Sean McCarthy: You’re welcome.
Operator: Thank you. One moment while we prepare for the next question. Our next question will be coming from Peter Lawson of Barclays. Your line is open.
Unidentified Participant: Hey. Good afternoon, guys. Thank you for taking our question. This is actually — this is Alex on for Peter. I just had two quick questions on the BMS collaboration. The first one is, can you comment or remind us the key differences that you saw in Phase 1 for the 218 molecule compared to the data we’ve seen for the 249 molecule?
Sean McCarthy: Yeah. Happy to comment on that. So, it does take a bit of time to sort of cover the various moving parts here, so just bear with me for a second, just overall on the same page. So 249 is the Probody version of ipi. The 218 is the non-fucosylated antibody, which is BMS’ antibody. And then, there’s 288 which is the Probody version of 218, the non-fucosylated. So the clinical data that BMS has presented previously relates to, as you rightly point out, to 249’s Phase 1 study and also the 218 Phase 1 study. No data has yet been presented for 288, which is a non-fucosylated Probody. I would say that the key learnings from the Phase 1 work on 249 and 218 are as follows. With the Probody 249, the Probody version of ipi, the dose escalation was able to achieve really very high levels of the mass ipi.
So, they achieved 30, 3-0 mg per kg of monotherapy and 15 mg per kg in combination with full . And you can see how — and I think this is pretty consistent with the work we’ve done over the years in the clinic that the masking shifts the dose response curve for toxicity, so they can get to higher levels and still have a well-tolerated drug. The other aspect of the Phase 1 data, and this was really the update last year at ESMO, clear evidence of clinical activity for 249 demonstrated in that poster presentation, including a response in MSS stable CRC, which was highlighted as a case study. The 218 poster was important, I think, for several reasons, demonstrated again that 218, the non-fucosylated ipi is clinically active. Again, a case study was put forward in MSS CRC, which is an area where we’re seeing a lot of progress by others, including HNS with their .
The other noteworthy data from the 218 poster is that this drug, you can see how it’s a lot more potent. It’s designed to be more potent than ipi and non-fucosylation leads to a more potent drug. And that meant that the doses administered are substantially lower than for ipi alone. So, I think that’s kind of an interesting take home. And the prioritization of 288, the masked version of that 218, I would think has the potential to evaluate higher doses of the non-fucosylated in mask form. So we don’t have a lot of visibility at this point in what BMS’ Phase 2 strategy will be for 288. But those are just a few thoughts from the data that’s been presented thus far.
Unidentified Participant: Okay. Great. That makes a lot of sense. And then, yeah, just I was also curious if you have any visibility in terms of — or should we assume that the current ongoing studies with the 249 will sort of stop enrolling patients and going forward and that’s it. Thank you.
Sean McCarthy: You’re welcome.
Operator: Thank you. One moment while we prepare for the next question. Our next question will be coming from Mitchell Kapoor of H.C. Wainwright. Your line is open.
Mitchell Kapoor: Hi, Sean and team. Thanks for taking the questions. Hope you are well. Just wanted to ask about CX-2029 and a little bit more on the discussions to reacquire the rights. What does that entail? And then secondly, what is the — what do you think the ability to more effectively treat esophageal cancers versus other cancers suggests about the profile and the mechanism of the drug with respect to the target?
Sean McCarthy: Yeah. Thanks for the questions, Mitch. I can’t really comment on the 2029 negotiation for obvious reasons at this point other than to say that those discussions have been initiated, and there’s a process laid out in the contract that we negotiated some years ago for how to go about that. So, we’ll see where it all goes. With regards to esophageal, it is really interesting to us. The signal that we’ve seen there, one of the intriguing features of esophageal that relates to the target is published data from others showing or suggesting that CD71 is amplified in certain squamous esophageal tumors. So one could certainly imagine that there’s a relationship between target level or more specifically target amplification and clinical activity.
And that is something that we’re aggressively pursuing, as to figure out whether there’s a potential patient selection strategy there. So speaking in general terms, of course, given the high incidence of anemia that we have with this drug, but also given its clinical activity, if we elect to move the drug forward in esophageal, let’s say, obviously, we’d be wanting to do everything we can to select patients in our favor to increase the likelihood of response and also, of course, continue to work to find ways to manage and mitigate anemia to give the drug its best chance of future success. So that’s something that we’re actively looking at that relates directly to the target.
Mitchell Kapoor: Okay. Great. Thank you very much for taking my questions.
Sean McCarthy: You’re welcome.
Operator: Thank you. One moment while we prepare for the next question. Our next question will be coming from Anupam Rama of JPMorgan. Your line is open.
Malcolm Kuno: Hi. Thank you for taking the question. This is actually Malcolm Kuno on for Anupam. Just one quick question. So given that some of your collaborations involve cost sharing agreements, what should we assume as being baked into your cash runway?
Sean McCarthy: I’ll pass that one over to Chris.
