Trastuzumab emtansine

We saw this trial in the second line setting.

It just blew TDM1 out of the water.

And then all of a sudden, people realized that the first line trials, which just got reported incidentally after four years, were going to be very promising.

They turned out positive neoadjuvant, adjuvant.

I had a double mastectomy about three weeks after that, and then they still found a little bit of residual cancer in my lymph nodes that they had removed, so then that meant nine more months of treatment.

I had to do 25 cycles of radiation and nine more months of a low-dose chemo called Kadcyla.

Wow.

Yeah.

And, of course, I don't have to tell this audience what else has been going on in HER2-positive disease.

First, the Catherine trial with TDM1, but then in the emergence of TDXD, eventually coming out to the last ASCO meeting a year ago where we saw Destiny Breast 09 really completely changing the whole apple cart.

But Lisa, one of the things I've been thinking about is that over the years, we've done so many programs on HER2, but yet we haven't talked that much about endocrine therapy.

I feel like there's been so much excitement about using anti-HER therapy that I wonder whether we kind of left it behind.

HER2 pathway inhibition is the dominant established driver of LV dysfunction.

What do the data show? TDM1 has low cardiac event signal.

T-DXd shows higher variable LVF decline.

Trop-2 directed SG and TATO-DXd show limited cardiac signals.

They've reduced it by 20%.

So why is that? Just to give me a bit more quality of life because this drug that I'm on, the TDM-1, is very much a – what did I say? It's very much – They say it makes you really, really tired and fatigued.

So he's been testing with his patients, being able to like, you know, if you're about to go on a holiday, for example, maybe two weeks before, get a massive dose of it and like ramp it up to like 150 and like you'll be really sick.

And then like you could probably have like six weeks off or something.