On the other side of the world.
Register for free to join our community of investors and share your ideas. You will also get access to streaming quotes, interactive charts, trades, portfolio, live options flow and more tools.
Register for free to join our community of investors and share your ideas. You will also get access to streaming quotes, interactive charts, trades, portfolio, live options flow and more tools.
TDAmerica is down. Reporting inability to login. I suspect other brokers are affected.
.28 is the wall .... until it’s not ... lol
Someone’s been moving the “brick wall” for 2 weeks. Seems an awful lot like moving goal posts. The brick wall is now .24...no, .25...wait, .26...no, .25...OK, .26....27... now, .28...just a minute, .27 is holding.
In your example, Remdesivir plus Brilacidin is better than Remdesivir alone. LR is correct on this point regarding the current trial.
The trial includes moderate to severe COVID-19. A prophylaxis can also prevent moderate from becoming severe and severe from becoming dead. The article laments the low efficacy of Remdesivir, meaning though it reduces the time for hospitalization, it doesn’t seem to sufficiently prevent a moderate case upon admission from advancing to severe before the cytokine storm finally overwhelms the virus.
The trial design will show a prophylaxis for disease progression, if B does sufficiently in clinical work what it did in lab studies.
Because this is Hydroxychloroquine all over again. And, don’t forget the sunlight and take your bleach.
I wasted my time going through some recommended studies. The one with numbers was a small double-blind, but the reduction in treatment time was only some 25%. Also, treatment had to be administered at the outset of symptoms. Why didn’t it get more clinical attention? In the study it was no better than Remdesivir.
FDA: Why You Should Not Use Ivermectin to Treat or Prevent COVID-19
https://www.fda.gov/consumers/consumer-updates/why-you-should-not-use-ivermectin-treat-or-prevent-covid-19
Plug this into your Google search and you’ll get dozens of animal studies for mRNA vaccines. Some studies go back to before the Human genome map completion.
peer reviewed mrna vaccine animal studies
Also note, some of these studies were designed to test safety and as such did kill animals in the studies in a search for toxicity. These studies were successful in that they did kill animals at higher dosages.
Finally, emergency authorization means extending studies into vast numbers of population. As I mentioned, this means constant review and tracking of data for adverse events. That’s how rare reactions are discovered and to under what patient physical conditions they occur and to what degree these rare events happen. That’s also when actuaries step in and assess the human cost of vaccination verses the toll of Covid-19 on populations.
Obviously you are unaware of Long Haul Covid. 20% of those who get Covid wind up with 3 months to a year of recovery including lung damage, kidney damage, joint damage, heart/pulmonary damage and brain damage. 40% of the population gets mild to severe Covid. Any of them can wind up with long haul.
People are misinterpreting emergency approval for vaccines. It doesn’t mean vaccines are not approved; it means the FDA and other world governing bodies agree that there is enough safety data to show few or no severe effects. Severe effects must be low enough that improvement over unvaccinated populations is a clear result and advantage. This is especially the case that a vaccine must show a clear log-scale reduction in deaths. Furthermore, emergency approval requires continued monitoring and reporting of all adverse events. It also demands that only approved demographics receive the jab.
These same procedures have been in place for 60 years of vaccine development. A good example was 1970s swine flu. It was approved for emergency use, then in expanded approval adverse events began to show. The swine flu vaccine was quickly pulled. The most recent example is the AstraZeneca CoV-2 vaccine, which has now been halted several times across the Atlantic.
There is no way to reliably predict efficacy in a blinded, new therapeutic drug verses a standard of care. Upon unblinding, efficacy is often measured in reduction of hours or days in therapy. Since blinding means also randomizing the groups (standard of care plus placebo and SOC plus test drug), there is no way to discern a reduction in time unless full treatment response is instantaneous where staff witness and report miracle healing.
You do realize that there are three false assumptions:
1) false assumption: CoV-2 particles are spread as particles. This is false because airborne CoV-2 is spread as a mucosal aerosol. It doesn’t matter what size CoV-2 particles are if the medium itself is a wet, viscous droplet measured in microns. Micron weaving stops micron droplets.
2) false assumption: some tests showed surgical masks don’t stop CoV-2. Several studies of aerosols at cough and sneeze velocities showed that the aerosols (which carry the virus) were stopped by N95 masks. Other lower standard masks were effective at greatly reducing the distance of the aerosol from the source. In published lab tests, simulated CoV-2 medium stopped the aerosol, which disproves the false assumption that micron filters won’t stop nano sized viruses, which cannot spread outside wet mediums.
3) false assumption: in the real world, masks don’t stop the spread. Vietnam, which had the greatest experience with both SARS-1 and H5N1 found that surgical masks were effective at preventing the spread along with other measures, such as aggressive quarantining of contacts. During SARS-CoV-2 outbreak, the Ministry of Health required masks and social distancing along with a policy of “hit hard and fast” for any outbreak. This same policy was equally effective in New Zealand and Australia, Australia after they realized they needed to follow policy other than that of the US. In a country of 100 million roughly the size of California, sharing a trade border with China, Vietnam after a year of fighting Covid-29 has less than 2600 cases and 35 deaths.
Masks work.
Seems a classic case of the Dunning-Kruger Effect, including the projection....
What complete bullshit and dismissal of hard science. I even provided a link to the journal Nature which published the study and included a ton of references.
“It pains me that well meaning people just passively listen to politically motivated crap. Read the science articles and stop buying into the agendas.”
Then your sources don’t know what they are talking about. It’s the false analogy of throwing sand (very dry and wet sand does not behave like CoV-2 laden droplets) at a mesh fence. That premise alone renders every other assumption false.
Then there are the raw statistics of who contained the pandemic and how it was contained. No country that didn’t mandate masks contained Covid. Every country that contained Covid mandated masks.
Wearing masks works. Not wearing masks doesn’t work.
Your post and source is not the truth about masks:
1) a mask is not a chain link fence and virus particles are not like sand. Transmission of SARS-CoV-2 is through aerosol dispersion where virus particles are contained inside varying sizes of micron level droplets. Each droplet can contain between 10 to the 2 and 10 to the 100 virus particles.
2) the mask prevents aerosol droplets from passing through as the droplets impact the fine mesh of these masks. N95 quality masks are able to prevent greater than 99% of aerosol from breathing, coughing and sneezing from passing through when worn and handled correctly.
3) CoV-2 transmission occurs when mucus membranes encounter CoV-2 laden aerosol droplets or direct contact with saliva or other mucus from infected people who are shedding virus particles. Preventing aerosol transmission greatly reduces exposure to Covid-19 transmission.
4) every nation that has effectively contained virus transmission has included mask wearing in its containment protocol. Every nation that has not included mask wearing has had a surge in cases.
One recent study: https://www.nature.com/articles/s41598-020-78110-x
What happens in April besides Easter?
National Burrito Day, National Peanut-butter and Jelly Day, International Art Day, International Mother’s Day, World Penguin Day (mandatory Happy Feet watching), Super Heroes Day, Arbor Day and (the big one) National Beer Day.
Any one of these important days could be consequential for IPIX.
Italy will impose a national lockdown for the 3 days of Easter, April 3 to 5.
Oh, I see. You think that it works differently because it’s COVID and not one of the other inflammatory diseases against which it was tested like ABSSSI? Is this healthy skepticism or cynical contrariness? Very hard to tell.
“I cannot find any”
Simplest Google search turned up 4 scholarly papers. Here’s a poster that includes immunomodulation. Lol
Which is interesting and worth remembering when we arrive at the post mortem in due course.
So, with this choice of words, you are predicting failure. Got it.
When “longs” belittle every advancement as fluff, and there are dozens who do it, what can you expect?
And, why change the subject?
Yeah! Who are these chumps?
At the top of the paper:
National Center for Biodefense and Infectious Diseases, George Mason University, Manassas, VA 20110, USA
Public Health Research Institute, Rutgers, New Jersey Medical School, The State University of New Jersey, Newark, NJ 07103, USA
Um, who is the “New England School of Medicine”?
Innovation Pharmaceuticals Announces Publication of Peer-Reviewed Scientific Article in the Journal Viruses on the Anti-SARS-CoV-2 Properties of Brilacidin
Emerging mutations to the coronavirus are unlikely to affect Brilacidin’s ability to inhibit the virus
Brilacidin currently is being evaluated in a Phase 2 clinical trial in hospitalized COVID-19 patients
WAKEFIELD, MA – March 2, 2021 (GLOBE NEWSWIRE) Innovation Pharmaceuticals (OTCQB:IPIX) (“the Company”), a clinical stage biopharmaceutical company, today announced the publication of a peer-reviewed scientific article—Brilacidin Demonstrates Inhibition of SARS-CoV-2 in Cell Culture—in the journal Viruses.
The article is accessible at the link below.
Bakovic, A.; Risner, K.; Bhalla, N. (et al). Brilacidin Demonstrates Inhibition of SARS-CoV-2 in Cell Culture. Viruses 2021, 13, 271; https://doi.org/10.3390/v13020271
https://www.mdpi.com/1999-4915/13/2/271/
In the paper, Brilacidin was shown to exert potent inhibitory effects on SARS-CoV-2 in cell culture by decreasing viral load in different cell types, including ACE2 positive human lung cells, and, importantly, in both the Washington and Italian strains of the coronavirus. Testing of Brilacidin against additional SARS-CoV-2 strains is planned.
Already with over a half-million deaths in the U.S. and over two million deaths worldwide attributable to COVID-19, the emergence of more transmissible and more virulent variants of the novel coronavirus is causing added concern. Last week, the U.S. FDA issued industry guidance outlining recommendations for developing vaccines, drugs and diagnostic tools based on variants.
Brilacidin’s ability to disrupt viral integrity suggests Brilacidin likely is not subject to resistance developing due to coronavirus variants—unlike current COVID-19 treatments, such as monoclonal antibodies and convalescent plasma, and first-generation COVID-19 vaccines. This mechanism of action supports Brilacidin as a clearly differentiated antiviral in clinical development.
Leo Ehrlich, Chief Executive Officer of Innovation Pharmaceuticals, commented, “Infectious disease experts have noted the next phase in the global fight against COVID-19 will be in developing potent antivirals that directly act on the SARS-CoV-2 virus—which is what Brilacidin has been shown to do in pre-clinical studies. The Company looks forward to continuing its scientific collaborations with government and academic researchers to further inform Brilacidin’s treatment potential as a broad-spectrum antiviral drug candidate targeting coronaviruses, regardless of mutation or strain.”
Currently, Brilacidin is being evaluated in a global Phase 2 clinical trial in hospitalized COVID-19 patients.
Brilacidin and COVID-19
Brilacidin, which has received FDA Fast Track designation for the potential treatment of COVID-19, is one of the few drugs targeting COVID-19 that has been tested in human trials (a total of 8) for other clinical indications, providing established safety and efficacy data on over 460 subjects, thereby potentially enabling it to rapidly help address the novel coronavirus crisis. Pre-clinical testing at independent laboratories supports Brilacidin’s antiviral ability to safely and potently inhibit SARS-CoV-2, and multiple strains of human coronaviruses (H-CoVs). In a human lung cell line against SARS-CoV-2, Brilacidin achieved a Selectivity Index of 426. A molecular screening study of 11,552 compounds also supports Brilacidin as a promising novel coronavirus treatment. Brilacidin antiviral research to date has been limited to laboratory-based experiments. Additional pre-clinical and clinical data support Brilacidin’s inhibition of IL-6, IL-1ß, TNF-a and other pro-inflammatory cytokines and chemokines, which have been identified as central drivers in the worsening prognoses of hospitalized COVID-19 patients. Brilacidin’s robust antimicrobial properties might also help to fight secondary bacterial infections, which can co-present in up to 20 percent of COVID-19 patients. Collectively, these data support Brilacidin as a unique 3-in-1 combination—antiviral, immuno/anti-inflammatory, and antimicrobial—COVID-19 therapeutic candidate, with pan-coronavirus treatment potential. The Company has initiated a randomized, placebo-controlled Phase 2 clinical trial of Brilacidin for treatment of COVID-19 in moderate-to-severe hospitalized patients.
Global COVID-19 Cases and Mortality
An online tool tracking COVID-19 cases and mortality, both in the U.S. and globally, can be found on the Company’s website (http://www.ipharminc.com), and at the following link:
Standard of care means nothing more than all approved procedures and treatments which are standard. When Remdesivir was clinically tested against SARS-CoV-2 there was no antiviral treatment for it. My understanding is the standard of care severe COVID-19 included corticosteroids (Dexamethasone) or one of several other steroids, plus supplemental oxygenation. Remdesivir was simply added to the standard of care after showing no problems when combined with corticosteroids. So, yes, withholding steroid in treatment while adding a placebo would have been unethical without very strong rationale.
Also, if I recall correctly from one of the PRs, or investor updates, the B trial adds B or placebo to the standard of care, Remdesivir plus steroids.
“At this point all I'm sure of is that, unless Kips files a 13G/A saying that their holding has dropped below 5% of the IPIX outstanding (like Leviston did), they would have to file one on 2/14/22 unless there was no change in their holding...”
Correct.
Only limit orders for both Ameritrade and Schwab.
Translation of the first line:
A study investigating the use of delayed-release tablets to deliver brilacidin to the colon in healthy volunteers
Phase 1 Single Dose Escalation Study to Study the Use of Delayed-Release Tablets to Deliver Brilacidin to the Colon in Healthy Volunteers
Different clinical trial.
“When is clinical trial considered to be started?”
Generally, a clinical trial begins at recruitment, but the definitive start varies depending on trial design. In the case of B, the trial would have started with clearance to recruit the first patient in ICU, ER, or elsewhere in a hospital setting. So, the start of the trial might be the same day as the final walk-through and final staff checklist/training for procedure according to protocol. That would all have happened on Dec 17, according to the board discussion these past 24 hours.
But, also, one must keep in mind differences between US and Russian systems for drug approval. The start of the trial would be under stricter guidelines in the US. This would easily account for a one month delay to January. However, the start of the trial would be under similar criteria, and begin at the first recruitment.
Thanks. Seemed a high concentration to me, but your numbers put it in the ballpark for safe and effective dose.
“By that math the Russian patients could have been treated and had their endpoints
determined already. Is that what you think?”
Yes, that’s what I think.
50mg/ml seems too concentrated. The most successful of the phase 2b ABSSSI trial was dosed at .8 mg/kg. So, I think there is a problem in the translation from Russian to English, or who knows?
Everyone is missing the point of this trial. This isn’t an advertise for enrollment clinical trial. Enrollees don’t just show up sick after enrolling and participate at a clinical site.
These are ER patients at hospitals who are then asked if they want to take an experimental drug for Covid-19. If yes, the screening is quick following confirmation of SARS-CoV-2 infection, and the first dose is administered within hours of hospital admission. Very few patients are going to turn down an experimental drug for a pathogen that had only a marginally effective drug, Remdesivir, as a treatment. A hundred patients could fully enroll and complete treatment in a week. Completion of the trial would be a month later.
2/21 is a Sunday. Monday, 2/22, would be the filing day.
Agree! Don’t bite the gap. Let it fill to .45, then buy like a mad man/woman.
Brilacidin’s method of action as defined by the Wiki entry: “Brilacidin is an antibiotic that works by disrupting bacterial cell membranes, mimicking defensins that play a role in innate immunity.”
The defensin mimetic (imitation of natural antimicrobiological molecules) also had anti-inflammatory properties, meaning it reduces swelling of tissues and membranes due to infection.