he might be communicating with (3) Q
*** is Gen. FLynn
might you have the timestamp with seconds on this tweet?
It's good that he is taking Remdesivir.
He seems to be asymptomatic.
Monitoring him to be on cautious side.
Between Feb 6, 2020, and March 12, 2020, 237 patients were enrolled and randomly assigned to a treatment group (158 to remdesivir and 79 to placebo); one patient in the placebo group who withdrew after randomisation was not included in the ITT population. Remdesivir use was not associated with a difference in time to clinical improvement (hazard ratio 1·23 [95% CI 0·87–1·75]). Although not statistically significant, patients receiving remdesivir had a numerically faster time to clinical improvement than those receiving placebo among patients with symptom duration of 10 days or less (hazard ratio 1·52 [0·95–2·43]). Adverse events were reported in 102 (66%) of 155 remdesivir recipients versus 50 (64%) of 78 placebo recipients. Remdesivir was stopped early because of adverse events in 18 (12%) patients versus four (5%) patients who stopped placebo early.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7190303/
That was earlier this year.
There are many more study outcomes awaiting results.
I think they know the results ahead of time.
It's most likely an excellent drug of choice for him based on it's mechanism of action….
Remdesivir’s antiviral activity, sterically interacting with the viral RdRp to induce delayed chain termination, has been demonstrated in vitro against multiple coronaviruses (SARS, MERS, contemporary human CoV and bat-CoVs).72 Remdesivir was also shown to perturb pan-CoV RdRp function by inhibiting viral replication of SARS, MERS, and the model β-coronavirus murine hepatitis virus (MHV), even in settings with intact exonuclease proofreading activity.45 Biochemical data from recombinant respiratory syncytial virus (RSV) RdRp suggested the primary mechanism of action was through delayed chain termination.73−75 Importantly, remdesivir inhibits viral replication (demonstrated with both Ebola and RSV) in cell-based assays with IC50 values of approximately 100 nM, whereas human RNA Polymerase (RNAP) II and human mitochondrial RNAP are not inhibited in the presence of compound,75 providing approximately 500-fold selectivity. This selectivity is achieved, at least in part, due to the nucleoside analogues being poor substrates for the human polymerases.76 Interestingly, in vitro assays demonstrate that the triphosphate form of the inhibitor was incorporated at increased rates compared to natural nucleotide pools,77 likely adding to strong antiviral potency of remdesivir through premature RNA synthesis termination.
Yes, Q confirmed she was marker 9.