Ensuring equitable access to targeted therapies: the regulatory perspective | S11E2

And, you know, I figure we'll kick things off just with an introduction for our audience on NTRK fusions.

You know, and I can kick things off.

And, you know, obviously the field of lung cancer has changed dramatically over the last, you know, 15 years with the recognition that lung cancer isn't just one disease.

It's really a distribution of various oncogenic drivers.

And we now have regulatory approvals of so many different targeted therapies.

And really, this has transformed management of disease for many of our patients.

NTRK fusions tend to be amongst the rarest.

We sometimes say in our clinic, Maybe you find one or two in a career, but these patients are out there and they really, really benefit from targeted therapies.

In some of the retrospective series, it looks like 0.1, 0.2% prevalence.

The nomenclature here can be a bit confusing.

So N-tracks are the names of the genes.

So N-track 1, 2, and 3 distinct genes.

The corresponding proteins are track A, B, and C.

And importantly, these drivers are mutually exclusive from others like EGFR or ALK.

And we also know that patients with N-track fusions really have distinct clinical pathologic characteristics.

We tend to see these in adenocarcinoma.

you know, never smokers, much like we do for many of our other targetable oncogenic drivers.

Critically, they confer sensitivity to targeted therapies.

And maybe Sanjay, you can tell us a little bit about kind of what you expect to see with these agents in clinic.

Yeah, thanks, Justin.

I mean, I think you're right.

The field of oncogene-addicted disease has been spawned by the finding of oncogenic drivers.

You know, EGFR was the first one in 2004.

And drugging a driver has been shown to cause rapid tumor shrinkage, which is durable.

And that has really stood the test of time with all of the drivers that we've identified, particularly when it comes to end track fusions in end track one, two, and three.