The pre-print was incredible.
This paper clearly demonstrates Dr. BP's brilliance in approach to the use of diagnostics for the sake supporting the mechanisms of action for Leronlimab in treating Covid. Here’s my breakdown:
Cytokine Quantitation – use of flow cytometry and subsequent ELISA confirmatory testing to measure the hypothesized reduction of cytokines post Leronlimab administration.
Immunorestoration – use of flow cytometry via anti-cell surface proteins measures quantity of certain immune cells (Cd8+/CD4+).
CCR5 receptor occupancy – use of flow cytometry to measure loss of signal of CCR5 due to binding of Leronlimab over time.
Plasma viral load quantitation – use of Qiagen Viral mini kit (Qiagen is an industry standard in nucleic acid sequencing. I know because I work in next gen sequencing and we use their kits) to extract viral RNA. Use of Digital droplet PCR to quantitate the actual viral cDNA.
Single Cell RNA sequencing – used NextSeq500 (also an industry standard used at my job) to identify gene expression of pro-inflammatory molecules and anti-viral molecules in healthy vs. 2 covid infected patients.
Methodologically, BP is making sure that every mechanism of action they SAY Leronlimab has, they can support with data. Calming cytokine storm, immune-restoration, plasma load reduction. Also, doing the Single cell RNA sequencing was a great move because it set up a control to compare gene expression against that confirms differential gene expression as a result of leronlimab administration.
But the real genius is the use of the receptor occupancy assay. This assay, in my opinion is the nail in the coffin with respect to any doubts as the whether or not it’s ACTUALLY Leronlimab causing these other metric changes.
The CCR5 occupancy assay clearly demonstrates that over the course of treatment, the more CCR5 is bound to monocytes, macrophages and lymphocytes (d. RO: Bulk T cells / e. RO: Monocytes) – the less cytokines you see (a), the more immune-restoration occurs (b) and the lower the viral load is (f).
I expect the scientific and medical community to rally in support of Leronlimab at this point. I also have no doubt that the interim analysis of our mild/moderate study will be impressive and primary endpoint will be met. Just a matter of time now
This paper clearly demonstrates Dr. BP's brilliance in approach to the use of diagnostics for the sake supporting the mechanisms of action for Leronlimab in treating Covid. Here’s my breakdown:
Cytokine Quantitation – use of flow cytometry and subsequent ELISA confirmatory testing to measure the hypothesized reduction of cytokines post Leronlimab administration.
Immunorestoration – use of flow cytometry via anti-cell surface proteins measures quantity of certain immune cells (Cd8+/CD4+).
CCR5 receptor occupancy – use of flow cytometry to measure loss of signal of CCR5 due to binding of Leronlimab over time.
Plasma viral load quantitation – use of Qiagen Viral mini kit (Qiagen is an industry standard in nucleic acid sequencing. I know because I work in next gen sequencing and we use their kits) to extract viral RNA. Use of Digital droplet PCR to quantitate the actual viral cDNA.
Single Cell RNA sequencing – used NextSeq500 (also an industry standard used at my job) to identify gene expression of pro-inflammatory molecules and anti-viral molecules in healthy vs. 2 covid infected patients.
Methodologically, BP is making sure that every mechanism of action they SAY Leronlimab has, they can support with data. Calming cytokine storm, immune-restoration, plasma load reduction. Also, doing the Single cell RNA sequencing was a great move because it set up a control to compare gene expression against that confirms differential gene expression as a result of leronlimab administration.
But the real genius is the use of the receptor occupancy assay. This assay, in my opinion is the nail in the coffin with respect to any doubts as the whether or not it’s ACTUALLY Leronlimab causing these other metric changes.
The CCR5 occupancy assay clearly demonstrates that over the course of treatment, the more CCR5 is bound to monocytes, macrophages and lymphocytes (d. RO: Bulk T cells / e. RO: Monocytes) – the less cytokines you see (a), the more immune-restoration occurs (b) and the lower the viral load is (f).
I expect the scientific and medical community to rally in support of Leronlimab at this point. I also have no doubt that the interim analysis of our mild/moderate study will be impressive and primary endpoint will be met. Just a matter of time now
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