Treatments for COVID-19: Drugs being tested against coronavirus
COVID-19, pandemic virus that has not only brought the world on its knees but as well wreaks havoc on the global economy.
Health experts around the world see coronavirus with code name COVID-19 as global fight, the war that must be won altogether.
Finding effective treatment has been a herculean task with Italy experiencing ugly side of the scourge more than other countries.
As numbers of cases rise in Italy, numbers of death recorded also beat human emotional imagination.
On her part, China is recovering albeit slowly but the authority have been able to reduce the virus from skyrocketing noting.
There are similar issue on cases and effective treatments.
Meanwhile, health practitioners and scientists are struggling to find effective drug to end the scourge but the journey has neither been easy not fruitful.
The only hope humanity has now is the COVID-19 answers to treatment. In terms of severity, it looks like there is no rule but a strong immune is a best bet.
According to www.livescience.com, as of Friday (March 20), 86 treatments or vaccines that are either ongoing or recruiting patients.
The drugs being tested range from repurposed flu treatments to failed Ebola drugs, to malaria treatments that were first developed decades ago.
Here are the treatments that doctors’ hope will help fight COVID-19.
Japan flu drug
So far, reports suggest the drug has been tested in 340 individuals in Wuhan and Shenzhen.
The drug, which works by preventing certain viruses from replicating, seemed to shorten the duration of the virus as well as improve lung conditions (as seen in X-rays) in tested patients, though the research has yet to be published in a peer-reviewed science journal.
Chloroquine and hydroxychloroquine
Chloroquine and hydroxychloroquine have been approved by the U.S. Food and Drug Administration for the treatment of malaria, lupus and rheumatoid arthritis, but preliminary research in and suggests that the drugs could effectively treat COVID-19.
found that chloroquine could quell the spread of SARS-CoV when applied to infected human cells in culture. SARS-CoV is closely related to the novel coronavirus, SARS-CoV-2, and caused an outbreak of severe acute respiratory syndrome in 2002.
The cell culture studies of SARS-CoV-2 revealed that the drug and its derivative hydroxychloroquine undermine the novel virus’ replication in a similar way.
Doctors in China, South Korea, France and the U.S. are now giving the drug to some patients with COVID-19 with promising, albeit anecdotal, results so far. The FDA is organizing a formal clinical trial of the drug.
In addition, the University of Minnesota is studying whether taking hydroxychloroquine can protect people living with infected COVID-19 patients from catching the virus themselves.
The authors reported that detectable concentrations of SARS-CoV-2 fell significantly faster in the study participants than coronavirus patients at other French hospitals who did not receive either drug. In six patients also given azithromycin, this promising effect appeared to be amplified.
However, that the small, non-randomized study “did not assess clinical benefit[s]” associated with the treatment; in other words, the study did not probe whether the treated patients were more likely to recover and survive their illness.
Additionally, the agency advised that doctors should be cautious when giving either drug to patients with chronic disease, such as kidney failure, and especially those “who are receiving medications that might interact to cause arrhythmias.”
A failed Ebola drug
A Gilead Sciences drug that was originally tested in people with Ebola, remdesivir, is being repurposed to see if it can effectively treat COVID-19.
The drug was found not to be effective in Ebola, but in lab studies, it has proven effective at inhibiting the growth of similar viruses, severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS).
The Food and Drug Administration has currently approved use of remdesivir for compassionate use, meaning only patients with severe COVID-19 disease can be approved for treatment.
In other countries, requirements to receive remdesivir may be less stringent.
Many doctors are excited about the drug’s potential.
“There’s only one drug right now that we think may have real efficacy,” Bruce Aylward of the World Health Organization said last month, as reported by STAT. “And that’s remdesivir.”
George Thompson, an infectious disease specialist at UC Davis Medical Center who treated an early, severe case of COVID-19, that their patient got better after getting the drug, about 36 hours after diagnosis. The doctors initially thought the patient would die, Thompson said.
However, such anecdotal evidence can’t demonstrate effectiveness, and the lab has yet to analyze blood samples to show that the patient’s clinical improvement following the administration of remdesivir coincided with a drop in viral load (concentration of viral particles).
The study, which was not peer-reviewed, found no clear time-dependent relationship between getting the drug and seeing improvements in symptoms. The patients also experienced rectal bleeding, elevated liver enzymes, vomiting and nausea, which could potentially be tied to the drug.
Another quandary is that antiviral drugs generally work better the earlier patients get them, but because remdesivir is not FDA-approved for general use, only patients with the most severe, and late-stage, disease, qualify for its use in clinical trials, Thompson told Science.
On Sunday (March 22), Gilead Sciences announced that they were temporarily halting compassionate use of remdesivir, due to “overwhelming demand.”
An HIV drug combination
The antiviral drug kaletra, a combination of lopinavir and ritonavir, generated early excitement. However, new data from China, published March 18 in the , could not detect a benefit when patients took the drug.
A total of 199 people with low oxygen levels were randomized to either receive kaletra or a placebo. While fewer people taking kaletra died, the difference was not statistically significant, meaning it could have been due to random chance. And both groups had similar levels of virus in their blood over time.
However, other studies are still ongoing, and there’s still a possibility this combination could show some benefit. As with other antivirals, this drug would likely work better if given earlier in the disease course.
An immunosuppressant and an arthritis drug
For some patients with COVID-19, the virus itself doesn’t do the worst damage.
That immune overreaction can damage tissue and ultimately kill people. To quiet such cytokine storms, doctors are now trying an immunosuppressant known as Actemra, or tocilizumab.
The drug is approved to treat rheumatoid arthritis and juvenile rheumatoid arthritis.
It blocks a cell receptor that binds something called interleukin 6 (IL-6). IL-6 is a cytokine, or a type of protein released by the immune system, that can trigger dangerous inflammatory cascades.
One group will receive the drug plus other standard treatments, while another group will receive a placebo, plus standard treatments.
Regeneron is enrolling patients in a clinical trial to test another IL-6 inhibitor, known as sarilumab (kevzara), for treating COVID-19 pneumonia. The logic behind using sarilumab is similar to that for tocilizumab.
A blood pressure drug
Losartan is a generic blood-pressure medication that some scientists are hoping could help patients with COVID-19.
The University of Minnesota has launched two clinical trials using the inexpensive, generic drug.
The first would evaluate whether losartan can prevent multi-organ failure in those hospitalized with COVID-19 pneumonia.
Losartan works by blocking a receptor, or doorway into cells that the chemical called angiotensin II uses to enter the cells and raise blood pressure.
SARS-CoV-2 binds to the angiotensin-converting enzyme 2 (ACE2) receptor, and it’s possible, the thinking goes, that because losartan might block those receptors, it may prevent the virus from infecting cells.
Complicating things, a paper published March 11 in the journal has raised the possibility that common drugs for hypertension, such as ACE inhibitors and so-called angiotensin II receptor blockers (ARBs), which includes losartan, might actually spur the body to make more ACE2, thereby increasing the ability of the virus to infiltrate cells.