Okay.

Talk about the concept.

What are we doing? Because that's also related to your previous question.

Like, what is the concept of a prayer? And then we can talk about the responses.

So synthetic lethality and targeted therapy, what does it mean? And how is that different than chemotherapy? I kind of touched on it, that chemotherapy kills every dividing cell.

In synthetic lethality, I said that we're matching the drug with the disease.

So think about a cell with two backup systems, two pathways, right? When the two backup systems are intact, they're functioning, the cell is alive.

I

What have you learned in practice and how you have a more meaningfully wider therapeutic window, do you think? What have you learned about the assets to date?

Chris, this is a key question and very important topic to discuss because as you said, conceptually, we're not the first one to show that by targeting V1, you can shrinkage tumor.

But the other drugs, they had some liabilities.

They couldn't get the therapeutic window to work.

That was ACD-1775, which before that was MK-1775.

So the toxicity was just too high.

And what we did, we went back to the drawing board.

Can you tell us a little bit about how that works and kind of where you are in clinical development with that product?

So what have researchers learned from those earlier programs, and how has APR-1051 of yours designed to address those limitations?

So, Erin, this is a great question because you touched on the liabilities that are associated with the other WEE1, and what we did, before we even started the program, we went and looked at every molecule, every program, every patients that has been treated with it, preclinical data as well, and we have identified an- another group of enzymes that is not WEE1 related.

It's a PLK.

It's another, um, um, group of enzymes that are-- seems to not have selected for.

So the other WEE1 seems to inhibit both WEE1 and the PLK family.

So we went back to the drawing board, and we created a molecule that is very selective to WEE1 with minimal effect on this family of, uh, enzymes, the PLK.

And that's what we saw-- Well, that's what we're seeing.

Okay, before I let you go, talk to us a little bit about where you see in the next handful of years, uh, w- what, what's on the roadmap for Aprea, and then from a, from a field-wide perspective, you know, how do you see precision medicine, whether it be from a clinician or researcher perspective or perhaps even, you know, just your perspective as, as your role at Aprea, where do you see it going over the next few years?