Monoclonal antibodies were first used in humans in the 1980s². They have gradually become more prevalent with Regeneron, producing and selling this treatment for those with severe COVID-19¹.

Monoclonal antibodies work like our own antibodies to “tag” targets to be attacked by our immune systems. This treatment works for COVID-19 by targeting the virus in the blood and marking it for destruction¹. While potentially life-saving for COVID-19, it comes with risks ranging from flu-like symptoms to an anaphylactic reaction³.

This is why the decision to start such a treatment must be made by a physician working with a patient or a patient’s family to determine if the benefits of the treatment outweigh the risk.

Most current antibody treatments target an aspect of the virus that helps it enter cells, the ACE-2 receptor binding domain¹. The authors created a model that studied how different mutations impacted this viral protein’s function and sensitivity to antibody treatments².

Using this analysis, the authors identified mutations that would prevent the antibodies from appropriately targetting this viral protein¹. While most mutations only prevented targetting by one of the two antibodies in these treatments, mutations that blocked both were identified, the key finding of this paper¹.

This paper’s conclusions are not alarming and do not suggest the current pandemic will immediately get worse. This paper demonstrated that current treatments may need to be revised or have deficiencies addressed where viral evolution to go in a particular direction¹. We already know that the virus evolves. This paper addresses one point that requires surveillance so we can respond appropriately.

Remarks:

The title of source 2 portrayed monoclonal antibodies as “magic bullets”². If not otherwise clear, this treatment has limitations just as other clinical treatments discussed in this article.

References:

1. https://science.sciencemag.org/content/371/6531/850/tab-pdf
2. https://link.springer.com/article/10.1023/A:1015860525341
3. https://pubmed.ncbi.nlm.nih.gov/23835249/

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He called it a blessing from God because he was able to get multiple treatments for COVID-19. He then went on to tout those treatments as a “cure” for the disease. The reality, however, is quite different. The treatments he received can hardly be characterized as “cures,” and here is the data behind each one.

Monoclonal Antibodies

The most high profile treatment President Trump received — under a “compassionate use” application — was monoclonal antibodies. These are proteins that are highly specific against SARS CoV-2, and they have the ability to latch on to the virus to prevent it from entering the cells.

The data behind using them is from a study of ambulatory patients, which means patients in a doctor’s office or clinic setting, not the hospital. Right off the bat, this tells me that those patients were not very sick, to begin with. If they were, they would have been hospitalized. The drug has not been studied in that patient population, as far as I know.

In that ambulatory setting, the greatest benefit was for those patients who did not have their own antibodies against the disease, so-called seronegative patients. Those who had antibodies already did not benefit as much. Furthermore, there is absolutely no evidence that this treatment will work in patients with severe disease requiring hospitalization or ICU care (such as patients whom I see).

What’s more, it seems that the highest dose of the antibodies — the same dose the President received — was not as effective as the lower dose. More of the patients receiving the highest dose had to seek medical attention, and it took them longer to achieve symptom alleviation. These findings, however, were not statistically significant.

So, really, this treatment is hardly a “cure” as the President claims. It is definitely promising, but we need to wait for more data to come out.

Remdesivir

President Trump also received remdesivir, an anti-viral drug that was originally developed for Ebola. Remdesivir may also be helpful in treating Covid-19. The final results were recently published in the New England Journal of Medicine.

All that remdesivir does is shorten the time to recovery from 15 days to 10 days compared to placebo. That’s it. I am not saying that this is not significant, but it is not a “cure.”

Now, there was a trend toward lower mortality in the patients who received the drug, but technically, it was not statistically significant. Thus, you can’t make this claim about Remdesivir, and the study authors did not make this claim in their study conclusions.

Dexamethasone

By far, the best data is for dexamethasone. In this randomized clinical trial, the number of days alive and free from mechanical ventilation during the first 28 days was significantly higher among patients treated with dexamethasone plus standard care when compared with standard care alone (6.6 days vs 4.0 days).

When they pooled all the data for steroids in a meta-analysis, the 28-day all-cause mortality was lower among patients who received corticosteroids compared with those who received usual care or placebo (summary odds ratio, 0.66). This odds ratio means that the group who got steroids had a 34% decreased risk of death.

Now, the President received other treatments such aspirin, famotidine, zinc, and vitamin D. The data for these treatments is even more sparse. That’s what makes it so frustrating with this disease: it such a horrific condition with few truly effective treatment options.

The treatments for seasonal influenza are also not blockbusters, but seasonal influenza is not nearly as deadly as COVID-19. So, at the end of the day, the studies behind the treatments that the president received were not blockbusters, and they showed some benefit. But, I would hardly characterize them as “cures.”

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