Good morning, and thank you everyone for joining us today. Today is the last day of JP Morgan's 40th Annual Healthcare Conference. My name is Tarun Soni. I'm a Vice President in JP Morgan's Healthcare Investment Banking Group.
Before I introduce you to our presenter for this session, I want to call your attention to the blue button on your screen which says Ask a Question. You may submit your questions here, and I can address it during the Q&A session. With that, I'm very pleased to introduce you to Nadim Ahmed, CEO of Cullinan Oncology. I know he's very excited to tell you a little bit about their story. Over to you, Nadim.
Good morning, Tarun, and everyone watching. It's great to be with you today. Let me start out by providing a little strategic background to Cullinan Oncology as a company. Starting with slide three, if I can move it. We have a very broad and deep pipeline. We now have eight programs across multiple platforms and multiple indications across hematology and solid cancers.
We have assets that have the potential to either be best in class or first in class. Our lead program, CLN-081, for non-small cell lung cancer patients with EGFR exon 20 insertion mutations, is currently ongoing in phase I/IIa. We recently provided a clinical update, which further supports the differentiated clinical profile that we're seeing for CLN-081.
Of course, we're very pleased to receive breakthrough therapy designation from the FDA recently, which further underscores the differentiated profile that we're seeing with CLN-081 in the clinic. In addition to CLN-081, we now have another two programs that enter the clinic at the end of December.
That was CLN-619 and CLN-049. CLN-049 is our FLT3 T-cell engager, and CLN-619 is our MICA/MICB antibody. We're fortunate to have a very robust cash on hand position at the company. This really allows us to deploy capital to advance the pipeline very expeditiously but continue to in-source innovation.
As we look at our preclinical pipeline also, we have a broad pipeline there too, with 2 assets that are currently in IND-enabling studies, which should enter the clinic in the next 12-18 months. Also, we continue to replenish the pipeline. We made an announcement earlier this week. We're excited about a collaboration that we have with Mount Sinai to work together on a novel HPK1 degrader program.
Very excited about that possibility as well. I think a couple of things I'd say that are unique about Cullinan Oncology, that we take a very disciplined approach to either insourcing innovation or the way we actually advance our program. Three key criteria I'd point out here. The assets have to have the potential, at least, to either be first in class or best in class.
We're really focusing on those molecules that can activate the immune system or target key oncogenic drivers. The molecule has to at least pre-clinically have the potential or promise of single-agent activity. I'm fortunate to be surrounded by a very experienced senior leadership team, very strong scientific capabilities that really allows us to target the assets that we're bringing in as well as the agents we're advancing.
As I mentioned earlier, we're very platform-agnostic. Within the company we have small molecules, biologics, T-cell engagers, fusion proteins, and where we're really focusing on are areas of differentiation. Whether it's a differentiated platform or a novel mechanism of action.
Across the broader Cullinan Oncology team, we have deep scientific expertise that really allows us to kind of push and accelerate our internal programs, but also allows us access to a network of collaborators, both in academia as well as company partners. You can see the pipeline here.
As I mentioned, eight programs. Obviously Oh Eight One is a very important program for us and is our lead program. You can also see beyond Oh Eight One, we have a very deep pipeline across solid tumors and hematology indications and across multiple platforms also.
Eight programs across various stages of development, with three already in the clinic, another three assets in IND-enabling studies, and then two other programs at the candidate selection stage, including the newly announced HPK1 degrader program.
Let me dive into the pipeline a little bit and start out by talking about CLN-081 on slide seven. CLN-081 is a very interesting molecule. It's a novel oral EGFR inhibitor with a unique chemical structure, which allows it to preferentially target mutant exon 20 versus a wild type variant.
We think this contributes to the therapeutic profile that we're seeing in the clinic. 081 is in an ongoing phase I/II-A trial, as I mentioned earlier, testing a broad range of doses from 30 to 150 mg BID in non-small cell patients harboring, again, the exon 20 insertion mutation. It's a heavily pre-treated patient population, with about two-thirds of patients having received two or more prior lines of therapy. This table summarizes the response rates that we've seen to date.
We see a confirmed response rate of 39%, which compares very favorably to other agents in this space. In totality, we see a 97% excellent disease control rate of 35 of 36 patients. Following ASCO, we're very pleased with the response rate we now see in a larger group of patients.
When you look at the 150 mg BID dose, we see a confirmed objective response rate of 27%, which we believe is perhaps driven somewhat by the tolerability profile, which I'll go on to discuss. Moving to slide eight, you can see here that CLN-081, especially at the 100 mg BID dose, really has a differentiated and favorable safety profile, which is especially important in the context of the efficacy that we just discussed.
This table breaks down key treatment-related AEs, especially those that are wild-type EGFR associated toxicities across the 100 mg dose, the 150 mg dose, and across all dose levels. At the 100 mg dose, you can see that no patients experience grade 3 or greater rash or diarrhea.
In fact, for rash and diarrhea, when you look at grade 1 and 2 toxicities, it's heavily skewed at a ratio of three to one for both rash and diarrhea towards grade 1, which we think is very encouraging. Also, with the protocol, all of these events were manageable with conventional supportive care, and we didn't require systemic GI prophylaxis to manage the diarrhea that was observed.
At the 100 mg dose, we did see one patient with grade 3 pneumonitis, which is known to be a toxicity with EGFR TKI inhibitors. However, you'll see in the footnote, this was a patient that had some confounding factors. At the 150 mg BID dose, we did expand enrollment since we presented the data at ASCO, now up to 11 patients.
What we found was grade 3 diarrhea in two patients, grade 3 rash in one patient, and we also saw two patients with transaminitis, either grade 3 or grade 4. And also we saw a patient with grade 3 pneumonitis at the 150 mg dose. Again, some confounding factors.
I think the most important aspect of the 150 mg dose, in addition to the step-up in toxicity, you can see on this slide that we see a significant increase in treatment-related dose reductions as well as treatment-related dose discontinuations.
When we look at the totality of the efficacy and safety dose data, it really supports moving forward with the 100 mg BID dose. Moving to slide nine now. I did mention the response rates earlier on. Obviously, quantity of response is important, but quality of response is equally important. We were pleased to see, for the first time, we were able to assess durability data from this study in the 13 patients in the phase I cohort.
Using Kaplan-Meier estimates, we saw a median duration of response of greater than 15 months and a progression-free survival or median progression-free survival of 12 months and a disease control rate of 92%.
Again, these durability data compare very favorably with other agents in the same class. Of course, we continue to follow up for the phase II A patients, and we'll have durability data to report on those patients in the future. We are very encouraged by the quality of response we've now seen in this study. I mentioned earlier, we're very excited about the breakthrough therapy designation we recently received from the FDA.
That really underscores the differentiated profile that we see with CLN-081. At the same time, it also encourages us regarding the regulatory pathway and the fact that accelerated approval is still open for us.
That's the summary of CLN-081. Based on the updated data, we see a very favorable profile in terms of efficacy, both quality and quantity of responses. We also are encouraged by the favorable safety profile we've seen so far in a heavily pre-treated group of patients with a significant unmet need.
Let me now turn to the other clinical stage programs. Slide 11, this is CLN-049, which is a novel T-cell engager targeting FLT3 in a phase I study for relapsed refractory AML patients. FLT3 is a very well-validated target in AML, and it's actually expressed in a substantial majority of AML patients, and fortunately, very low expression on normal myeloid cells. The unique approach we have with 049 is that it targets the extracellular domain of FLT3.
That allows it to target both mutant and wild type FLT3. It expands the addressable patient population to 80%+ versus the mutant FLT3 kinase population of around 25% that's addressed by currently approved agents.
The fact that we see low FLT3 expression on normal myeloid cells is good relative to other targets like CD33, CD123. Also the constructs of the antibody is in line with other T-cell engagers that we've seen in the lymphoma space that are encouraging high levels of activity and low levels of CRS.
We also have a silent Fc backbone in this molecule, so that will prolong the half-life and allow potentially for less frequent dosing and no need for continuous infusion, for example. As I mentioned, CLN-049 is in the clinic now in relapsed refractory AML patients.
The study just opened for accrual in December, so we look forward to sharing those data with you in the future. On slide 12, you can see some of the proof points we've seen preclinically with zero four nine.
We've seen promising preclinical activity. In the upper left chart, you can see the activity of zero four nine in both wild type and mutant FLT3, and the complete in vitro eradication of AML cells in these FLT3 lines. Very encouraging data that shows that the agent targets both mutant and wild type FLT3.
On the top right graph, you can see, compared to control CD3 antibodies, you don't see activation of T cells with CLN-049 in the absence of target FLT3 cells, which potentially portends for a favorable safety profile. In the bottom left, in the xenograft model, you can see a nice dose-dependent survival curve, showing improved survival with increased doses, and this is at very low doses.
We also, in the bottom right graph, transplanted human AML blasts directly into mice. As you can see from this graph, we see a complete eradication of AML cells from the bone marrow. Very encouraging preclinical data. Of course, now we're in the clinic. Let's now turn to our third clinical program, which is CLN-619 on slide 14. CLN-619 is a first-in-class molecule targeting MICA and MICB.
MICA and MICB are ligands for NKG2D, which really activate receptors in the immune system, but especially mainly on NK cells. MICA and MICB is broadly expressed on tumor cells. They actually send a kill me signal to the immune system, especially NK cells.
However, what happens in the tumor microenvironment is that tumor cells are very clever, and they send proteases that cause cleavage on the cell surface, which sheds MICA and MICB, essentially evading the immune system and masking these cells. These cells essentially become invisible to the immune system.
That's a way that these tumors evade and escape the immune system. Now, MICA and MICB is broadly expressed across solid and liquid tumors. Soluble MICA and MICB has actually shown to be a prognostic marker, and I'll show you that in the subsequent slide.
We believe with six one nine we have a first in class potential here with the first monoclonal antibody targeting this agent now in the clinic. Essentially, what six one nine does is it keeps MICA and MICB on the cell surface, which allows elimination by the immune system through various mechanisms, including invoking both the innate and adaptive immune system through multiple mechanisms, including ADCC.
Those tumor cells that escape the immune system when MICA and MICB is shed are no longer able to escape the immune system because six one nine keeps MICA and MICB on the cell surface. We also have very broad allele coverage of MICA and MICB of over 95%.
As I mentioned, 619 is now in the clinic, and we're doing a parallel evaluation of this novel agent as both monotherapy and combination therapy across a range of solid tumors. In the next slide 15, you can see both the biological rationale for the target, MICA and MICB, as well as the interesting preclinical data that we've generated to date. In the top right graph, you can see a heat map which shows a range of NKG2D ligands across a range of tumors.
The red and the pink denote the very high expression levels we see of MICA and MICB, again, portending for pan-cancer activity with this novel agent. In the top left, I mentioned that shed MICA is a negative prognostic indicator.
You can see in this study in patients, a retrospective study, that patients that had shed MICA, shown by soluble MICA in the plasma, did much worse in terms of survival when patients had high levels of shed MICA versus those that had low levels. Turning to the bottom half of this graph, we can look at the preclinical activity now.
In the left graph, you see complete tumor eradication in a xenograft model at all doses of CLN-619. At the same time, pharmacodynamically, in the right graph, you see that at all doses of CLN-619, you see complete prevention of shedding of MICA and MICB. Again, the preclinical package is very strong here, and of course, we'll see the data from the clinical studies in subsequent months.
Now, I'll also talk about two assets in our preclinical pipeline, given the time constraints of the presentation. We're very excited about CLN-617, which is a first-in-class cytokine therapy combining IL-12 and IL-2. IL-12 and IL-2 are very well described in the literature having potent activity.
The problem with these cytokines is the systemic toxicity that we're seeing with these agents. We believe we have a unique molecule here that combines both IL-12 and IL-2, but we also include a collagen-binding protein in the construct, which allows the tumor to actually retain the cytokine so you don't get leakage. With CLN-617, you see a co-delivery of both IL-12 and IL-2, which means we get synergistic activity. This is an intratumoral approach.
As I mentioned, we have a unique retention strategy here because of the collagen binding domains. The other interesting aspect of this molecule is that we have potential for memory T cell response and abscopal effect, which is important because just having activity at the site of the tumor injection is obviously not as important as having systemic effect.
The other thing is that we have in the construct native IL-12 and IL-2, so reduces the risk of immunogenicity. Also, just as importantly, unlike other intratumoral approaches, CLN-617 doesn't rely on viral or nucleic acid delivery. It really allows us to control the dose that's being delivered. With CLN-617, we have a pan-cancer opportunity as monotherapy and also in combination with checkpoint inhibitors.
On slide 18, you can see some of the data that we've generated already that we're very excited about. In a very refractory primary tumor xenograft model, you see a 100% complete response rate.
Essentially, these mice are cured when injected with CLN-617, and you see a minimal effect with a checkpoint inhibitor in this setting because of how tough this refractory model is. Now, when you look on the right-hand side, which is even more interesting, you see that we induce a very strong systemic T-cell memory response.
We take the mice that have been cured in the top right corner, re-inject tumor into those patients with no treatment, and you see that in nine out of ten cases, the tumor is completely rejected, and even in the tenth case, you see a significant delay in progression of that tumor. Inducing a strong memory T-cell response, which is very encouraging.
In the bottom panel, you see a systemic immune response with both monotherapy and combination therapy in a similar model. We take mice and graft two tumors. One tumor is injected with both anti-PD-1 and the combination of CLN-617 as well as monotherapy. You see a nice effect for both monotherapy and CLN-617 combined with checkpoint inhibitor, where you see complete tumor regression.
Even more encouragingly, in the untreated tumor, you see an abscopal effect here, where monotherapy, you see a significant eradication of the tumor, and you see synergistic activity with complete eradication of the tumor with the combination therapy approach.
We're very excited by the very robust preclinical package we've generated for CLN-617. The last molecule I'll talk about is CLN-978, which we believe has best-in-class potential for hematologic malignancies. It's a CD19/CD3 T-cell engager.
Now, of course, CD19 is very well-validated now, clinically and commercially, with agents that have been approved. And T-cell engagers as a modality have also been very well-validated. We believe we have a best-in-class potential here with this construct. You see we have an engineered molecule here that has very high affinity for CD19 and a long half-life.
From a differentiation perspective, this means that this agent has the potential to really target low-expressing CD19 cells. For example, this may be a mechanism of resistance for CD19 CAR T and other T-cell engagers. In that post-CAR T setting, you can imagine the potential to salvage patients with this T-cell engager that is activated by low levels of CD19.
At the same time, in other settings, you can imagine having this off-the-shelf therapy can make this agent very accessible to a broad range of patients relative to, for example, autologous approaches.
The fact that this targets very low-level expression CD19 is potentially favorable relative to, for example, CD19-targeted ADCs, where you need a relatively high level of target expression so that you can deliver the payload in a safe environment.
You can see in the bottom right here, in this antitumor study in an in vivo model, we compared 978 directly with an approved CD19 agent, and you see superior antitumor activity. We're very excited about CD19, CD3 978 entering into the clinic in 12-18 months.
Hopefully I've given you a flavor of all the work that the company's been doing in the past 12 months. We've had a very busy year of achievements in 2021, so I'd really like to thank the team for that. We also have a significant number of milestones coming up in the next 12-18 months.
Reflecting on the year, as I mentioned, we've made significant advancement, especially with CLN-081, where we were able to update the phase II-A data, and we also now have breakthrough therapy designation, which is really important. We also took two additional molecules into the clinic, so the pipeline continues to advance with CLN-049 and CLN-619 entering the clinic.
Over the next 12 to 18 months, we're very excited about the key value creation milestones ahead of us. For example, regulatory activities with CLN-081, which will allow us to initiate a pivotal second-line study, of course, but at the same time, also initiate a front-line study, which will allow potentially even more patients to benefit from CLN-081.
With CLN-049, our FLT3 T-cell engager, and CLN-619, our MICA/MICB antibody. Hopefully, we're planning to present clinical data updates over the next 12-18 months. Our fusion protein, IL-2/IL-12, will enter into the clinic in the next 12-18 months, as well as our next-generation best-in-class CD19 T-cell engager.
Lots of activity ahead, promising future. In conclusion, I'd say again, we have a very broad and deep pipeline of eight programs that are either best-in-class and/or first-in-class potential. We're of course very encouraged by the CLN-081 data that we've seen to date, including the breakthrough therapy designation. Beyond CLN-081, which is of course a very important program for us, you can see a range of best-in-class, first-in-class molecules across hematology and solid tumor indications.
We have a very deep and rich pipeline beyond oh eight one. In the next 12-18 months, we'll have five highly differentiated assets entering into the clinic, which really reflects our evolution into a later-stage oncology company. I would say the progression of our pipeline will really drive significant value for our investors, but more importantly, allow us to deliver innovative medicines for cancer patients.
In closing, I'd really like to thank my colleagues at Cullinan Oncology for their relentless dedication, especially during this global pandemic, as well as our colleagues at J.P. Morgan that provided the opportunity today for us to present the exciting story of Cullinan Oncology. With that, thanks for your attention. Tarun, I turn it over to you for the Q&A session.
Thank you, Nadim, for the great presentation. I just want to call out again if you want to ask any question, please use the feature on our conference portal that says ask a question, and I can ask your question to Nadim. I don't see any questions, Nadim, for the moment, but I would begin with one of the key questions, which is that, you know, in your new role as the CEO at Cullinan, how are you thinking about the strategic direction of the company changing, if at all? You know. With that, the second part of the question is that you recently had a deal with Mount Sinai for your HPK1 degrader, so shall we expect more such deals, and how are you thinking about it? Thank you.
Sure. Thanks, Tarun. I would say, in general, the overall strategic direction of the company is not changing. We have a continued focus, as I mentioned, on first in class, best in class assets, and that remains in place, and we'll continue to both in-source innovation that meet our criteria and also advance assets that meet our criteria as well, both internally and externally. The one thing I would add, though, with the board bringing me in with my experience, especially in late-stage development and commercialization, is we now have an additional option to actually take molecules all the way through to late-stage development and ultimately commercialization, which is based on my experience. Yeah, ultimately, we do have an ambition to become an end-to-end, fully integrated biotech company.
You know, for the right molecules under the right circumstances, we'll take them all the way through to commercialization. At the same time, we'll also continue to partner and in-source innovation. To the second part of your question, look, you know, in this business, while we would like everything to succeed, in R&D, everything doesn't succeed. For me, it's really important to continue to replenish our pipeline. As I mentioned, we do have a robust cash on hand position, which does allow us to continue to do both the deals like Mount Sinai, as well as advance our all of our programs that we have today, either preclinical or clinically on into the clinic or late-stage development as well. Very excited about the future.
No overall, big change to the strategic direction of the company, but we now have the added option of going all the way through to commercialization.
Got it. Thank you. That's great. Just a quick check on that. Would you say your partnership is essentially going to be with academia or more, or you are planning to do it like with big pharma or someone like other players? How are you thinking about it?
Yeah. Look, I mean, we're open for business. I mean, we're willing to talk to anyone that has interesting assets that meet our criteria. You know, we continue to have discussions with large pharma partners as well as smaller biotech companies. We also continue our academic collaborations, which I think we have very strong network based on the people at Cullinan Oncology that have these relationships. It's actually more about the profile of the asset as opposed to where it comes from.
Got it. Thank you. That makes sense. Just moving on to your lead asset, probably, CLN-081 for exon 20 EGFR and NSCLC patients. The market is becoming a little bit competitive, I guess, and there are some approved agents in combination therapies, which are already there. How are you thinking about positioning or, you know, differentiating your asset, compared to these agents and you know, similar other products in the market as well?
Sure. Look, the first thing I would say is, you know, I think we have good molecules that are approved in this setting, and we need more therapies for these patients because there's clearly an unmet need. So let me say that first.
Secondly, I would say, look, based on the emerging data that we've seen now with CLN-081, I think we see a favorable safety profile, certainly, based on our mechanism of action, which I think provides differentiation. I spoke earlier about the quantity of response, but now for the first time, we're seeing the quality of response. So I'm very encouraged by the durability we're seeing, both in terms of median duration of response and progression-free survival.
Although, you know, I'm a very competitive commercial guy, I always like to be first in class and best in class, but if I can't have first in class, I think the potential to be best in class is exciting for us. We do feel we have a potentially strong competitive position with the profile of CLN-081.
Got it. Thank you. Just related to it, you know, the data, I guess what you presented is in previously, you know, heavily treated patients, I believe. What's your view in terms of are you exploring this agent in the frontline setting as well?
Because probably, Tagrisso or, you know, some of the other TKIs may be, the first, you know, line of defense for these metastatic patients. How are you thinking about, taking this, product in the earlier lines of setting, if at all, and, you know, moving maybe, I don't know if it has any value in the adjuvant setting as well. Any color on that?
Yeah. Look, I think with CLN-081, based on the profile we're seeing, you know, our clinical development team is really looking at how can the maximum number of patients benefit from this therapy. I think the fact that we're seeing such robust efficacy and safety data in the heavily pretreated setting, of course, the natural next step is to bring this into the first line trial setting.
That's part of the milestones that I mentioned over the next 12-18 months. We would want to start to initiate a front line trial so that even more patients can benefit. Of course, you know, we'll have to discuss study design, et cetera, with the FDA, but that's certainly in our plans because we wanna make sure that as many patients as possible can benefit from CLN-081 in the future.
Got it. Thank you. You know, first of all, congratulations on getting the breakthrough therapy designation for this asset. How does it expedite any process for you in terms of your discussions with the FDA or, you know, what are the next steps for it?
Sure. First, Ian, let me say we are still planning to provide a regulatory update in first Q of the first quarter of this year, which we've said previously. I think for us, the BTD designation was somewhat of a de-risking event. One, I think it further validates the differentiated profile of CLN-081.
Now we have external validation of that which we're pleased with, but at the same time, it also clearly indicates that the accelerated approval pathway is still open to us. I think on both those fronts it was quite a de-risking event for us. Of course we'll continue to engage with the agency.
The third aspect of breakthrough therapy designation, of course, is that it gives you the opportunity to have enhanced discussions with the FDA because they wanna help you expedite your program. That's why they give that sort of designation because of the unmet needs. We'll look to avail ourselves of the opportunity to continue to have even more enhanced discussions with the FDA, and then we'll provide a regulatory update in Q1 of this year.
Got it. That's a nice segue. What shall we expect in this regulatory update?
Sure. You know, the things that obviously we're interested in is if you assume that the accelerated approval pathway is still open, part of the discussion will be the study design, for example, for our pivotal study and what that looks like.
Clearly we'd wanna have agreement with the FDA on that. That'll give us an idea of timelines also of initiating study and when study will be complete. I think there are a few things that we really wanna get engagement with the FDA on in terms of moving forward from a regulatory perspective and ultimately approval.
Got it. Just maybe a last question on this asset itself. How are you thinking of, you know, bringing this asset into the market? First, from a clinical perspective, do you think a combination with some of the EGFR TKIs would make sense if you are moving in the frontline setting that can enhance the value? Or, and the second part of the question is, are you going to partner with some other agent, for, you know, for this agent?
Sure. You know, our near-term immediate focus, of course, is the pivotal study that will ultimately get us to approval in the second-line plus setting, which is a monotherapy approach. A heavy focus on that for now. You know, we need to continue to drive the momentum there.
You know, you'd asked a question about the frontline setting, so I can use that as an example. Of course, there are a range of study designs that the clinical development team is looking at. Without revealing our cards too much, I think they can range from, you know, different types of combination approaches.
Got it. Any particular combination that you feel, you know, based on your knowledge? I don't want to reveal all your cards, but, anything that you can share with us that looks exciting to you.
I think there are a range of options on the table, Tarun.
Okay. Got it. Thank you. Probably, I would move to some of the other agents, you know, which is for CLN-049 for AML. How this space is kind of evolving a lot, and what can you tell us more about the specific, you know, bispecific landscape, and how does your molecule again differentiate compared to the rest of, you know, other molecules in development?
Sure. I think first, I would say we have some very good agents that target FLT3 that are already approved on the marketplace and obviously serving an important unmet need. With CLN-049, as I mentioned earlier, I think the fact that we bind to the extracellular domain of FLT3 allows us to target both mutant and wild type FLT3, which actually opens up a much bigger pool of addressable patients of 80% plus compared to the 25% or so patient population targeting mutant FLT3. So that's obviously an advantage.
Two, we are the first in clinic now antibody that's targeting FLT3 in this way. We're excited about that first in class potential. Look, AML is a very, very tough disease. I know personally, I've launched two drugs in that space and one more recently, and so I do think the potency of this molecule will be important for this type of disease where we still see very dismal prognosis.
I think if you have a potent agent that targets a larger addressable patient population, you have the opportunity to significantly impact this disease. Of course, we've just started the clinical study, so we hope to see the preclinical data translate into the clinical setting moving forward. This is one of those agents that has the potential to be both first in class and or best in class as well.
Got it. It's a kind of a nice segue as you are saying that we are moving from preclinical to clinical. What is like you have mentioned in your presentation some of the timelines for the clinical data, and what is the benchmark that you think, which is there that you are targeting or hoping to achieve, in your data set?
Yes. I would say at the moment, because we've only just started the studies for both CLN-049 and CLN-619 in December, it's a bit early to give guidance other than saying, you know, we would plan to have a clinical update in the next 12 to 18 months, but we've really got to, you know, accrue more patients and dose more patients.
As it pertains to benchmarks in AML specifically, I think when you kind of look at some of the approved agents in the relapse refractory space, and as I mentioned, some of those I've launched myself, you know, it's clear that there's a need for a higher complete response rate. I think, you know, we'd be looking at the complete response rates that we induce in relapse refractory AML patients, for example.
Got it. Thank you. I want to talk about, you know, the other asset that you have in your pipeline, and that looks pretty exciting because there's a lot of, you know, others, your colleagues or peers, I would call it, which are also developing, which is CLN-619 for solid tumors.
Fate Therapeutics has announced, you know, allogeneic CAR NK cell therapy that has the MICA and MICB targeting. How do you see, again, your product differentiated with, you know, your competitor's product and, what would you call it? You know, it's kind of really appealing in this domain.
Sure. Let me start out by saying I know Scott Wolchko and the team at Fate. They're good friends and former colleagues of mine, and they have a really strong scientific team there. Let me start out by saying that first. I think a couple of things I would say is, yeah, having an antibody that is completely off the shelf is something that, you know, oncologists are used to doing from a modality perspective.
Presumably there's obviously a convenience factor there as well. You know, we also invoke both the innate and the adaptive immune system. I think there's a potential advantage there as well. You know, we won't need to have, you know, conditioning chemotherapy with each cycle of treatment.
I think there are some aspects of CLN-619 that are different, but at the same time, I think Fate is doing great science and especially pushing the boundaries of what we can do with NK cells and allogeneic approaches.
All right. Just in the interest of time, I just want to call attention that if any of our viewers have any questions, please feel free to use the feature on our portal to ask a question. We are just going to wrap up the session in a couple of minutes.
There are no questions, Nadim, from the portal at this point of time, but I would love to hear your thoughts on your CLN-978, which is a CD19 by CD3 targeted approach that you have. There are a lot of CD20 and CD3 approaches by different, you know, players, which is there in the market. How do you see your approach kind of differentiated with that? Maybe, you know, if there are any read-throughs that we can draw or parallels from the CD20, CD3 products from other agents.
Sure. Look, I would say, I'm somebody who's been very close to the CD19 market and involved in the development and approval of at least one CD19 CAR T, which I'm very proud about, actually. I would say, you know, the fact that this antibody construct has been engineered to really target low levels of CD19.
For example, you know, CD19 loss has been implicated in certain patient subtypes, for example, with CAR T, where, you know, we do see relapses in patients. You can envisage a setting where in the post-CAR T setting you could have activity with an agent that targets very low levels of CD19 expression, for example.
In addition to the broader group of patients, you know, this is an alternative approach, again, an off-the-shelf approach that could be applied and accessible to a broader group of patients. Then for example, relative to CD19 ADCs, where you need a relatively high expression level of CD19, you could see a CD19 that targets low expression levels could have utility there also.
I think as we think about the future, it's really good that we're seeing so many treatments in lymphoma. You know, you may see a future where you see CD19 and CD20 approaches combined to push efficacy even further. I do think all of this research is actually great news for patients as we kind of create more modalities and look at combination approaches moving forward.
Got it. Thanks a lot, Nadim, for sharing all your views, and it has been great speaking with you. We are almost there for the time for our session, so I want to thank all of our viewers, and thanks a lot to you, Nadim, as well, for sharing your views with us. I hope everyone enjoyed our conference, and today is the last day of our conference, so wish you best of luck and have a great rest of the conference. Thank you.
Thanks, Tarun.