An Urgent Message to President Biden and Members of The Biden COVID-19 Taskforce: On Cyclosporine

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President Biden’s COVID-19 task force has an opportunity to recognize that the NIH’s therapeutic search response to COVID-19 has vastly underplayed the role of inflammation as COVID-19’s dominant “kill-mechanism”. At this late hour, this task force’s clarity on the role of inflammation in the thousands of American deaths daily, could balance our nation’s therapeutic approach to COVID-19 disease.

Honorable Mr. President and members of the Biden task-force,

I write this public letter to you on this November day, as yesterday our nation reached another tragic milestone during the COVID-19 pandemic: 180,000 new Americans infected in a single day!

I am writing to you as an American physician, a cellular immunologist and a public health advocate.

With this letter I am specifically informing you that our nation’s efforts against COVID-19 on the therapeutic front have been radically imbalanced away from anti-inflammatory drugs. This, despite the fact that the only partially effective therapeutic agent against COVID-19 is the anti-inflammatory drug, dexamethasone. But, as you know, even this drug was not an American contribution to COVID-19 therapy, it was a British one.

The error in strategic scientific thinking about COVID-19 disease in the United States has been the NIH’s prejudice against anti-inflammatory therapy, and in favor of anti-replication, virus neutralization and vaccine agents. Of course, I am NOT critiquing the latter focus. Anti-viral replication, neutralization and vaccination are critical components of a cogent defensive strategy against COVID-19 — but the American strategic blunder is that: NIH’s efforts to treat COVID-19 disease, as a dominantly inflammatory disease, have been dangerously anemic, at best.

Here I write you to specifically highlight the potential critical importance of immediately focusing on the inexpensive and widely available generic drug, cyclosporine — This, as a reasonably safe and very well-known therapeutic agent, whose transient use, like an “antibiotic” (i.e., a 5–7 day oral course), is highly likely to curb progression of COVID-19 hyper-inflammatory disease to critical illness.

Importantly, cyclosporine resides in a well-lubricated supply chain in the US, already funded by the prescription insurance plans of the vast majority of Americans — literally every corner CVS or Wallgreens can supply a 7 day course of this drug to ANY patient for whom it is prescribed at somewhere around $20 per regimen. What’s more, is that cyclosporine is globally scaleable.

Sine last April, I have been engaged in a serious public health campaign to highlight the likely need for this drug to be quickly tested and deployed — using our conventional “evidence-based” and emergency mechanisms. Unfortunately, however, a combination of competition with monied drug choices in the US and professional prejudices in favor of anti-viral replication and neutralization agents has introduced resistance to progress on cyclosporine.

But, irrespective, we have managed to initiate two small clinical trials, which are now recruiting COVID-19 patients for testing of cyclosporine — one at the University of Pennsylvania, under direction of Professors Carl June and Emily Blumberg, and a second at Baylor College of Medicine, under the guidance of Professor Bryan Burt. A grand total of only FOUR, yes FOUR, patients have been enrolled in these trials since June 2020. Anemic, indeed! All four patients were discharged from the hospital within 5 days and are doing quite well now.

Simply put, America is insufficiently attuned to the fact that COVID-19’s “kill-mechanism” is driven by a hyper-inflammatory response mediated by T-cells and Macrophages. The exact cell subsets whose activation can be efficiently modulated by the well known drug we call cyclosporine. A drug, which most clinicians know revolutionized the worldwide treatment of hyper-inflammatory and autoimmune diseases — and organ transplantation. This, by dampening the vigor of T-cell and Macrophage activation.

Dr. Janet Woodcock of OWS and Dr. Anthony Fauci are both aware of the potential critical importance of this drug in curbing COVID-19 hyper-immunity. However, because of monied priorities driven by corporate players in Pharma, and because of Dr. Fauci’s past success with anti-replication agents in the HIV/AIDS playbook, a major focus on anti-inflammatory agents, prominent amongst them cyclosporine, remains dangerously absent from our American strategic approach.

I write to inform you, as a cellular immunologist and clinician with experience in the use of immunomodulatory drug agents like cyclosporine, that it is more than highly likely that a combination of dexamethasone and cyclosporine will block the progression of COVID-19 disease in a large majority of patients with unremitting disease, who are moving towards critical illness daily across America.

At this late hour in the American pandemic, I ask for your urgent voice of support in engaging cyclosporine as a defensive weapon. And I can only hope that you have the clarity to see that this major defensive weapon in our generic pharmaceutical arsenal remains unacceptably siloed — as American lives begin to burn at an unprecedented rate daily.

I ask for your urgent voice of support in casting cyclosporine into the limelight of professional, public and regulatory discourse as a likely candidate for blockade of COVID-19's deadly inflammatory phase.

Yours with respect and in defense of the United States and global public health,

Hooman Noorchashm MD, PhD (For Amy and the others).

Hooman Noorchashm MD, PhD is a physician-scientist. He is an advocate for ethics, patient safety and women’s health. He and his 6 children live in Pennsylvania.

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