Dr. Peter Attia
speaker
5,258 appearances
36 recordings
6 series
first heard Jan 2024
last heard Jun 2025
Dr. Peter Attia’s voice in public audio — every appearance, attributed to the second.
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Appearances
And why do those patients with marrow that's still producing CD20 positive cells not go on in a constant state of lymphoma requiring? In other words, why is it that you can treat this and create a durable remission?
So it's just getting rid of enough of the diseased B cells until you get the load down low enough that the immune system can wipe out the clone.
What was the price of these drugs at the time they came out? Were these the first chemotherapeutic agents, or you kind of want to distinguish them from traditional chemo, but were these the first oncology drugs that came with big price tags?
And about this time, we get the whole anti-VEGF story, right? Yeah.
That was... So Judah Folkman over at Boston Children's.
Yeah. I never had the chance to meet him.
I've never met Judah. He wrote a fantastic book that I read in medical school, poured over the book. I'm blanking on the name of it. Do you remember the book? It was his story.
Again, a beautiful story.
You know, the saying that I love is it's the description of science as a beautiful, compelling hypothesis slayed by an ugly fact.
Mostly human.
This was the first phase one. So you're going very low dose. We're going to dose- Very low. That's the first time it's going into a human.
And this is also mid-90s. Yeah, yeah. This is all happening when you arrive.
I mean, what a time to be a Genentech.
Wow.
How are you picking the cancer to study something like this? Herceptin's obvious because you're targeting a receptor.
Yeah, they're easy. You know what you're doing. But here you could be targeting anything.
Why is that? You've got the IL-2 stuff going on where you've got 10% of people will respond to it, but 90% won't.
These were patients with metastatic breast cancer?
And the standard you're going to hold yourself to in the phase two is 50% shrinkage?
This is a great time to actually hit pause. I wanted to do this later, but I think this is the right drug to go through two things. One, even though I've done this probably half a dozen times on the podcast, you should never assume somebody remembers it. I want people to understand what the difference is between a phase one, a phase two, a phase three study. Also understand what's preclinical.
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