I would say, the type of rash that we see, cetuximab rash is typically the acne form rash. We see some of that, Grade 1, Grade 2. There are also, as Wayne mentioned, maculopapular rashes, which are maybe more T-cell, involved T-cells. So I think we’re going to have to learn more about it, but we’re not worried about it because it’s mostly Grade 1, 2. In fact, across the entire study, the incidence of rash across the entire 35 patients was 40% and just about all Grade 1, 2 are manageable. So we’re really encouraged by the AE profile here, not to mention the CRS profile, which really quite frankly surprised us to the upside.
Joe Catanzaro: I guess maybe my follow-up for the pancreatic cancer patient that had that deep response and then subsequent progression, wondering if you could maybe elaborate a little bit more on that progression event. Was it a new lesion, growth of a target lesion? If it was a new lesion, maybe you’re able to sort of profile it and see what’s going on? Just anything you could say there, I guess, would be interesting.
Chris Ogden: Yes. I could provide some details on that. This is a patient that was treated with the 6 milligram non-step-dosing, had a confirmed partial response that’s strikingly with over 80% reduction in measurable tumor burden. The patient did progress based on growth of the target lesion from the nadir as well as the appearance of, I think, of one new target lesion, I’m sorry, one new lesion. So, that was the nature of the progression on that particular patient. But all through that treatment course, the patient did quite well clinically. It was just based on the radiographic progression there.
Joe Catanzaro: And maybe if I could just squeeze in one more quick one, maybe going back to an earlier question. Just if you could maybe speculate more on what you think is maybe going on in MSS CRC. It seems mechanistically like you are seeing T-cell in filtration but that’s not translating to tumor reduction. So I’m wondering if you have any other sort of hypotheses of what may be going on in those patients? Thanks.
Sean McCarthy: I think mechanistically, it’s really interesting, when we think about how T-cell engagers work overall, right, CD3 combined with the tumor antigen, we think of these typically as being MHC non restricted mechanisms that may very well be what’s going on, but there could be more that’s necessary to really mount an anti-tumor response. I think we’re again in the field, I think there’s more to be learned about specifically how CD3 T-cell engagers kill cancer cells. Clearly, we’re doing it in pancreatic cancer. We’re getting the T-cells there in CRC, but it draws one’s attention to thinking about what combination strategies could get you to actual objective tumor responses. So, I think more work to do there in some of the basic science and then also clinical work that we can do in terms of clinical combinations It’s quite intriguing.
Operator: And for your next question, it comes from the line of Etzer Darout from BMO Capital Markets.
Etzer Darout: Just wondered if you could maybe talk through your current thoughts on sort of the step versus the non-step dosing, particularly in the pancreatic patients that sort of had to response and how you’re kind of thinking about potentially moving one or the other option forward as you sort of expand the patients? And then, I don’t know if you said this specifically, but about sort of the EGFR expressions across sort of the patients that you’ve seen so far? Is it that you’re going to moving forward you will look at EGFR expressions or is there an opportunity to kind of look at EGFR expressions across the folks that you’ve already sort of enrolled in the study? I don’t know if I caught that correctly. Thank you.
Sean McCarthy: Yes. Thanks, Etzer. In terms of moving forward with step or non-step, we obviously haven’t made a decision on that yet. But I would say based on our experience today, more likely that our Phase 1b doses will be step strategies, because it’s allowing us to get to significantly higher target doses. And we do think there’s a dose response here of sorts. So, more to be learned there. We’ll also likely take when you think about project optimist considerations, we’ll likely want to take more than one dose and schedule into Phase 1b to gain further experience of the drug candidate, not only in pancreatic, but also in other tumors as well. In terms of EGFR, it’s surprising actually how should I put this. The available assay for EGFR or assays for EGFR by IHC, let’s just say it’s not perfect.
And so we’re not sure how much one would want to rely on it moving forward, particularly because it doesn’t seem from our early data that this is a straightforward ADC type thing where you high target is required for activity. These drugs like T-cell engagers just would be predicted to be active at low target levels because of the mechanism of the amplified mechanism of tumor killing where one T-cell can kill multiple tumor cells. So I think we’ve got more to learn there and that’s why we’re we may not be needing or leveraging each of our selection on a go forward basis based on what we’ve seen so far.
Operator: Your next question, it comes from the line of Anupam Rama from JPMorgan.
Anupam Rama: Thanks so much for the data update. Can you comment, was there anything in the baseline characteristics, number of prior treatments, I think the PDAC case study that you said was three lines of therapy or otherwise that might be predictive of a response. I think based on the first question, EGFR expression did correlate. And then can you comment and I’m sorry if I missed this, the other three stable disease patients, what was their duration? Thanks so much.
Sean McCarthy: I’ll take the first question in terms of which I think was anything in the patient characteristics that could have been predictive of response, and I’d say no, not really. Again, these are all pretty late line patients. And aside from EGFR, we did show, that said, Wayne showed a slide of a pretreatment biopsy of a patient with pretty high levels of pretreatment, CD8 positive cytotoxic T-cells, which is intriguing and certainly could have contributed to the response. And so that’s something that we have observed. We don’t have that data systematically across the whole study. That’s difficult data to get for every patient, but it is intriguing. In terms of the stable disease, Wayne can address that question real quick.
Wayne Chu: Yes. So, as we showed in the swim lane plot during the presentation, there were a number of patients who were able to maintain a stable disease through at least one tumor response. And that included smattering of patients that had durable stable disease to tumor responses. But for otherwise patients were able to achieve a stable disease, and then it was followed by progressive disease.
Sean McCarthy: I do think it’s important to reemphasize that these again, pancreatic is a very as everyone knows, it’s a very rapidly progressing disease. These are patients who for the most part have had three or four priors. And so, this, so we think this is really exciting data.
Operator: [Operator Instructions] And for the next question, it comes from the line of Mitchell Kapoor from H. C. Wainwright.
Mitchell Kapoor: I wanted to ask, about the total eight patients with tumor reductions. The, others, well, I guess, if you could just broadly comment on what a spider plot for these patients might look like? Are you seeing a trend in-depth of response over time? Or how are we seeing those tumor reductions evolve?
Sean McCarthy: Yes. I mean, it’s early days. I think those eight patients, there was the two of them with the pancreatic patients, and you can see them in the waterfall plot. I think there’s encouragement there in terms of the fact that escalation continues. We’ll keep pushing the dose here. So at this point, I think it’s fair to say the spider block will be relatively immature.
Mitchell Kapoor: And could you just comment on the other confirmed partial response patient and how much duration of follow-up that patient had?
Wayne Chu: That patient, again was treated at the 6 milligram non-step dosing schedule, had confirmed partial response. And that patient remained on study about on study treatment approximately 18 weeks before having progressive disease.
Operator: Thank you. And I’m showing no further questions. I would now like to turn the conference back to Dr. Sean McCarthy, CytomX’s Chairman and CAO for closing remarks.
Sean McCarthy: Great. Thank you very much, and thanks everyone for listening in today. CytomX has made terrific progress so far in 2024, and we look forward to providing additional updates as the year proceeds and as we continue to build our company for the long-term to make the biggest difference we can for patients. And so thank you very much. Have a good evening.
Operator: This concludes today’s conference call. Thank you for participating and you may now disconnect.
