So does the patient illness even further delay the

So does the patient illness even further delay the escape of leronlimab from the subcutaneous compartment to the bloodstream?

MDV, I remember you made a comment that a sick covid patient's circulatory system was not the same as a regular person, and that the displacement from normal circulatory paramaters indicated a need for intravenous rather than subcutaneous injection.

Your description was highly technical, I couldn't understand it, but my takeaway was that sometimes sick patients need IV for a medicine they would normally get subcutaneously.

I looked at the old PRO140 HIV clinical trial papers. Lalezari is on all of them so google scholar "lalezari ccr5 pro140 pharmacokinetics" brings them up.

When LL was given by IV, peak blood concentration was obtained basically at the end of the 30 minute IV infusion and then serum LL decayed exponentially with a half-life time constant of about 3.1 days.

When LL was given by subcutaneious injection, the identical exponential decay half-life time constant of about 3.1 days was also observed.

What was different in the subcutaneous trial reports is that the peak leronlimab concentration was not achieved until two days after the injection.

In other words, it is clear that IV infusion shortens the time it takes to get LL into the bloodstream by about two days.

If memory serves, the peak LL blood concentration is also different, over 100 micrograms per milliliter in IV and only about 10 micrograms per milliliter in subcutaneous.

So looks to me like in healthy people, LL works faster by two days in IV vs. subcutaneous.

But thats healthy people. I have no clue, but if subQ absorption into the bloodstream is impaired in sick covid patients maybe it gets really bad?

A factor of two would effectively delay LL activity by four days compared to intravenous.

Seems like the subQ patients should be checked for serum LL levels to make sure the subQ absorption is OK?