Michael R. Bloomberg Accelerates Fight Against Global Coronavirus Pandemic
Bloomberg Philanthropies Announces New $40 Million Coronavirus Global Response Initiative

Coronavirus Local Response Initiative to Begin Virtual Convenings of U.S. Mayors on March 19

NEW YORK — Just days after Mike Bloomberg launched a program to help American mayors improve their coronavirus response, Bloomberg Philanthropies today announced additional actions and funding to combat the pandemic on a global scale. The new $40 million global initiative will support immediate action to prevent or slow the spread of COVID-19 in vulnerable low- and middle-income countries. Bloomberg Philanthropies will partner with the global health organization Vital Strategies on global response efforts, along with the World Health Organization (WHO), to support lower income countries and cities respond to the COVID-19 pandemic.

How does Ifenprodil work as a therapy for patients who experience respiratory complications?

Keep in mind that all of our data has been developed from animal models that mimic or match the human disease for which we are working to develop a treatment. In our initial research stages, we were investigating Ifenprodil for a disease of the lung called idiopathic pulmonary fibrosis (IPF). We used a murine animal model that created fibrosis tissue/scarring conditions in the lungs of the mice that we were studying. Ifenprodil showed a dramatic reduction in fibrosis in the treated arm of the study. We also put Ifenprodil up against two leading human treatments and it outperformed these two drugs. This told us that the drug is active in the lung and is reducing the amount of fibrosis that can build making breathing more difficult and reducing the oxygenation capacity of the lung tissue.

An independent study of Ifenprodil in H5N1 infected mice showed that the drug reduced mortality by 40%, reduced the acute lung injury and inflammation that occurs in the lungs after being infected. H5N1 is far more lethal a form of flu than COVID-19 and so the data suggests that we may see a similar if not a stronger response in humans infected with a far less aggressive or lethal form of the flu, being COVID-19.

We believe that the mechanistic activity of the drug is lessening the inflammatory response called the cytokine storm and as a result can possibly reduce the duration and severity of a COVID-19 infection.

Ifenprodil is an inhibitor of the NMDA receptor,[1] specifically of GluN1 (glycine-binding NMDA receptor subunit 1) and GluN2B (glutamate-binding NMDA receptor subunit 2) subunits.[2] Additionally, ifenprodil inhibits GIRK channels, and interacts with alpha1 adrenergic, serotonin, and sigma receptors.[3]

NMDA receptors are multimeric ionotropic glutamate receptors composed of four subunits. GluN1 is obligate for functional expression. Other subunits include GluN2A, GluN2B, and the more recently discovered GluN3 subunits. Ifenprodil selectively blocks NMDA receptors containing the GluN2B subunit.

An anti-inflammatory drug developed at Scripps Research 25 years ago is now being tested as a way to prevent acute respiratory distress in patients with COVID-19, the pandemic disease caused by the novel coronavirus.

The drug, a monoclonal antibody now owned by the pharmaceutical company Implicit Bioscience, is planned to be used in a small clinical trial taking place at four sites in Italy, Spain, Australia and Singapore.

The trial will assess whether the drug, known as IC14, can temper the immune system's response to coronavirus infection of the lungs, thus preventing dangerous levels of inflammation seen in patients with severe cases of the disease.

"Patients with severe COVID-19 often progress to acute respiratory distress, where inflammation results in lung damage and subsequent multiple organ failure," says Richard Ulevitch, Ph.D., a professor and former chairman of Immunology at Scripps Research, who originally developed the drug. "By dampening the innate immune system's response to the infection, IC14 may prevent patients from spiraling out of control and improve their chances for recovery."

The drug targets an immune system protein called CD14, that Ulevitch and Scripps Research colleagues first linked to innate immunity and inflammation in work started in the mid-1980s.

Charlotte's Atrium Health is participating in an international clinical trial to treat coronavirus (Covid-19) patients.

The trial is with Selinexor, an oral drug used to treat multiple myeloma, a type of cancer in bone marrow. The anti-viral and anti-inflammatory drug has also been shown to kill the Covid-19 virus. This trial, known as the XPORT trial, spans about 15 countries, including more than 10 sites in the United States, said Dr. Zainab Shahid, medical director of bone marrow transplant infectious diseases at Levine Cancer Institute. Shahid is the trial's principal investigator.

Patients at Carolinas Medical Center, Atrium Health-Cabarrus, Atrium Health-Pineville and Atrium Health-University may be eligible to participate. They take the pill every other day and can do so at home. The trial lasts two weeks.

Shahid hopes to enroll one to two patients per week. Atrium screened its first patient on Tuesday morning, she said. Part of her role is to work with doctors to find eligible patients and then connect those patients with the clinical trial team. The trial is for patients with more serious Covid-19 symptoms — they could be hospitalized with upper-respiratory issues, for example. Supportive care is more appropriate for mild cases, Shahid said.

Selinexor (INN, trade name Xpovio; development code KPT-330) is a selective inhibitor of nuclear export used as an anti-cancer drug. It works by binding to exportin 1 and thus blocking the transport of several proteins involved in cancer-cell growth from the cell nucleus to the cytoplasm, which ultimately arrests the cell cycle and leads to apoptosis.[1] It is the first drug with this mechanism of action.[2][3]

Selinexor was granted accelerated approval by the U.S. Food and Drug Administration (FDA) in July 2019, for use in combination with the corticosteroid dexamethasone for the treatment of adult patients with relapsed refractory multiple myeloma (RRMM) who have received at least four prior therapies and whose disease is resistant to several other forms of treatment, including at least two proteasome inhibitors, at least two immunomodulatory agents, and an anti-CD38 monoclonal antibody.[4] In clinical trials, it was associated with a high incidence of severe side effects, including low platelet counts and low blood sodium levels.[3][5][6]

Xpovio's price tag also raised eyebrows. Steensma called it “ridiculous to charge $22,000 per month for such a marginal drug.” Rajkumar went further. “It's laughable to think selinexor is worth $22,000

The only colour piercing the dimness of the hotel bar was the amber liquid flickering in the glass before him. As I approached, he raised his eyes to greet me with a nod before staring back down into his tumbler of whiskey. I sank onto the plush sofa, exhausted. On cue, his familiar voice sounded imposingly morose. ‘Yanis,’ he said, ‘you made a big mistake.’

In the deep of a spring night a gentleness descends on Washington, DC that is unimaginable during the day. As the politicos, the lobbyists and the hangers-on melt away, the air empties of tension and the bars are abandoned to the few with no reason to be up at dawn and to the even fewer whose burdens trump sleep. That night, as on the previous eighty-one nights, or indeed the eighty-one nights that were to follow, I was one of the latter.

It had taken me fifteen minutes to walk, shrouded in darkness, from 700 19th Street NW, the International Monetary Fund’s building, to the hotel bar where I was to meet him. I had never imagined that a short solitary stroll in nondescript DC could be so restorative. The prospect of meeting the great man added to my sense of relief: after fifteen hours across the table from powerful people too banal or too frightened to speak their minds, I was about to meet a figure of great influence in Washington and beyond, a man no one can accuse of either banality or timidity.

All that changed with his acerbic opening statement, made more chilling by the dim light and shifting shadows. Faking steeliness, I replied, ‘And what mistake was that, Larry?’ ‘You won the election!’ came his answer.

It was 16 April 2015, the very middle of my brief tenure as finance minister of Greece. Less than six months earlier I had been living the life of an academic, teaching at the Lyndon B. Johnson School of Public Affairs at the University of Texas at Austin while on leave from the University of Athens. But in January my life had changed utterly when I was elected a member of the Greek parliament. I had made only one campaign promise: that I would do everything I could to rescue my country from the debt bondage and crushing austerity being imposed on it by its European neighbours and the IMF. It was that promise that had brought me to this city and – with the assistance of my close team member Elena Paraniti, who had brokered the meeting and accompanied me that night – to this bar.

Smiling at his dry humour and to hide my trepidation, my immediate thought was, Is this how he intends to stiffen my resolve against an empire of foes? I took solace from the recollection that the seventy-first secretary of the United States Treasury and twenty-seventh president of Harvard is not known for his soothing style.

Determined to delay the serious business ahead of us a few moments more, I signalled to the bartender for a whiskey of my own and said, ‘Before you tell me about my “mistake”, let me say, Larry, how important your messages of support and advice have been in the past weeks. I am truly grateful. Especially as for years I have been referring to you as the Prince of Darkness.’

Unperturbed, Larry Summers replied, ‘At least you called me a prince. I have been called worse.’

Nicotine is a nonselective agonist of the ?7Ach receptor and is able to suppress the production of proinflammatory cytokines by mimicking the binding of acetylcholine. It has been demonstrated that nicotine can selectively reduce the inflammatory response in a number of infection scenarios, including Legionella pneumophila (54) and Chlamydia pneumoniae (55) infection; however, it is highly unlikely that nicotine will ever be used clinically due to its toxicity, addictive nature, and lack of specificity.