An Urgent Message To All COVID-19 Healthcare Providers, To The Citizens of New York City, And To The American Public: Stopping The COVID-19 Kill Mechanism, Using CYCLOSPORINE.

Hooman Noorchashm
4 min readApr 1, 2020
Tolypocladium inflatum — the fungus from which CYCLOSPORINE is derived.

Today, as we have passed the threshold of 3000 American lives lost, I am compelled to write publicly. Because I fear that our government, our major academic medical centers and our press are likely to fail in acting with sufficient speed and vigor to protect us systemically — using ALL reasonable available means.

I write to inform you that all clinical and pathology data available so far almost certainly point to the fact that COVID-19's “kill mechanism” is a “HYPERIMMUNE state” consisting, in large part, of over-activation of T-cells that normally serve to protect us from infection.

In the case of COVID-19, this immunological overdrive, itself, is responsible for causing the patients’ lungs and other organs to fail in the advanced stage of infection— with the deadly consequences we are witnessing in New York City and elsewhere.

At present, our healthcare establishment and the US Food and Drug Administration (FDA) have yet to take ANY steps in the direction of opening the door to use of a widely available pharmacological arsenal of T-cell inhibitory drugs for treatment of COVID-19 mediated HYPERIMMUNITY.

Additionally, our prominent press outlets, though fully aware of the possibility, are also slow to urgently initiate the necessary national conversation about this issue in any meaningful way — to facilitate focus.

THIS IS AN HISTORIC ERROR IN JUDGEMENT on many levels — with time running out for America to prevent irreversible harm.

Here, for history’s sake, I am writing as a physician-scientist, as an immunologist and a citizen of the United States of America, to inform you that if we interrupt the hyperimmune T-cell activation state that is underway, by the time COVID-19 positive patients first require hospital care, we may stand a chance of protecting lives.

How do we do this?

A class of drugs, known as Calcineurin Inhibitors, the main trade-name for the generic version of which is CYCLOSPORINE, are the central player. With over 40 years of experience with this vastly available and scalable drug, we already know that it has a tolerable safety profile for transient use in patients — even in most those with co-morbidities.

CYCLOSPORINE, is derived from the fungus Tolypocladium inflatum — and is traditionally used in the case of organ transplants, psoriasis, Rheumatoid arthritis and Ulcerative Colitis to specifically dampen pathological T-cell responses by inhibiting the cytokine, Interleukin-2, which is central to the T-cell activation process. Additionally, this class of drugs are used as a key component of therapy in the case of a serious disease process known as “Cytokine Release Syndrome” (or, “Cytokine Storm”), which is nearly identical to what is being seen in critically ill COVID-19 positive patients. These drugs are easily tolerated by mouth and IV, especially in transient dosing — they are no less difficult to administer than antibiotics, most of which are also fungal derivatives.

In addition to their ability to specifically dampen T-cell responses well, Calcineurin Inhibitors have been shown to also specifically inhibit Coronavirus replication in several well-done experimental studies.

Here, I am informing you that treatment of COVID-19 positive hospital inpatients, at the Pre-ICU stage of their disease process, is highly likely to arrest the progression of the hyperimmune state that renders these patients critically ill and ultimately kills them.

I propose, here, that every symptomatic COVID-19 positive patients at the stage requiring hospitalization, be treated with:

Cyclosporine (2.5–4mg/kg/day in two divided doses — PO or IV)-plus-a Medrol steroid pack.

I propose, here, that every critically ill COVID-19 positive patient at the stage requiring ICU care be treated with:

Cyclosporine (4–10mg/kg/day — IV)-plus- the steroid, Decadron.

Unless we dampen the hyperimmune state that emerges in the later stage of COVID-19 infection (i.e., 7–10 days post exposure when symptoms start to worsen), we will continue to lose many precious American lives.

As of this writing, the T-cell specific inhibitory drug CYCLOSPORINE rests undeployed in our national and international arsenals — as COVID-19 drives a T-cell hyperimmune response that the POTUS has promised will kill well over 200,000 Americans in the next 2 months — and many more globally.

Why?!?

It is up to each and every one of you reading this article to use the word CYCLOSPORINE — and ask why it remains undeployed against COVID-19 disease….I suspect we will be sorry if we don’t.

Finally, if anyone reading this message is in a desperate position with worsening symptoms, you may reach me at noorchashm@gmail.com — I will discuss this potential treatment with you and will determine if you are candidate for transient off-label Cyclosporine use. In that case, I will do all I can to help get you this treatment efficiently.

Your friend in defense of the United States of America — and all those fighting to preserve precious lives in harms way across the world,

Hooman Noorchashm MD, PhD.

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Hooman Noorchashm

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.