“preclinical data for OnCarlytics is showing the same as single-agent CF33”
Well yea, that’s because OnCarlytics is CF33 + a gene to cause expression of CD19 on solid tumours. So it makes sense it performs similarly in the absence of the CD19 therapy?! The whole point of the therapy is to allow CD19 directed therapies previously only effective in blood cancers, to be effective against solid tumours.
So you stating “there’s only meaningful anti-cancer activity when you add an approved therapy in Blincyto” is actually confirming the value in the therapy. It confirms that oncarlytics allows a powerful CD19 targeted therapy currently only effective in blood cancers can now be used against solid tumours… I’m glad we are on the same page. It’s totally novel and never been done before!
If only it was as simple as treating fast growing tumours. The model you show is melanoma, which has more aggressive growth, but also has many therapies that can target it. The mouse model used in the oncarlytics preclinical data you quote (MDA-MB-468) is a proxy for triple negative breast cancer. I’m sure you’d agree if you plan to produce a therapy for hard to treat cancer like TNBC, it makes sense to use a mouse model that is representative/best suited to that cancer?! Similar to TNBC the mouse model used lacks estrogen, progesterone receptors and Her2 expression making it a very hard cancer to treat but also A GREAT MODEL TO USE TO TEST TNBC. It’s a reason why there are no therapies inclusive of immunotherapies that are effective against it. So showing clear efficacy preclinically is significant.
I wonder whether you are willfully ignorant or genuinely don’t have a good enough grasp on the science?! Not sure….but I’ll stick to valuing the word of the world renowned scientist and clinical experts.
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