Disc Medicine, Inc. Common Stock H.C. Wainwright 28th Annual Global Investment Conference

Yeah. Thanks for having us here, Doug. Last week at SOHO, very exciting data for us. It's a very exciting moment for the company at large. This is the third program now where we've shown POC data with the anti-TMPRSS6 antibody, our drug's called DISC-3405, was that by inhibiting this target, you're able to induce the body's own production of a hormone called hepcidin, which is the master regulator of iron. In polycythemia vera, these patients have systemically low levels of hepcidin, and the disease is characterized by uncontrollable growth of red blood cells, or called erythrocytosis. The thesis has always been, if you're able to increase hepcidin production and restrict iron, that can slow down this uncontrolled growth of red blood cells.

What we saw in this initial data cut is just that the drug is doing exactly what we expected it to do, across all the different parameters. We're able to see that the drug is able to induce hepcidin production. This results in iron restriction. That translates into very strong hematocrit control, which is very important for these thrombotic events. We reported that patients are feeling better, and that also that we're able to reduce phlebotomy burden. It was exciting to see this just in the first cut of data. We'll have an update at the end of the year. The profile is looking excellent. I should add that also the safety and tolerability, which we think is going to be something that is going to be important to be able to differentiate in this field, also looks stellar.

We believe we may have a leading profile here.

That's right. So this study studies 2 different dose regimens. One is Q2W, subQ Q2W, and the second cohort B, is also a single subQ injection, Q4W. Why we like the antibody approach so much is the PK/PD relationship is very tight. What we saw in the phase I study, in the healthy volunteers, is we're able to see iron restriction that should be relevant for a once monthly dosing. I should add that, in this study, there was a dose escalation portion, which started off at Q4W. Even at a Q4W dosing, it was a lower dosage, we were already able to see the mechanism engage. So there's reason to certainly believe that Q4W dosing, the drug will be active.

Sure. I think being able to control hematocrit fairly quickly does matter. I will say that there is a nuance about this study design that maybe might lead you to believe that there is an onset of action liability. We don't think that's the case. Just because there is a dose escalation portion, we started off at lower doses because this was the first patient study with the drug. Even at the lower doses, we were able to see the mechanism engaged in the first week. We see hepcidin increasing in the first week. In the healthy volunteer study, we were able to see hepcidin increase and iron reduce in the first week. We don't, in fact, even in some of the patients, we already saw phlebotomy reduction early on.

I think just sometimes the numbers get obscured because you're looking at phlebotomy, which is a downstream readout of the drug's activity. We expect the drug to be acting from the onset.