David Southwell
speaker
275 appearances
1 recordings
1 series
first heard Feb 2026
last heard 28 Feb
David Southwell’s voice in public audio — every appearance, attributed to the second.
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recordings per month · last 12 monthsRecordings per month over the last 12 months — 1 in all, peaking in Feb 2026 with 1.
Appearances
So one of the things that's interesting about our drug is it leaves normal cells alone and we leave T cells alone.
So immunotherapy for cancer almost universally involves T cells, CD4 and CD8 T cells.
And you don't want to mess with those because that is the body's natural immune response to a foreign
invader, otherwise known as a tumor.
And there are different approaches to doing it.
One is to overcome the checkpoints, you know, PD-1, PD-L1 inhibitors, for example.
The difficulty with T cells is that oftentimes the T cells inside a tumor are exhausted.
And which is why the response rate on some of the checkpoint inhibitors is not as much as you might like.
So there's a whole different ways of dealing with immunotherapy.
We're really different.
We're a totally different mechanism of action that applies in hot tumors, you know, hot tumors being ones that are very prone to immunotherapy, cold tumors and others.
And there are some tumors that are not particularly chromosomally unstable, colon cancer being an example, but 80% of tumors are chromosomally unstable.
So that creates a huge market for us.
And the question from a business perspective is, where do we go?
And we started in ovarian cancer, platinum resistant ovarian cancer.
And our approach there is to sort of go after that.
But now that we've discovered a biomarker, the goal is to look at, we've also figured out the prevalence of that biomarker.
In other words, how many other cancers is it expressed in?
Well, I think what we're doing is relatively straightforward.
It's straightforward to explain.
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