Hello, and welcome to the Nurix Seagen Collaboration Conference Call. Participants are in a listen-only mode. After the prepared remarks, there will be a Q&A session. If you wish to ask a question, please enter star 11 on your touchtone phone. I would now like to turn it over to the host of today's call, Arthur Sands, President and CEO of Nurix. Arthur?
Thank you, Liz, and welcome to today's call, announcing a very exciting and innovative collaboration between Nurix and Seagen. I'm joined on the call today by Gwenn Hansen, Nurix's Chief Scientific Officer, who will provide the scientific rationale for the collaboration, and Hans van Houte, Nurix's Chief Financial Officer, and Jason Kantor, Nurix's EVP of Finance and Business Strategy, who will be discussing the financial and business terms of the collaboration. Turning to our risk factor slide, slide 2. Before I continue, I would like to remind everyone that we will be making certain forward-looking statements, and I refer you to our most recent filings with the SEC for a full list of our risk factors. So on slide 3, I'm very excited to share this news with you today.
This is a first-of-its-kind collaboration, which combines Nurix's industry-leading technology and proven track record in targeted protein degradation, or TPD, with Seagen's technological, clinical, and commercial leadership in Antibody-Drug Conjugates, or ADCs. With this collaboration, Nurix and Seagen will advance a new class of cancer therapeutics called Degrader-Antibody Conjugates, or DACs, for short. This is a very unique and strategic collaboration for the industry. It represents a next-generation drug class for both TPD and the ADC fields, with the potential to improve treatment options for people suffering from a wide range of solid tumors and hematologic malignancies. For Nurix, it expands the use of our DELigase platform, while also expanding our drug pipeline into the area of biologics through a partnership with one of the leaders and innovators in this space.
Indeed, the value of this collaboration beyond the financials to our Nurix pipeline is very significant, since the structure allows Nurix certain options to participate commercially via profit sharing and co-promotion, which is a critical component of all of our deals. We will be discussing the financials and the structure of the collaboration later in this presentation. Turning to slide four, let's take a closer look at what a Degrader-Antibody Conjugate, or DAC, looks like. On the right and not drawn to scale, you'll see the basic concept of the attachment of the degrader molecule via linker to an antibody. In this figure, we are showing a single degrader attached to the antibody, but in actuality, each antibody will have a payload of multiple degrader molecules attached at separate sites.
As with ADCs, the antibody provides tumor or tissue-specific delivery of the payload, the DAC, the degrader molecule. The unique aspect of the DAC is the nature of the payload, which is a highly engineered targeted protein degrader molecule depicted as a barbell shape structure to the left of the antibody. This approach, using a degrader as the payload, vastly increased the potential target universe of ADCs. In addition, a single degrader molecule could be attached to multiple different antibodies, providing a multiplicity of product opportunities under this collaboration. So with that, I am now going to turn the call over to our Chief Scientific Officer, Gwenn Hansen, to describe the technology in greater depth, its potential advantages, and our collaborative relationship with Seagen to build a pipeline of novel DACs. Gwenn?
Thank you, Arthur. I am also thrilled about this new collaboration, particularly in how it will allow Nurix and Seagen to create a synergy between two very powerful and selective technologies, advancing both the field of targeted protein degraders and the field of ADCs, with an innovative new class of therapeutics called DACs. There are many potential advantages of this approach, but the key message I want to convey is that DACs combine the potency and catalytic activity of a targeted protein degrader with the cellular specificity of an antibody. And as such, DAC drugs have the potential to enhance efficacy and improve safety relative to current ADC technologies. On slide 5, we depict the basic concept of selective delivery. The DAC shown at the top consists of an antibody with multiple degrader molecules attached as payloads. Here we are showing four.
The antibody is designed to selectively bind an antigen, shown here on the surface of a cancer cell. By binding directly to the antigen, the antibody will discriminate between healthy and diseased tissues, delivering degrader payload selectivity to relevant cells. Once inside the target cell, the degrader payload is then released, initiating catalytic degradation of its respective target protein, which could represent nearly any intracellular protein associated with disease. In this particular illustration, the target protein of interest represents a key driver of cancer cell growth. The result is highly selective destruction of cancer cells while preserving healthy cells and tissues....
Overall, by utilizing degraders as payloads, we hope to generate medicines that are both highly efficacious and potentially safer than current ADC drugs. To understand, understand why degraders make such attractive payloads for antibody delivery, it is important to review how these molecules work.
In this figure on slide 6, the degrader is shown in the top middle as a barbell-shaped bifunctional molecule. One end of the molecule binds to the target protein that you want to eliminate, and the other end binds to a protein called an E3 ligase. The ligase is part of the cell's natural machinery for controlling protein levels. The dual binding of the degrader brings the target protein in close proximity to an E3 ligase. This ligase then catalyzes the covalent attachment of a chain of ubiquitin molecules to the target protein, creating a molecular tag that marks the protein for destruction by the proteasome depicted on the far right of the figure. There are several very important characteristics of degrader functionality that make their incorporation into DACs potentially advantageous over existing ADCs.
First, the degrader binding elements are highly specific for, one, a particular protein target, and two, a particular ligase. So in addition to the exquisite selectivity afforded by antibody delivery, the proteins and ligases targeted by degraders may also confer selectivity through their inherent restriction in tissue distribution or activity, thereby adding yet another level of specificity for DAC drug action overall. These two layers of specificity may allow for the degradation of oncogenic driver proteins that would otherwise be too toxic for drugs in an unconjugated small molecule form.
Second, degraders are catalytic, displaying event-driven pharmacology, which means that each degrader molecule has the potential to eliminate many target protein molecules, as they require only brief interaction with the target protein, after which their reactivity is recycled to function again and again, increasing their effective potency against the disease target.
This can provide a major advantage over existing ADCs, which generally deliver a payload that is a toxin or a molecule that acts through occupancy-driven pharmacology, essentially 1:1 stoichiometry. Third, by destroying the protein target, the degrader completely removes the function of its target. This includes both the enzymatic activity, along with any scaffolding function of the protein. By eliminating the target protein, the therapeutic effect may be very long-lasting because the cell must resynthesize the protein in order to restore its function. Fourth, the protein target that can be addressed by degraders do not require well-defined enzymatic active sites in order to be targeted by bifunctional degrader, so the target universe for DACs is extremely large.
Lastly, as Arthur mentioned previously, the modular nature of DAC construction means that any one degrader payload may be combined with any number of tumor-targeting antibodies, generating the potential for multiple product candidates for each degrader that is developed. Hence, we anticipate a high pipeline value as a consequence of the potential for multiple product candidates emerging from the collaboration. On slide 7, we put these pieces together to depict the entire cycle. The DAC binds selectively to the surface of a cancer cell and becomes internalized. The degraders are released from the antibody and enter the cytoplasm of the cell. These degraders then bind to their target proteins, inducing proximity between the target and the E3 ligase, and then the proteins are tagged and destroyed.
The degrader can then go on to do this again and again, and if we have chosen our targets correctly, the tumor cell will be selectively destroyed. Turning to the drug discovery workflow captured in our agreement, this is on slide 8. The deal is designed to be a true collaboration, with each party bringing a specific technology and expertise. Nurix is responsible for discovery of small molecule degraders against an agreed-upon set of targets. These highly potent and targeted degraders will be designed and optimized for efficient conjugation to antibodies.
Seagen will then take the lead on conjugating these degraders to antibodies to generate the DACs, with both parties collaborating on subsequent optimization to achieve potent in vitro and in vivo activity. Seagen will ultimately be responsible for preclinical testing and for bringing these future drug candidates to the clinic.
Because each degrader can be used with multiple antibodies, the collaboration has the potential to generate any number of DAC drug candidates. I would like to now turn the presentation over to Jason Kantor, who will discuss the commercialization of DACs that arise from the collaboration and the associated financial terms of the agreement. Jason?
Thank you, Gwenn. As Gwenn mentioned, we anticipate multiple DAC product candidates emerging from this multi-year collaboration. Seagen will be responsible for the clinical development of these DACs, and if successful, will also be responsible for global commercialization. Similar to our existing partnerships, Nurix is eligible to receive milestones and royalties, and retains an option for U.S. profit sharing and co-promotion for up to two products emerging from this collaboration. On slide 9, we list the terms of the deal. Nurix will receive an upfront cash payment of $60 million. In addition, Nurix has the potential to receive up to $3.4 billion in future milestone payments, which include milestones in the research phase of the collaboration, clinical development milestones, regulatory milestones, and sales milestones.
Nurix will also be eligible for tiered royalties from mid-single digits to low double digits on any number of DAC products that utilize the Nurix degrader. Importantly, Nurix retains the option for U.S. profit sharing and co-promotion for up to two DAC products developed within this collaboration.
... I would now like to turn it over to Nurix's Chief Financial Officer to discuss the impact of this transaction on our capital strategy. Hans?
Thank you, Jason. Business development has always been an important component of Nurix's capital strategy. To date, and with this transaction, Nurix has received approximately $400 million in funding through our partnerships. In 2015, Nurix received $150 million upfront from Celgene for a multiyear research alliance. In 2019 and 2020, we added discovery deals with Gilead and Sanofi. From 2021 through 2023, we have received a steady flow of research milestones, and now today we're announcing a new discovery alliance with Seagen. This partnership funding is critically important for Nurix and provides an alternative to dilutive equity financings. It also builds our pipeline with options for profit sharing on up to six programs and up to $8.2 billion in potential future payments.
I'm happy to announce that with today's transaction, we are updating our financial guidance and now expect current cash to provide runway into the second quarter of 2025. I would now like to turn it back to Arthur for closing remarks.
Thank you, Hans, and thank you, Gwenn and Jason. Today is truly an exciting day for us, and I believe for our future patients. It's an important first step towards bringing a new class of drugs to patients with cancer. As you can see on this slide, Nurix's pipeline continues to grow. We now have three wholly owned drugs in the clinic for hematologic malignancies and solid tumors. As announced earlier this year, our partner, Gilead, is now advancing an oral IRAK4 degrader toward the clinic for the treatment of immunologic and inflammatory diseases, such as rheumatoid arthritis. In addition, we continue to advance a large portfolio of preclinical programs, well over a dozen now, internally and with our partners, Gilead and Sanofi, and now adding novel antibody-based DAC programs as well to our preclinical pipeline.
With that, I'd now like to turn the call back to the operator and start our Q&A session.
As a reminder, to ask a question, please press star 11 on your touch-tone telephone and wait for your name to be announced. To withdraw your question, please press star 11 again. Please stand by while we compile the Q&A roster. Our first question comes from the line of Gregory Renza with RBC Capital Markets.
Hi, this is support for Gregory. I was wondering if you can speak a little bit more about, you know, if there are certain cancer indications that you know might be more attractive for DAC. And are you thinking about the, you know, Seagen- are you thinking about more of a traditional cancer targets or that's you know ADCs open doors to you know potentially newer classes of cancer targets? Thank you.
Well, definitely the collaboration is focused on oncology targets. So first off, we can say that any current ADC, you know, target, tissue target or tumor target is really viable for a DAC, a degrader approach. So that's a large universe of existing drug targets for ADCs are available. In addition, any new target on the cell surface could also be explored. And so that, I think, is you know what could be included in the collaboration. Most importantly, though, it's the degrader molecule that I think vastly expands the target universe for ADC technology. And I think that does open a new door of targeted therapeutics for ADCs.
And so that, that really, I think, is what is gonna be the major strategic advantage for the degrader antibody conjugate technology. Thank you for your question.
If I may ask just another question. I'm just curious, in terms of what could we expect in terms of the therapeutic windows for DAC, you know, as opposed to traditional ADCs? Do you also expect the same levels of bystander effects? Thank you.
Gwenn, would you like to answer that question, please?
Sure. So, I don't think that we can comment yet on whether or not there will be an increased or decreased amount of bystander effect. I think one of the advantages of combining the degrader modality with the antibody is that the degraders are inherently more selective and therefore less toxic. And so a bystander effect in, in terms of how you thought of it in, in the ADC world with the conjugation of toxins, I think it will not be as significant with respect to its impact on the therapeutic index. So I would expect that we would have an increased therapeutic index for actually both agents, as you would think of them in their, in their classic form.
Thank you so much.
Thank you.
Our next question comes from the line of Joel Beatty with Baird.
Hi, congrats on the deal, and thanks for taking the questions.
... With the pending partnership of Seagen and Pfizer, could you comment, is this a collaboration that was reviewed by Pfizer at all, or do they have input into this?
Our understanding is, yes, it was reviewed by Pfizer, and so that is, you know, an important aspect of this.
Great. And then with the agreement with Seagen, does Seagen have the right to veto Nurix opting in on a target, similar to the way it's laid out in the Gilead agreement?
We have not disclosed the mechanics of the option arrangements, so I can't really comment on that at this time.
Great. Thank you.
Thank you.
Our next question comes from the line of Stephen Willey with Stifel.
Yeah, good morning. Thanks for,
Good morning.
-taking questions. This sounds like a pretty interesting concept, but I guess, can you speak to some of the work that you've done thus far just to establish technical proof of concept?
Well, I'll take the first part of that question, Steve, which I'll answer it with the fact that we're in the clinic with the degrader molecules that work quite well. So we've established that these molecules have catalytic activity. They, when administered, hit their target very efficiently and cause complete degradation of the target. I'm referring to the BTK programs we have. So I think that's probably the most important proof of concept. And then adding to that will be the specificity of antibodies. There have been others in the field that have worked on preclinical programs around DACs, and I'll hand it to Gwen to talk about what's been done in the early days of this DAC technology.
Thank you, Arthur. So there is a little bit of literature out there describing how you can conjugate degraders to antibodies, and you can get effectively enough concentration of degrader into cells to basically have that target coverage or elimination of target proteins that we expect with our degraders. I think we won't comment about what we have done internally or what Seagen has done internally to vet the technology, but we feel very confident that we'll be able to take the effectiveness of the degraders that we have seen in our testing into this setting. And then we really do think that we can also innovate on this technology. In this format, we have a little bit more flexibility in our degrader design because we're afforded the ability not to have to optimize for oral bioavailability.
So in ways, that we haven't even explored yet, we think this has a lot of potential to allow us, more chemical flexibility, more chemical, exploration, to really achieve some really innovative degrader designs, that will work very effectively in the DAC format.
Thanks, Gwenn. And if I could just add, I just wanna be clear, I mentioned our BTK degraders. They are not part of this collaboration. This collaboration is focused on novel targets.
Okay, that's helpful. And maybe a bit of a naive question, but presumably, within anybody's scaffold, you can leverage less frequent dosing. And I guess I'm kind of wondering if you need to kinda tweak the PK profile of the degrader that you're delivering in order to accommodate the resynthesis rate of the target protein. And then you talked about the multiplicity feature here, I guess being able to use the same degrader across multiple different antibody scaffolds. But I'm guessing that the resynthesis rates for some of these target proteins are probably different across different target tissues and organs. So I guess I'm just trying to think about the degrader part of this, the pharmacology, and then how that ties into less frequent dosing.
Okay. Well, thanks, Steve. I'll start out and give you a, you know, really largely theoretical answer, I would say. But as with our, you know, bare degrader molecules, our current degrader molecules, we have been exploring and establishing fundamentally new PK/PD parameters. These are fundamentally different molecules, as you know. And in that exploration, we've been quite successful in identifying, you know, these once-daily dosed compounds that do in fact have long half-lives in and of themselves. So I would expect, at a theoretical level, that the PK/PD we're exploring here will also be new and will be long-lasting, given that antibodies do have long half-lives.
So it is yet to be determined, but I would anticipate it, it being a long PK and PD relationship, and perhaps accentuated by the fact that we're degrading the targets, and as you cite, the resynthesis rates will have to be accounted for as well, which take the cell longer to do than simply inhibitors acting on the target. So that is a theoretical answer. I'd anticipate long half-lives for these compounds.
Okay. And then just on the multiplicity side, I guess this is just a, again, another naive question, but do you typically see pretty distinct resynthesis rates of the same protein within different target tissues?
Gwenn, do you want to take that question?
Yes, you can. Typically, it's hard to say typically, you know, we've pursued many different targets, but, I think that's, that's a hard thing to answer unless you've maybe seen 20 or more drugs. I would say that in general, what you're trying to target is your disease tissue, so, so it, you're really thinking about the disease setting, and the disease setting, isn't as multiplicative, I guess, as, as you might think.
So, eliminating the target in the disease tissue is a real focused way to look at your PD, and I think that's one thing that we have really learned with our BTK program, by focusing on the PD and the elimination of the protein within your disease cell type, you really can have kind of a laser focus on trying to get your dosing and scheduling right.
Okay. Thanks for taking the questions, and, congrats.
Thank you, Steve.
Our next question comes from the line of Eric Joseph with J.P. Morgan.
Yeah, good morning. Thanks for taking the questions. Just to clarify, are there specific targets or cell antigens that are predefined under the collaboration agreement with Seagen? And I could see how like the DAC approach could be an end run around, you know, the limited bioavailability for some TPD chemistry. That said, are you precluded from developing an oral degrader for any target within the Seagen collaboration if, you know, if you are sort of able to innovate around any bioavailability issues?
Yeah, excellent questions. So first off, there are specific targets under this collaboration that are identified, and we have not disclosed what those are. Those are new targets to the Nurix pipeline. That's what I can tell you. They are focused on oncology. So the second part of your question is an interesting one as well. The collaboration is exclusive on those targets, irrespective of what drugs ultimately come out of it. So if an oral drug were to be developed, independently, that would be under the collaboration. But the intention is for these to be DAC products, to be antibody-based products.
Okay, great. I know it's super early stage with the, with the announcement here, I guess, is there a general sense of when a first development candidate might be nominated? I guess, how far out should we be thinking on that front?
So I guess I would answer that, Eric, by saying, as with our other collaborations, we expect within the term of the collaboration to have our first development candidate, which we achieved with Gilead. And so we're excited to see these advance into the clinic.
Okay, great. If I could, maybe just one quick question on the proprietary pipeline. Any update regarding regulatory actions for NX-2127 to provide on this call, I guess, or when you might sort of narrow, are you narrowing guidance at all as to when you might be updating investors on that front?
So we're gonna remain focused on this topic for today's call, Eric. We did update our financial guidance. That's the only thing I think I'd point out.
Okay, great. Thanks very much. Thanks for taking the questions.
Thank you.
Our next question comes from the line of Gil Blum with Needham & Company.
Hey, good morning, everyone, and thanks for taking our questions. So generally, use of ADCs, you know, improves the therapeutic window. So maybe a different way of asking questions that was asked here before. Does this provide you access and the ability to maybe look at protein degraders that previously you wouldn't have because the target is essential?
I think that's a fair statement. Gwen, do you want to elaborate at all?
Theoretically, absolutely. I think the antibody conjugate gives us the ability to expand the range of targets that are now relevant for degraders. So, in an example like you suggest, an essential protein that if you eliminate it, even in healthy cells, you would have a negative impact. If you can then restrict the delivery of that degrader only to the cells, the disease cells, then you can use that target, and that could be a real advantage, right, to expand the repertoire of places that you can take degraders.
So we are not gonna comment on what targets that we're gonna start with, but I do definitely think that is, it's a point to be made that, we're trying to enable both of these technologies by taking advantage of the best parts of either one, which is why I think we're so excited about it, about running this collaboration.
Great. And maybe another topic that was touched upon a little bit also in your own presentation. So it feels like there's potential here to overcome certain resistance mechanisms that are typical for some other agents, both through, you know, the differences in PK/PD and the fact that the protein degraders remove a protein. I'd love to hear your thoughts on that.
... Gwenn, would you like to go ahead?
Sure. I mean, we absolutely think that the degraders have the potential to really address resistance as it happens within the target protein itself. We've learned this really extensively with our BTK program, in that even, you know, minor changes on the surface of the protein that would otherwise render inhibitors completely ineffective can be solved through removal of the protein itself and retention of the interaction of the ligase and the protein in that event-driven pharmacology that these degraders work in. So absolutely targets that otherwise show mutational resistance to inhibitors would be great fodder for this technology.
But this technology also, you know, adds that extra layer of new routes to selectivity so that you can more effectively get to your target tissues and more effectively eliminate some of the, the limitations of therapeutic index that would happen through either ADCs alone or, in some cases, degraders. But I think ADCs are where we're really adding the advantage of the degrader.
All right. Thanks for taking our questions, and let me also add my congratulations.
Thank you, Gil.
As a reminder, that is star one one to ask a question. Our next question comes from the line of Peter Lawson with Barclays.
Thanks for taking my questions. I guess just around IP protection, is there anything there we should be thinking about that can hinder other degrader or ADC companies from entering the space? And then a question about toxicities and kind of your thoughts if there could be a potential drug class toxicities for these DACs.
Okay. Thanks, Peter. So first off, on the IP side of things, really, the intellectual property associated with these kinds of molecules is quite intense, I would say, in incorporating both, ADC, intellectual property and, of course, degrader intellectual property, and then ultimately, the molecule-specific intellectual property. So, these are, I believe, will ultimately be, you know, very well protected, unique and proprietary molecules. So that's, the first, part of your question. With regard to the second part, I'll turn that over to Gwenn with regard to any class, toxicology, I think it was. Gwenn?
Right. So I think it's a little early to speculate on that. I think we'll have to go quite a bit further down the line of exploring our targets to understand. But I think we feel pretty comfortable that the degrader itself affords you quite a bit of control of toxicity. You're going after a single target, you're going after a disease driver target, and therefore, unlike toxins, which are, you know, typically associated with the ADC field, you're not expecting deleterious effects everywhere the drug is exposed. So just by virtue of that, I think we've eliminated some of the possibility of that kind of class effect, but we won't, you know, we won't know until we go in farther.
I think there was a lot of speculation with the degrader field itself, whether there would be any class effect of general issues, and I don't think we've seen that yet, and obviously, more degraders need to get into the clinic to understand that. I think we're very hopeful that, you know, this is a combination of two different types of selectivity, and by virtue of that, I think a therapeutic index and a reduction of tox is kind of what we're after.
Gotcha. And then just a final question, and it kind of touches upon prior questions of whether the delivery of the degrader via this antibody and, you know, through the endosome and, or, and the conjugation itself, if that changes the level of degradation and the speed of activity of the degrader.
Gwenn, do you wanna keep going with that line?
Sure. So, there may be a slight reduction in the speed of degradation, I suppose, right? Because there are multiple steps now that have to take place to move from the conjugate all the way into degradation. But, I don't know that we'd wanna speculate too much on that. I think there's a huge advantage of having the degrader not have to, you know, basically be orally bioavailable. You have direct delivery on attached to the antibody into the system. So, that may afford us speeds in ways that we haven't seen it in the oral realm, and it certainly gives us a lot more chemical flexibility. So I think we're opening up a number of doors here, and we're kind of defining some new space.
I think some of those parameters are gonna come out when we've nominated our first candidate, and we get to see the action in the clinic.
Great. Thank you so much.
Thank you.
Our next question comes from the line of Joe Catanzaro with Piper Sandler.
Hey, everybody. Thanks for taking my questions, and congrats on the deal. I guess maybe a couple follow-ups on some things that have already been discussed. First, Gwenn, I know you mentioned, you know, potentially more chemical flexibility, but just wondering if there's any other specific different considerations around degrader design when thinking about potential conjugation, you know, obviously relative to what you've done with bare degraders. I guess I'm thinking whether a conjugation handle needs to be incorporated and how that impacts the screening process, but any additional thoughts there would be appreciated. Thanks.
Gwen?
Sure. Thanks for the question. I don't think we can share a lot of our planning, but I will tell you we're doing a lot of planning in that regard, and we will be changing a bit of how we design and test and evaluate the degraders to allow for this process. So yes, I mean, we have to be able to very effectively conjugate these degraders to antibodies, and therefore, we will have to have handles for that conjugation, and so we'll have to be screening our degraders in that context. So, you know, is there anything particular that we could tell you about the efficiency of that yet? No, I don't think so.
But, one of the advantages I think we have in this space is we set up automation, chemical automation very early. So we really do have the capacity to create, hundreds of, new degrader molecules and test them for whatever we're focused on. So in this case, we're focused on, mechanisms of design that will allow us easy conjugation. So we're really looking forward to that, and we'll absolutely share, learnings from that as we go.
Thanks. And then maybe my second quick question, I guess, a follow-up on this PK/PD discussion, but just a little bit different. I know with traditional ADCs, there's usually like a hit to pharmacokinetics as you conjugate more payload. So just any thoughts around how many degraders you think you could potentially conjugate and still maintain favorable PK properties? Thanks.
Gwenn, further scientific speculation, Gwenn?
Sure. So, we don't know yet. We do think it's going to be an antibody degrader target, a specific event. There isn't going to be a set number of degraders per antibody that will always be relevant. And, you know, the beautiful thing about this degrader modality is that event-driven pharmacology, the ability to get highly potent removal of protein from the cells, it affords you not to have to have a heavy load of drug on board. And therefore, in this context, I think, the existing technology, the existing number of conjugates per antibody that has been exemplified by the ADC field, is basically sufficient.
So I don't think we have to go through any sort of unusual number ratios to get a proper amount of drug onto the antibodies and therefore exposed and in the cell.
Okay, got it. Appreciate your thoughts, and thanks for taking my questions.
Thank you.
That concludes today's question and answer session. I'd like to turn the call back to Arthur Sands for closing remarks.
Thank you. Well, to summarize, we believe the Nurix-Seagen collaboration announced today is truly a strategic landmark event for both the TPD and the ADC fields, as we embark on a new chapter in the development of highly specific and effective cancer therapeutics. With that, I'd like to thank everyone for participating in today's call. Bye-bye.
This concludes today's conference call. Thank you for participating. You may now disconnect.