Replies to post #189669 on Biotech Values

[poorgradstudent]

CLDN:

Do you think the basis for this could be endothelial expression of SERCA, or simply cardiomyocyte expression of SERCA that simply loses expression over time? I do understand at least partly the potential issues with AAV and potential carbohydrate recognition mismatch between species.

Perhaps for the endothelial expression, but my gut says unlikely. Myocardium is a mixture of cells, and unless they did some type of cell dissociation and sorting prior to the PCR, their persistence data would include all cell types. If there was disproportionate expression in endothelial cells or fibroblasts or whatnot, my expectation is that it would have registered in the PCR.

Having said that, this SERCA isoform is one of the best ways (if not THE best) to deal with CHF if expression can be directed and exist for the long haul.

We part ways here somewhat. Having read the HF literature for a while now, it seems that downregulation of proteins is a general trend during the heart's decompensation. I think the important question towards SERCA is whether its decrease is causative for altered cardiac function, or if there is another initiator(s) of declining cardiac function that, as part of the impact on cell phenotype, causes a change in cell phenotype that has an accompanying decrease in SERCA. Simply put, the old causation versus correlation problem.

In a similar vein, do you have a view on QURE?

Not too much. I had not followed their non-CV programs and, to my knowledge, there aren't many data available yet for their CV program.


For those interested, my twitter handle is @Ogut_Ozgur. The rest can be found from the profile on twitter..