Yep that is very strong piece of 'proof of concept' that CLTX...

Yep that is very strong piece of 'proof of concept' that CLTX CAR-T was responsible for the tumor control, as the resected tumor should have regrown at the same pace of the distant reoccurrence.. instead tumor growth was contained at the injection site for 2 months.

That's exactly what you want to see and gives us a good steer as to what we can expect when we ramp up the dose as well as introduce intraventricular administration, which has shown to be able to reach distant reoccurrences in the brain as well as the spine.

A higher dose is important because what you want for CAR T therapy is to destroy as much of the tumor as quickly as possible, to avoid antigen escape/reoccurrence. This is what they term, persistence, and is a known limitation in the therapy, which basically means you only have a certain window in which the CAR T persists at the target region and kills tumor cells, before the level of CAR T cells diminishes over time, as well as the T cell / immune response. Once that declines, the tumor has a chance to regrow if it hasn't been adequately killed off.

It's shown that while a certain % of cancer cells need to express the 'target' ... once your immune system ramps up ... it is able to kill tumor cells with or without the 'target' i.e. there are so many T cells, NK cells and macrophages present on site.. that it is able eradicate the tumor cells expressing as well as not expressing the target (that is why we only need >20% MMP2 expression as a selection criteria).

And increasing your dose as well as introducing intraventricular administration is exactly how you can address this.

CLTX appears to kill tumor cells preferentially with MMP-2 expression is an important point, and speaks to potency assays...