Skip to main content
Menu

Current Events

Coronavirus: Some Clinical Trial Data

We’re starting to see some clinical trial data on possible Covid-19 therapies, specifically some of the ones mentioned in this earlier post on small-molecule approaches. First, the bad news (although I have to say it’s not unexpected). A trial of the lopinavir/ritonavir combination has shown no benefit. I say “not unexpected” because these antiretroviral drugs are not at all targeted to coronavirus proteins – this was always something of a long shot.

The second report is a bit secondhand; no paper or preprint with full data has yet appeared. The Chinese authorities report that favipiravir shows useful effects in trials of the drug. I’ll give people the choice of links for that one: the original is China Daily, but you’ll have to deal with the little box up in the right corner labled “Xi’s Moments”, where a smiling Xi Jinping urges joint efforts to fight the pandemic. The report at the Guardian is actually more complete, and is Xi-free (as far as I can tell).

. . .Patients who were given the medicine in Shenzhen turned negative for the virus after a median of four days after becoming positive, compared with a median of 11 days for those who were not treated with the drug, public broadcaster NHK said.

In addition, X-rays confirmed improvements in lung condition in about 91% of the patients who were treated with favipiravir, compared to 62% or those without the drug. . .

. . .But a Japanese health ministry source suggested the drug was not as effective in people with more severe symptoms. “We’ve given Avigan to 70 to 80 people, but it doesn’t seem to work that well when the virus has already multiplied,” the source told the Mainichi Shimbun.

I’m surprised that it works at all, but the data should speak for themselves, when we can see all of it. The good news is that the compound (an RNA polymerase inhibitor) seems to have a good safety profile.

Update: here’s the paper itself. I note that it is open-label, 35 patients in the treatment arm, so like the study below, not enough to base a large decision on yet, other than one to do a bigger and more controlled trial. Second update: it’s been pointed out (I missed this) that the control patients were enrolled in the last week of January, while the treatment group was enrolled during the first two weeks of February. That’s not exactly randomization, but the effect of this on the data is up for debate). Here’s the explanation for this, and I can see their point:

. . .given the high number of patients presenting simultaneously and the very high infectivity of the disease, it was ethically unacceptable to allocate patients to receive a different experimental drug using a randomization process impossible for most of the patients to understand. Furthermore, in the context of rumors and distrust of hospital isolation, using a randomized design at the outset might have led even more patients to refuse being isolated.

Next up is remdesivir. There are scattered reports from on-the-spot use in several countries, but we need better quality data on this one. Trials are underway from the NIH, from a WHO consortium, and from Gilead itself, among others, so we should have a clearer picture soon. Do not expect a cure. But it would be good if this compound can slow things down.

Finally, there are some potentially very interesting results from France on hydroxychloroquine. That compound (and chloroquine itself) have been the subject of much interest, and these are the first trial data that I’ve seen. A number of things need to be said up front: first of all, this was a small trial. Second, it was open-label. Third, there were significant patient drop-outs in the treatment group, making the sample even smaller. Under normal circumstances, to be honest, I would be looking askance at this, but (1) these ain’t normal circumstances and (2) the effect size seen in this work may be significant.

In summary, 26 patients were enrolled in the treatment group, with 16 controls. Six patients dropped out of the treatment group: 3 went to the ICU, one dropped out due to nausea, one left the hospital (apparently recovered?) and one died. No one left the control group. There were 15 male and 21 female patients. 6 of them were asymptomatic, 22 had upper respiratory symptoms, and 8 had lower respiratory tract symptoms (all of those had confirmed pneumonia by imaging).

The treatment group got 200mg of hydroxychloroquine sulfate three times a day, and six of those patients were also given 500mg azithromycin in addition. The paper says that this was the deal with possible bacterial superinfection, and the lead author also makes mention of possible antiviral effects of the compound. I hadn’t heard of these – azithromycin is, of course, more famous as an antibacterial – but there seems to be a pretty established literature on this, although the mechanism doesn’t seem to be well worked out.

The results are shown at right. As you can see, there appears to be an effect of hydroxychloroquine (although I would like to see some error bars), and a notably stronger effect (down to zero virus as measured by nasal swab) of the hydroxychloroquine – azithromycin combination. That’s the result that’s getting the attention, and justifiably so.

I would expect this to start some larger trials, and that looks completely justified. This by itself is not enough to recommend that people start using this combination – again, it’s a very small trial and open-label at that. But it points the way to something larger and more controlled. These are two inexpensive generic drugs with a long history of use in humans; if they can be repurposed in this manner we need to know as soon as possible. Chloroquine and hydroxychloroquine both can have notable side effects, but this is not a long course of treatment, either. Let’s see if this is real!

Update: a closer look at the data. Broken down like this, it’s messier, and makes it all the more imperative to run a better trial as quickly as possible.

 

79 comments on “Coronavirus: Some Clinical Trial Data”

  1. Barry says:

    “There is no solid evidence yet that anything works, but the epidemic is moving so fast that doctors are trying approaches where even preliminary data suggests there may be a benefit. Many feel they are on their own to develop treatment protocols. Federal health authorities like the Centers for Disease Control and Prevention recommend supportive care, but have said there is no evidence yet to support antiviral drugs or treatments for inflammation…For critically ill patients suffering from intense inflammatory reactions, called a cytokine storm, some centers are trying a drug called tocilizumab.”

    https://www.nytimes.com/2020/03/18/health/coronavirus-antiviral-drugs-fail.html

  2. A Nonny Mouse says:

    My contacts tell me that there are now 6 Indian companies starting to make favipiravir. Also, a company that was making chloroquine and had a very bad FDA inspection has now had the decision reversed and been asked to ramp up production for the US.

    Strange times….

  3. bks says:

    Fauci has been missing from the last two WH briefing sessions. Not a good sign.

    1. Barry says:

      Trump is very insecure about appearing with people who are smarter than he his.

      1. Who Dr. says:

        My boss gets like that too

      2. Polynices says:

        Don’t make stuff up. Really not helpful in this circumstance. Pretty sure Trump routinely appears with experts of various sorts. Also making a typo in a post criticizing someone’s intelligence: priceless.

        1. the texas carbon says:

          …what?

          Trump has fired anyone who remotely disagrees with him and has chosen instead to surround himself with sycophants and morons. How else do you explain that the one person he charged with the pandemic response doesn’t believe smoking kills people?

          No, I don’t think it is any coincidence that Fauci has disappeared, given that he publicly corrected Trump’s laughable understanding of drug development timelines.

          Also laughable that you conflate typos with intelligence. Give me a break.

      3. Former Merckoid says:

        uhmmm that would be everyone?

      4. Sharon wong says:

        . . . but everyone including my goldfish is smarter than Trump . . .

      5. Dennis K Yavorsky says:

        Barry et al – President Donald J. Trump seeks and recruits people more competent than himself (a very high standard) and does not suffer incompetence in his organizations. The US Presidency is such that it it more difficult to enforce that policy within government culture inculcated with deception. Still, he acts and acts quickly to assemble teams for success. Get use to the concept that President Trump doesn’t fit into your familiar circles and adapt to a better, more honest agenda he will enforce.

        1. the texas carbon says:

          you’re essentially regurgitating what Polynices stated without providing a single verifiable claim. All other offices and briefings temporarily aside, can you even address how Trump appointed leadership for the pandemic response who doesn’t even believe in evolution? If you really believe that Pence was a judicious choice, I think you might be letting politics override any scientific inclination you might have.

        2. Texas Carbonyl says:

          Zdraste Russia!

        3. Suzanne Roy1 says:

          Oh please…

        4. Silence Hand says:

          So, what we’ve seen is “success”? Then wait ’til we see failure…

          In seriousness, we have here an exemplary Trumpian argument. When confronted by critique that’s plainly (even hilariously) accurate, STRONGLY ASSERT THE EXACT OPPOSITE. Do this unblinkingly, immediately, with total authority: evidence is for losers. While your opponent is responding, move on to a different baldly false statement (or say something rankly offensive).

          It disorients those of us with a scientific bent. That’s the point. Yavorsky’s statement is just one snowflake in a howling blizzard of deceit that numbs and buries us. It’s particularly intense now, as Trump and his enablers struggle to bend reality to “I HAVE ALWAYS BEEN AT WAR WITH CORONAVIRUS”.

      6. Maybe the most ignorant thing I’ve seen written.

    2. TallDave says:

      We can’t be sure Fauci hasn’t been at the briefings, the evidence is only anecdotal.

  4. Sunyilo says:

    I wonder why are you skeptical on remdesivir? To my superficial understanding the biggest problem would be insufficient PK to target a respiratory virus (as it was optimized for hemorrhagic viruses). But the change of formulation and delivery (to nasal spray/inhalator) seems quite straightforward to me. Am I missing something?

    1. WFH says:

      Remdesivir likely doesn’t have a PK problem. In their Nature paper from last year (doi:10.1038/nature17180), they showed that the parent prodrug compound clears relatively rapidly from serum, but that the nucleoside itself clears fairly slowly. They also showed that it has a long half life in peripheral blood monocyte cells (PBMCs). Human dosing is 200mg on d1 and then 100mg IV qd subsequently, again suggesting that PK is not an issue.

      1. Sunyilo says:

        ….actually, I meant the exposure in the respiratory tract.

    2. Calvin says:

      The issue, I think, is that in Ebola it did not work anywhere near as well as we’d hoped. It does have efficacy, just not enough to merit it progressing. The two Mabs in the other arms of that trial were far superior (which is still a little bit of a surprise, but the data is the data).

      The general feeling is that the compound needs to be given as early as possible in the course of the infection and given the way testing is going (in the US it’s just not happening) it’s likely that people might be getting it too late in the course of the disease to show an effect.

      It does not have a super clean tox profile, prophylactic use is not going to be ideal either.

      We’ll just have to wait and see how it plays out. I suspect we’ll see efficacy that is in the 30% range.

      1. Silence Hand says:

        A disappointment to be sure. Frankly I worry about adenosine analogs given that they’re always gonna be competing with ATP,. Selectivity of ATP over Remdesvir wasn’t huge (3 – 4x I think), but ATP concentrations in cells can be pretty high. I’ve wondered if a different nucleoside analog (like cytosine) would skirt this problem.

  5. bhip says:

    very much hopes this/these work for the obvious selfish & altruistic reasons. That said, biologists only leave std deviations off a graph when the data sucks

    1. Standard Deviant says:

      There can be no error bars on qualitative data. I’m having trouble finding their exact method (they reference a pre-print), but I imagine that finding a relevant ‘reference gene’ to normalize the CT is a bit of a challenge as well making the quantitative data somewhat arbitrary. I suspect that’s part of the reason people aren’t considered ‘cleared’ until they’ve had two consecutive tests come back negative.

    2. Silence Hand says:

      The data in the French study are incredibly problematic. Most of the control group were tested with lower frequency at a different site, with only pos / neg indicated. Not clear what error rates are at that site and with that assay, or what the threshold is for scoring positive. Thanks for linking to twitter thread – provides crucial analysis.

      This paper was accepted after 1 day of “peer review”. The journal’s Editor-in-Chief is one of the paper’s authors. Red flags all over the place; this needs serious scrutiny.

    1. Lars says:

      Actually, Derek covered that yesterday. It’s complicated.

  6. charlie says:

    if you can reduce viral counts to near zero, that would be great for mild cases. 7 days recovery instead of the 14-21 that you’re seeing now.

    Still not clear to me how the virus is being distributed by asymptomatic patients but it seems to be.

    1. Old Timer says:

      My understanding is that all patients–asymptomatic, mild, bad, ICU–have amazingly massive throat/mucus titers of virus. That’s the big problem.

  7. cynical1 says:

    Is there any reason to believe favipiravir might be just as effective in viral clearance as mono therapy without alpha interferon? I am guessing that alpha interferon Ribavirin combination didn’t work??? So they tried this??

  8. loupgarous says:

    Is anyone tracking lung inflammation in the azithromycin + hydroxychloroquine arms of the last study mentioned?
    I ask because azithromycin’s been studied for its effect on COPD. Perhaps that was an endpoint and I just didn’t catch it?

  9. Mark says:

    Please keep on being a voice for reason. People appear to have very uninformed ideas about the difference between an attractive molecule and a medicine. Most, the majority, almost all hypothetical treatments wind up not working. Some brilliant guy with shaggy hair who just thinks up a miracle drug is only found in the movies.

    1. milkshake says:

      In real world, it is done by teams of shaggy technicians with brilliant hair, working under the inspired leadership of project manager – who is covering his butt, servile and paranoid in equal measure

      1. AR says:

        Yes but what does the project managers hair look like

  10. Bill Sellers says:

    The dropouts in the treatment arm are a major problem for interpreting the data. So I would be extremely cautious on the hydroxychloroquine data. At the moment it looks ambiguous to me. Also it would be much more interesting to see the actual viral titers in the patients rather than percentage of patients as the endpoint.

    1. MTK says:

      Bill,

      Exactly what I was thinking re: viral titers.

      The cutoff for a positive was <35 CT and some of the positives were 34, so looking just at a binary signal outcome seems like it could skew things considerably.

    2. MTK says:

      I also don’t understand how some of the positive results are just listed as “POS” while some provide the actual CT value.

    3. Bruce says:

      “Six hydroxychloroquine-treated patients
      were lost in follow-up during the survey because of early cessation of treatment. Reasons are
      as follows: three patients were transferred to intensive care unit, including one transferred on
      day2 post-inclusion who was PCR-positive on day1, one transferred on day3 post-inclusion
      who was PCR-positive on days1-2 and one transferred on day4 post-inclusion who was PCR
      positive on day1 and day3; one patient died on day3 post inclusion and was PCR-negative on
      day2; one patient decided to leave the hospital on day3 post-inclusion and was PCR-negative
      on days1-2; finally, one patient stopped the treatment on day3 post-inclusion because of nausea
      and was PCR-positive on days1-2-3.”

      It seems disconcerting that that 4 people in the treatment group dropped out due to progression to ICU or death, while none of that happened in the control group. But the people in the treatment group were older (51.2 yo vs. 37.3 yo), and that may account for it.

  11. Pajas says:

    Combo favipiravir/chloroquine would be interesting to test then.

  12. brian says:

    Hydroxychloroquine is also used to suppress autophagy. Is that help WRT fighting a viral infection?

    Or would combination therapy with something that promotes autophagy, such as Ambroxol, be useful?

    1. Silence Hand says:

      Azithromycin also blocks autophagy!
      https://www.ncbi.nlm.nih.gov/pubmed/21804191

      …except when it induces autophagy..
      https://erj.ersjournals.com/content/34/3/721

      ….sigh

  13. Biobass says:

    Looking at the Gautret paper. Shouldn’t the hydoxychloroquine alone data be the same for figures 1 & 2?

  14. Al says:

    I’d be a bit careful with the Raoult results too – the guy said in an interview today that a 20-people trial is more significant than one on 10,000 patients, and his usual reply to any critique of his methods is that he doesn’t care. Not to say the test was completely useless, but the cynic in me can’t help but wonder if he was trying to secure a spot in posterity for when this all blows over and pats in the back are a handed out. I’ll remain sceptical until more data is out there.

    The French daily Marianne has a decent general public write-up (in French), with a lot of conditionals in the text: https://www.marianne.net/societe/la-chloroquine-guerit-le-covid-19-didier-raoult-l-infectiologue-qui-aurait-le-remede-au

    1. Jim Y says:

      I see China is pushing for prevention studies using HCQ. I can’t find any for the U.S.

      https://academic.oup.com/jac/advance-article/doi/10.1093/jac/dkaa114/5810487?searchresult=1

  15. Giannis Zaxarioudakis says:

    Am I the only one that is far more interested for Pre exposure prophylaxis? The only drug combo that could be used for PrEP is HCQ+AZ. This would be a gamechanger since it transforms the disease completely. As long as you take your meds you cannot get sick. I hope that HCQ + AZ will be used in randomized PrEP trials.

    1. Barry says:

      handing out azithromycin as a prophylactic has other foreseeable consequences. You’d need a compelling case before you start cultivating resistant (bacterial) pathogens like that.
      But if Azithromycin has real anti-viral efficacy and that’s not mediate by bacterial ribosomes, it may be–long term—an exciting lead.

      1. Giannis Zaxarioudakis says:

        Low doses of AZ are routinely given to asthmatics for preventing exacerbations. Anyways we might create an inhaled HCQ + AZ formulation.

        https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(17)31281-3/fulltext

    2. BoneyAA says:

      I would like to see if mefloquine works for this – it would be an ideal pre-exposure prophylaxis agent – 250mg once or twice weekly (maybe with azithromycin 600mg twice weekly) the PK for mefloquine is great for this type of prescription – controlled trial in emergency medical workers would be easy to set up and fast to get results – assuming these anti malaria meds for for this virus

  16. RiRa says:

    Hi Derek, The host receptors from COVID-19 are ACE2 and TMPRSS2. Do you know of any trials planned on these targets? JAK inhibitor Olumiant purportedly has activity at ACE2 and Camostat Mesilate is a TMPRSS2 inhibitor approved in Japan.

  17. Sean says:

    Azithromycin is a macrolide antibiotic with well-described anti-inflammatory properties which can be attributed, at least partially, to its action on macrophages.
    https://pubmed.ncbi.nlm.nih.gov/22766077/

    So ibuprofen not good but maybe the right anti inflammatory

  18. Barry says:

    if azithromycin boosts expression of various interleukins as reported, it might actually exacerbate a cytokine storm, depending on when it’s dosed?

    1. loupgarous says:

      Azithromycin’s anti-inflammatory properties seem mainly to have been demonstrated in vivo, it’s entirely possible treating late-stage Covid-19 patients could touch off a cytokine storm – has anyone looked at the potential for that in the in vivo studies?

      We need to look harder at the three deaths in elderly patients receiving azithromycin in the Rouault study to affirm or rule out cytokine storm.

  19. matt says:

    Agree someone (independent) should replicate the French hydroxychloroquine results (which follow earlier Chinese testing as well) in a larger, much better trial. Having the control group only in different facilities from the treatment group, with no randomization of patients meaning the active arm may actually have been receiving patients more likely to be recovering, having patients “drop out” of the results when dropping out means they got worse on the measure being tested…seems like a whole lot o’ sketch.

  20. jeffrey r brender says:

    Italian group claims they cannot find any record of the chloroquine results in the clinical trial registry.
    ” A narrative letter by Chinese authors reported that a news briefing from the State Council of China had indicated that “Chloroquine phosphate… had demonstrated marked efficacy and acceptable safety in treating COVID-19 associated pneumonia in multicentre clinical trials conducted in China” [5]. The authors also stated that these findings came from “more than 100 patients” included in the trials [5]. We sought for evidence of such data in the trial registries we reviewed and found none.”
    https://www.sciencedirect.com/science/article/pii/S0883944120303907

  21. Fez says:

    While the mechanism of antiviral action of Azithromycin is not well worked out, Teicoplanin -a gram positive antibiotic- “potently prevents the entrance of 2019-nCoV-Spike-pseudoviruses into the cytoplasm” http://m.jbc.org/content/291/17/9218.full – So, I await a SNY sponsored trial of Teicopanin and Hydroxychloroquine.

  22. Zinc says:

    Zinc should be looked at more. I’ve attached a link to a Youtube video talking about how zinc and chloroquine together is a highly effective antiviral. Zinc is known to inhibit the viral RNA polymerase and the chloroquine acts as a zinc ionophore to rapidly transport zinc ions through cell membranes into the cytoplasm where they are needed. For most normal healthy people, there is no need for ionophores, our natural zinc transporter proteins are good enough for the job. Keeping zinc levels well maintained by zinc supplementation will indeed help prevent the rapid multiplying of viruses. Many people have seen the effects of zinc lozenges to beat the common cold. Zinc is truly great in this regard, I’ve experienced it many times myself.

    1. x says:

      Thank god for glowing testimonials for sketchy cures made by people named after the purported cures.

      1. Chris says:

        Thank god for glowing trolling done by people named after a math variable… What a contribution!
        It is perfectly reasonable to propose that zinc and chloroquine could have synergistic effects. Synergy does not require individual efficacy. Considering the properties and MoA at work it is something at least worth looking into.

      2. H.Saint says:

        He is correct. The ionophore makes the cell membrane porous to the Zinc ion ZN+2. The RNA of the virus needs to be converted into proteins for the virus to replicate. The Zinc is the hero of the story as it inhibits this process. The viral RNA is inhibited from creating a new copy of the viral body. The virus data is transcribed in multiple runs over the viral rna.

    2. Silence Hand says:

      Alex Jones and Jim Bakker are hawking some kind of “silver” miracle stuff, and I’m sure that they’ll be super interested in zinc as well. At least one animal study has found zero effect of dietary zinc on CoV etiology. Different one, though.

      1. Some Potential says:

        Silver Zinc batter!

      2. Shinkiba says:

        Jones is already pushing zinc aggressively, probably because he has pallets of a slow moving supplement that contains a bit of zinc gathering dust in his warehouse.

    3. S.K says:

      1. Zn2+ Inhibits Coronavirus and Arterivirus RNA Polymerase Activity In Vitro and Zinc Ionophores Block the Replication of These Viruses in Cell Culture
      https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2973827/

      2. Chloroquine Is a Zinc Ionophore
      https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0109180

    4. Ria says:

      What dsage and what type of Zinc should be used with Hydroxychloroquine?

  23. Me says:

    Azi is a pretty obvious choice to co-dose. I know nothing of it’s anti-viral properties (if any) but it seems to be a fairly powerful pulmonary anti-inflammatory. Indeed, many asthma/COPD docs have been asking for many years to have a non-antibiotic azi analogue. Something that GSK were developing when the great Patrick Vallance, the UK’s Chief Scientific Officer, no less, decided to terminate when he shipped out the Zagreb group.

    1. PV=nRT says:

      Chalk up another spectacularly bad call for Vallance, Witty and Slaoui. JP would have known better.

  24. jz78817 says:

    These drugs are inexpensive, that is until another Shkreli comes along and gets his hands on it.

    1. Brian says:

      Zithromax is sold out all over the place online. I wonder why?

  25. DTX says:

    FDA is advising against the use of anti-inflammatories such as aspirin & ibuprofen (NSAIDS) because they may exacerbate Covid-19 and increase mortality.

    Clinical evidence also does not support the use of steroids for Covid-19 (Lancet 7 Feb 2020). Steroids have many many effects, but a primary one is anti-inflammatory. (their adverse effects could also be the result of immune suppression)

    The half-life of azithromycin is very very long, 68 hours, so if its anti-inflammatory makes Covid-19 worse, it will make it worse for a very long time (maybe until they pass away & speeding the time to death). I’d want much much much more information on how anti-inflammatories impact Covid-19 before I’d ever suggest giving azithromycin to patients.

    Hence, as others as noted, we need to be careful about recommending treatments without good data, particularly when available data suggests the treatment could make patients worse.
    https://www.fda.gov/drugs/drug-safety-and-availability/fda-advises-patients-use-non-steroidal-anti-inflammatory-drugs-nsaids-covid-19

  26. Unintelligible says:

    Also linked on the China Daily page — not exactly a confidence builder…
    https://covid-19.chinadaily.com.cn/a/202003/21/WS5e7543eaa310128217280de5.html

  27. Pat Morgan says:

    26 patients were enrolled in the treatment group, with 16 controls. Six patients dropped out of the treatment group: 3 went to the ICU, one dropped out due to nausea, one left the hospital (apparently recovered?) and one died.”

    1/26 died = 3.8% mortality among infected….appx. the same 3.4% mortality among infected that the WHO reports….so it is definitely not a “cure”.

    So at best this small non-random open label study means nothing more than more research is needed ….

    https://drive.google.com/file/d/186Bel9RqfsmEx55FDum4xY_IlWSHnGbj/view

  28. rtah100 says:

    There is a paper doing the rounds about a soluble derivative of aspirin with in vitro activity against SARS2 and potential for inhalation administration (when they say potential, note the IV dose would be lethal…).

    https://www.longdom.org/open-access/d-llysine-acetylsalicylate–glycine-impairs-coronavirus-replication-jaa-1000151.pdf

  29. Malcolm says:

    New here and late to the party, but I thought I’d mention an article I came across about a drug called Retromad1. It is a Furin protease, and has been used to successfully treat feline infectious peritonitis, which is caused by the coronavirus FeCoV. https://www.scmp.com/news/asia/southeast-asia/article/3075604/coronavirus-singapore-start-thinks-cat-leukaemia-drug.

    Genome analysis shows that SARS-Cov-2 has a possible Furin cleavage site at the boundary of S1 and S2 domains of Spike Protein. https://www.sciencedirect.com/science/article/pii/S0166354220300528?via%3Dihub
    http://www.virology.ws/2020/02/13/furin-cleavage-site-in-the-sars-cov-2-coronavirus-glycoprotein/

    site)

  30. JB says:

    Here’s another idea using an already approved drug:

    Cell. 2020 Mar 4. pii: S0092-8674(20)30229-4. doi: 10.1016/j.cell.2020.02.052.

    SARS-CoV-2 Cell Entry Depends on ACE2 and TMPRSS2 and Is Blocked by a Clinically Proven Protease Inhibitor.

  31. RA12 says:

    Noticed new chinese trial on “Carrimycin” vs polyermase inhibitor or chloroquinine. Is carrimycin a man made macrolide? Obviously the combination of QT prolonging drugs sounds dangerous. The french study, right or wrong, suggests that azithromycin might be the bigger addition. Would love to see study on azithromycin alone, as this drug is generally well tolerated and would not produce the combination QT side effect. Scary to see mass use of azithromycin without significant proof, especially with this drugs tendency to promote resistance.

  32. Tom says:

    HCQ has a 22 day half life in the average human, so the french study would be gradually building up a dose, which eventually is therapeutic. A lot of this puzzle has to be in the loading dose that is eventually needed if the effect is happening.

    Anyone know if people on high dose long-term HCQ in the RA or Lupus community are mysteriously not getting sick despite being immunocompromised?

  33. Rob Decker says:

    Azithromycin (Zithromax) is also an anti-inflammatory, used for treating lung problems. https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(17)31281-3/fulltext

Leave a Reply

Your email address will not be published. Required fields are marked *

Time limit is exhausted. Please reload CAPTCHA.