Beyond its effects on inflammation and complement and their relation to cytokine storm, here is another article that at least SEEMS to add credence and plausibility to the idea that Apabetalone could help w COVID-19.

I dearly hope Don has some genuine progress on this and will report soon.

Or, to the more clinically minded - am I wrong here?

https://www.medscape.com/viewarticle/929496

Some COVID-19 patients have very low oxygen, but don't seem to know it. They aren't breathing hard, and while they're sick, they can talk and sit up and generally seem to be functioning better than someone whose body is starving for oxygen. 

When doctors check their lungs on CT scans, they seem mostly clear, a marked contrast from the images seen in pneumonia patients whose lungs are cloudy and filled with fluid.

These patients are presenting a challenge to doctors who are scrambling to understand how they could have such low oxygen but also lungs that appear to be open. 

In a clinical update posted in JAMA, John J. Marini, MD, professor of Medicine at the University of Minnesota and Intensivist at Regions Hospital in Minneapolis/St. Paul and Luciano Gattinoni, MD, at the Medical University of Gottingen, in Germany, say the problem for these patients doesn't only lie in the tiny air sacs of the lungs, but also in the legions of blood vessels that ferry blood through them.

Normally, when a part of the lung becomes damaged, tiny blood vessels constrict to redirect blood to areas of the lung that are still working. This mechanism protects the body from a sudden drop in oxygen.

Emerging evidence suggests that the virus that causes COVID-19 can infect the lining of blood vessels. That infection plus an outsized immune response by the body, prevents the vessels from constricting the way they normally would. This causes blood to flow through damaged parts of the lungs where it can't pick up oxygen. Oxygen levels fall.

WebMD spoke with Marini about why this happens and how doctors might need to adapt their treatment plans to improve outcomes for patients.

WebMD: What are you hearing from you colleagues who are treating COVID-19 patients?

Marini: Doctors that I know personally are very concerned because they do not understand what's going on. These patients are not responding in the expected ways to their usual interventions.

WebMD: I know this is mostly a debate that's happening between doctors, but can you try to explain what's going on in a way that patients might understand?

Marini: I think I can. The viral infection is of the endothelium, the lining of the blood vessels, throughout the body. The lung gets the most blood flow of any organ of the body, so the potential for trouble to develop in the lung due to the vascular insult is very high. 

Once that happens, it destroys normal mechanisms that match oxygen need to oxygen availability in the air, and people become blue.

However, unlike most cases of severe pneumonia, the lung stays flexible. Doctors call this respiratory system compliance. In the early phase of the disease in many COVID-19 patients, lungs are highly compliant, which is not usually the case in acute respiratory distress syndrome, or ARDS.

Many people don't even feel very short of breath. They know something is wrong, but they don't feel very short of breath, despite the low oxygen going to their organs.

Later in the infection, when the lung becomes very damaged from the virus, and the patient starts to really make strenuous efforts to breathe, the lung begins to pick up fluid. The lung shrinks, forming what we call a baby lung, and you get the more conventional ARDS.

WebMD: There are guidelines that doctors use to treat ARDS. They tell doctors how to use a ventilator. 

Marini: Yes. They try to make sure that enough air sacs of the lung stay open, but not too stretched, since too much pressure from the ventilator can damage the lung.