Okay, Shell has been mulling this over and over and its...

Okay, Shell has been mulling this over and over and its beginning to bug me!

Here we have similarly impressive ORR and PFS results with zero SAE in the two main sub-types of TCL. Now the expansion trial was supposedly a study primarily to focus on PTCL. However, we ended up with a few more CTCL patients being recruited during the expanded trial. Is this because the original CTCL patient continued to keep living on the low dose that it warranted further investigation since we already had ODD for PTCL and recruitment for rare diseases must be difficult?

My main questions are: What differentiates PTCL and CTCL cancer on a molecular level? What particular RAS pathway or Rho, Rac or Ral particular circuits does PTX100 inhibit in these two different subtypes of TCL... or is it the same and could it offer targeted therapy for all TCL cancers?.... hence why the broader TCL granted ODD?

Help! Not complainig Promise