Why not ? She was front and centre of some pretty ordinary vitriol from some share holders in the past.
again from the research paper...That lead to the study that we are awaiting news for..
Despite the success of preventive vaccination, and the current antiviral treatment options, major public health and economic challenges of SARS-CoV-2 remain and may be expected to further intensify with continued virus evolution.BIT225, or related drug candidates targeting SARS-CoV-2 viroporin activity may have a meaningful clinical impact, with the potential to deliver simple and efficacious oral therapies that provide broad-spectrum protection across the coronaviruses.Further study of SARS-CoV-2 viroporin antagonists, as novel antiviral targets, and as a means of favourably modifying immune effectors are warranted. Such studies, whether proof of principle, or proof of concept hold potential to advance coronavirus therapeutics.
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it is a very inclusive document and happy to be accused of cherry picking tracts from it but it is to me a tour de force doc that highlights how good this drug could be.
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BIT225 showed similar antiviral activity against six different SARS-CoV-2 strains, supporting the broad-spectrum potential against SARS-CoV-2 variants. Antiviral activity was also similar in two different cell lines, consistent with the antiviral effect in cell culture being conferred by interaction with a viral protein.
The in vivo data presented here support the investigation of BIT225 for the treatment and prophylaxis of SARS-CoV-2 infection in humans.
And lastly...
The high efficacy of BIT225 treatment even when treatment was delayed for 24 or 48 hours after infection is notable, as monoclonal antibodies and other direct-acting antiviral agents have previously shown significant losses of efficacy when treatment initiation was delayed in lethal SARS-CoV mouse models. Treatment of SARS-CoV infection in the MA15 mouse model with GS-5734 (Remdesivir) showed outcomes similar to vehicle control when treatment started on Day 2 after infection [41]. Early treatment start was required for differentiation from vehicle, but even that could not fully protect mice from weight loss during treatment [41]. Similarly, treatment with EIDD-2801 (Molnupiravir) in this mouse model showed a significant loss of efficacy when treatment was delayed by 24 or 48 hours after infection [42]. When mice implanted with human lung tissue and infected with SARS-CoV-2 were treated with Molnupiravir, the treatment efficacy measured as a reduction of lung virus titres was lower when treatment was started at 48 hours after infection, as compared to earlier treatment starts [43]. Reports on treatment of hACE2 transgenic K18 mice infected with SARS-CoV-2 with Remdesivir, Molnupiravir, Nirmatrelvir or the 3CL protease inhibitor GC376 demonstrate the difficulty of protecting SARS-Cov-2 infected K18 mice from weight loss in this challenging mouse model of severe virus-induced pathogenicity. A 5-day treatment starting 6 hours after infection with Remdesivir, Molnupiravir or Nirmatrelvir protected < 50% of mice from death and could not protect mice from weight loss during treatment. A combination of Molnupiravir and Nirmatrelvir could achieve 80% survival [44]. A 10-day treatment with a deuterated analog of GC-573 starting 24 hours after infection of K18 mice with SARS-CoV-2 could protect all mice from death, but mice still showed significant weight loss during treatment [45].
BIT225 was initially designed as an HIV-1 Vpu viroporin inhibitor [8,37,38], and subsequently, demonstrated activity against Bovine viral diarrhea virus (BVDV) and Hepatitis C virus (HCV) p7 viroporins [9]. BIT225 has shown antiviral activity against both HIV-1 and HCV in the clinic, as well as potential to reverse adverse viral-induced immunopathogenesis [39,40]. SARS-CoV-2 may be particularly sensitive to viroporin inhibition, considering that this virus encodes not only one but several viroporin-like proteins, including the highly conserved E protein, as well as 3a, ORF7b and ORF10 proteins, suggesting an exceptionally high importance of viroporin functions in the Coronavirus life cycle [16–18].
The results obtained here indicate that BIT225 is an inhibitor of SARS-CoV-2 E protein ion channel activity.
As quoted from
Citation: Ewart G, Bobardt M, Bentzen BH, Yan Y, Thomson A, Klumpp K, et al. (2023) Post-infection treatment with the E protein inhibitor BIT225 reduces disease severity and increases survival of K18-hACE2 transgenic mice infected with a lethal dose of SARS-CoV-2. PLoS Pathog 19(8): e1011328. doi:10.1371/journal.ppat.1011328
Editor: Nicholas Heaton, Duke University, UNITED STATES
Received: March 30, 2023; Accepted: July 6, 2023; Published: August 7, 2023
Copyright: © 2023 Ewart et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Data Availability: The authors confirm that all data underlying the findings are fully available without restriction. All relevant data are within the paper and its Supporting Information files.
cheers all
