Release Date: May 08, 2024
For the complete transcript of the earnings call, please refer to the full earnings call transcript.
Positive Points
- CytomX Therapeutics Inc (CTMX, Financial) announced positive initial Phase 1a dose escalation data for CX nine oh four, showing promising anti-cancer activity, particularly in pancreatic cancer.
- The company maintains a strong financial position with $150 million in cash, providing a runway to the end of 2025, excluding potential milestone payments and partnership funding.
- CytomX Therapeutics Inc (CTMX) has a broad and deep pipeline with over 15 active programs, including three clinical-stage molecules, and significant commercial rights retained.
- Strategic partnerships with major pharmaceutical companies like Bristol-Myers Squibb, Amgen, Astellas, Regeneron, and Moderna, enhancing the development and potential commercialization of Probody therapeutic programs.
- The Probody platform demonstrates a reduced risk of toxicity in normal tissues, as evidenced by limited cytokine release syndrome (CRS) and neurotoxicity in the CX nine oh four trials.
Negative Points
- The complexity and inherent risks of developing novel cancer therapies, which involve lengthy and costly clinical trials with uncertain outcomes.
- While initial data is promising, the efficacy and safety of CX nine oh four and other pipeline candidates need further validation in larger, more diverse patient populations.
- Dependence on the success of strategic partnerships, which might affect the company's ability to control the development and commercialization of its products.
- Potential regulatory challenges and delays, which can affect the approval and market introduction of new cancer therapies.
- The need for continuous innovation and adaptation in a highly competitive oncology market, where new treatments and technologies frequently change the therapeutic landscape.
Q & A Highlights
Q: Thank you so much. Thanks for sharing the data. I'm really excited the mask and benefit you've seen. Do you think that can also extend to other T cell engagers and then the responses you've seen so far and do you think is something special about pancreatic cancer? Or do you think you can get deeper responses in other tissues as well?
A: Hi, Peter. Great. Great questions. Thanks. And regarding that the extension and the read through to other programs, we're obviously very optimistic that that will be the case. You got to start somewhere in nine oh four, I think is a very strong start for us. We've learned a lot with this one in the clinic and as we mentioned, both internally and with our with our partners, we're doing a lot of work in T-cell engagers. We've got multiple programs. In fact, the majority of our partnered work is in T cell engagers so we would expect to make substantial additional progress here over the next few years.
Q: Thank you. And then, Steve, the depth of the responses is that correlated with EGFR expression was it tumor microenvironment?
A: So one thing we have not shown was up this shown in this presentation, but we continue to evaluate is the level of EGFR expression as assessed by immunohistochemistry assay, and we've been doing this on a retrospective basis for all the patients that have enrolled to gauge based on our early data with EGFR by this IHC assay, we have not seen a clear association between EGFR expression and the left and the depth of the response. And just as an example, on the two patients in pancreatic cancer, whilst we had a confirmed partial response, one patient had a moderately high level of EGFR expression by IHC. But then the other the other patient had a very low level of EGFR expression. And it's actually the patient who had the 83% reduction and measurable tumor burden that had the low level of EGFR expression.
Q: Great. Congrats for the data and thank you for taking my question and a few questions from us on the first one related to that, those relationship seems the are the efficacy or antitumor PBT is not clearly collared with the dose level. My question is how do you think about as you dose higher even beyond TIM AG. Now you're at the 15. How do you think about the balance between the efficacy and the?
A: Yes, thanks, Roger. Let me kick that one off year. I'd say I think that there is a dose response in the that the responses that we're seeing, the confirmed resist responses. We've seen a five and six milligrams of remember that we began this dose escalation at seven micrograms. So, you know, the range of doses where we're seeing activity is actually really consistent with our from our predictions and for modeling of where the biologically effective range would be. So we think we're in the zone.
Q: Thanks for taking my questions and exciting data here. I guess maybe first one on the EGFR mediated tox that you're seeing. I guess my question is like what do you think is happening? Is that some small amount getting unmasked in periphery or maybe a small amount getting unmasked in the tumor and then reentering circulation? And is that tox that you're seeing typical of sort of historical EGFR experience a cetuximab? Or is there anything indicative that it's T cell targeting of EGFR on normal tissue? Thanks. And I may have one follow-up?
A: Yes, Joe, thanks for the question, um, the um, what first of all, let me say that we're really, really pleased with the very low incidence of Grade three rash in this study, we only have one patient over the 35 patients with a grade three treatment-related rash, and that's a significant achievement. We think come because this unlocks the opportunity to use this mechanism. It just requires that otherwise couldn't be sure exactly whether the Gevaert. So we're very, very pleased about that.
Q: Thanks for taking the question. Just, Dan, if you could maybe talk through on your current thoughts on sort of the STEP versus the nonstop dosing, particularly in the pancreatic arm, Coca-Cola patients that sort of had a response and how you're kind of thinking about potentially moving one or the other option forward as you sort of expand on 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 and that 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 expression across the folks that you have already sort of enroll in the study. I don't know if I caught that correctly. Thank you.
A: Yes, thanks. Thanks answer. In terms of moving forward, which type of loans that we obviously haven't made a decision on that yet. But I would say based on our experience to date, we are more likely that our fees, 1B doses will be set as 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 will also likely take when you think about Project Optimus considerations will likely want to take more than one dose and schedule into Phase Ib to gain further experience of the drug candidate, not only in pancreatic, but also at other in other tumors as well in terms of EGFR and is surprising actually how on earth, how should I put this the available assay for EGFR assays to EGFR. But I see 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 yield, ADC type thing where you have high target is required for activity, yes, these drug drugs like T cell engagers just up would be predicted to be active at low target levels because of the mechanism of the amplified mechanism of tumor killing one T cell can kill multiple GMSL. So I think we've got more to learn there. And that's why we're where we may not be needing or leveraging EGFR selection on a go-forward basis based on what we've seen so far.
Q: Hey, guys. How are you and thanks so much for the data update. Can you comment was there anything in the baseline characteristics, number of prior treatments?
A: I think the PDX 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 didn't correlate. And then can you comment in I'm sorry, if I missed this, the other three stable disease patients,
For the complete transcript of the earnings call, please refer to the full earnings call transcript.
