IDH2

And you can see that quicker.

You know, if you, early days of, Adifa and Acidna basically it was like there's AML where they needed IDH2 testing and it was you look at the fact that prior to launch even there was no testing going on for the IDH2 and there was a big effort on the part of the medical team to kind of help drive that but that was all based off of insights coming in from the medical team saying hey this pathologist is not doing this testing or This group doesn't even have it on the gene panel.

These people don't even know that IDH2 is involved in AML.

You know, there's a number of different issues there, and that has to come together.

Now, those insights kind of get passed over the fence, let's say, to the market access team to, you know, to make sure that testing is reimbursed properly.

And so you can sort of track when that, when those insights come in to show how that directly derives.

Now, when the launch actually comes, everybody's testing for IDH two up to like 97% testing.

And now you don't have that as a, as a, as a, as a barrier that needs that, that, you know, those patients that actually are IDH2 positive get the N-acidinib that they are, they benefit greatly from that effort.

Targeted drugs, targeting certain proteins and certain gene mutations are another avenue.

For example, some patients with MDS may have something called an IDH1 or IDH2 mutations.

We have drugs that can target these mutations, and there's still more research going on to how to optimize that type of targeted therapy.

There is a lot of thought that inflammation is a unique part of MDS, meaning inflammation can lead to the development and progression of MDS and inflammation can cause your blood counts to be lower.

And it's best in patients under the age of 60 with less than 5% blasts and if they have PNH clone that is positive.

And then IDH mutated lower risk after failure of ESAs, you can also consider the IDH1 inhibitor ivosidenib or enasidenib, which is a IDH2 inhibitor.

Definitely.

So I have to laugh because even though we've taken our boards now five years ago, when you, when I read or when you read the lenalidomide for deletion 5q low-risk MDS, I immediately thought, "I know that because there was a question on it." [laughs]

So that's azacitidine, which is 75 milligram per meter squared for seven days every four weeks, category one, and it's the only agent with a phase 3 survival benefit, or decitabine 20 milligrams per meter squared for five days every four weeks for at least four to six cycles.

And then there's also oral decitabine, cedirotinib, which is an acceptable substitute, uh, for the IV decitabine.

And then venetoclax may be added to the hypomethylating backbone in select patients, as well as IDH inhibitors, the ones we just talked about, ivosidenib, as well as here is olutasidenib for mutated IDH1, and then enasidenib for mutated IDH2.

And then transplant-eligible patients may go directly to transplant or receive hypomethylating chemo agents to bridge to get the blast under 5%.

You know, the other portion that was part of the passion project for me is they came to me originally for gliomas and brain cancer mutations.

And so we have a product called NeuroInsight that's for IDH1, IDH2.

IDH2 doesn't have a really good IHC around it, so immediately we would add 15% market share to a couple companies that already have IDH drugs out.

And our initial studies in that show that we're better than the IHC, very quickly.

And my father passed away of aglemo brain cancer.