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Once other key biomarker is molecule Vascular Cell Adhesion Molecule VCAM is very important because VCAM allow immune cells to migrate through blood vessel walls . We did not know that LRM reduces VCAM until NASH, but now we have now observed a reduction from mean change to baseline in week 14 for the NASH 350 mg for VCAM and this is important because it has application to other inflammatory markers that are reduced. So further trials need to be conducted with larger numbers, but the exploratory biomarker analysis may be very relevant for informing about future research in other disease states including cancer. Dr. Kelly can you provide an update in oncology.

My statement:

This reduction in VCAM is very small though, minimal, if you look at the heat map. To me it looks negligible.
https://www.postersessiononline.eu/173580348_...8274_3.png
But I guess if you have the actual values, it may be more significant.
Now since it is reduced, modestly, more reduced in 350mg than 700, it would point to the fact that when the systems are in the mode of metabolizing fibrosis, VCAM is reduced and when in the mode of macrophage attack of the dying hepatocytes, VCAM would remain same or modestly increase.

32:20 Dr. Scott Kelly: Yes, Chris left with a perfect thing about VCAM b/c we do believe VCAM is important for oncology in LRM. What we are doing now, we are currently evaluating opportunities KOM Smithing ford, in mTNBC program for LRM in combo with a current SOC as well as colon cancer trial , we have animal and human data for mTNBC as well as animal data on the effects of LRM on colon cancer.

We are very encouraged by the exploratory biomarkers data from NASH at the 350mg dose as many of the biomarkers that LRM appeared to effect in NASH are important for oncology program and this exploratory data may inform future trials in oncology.

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from: https://www.reddit.com/r/LeronLimab_Times/com...;context=3

If you lower VCAM, you lower the capacity for the immune cells to pass through the vessel walls. You also lower the capacity for tumor cells, circulating tumor cells, CAMLs, Cancer Associated Macrophage Like cells, metastasis from passing through the vessel walls and causing metastasis to another areas. So we will be using this reduction in VCAM, albeit, minimal as per the heat map, but may be more definitive once we can see the data. Right now, we only have the difference from start of trial to end. We will be using this to determine effectiveness of LRM treatment in colon cancer and mTNBC.

Did anyone understand this?: KOM Smithing ford

and:

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36:07 Scott Kelly: Sure, I'll take the positive news on the Science 1st. We are very encouraged by the fact of LRM on the biomarkers and NASH. Many of these same biomarkers are supported by the literature to be important in our oncology program including CCL2, CCL5, CCL18, VCAM and VEGF. Some of these biomarkers also correlate with the potential to decrease metastasis, control the tumor microenvironment and correlate with antifibrosis and NASH . We are also seeing some potential benefits of certain biomarkers in cardiovascular disease .

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taken from:
https://www.reddit.com/r/LeronLimab_Times/com...;context=3

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The VCAM-1 protein mediates the adhesion of lymphocytes, monocytes, eosinophils, and basophils to vascular endothelium. It also functions in leukocyte-endothelial cell signal transduction, and it may play a role in the development of atherosclerosis and rheumatoid arthritis.

Upregulation of VCAM-1 in endothelial cells by cytokines occurs as a result of increased gene transcription (e.g., in response to Tumor necrosis factor-alpha (TNF-α) and Interleukin-1 (IL-1)) and through stabilization of Messenger RNA (mRNA) (e.g., Interleukin-4 (IL-4)). The promoter region of the VCAM-1 gene contains functional tandem NF-κB (nuclear factor-kappa sites. The sustained expression of VCAM-1 lasts over 24 hours.

Primarily, the VCAM-1 protein is an endothelial ligand for VLA-4 (Very Late Antigen-4 or integrin α4β1) of the β1 subfamily of integrins. VCAM-1 expression has also been observed in other cell types (e.g., smooth muscle cells). It has also been shown to interact with EZR[7] and Moesin.[7]

VCAM-1 is also up regulate if vWF (Von Willebrand Factor) is given in Knock out ADMATS13 mice but not on mice without KO. [8]

CD106 also exists on the surface of some subpopulations of mesenchymal stem cells(MSC).[9]

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from: https://en.wikipedia.org/wiki/VCAM-1

I don't see the correlation of VCAM to asthma. Even if LRM lowers it a bit, asthma has more to do with reduction of air flow due to inflammation of air ways and thickening of the walls of the air ways so air can't get through. That's not related to passing macrophages through arterial walls. It is also not related to the thinning of the blood which is what aspirin does.
Yes, aspirin can be all those things and more so with increased dose.