidine use with improvements in mild to moderate symptoms such as cough and shortness of breath. While a prospective, multi-center clinical study is ongoing, two parallel in silico studies have proposed one of the two SARS-CoV-2 proteases, 3CLpro or PLpro, as potential molecular targets of famotidine activity; however, this remains to be experimentally validated. In this report, we systematically analyzed the effect of famotidine on viral proteases and virus replication. Leveraging a series of biophysical and enzymatic assays, we show that famotidine neither binds with nor inhibits the functions of 3CLpro and PLpro. Similarly, no direct antiviral activity of famotidine was observed at concentrations of up to 200 µM, when tested against SARS-CoV-2 in two different cell lines, including a human cell line originating from lungs, a primary target of COVID-19. These results rule out famotidine as a direct-acting inhibitor of SARS-CoV-2 replication and warrant further investigation of its molecular mechanism of action in the context of COVID-19.
    Keywords Medicine ; R ; Science ; Q
    Language English
    Publishing date 2021-03-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: The Effect Of Famotidine On SARS-CoV-2 Proteases And Virus Replication

    Loffredo, Madeline / Lucero, Hector / Chen, Da-Yuan / O'Connell, Aoife / Bergqvist, Simon / Munawar, Ahmad / Bandara, Asanga / DeGraef, Steff / Weeks, Stephen D. / Douam, Florian / Saeed, Mohsan / Munawar, Ali H

    bioRxiv

    Abstract: The lack of coronavirus-specific antiviral drugs has instigated multiple drug repurposing studies to redirect previously approved medicines for the treatment of SARS-CoV-2, the coronavirus behind the ongoing COVID-19 pandemic. A recent, large-scale, ... ...

    Abstract The lack of coronavirus-specific antiviral drugs has instigated multiple drug repurposing studies to redirect previously approved medicines for the treatment of SARS-CoV-2, the coronavirus behind the ongoing COVID-19 pandemic. A recent, large-scale, retrospective clinical study showed that famotidine, when administered at a high dose to hospitalized COVID-19 patients, reduced the rates of intubation and mortality. A separate, patient-reported study associated famotidine use with improvements in mild to moderate symptoms such as cough and shortness of breath. While a prospective, multi-center clinical study is ongoing, two parallel in silico studies have proposed one of the two SARS-CoV-2 proteases, 3CL<sup>pro</sup> or PL<sup>pro</sup>, as potential molecular targets of famotidine activity; however, this remains to be experimentally validated. In this report, we systematically analyzed the effect of famotidine on viral proteases and virus replication. Leveraging a series of biophysical and enzymatic assays, we show that famotidine neither binds with nor inhibits the functions of 3CL<sup>pro</sup> and PL<sup>pro</sup>. Similarly, no direct antiviral activity of famotidine was observed at concentrations of up to 200 μM, when tested against SARS-CoV-2 in two different cell lines, including a human cell line originating from lungs, a primary target of COVID-19. These results rule out famotidine as a direct-acting inhibitor of SARS-CoV-2 replication and warrant further investigation of its molecular mechanism of action in the context of COVID-19.
    Keywords covid19
    Language English
    Publishing date 2020-07-15
    Publisher Cold Spring Harbor Laboratory
    Document type Article ; Online
    DOI 10.1101/2020.07.15.203059
    Database COVID19

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    Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

  5. Article ; Online: The Effect of Famotidine on SARS-CoV-2 Proteases and Virus Replication

    Loffredo, Madeline / Lucero, Hector / Chen, Da-Yuan / O’Connell, Aoife / Bergqvist, Simon / Munawar, Ahmad / Bandara, Asanga / De Graef, Steff / Weeks, Stephen D. / Douam, Florian / Saeed, Mohsan / Munawar, Ali H.

    bioRxiv

    Abstract: The lack of coronavirus-specific antiviral drugs has instigated multiple drug repurposing studies to redirect previously approved medicines for the treatment of SARS-CoV-2, the coronavirus behind the ongoing COVID-19 pandemic. A recent, large-scale, ... ...

    Abstract The lack of coronavirus-specific antiviral drugs has instigated multiple drug repurposing studies to redirect previously approved medicines for the treatment of SARS-CoV-2, the coronavirus behind the ongoing COVID-19 pandemic. A recent, large-scale, retrospective clinical study showed that famotidine, when administered at a high dose to hospitalized COVID-19 patients, reduced the rates of intubation and mortality. A separate, patient-reported study associated famotidine use with improvements in mild to moderate symptoms such as cough and shortness of breath. While a prospective, multi-center clinical study is ongoing, two parallel in silico studies have proposed one of the two SARS-CoV-2 proteases, 3CLpro or PLpro, as potential molecular targets of famotidine activity; however, this remains to be experimentally validated. In this report, we systematically analyzed the effect of famotidine on viral proteases and virus replication. Leveraging a series of biophysical and enzymatic assays, we show that famotidine neither binds with nor inhibits the functions of 3CLpro and PLpro. Similarly, no direct antiviral activity of famotidine was observed at concentrations of up to 200 μM, when tested against SARS-CoV-2 in two different cell lines, including a human cell line originating from lungs, a primary target of COVID-19. These results rule out famotidine as a direct-acting inhibitor of SARS-CoV-2 replication and warrant further investigation of its molecular mechanism of action in the context of COVID-19.
    Keywords covid19
    Publisher BioRxiv; WHO
    Document type Article ; Online
    DOI 10.1101/2020.07.15.203059
    Database COVID19

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    Inter-library loan at ZB MED

    Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

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