Asthika Goonewardene: Got it. And then
Fred Schwarzer: And then I’d also that we’ve looked at those specific patients.
Asthika Goonewardene: Oh, yes, yes. And then
Fred Schwarzer: How they’re relative fold increase in caspase
Chris Takimoto: Yes, so we have those data. We’ve looked at things in terms of those patients that have shown seem to see clinical benefit and things. And again, it’s just small numbers, so we really can’t draw any conclusions. So we don’t really have anything to share with you right now, although obviously we’re going to be looking at this pharmacodynamic biomarker and correlating that with all different sort of other clinical endpoints in this study, particularly as we move forward.
Asthika Goonewardene: Got it. Okay. And then Chris, I mean, the slide with the biomarkers suggests that there’s 17 patients or so who’ve been treated at 10 milligrams per kg. Could you maybe give us some color on that about what €“ how many of those patients had colorectal cancer? Or if you can’t tell us that, was the distribution similar the percentage of colorectal cancer patients? Was the distribution similar to that seen as a 3 mg/kg dose?
Chris Takimoto: Yes. Yes. So the answer to the last part of your question is no, it’s actually different. So the data that we’re showing you here is a combination of the monotherapy dose escalation patients, which were in all tumor types, as well as patients that were in the FOLFIRI combination arm. And we previously disclosed that we only treated three patients with at 10 milligrams per kilogram in combination with FOLFIRI, not only one of those was a colorectal cancer patient. And because of the expansion at 3 milligrams per kilogram with FOLFIRI, the majority of patients that were showing you with these biomarker changes in the 3 milligram per kilogram cohort are actually colorectal cancer patients that are being treated with in combination with FOLFIRI.
But that being said, one of the things obviously that is a key question is how much, particularly for the combination patients, how much of this biomarker change is being driven by our IGM-8444 molecule, and how much is being driven just by chemotherapy. And what we’ll say, again, with small numbers, but when we look at this in our dataset. We don’t see much of an effect of FOLFIRI chemotherapy on this marker. So we think it is likely more specific for the action of IGM-8444. But in our randomized study, we will have a control arm and we will obviously continue to measure this. We will have more definitive data to share with you to really address that question.
Asthika Goonewardene: Great. Thanks for the call there, Chris. Fred, I got one last for you. You said at some point, I’m using air quotes here for presenting data from the Phase 1 study on the different cohorts. Can I, easy to say at least one of them in some point this year.
Fred Schwarzer: What are you talking? The imvotamab study?
Asthika Goonewardene: No, IGM-8444.
Fred Schwarzer: IGM-8444. We have €“ I’m being really honest in saying we have not made a decision when we would do that. I would say that sometime this year is a €“ would be a reasonable hope, at least for some of those. But we honestly just have not decided. We’ve been so focused on getting the randomized study up and running and these new biomarker data that’s really been our focus. And we’ll turn to that question that you’ve asked shortly I think.
Asthika Goonewardene: Excellent. Thanks guys. I really appreciate the questions.
Fred Schwarzer: Okay. Thank you.
Operator: Thank you. And I would now like to turn the conference back to Fred Schwarzer, Chief Executive Officer for the closing remarks.
Fred Schwarzer: I’d like to thank you all for joining us on today’s call, and we greatly appreciate your support. Thank you.
Operator: And this concludes today’s conference call. Thank you for participating. You may now disconnect.
