Immuneering Corporation Class A Common Stock 12th Annual Cantor Fitzgerald Global Healthcare Conference

Sure. Well, thanks, Lee, for having me today. Thanks to the whole Cantor team, and thanks to everyone joining us. I co-founded this company 18 years ago, and the idea was really to engineer overall survival.

Figure out how to help cancer patients live longer. When you just come in as an engineer and you look at the data, the data shows that there's really two ways to keep cancer patients alive longer. You can attack the tumor, and you can protect the patient. But 99% of all the work in the field to date is focused on attacking the tumor.

We said, "What if you could do both? What if you could attack the tumor while protecting the patient? Could you help patients live longer and have better quality of life?" When I say protect the patient, I mean minimizing the side effects so patients can have better performance status, so they can be more likely to go on to second-line treatments- You can combine better.

I mean helping patients maintain their weight, their body mass, their strength, their stamina. I mean not driving the genetics of the tumor to be more aggressive. Right? All those things are about protecting the patient. We said if we can do that, protect the patient while attacking the tumor, we can help patients live longer and also help them live better, have better quality of life.

I think the technology that we developed really enabled us to pursue that strategy.

Absolutely. Yeah. So atebimetinib is our furthest along program.

It is a Deep Cyclic Inhibition of MEK and the MAPK pathway.

The MAPK pathway is the most common pathway in cancer. Within that pathway, MEK is a great target. It is downstream of RAS, it is downstream of RAF, and it is really hard for the tumor to get around an effective MEK inhibitor. It is kind of like you are targeting the narrow point of the funnel, or you are trying to blockade the Panama Canal as opposed to the Caribbean Sea.

So it is a really strategic target. In fact, it is a validated target, both clinically and commercially. First-generation MEK inhibitors have been shown to extend overall survival in BRAF mutant cancers in combination with RAF inhibitors. They have demonstrated themselves commercially as well. In 2025, there was $3.7 billion in revenue driven by MEK inhibitors, either alone or in combination with RAF inhibitors.

It is a target that is validated both clinically and commercially, and yet it has really only lived up to a fraction of its full potential. There are two main reasons why. Number one, the first-generation MEK inhibitors have all been really toxic, really poorly tolerated, and they have been limited mainly to BRAF mutant disease. When we designed atebimetinib, we focused on overcoming those two limitations.

It is novel composition of matter. We created it in-house. Brett Hall, our Chief Scientific Officer, is the lead inventor on the composition of matter patent, which was granted in the U.S. last summer. We designed it to work more broadly, to work not just in BRAF mutant disease, but also in RAS mutant disease, which is about 3 times as many patients as BRAF mutant disease. We did that by changing how it sits in the pocket so that it blocks RAF-mediated phosphorylation of MEK. That was the first thing we did, and then we said we need to give this much better tolerability.

in order for it to be combined, in order to protect patients, as I talked about earlier. In order to do that, we developed a new technology called Deep Cyclic Inhibition.