All right. I guess we'll get started.
I've had it. My name is Eric Musonza . I'm one of the SMID biotech analysts here at UBS. Pleasure to have Martin Lehr from Context Therapeutics with us.
Thanks for having me.
I guess just to get us started, maybe for those less familiar, could you give us an overview of Context and what you're working on?
Absolutely. So Context is an emerging biopharmaceutical company developing T-cell engagers for solid tumors. T-cell engagers, simply put, are antibodies where one arm of the antibody binds to a cancer cell, the other arm binds to an immune cell. There's a variety of different ways of binding and activating an immune cell. Our preferred choice of doing that is using what's referred to as a high-affinity CD3. And so that's a very potent method of activating the immune cell. And what we've seen over the last year from companies like Harpoon, Janux, and Amgen, when one uses high-affinity CD3, you really give yourself a great chance of seeing profound efficacy, in solid tumors, which has been seen across prostate as well as small cell lung cancer in those references I just gave.
Our portfolio is growing. At the start of this year, we had one asset. Over the summer and early fall, we bought assets number two and three. We have a Claudin 6 by CD3 that is in the clinic, and we're actively enrolling for that phase I clinical trial. We have a second asset targeting mesothelin that will be entering the clinic in early 2025. We most recently acquired a Nectin-4 by CD3 asset from BioAtla. Nectin-4 is a very hot ADC target that we think carries great potential as a T-cell engager, and that we're projecting to enter the clinic in the next 18 months. A really exciting time for Context, a growing pipeline, and looking forward to telling you more about it.
Great. The T-cell engager space is getting increasingly competitive. What parts of your platform do you think differentiate you?
Yeah. I always think frame of reference is important. So where we were a year ago within T-cell engagers, absolutely, there's more competition. On a relative basis, T-cell engager competition versus ADCs, T-cell engagers are not very competitive. There's relatively few programs. And we think that's really the key one of the key value drivers here is the scarcity component.
As we think about the competitive landscape where we differ, what we are particularly focused on is targets that are clinically validated by antibody-drug conjugates. So ADCs, large pharma has invested tremendous amounts of capital in that space over the last couple of years. And as we think about the next three to five years, those investments will be in the life cycle management stage for large pharma. So how do they create a moat around those investments? We think T-cell engagers could really be a core part of that strategy. A T-cell engager can be used after an ADC. It can be used in combination with an ADC.
And so that, that logic to us makes sense. Scientifically, there's a good rationale too. An ADC versus a TC is a different mechanism of action, different adverse event profile, and different resistance pathways. It, you know, the way we think about it, Eric, is sort of a yin to the yang. An ADC, because that uses a very potent chemotherapy attached to an antibody, that requires to work internalization in the cell. So you need very high target density to get sufficient internalization. And if you're using chemo, you need a rapidly dividing cell. A T-cell engager works very differently. It's 50x to 100x more potent than an ADC. It can work in low, medium, and high-expressing cells. And generally speaking, prefers a cell that's maybe dividing a little bit more slowly.
And so if you combine the two strategies, you basically can address the gamut of cells within the tumor that one would like to kill. So from a competitive standpoint, I don't think a lot of companies in our space or really any are thinking about that combination potential. And so in our case, all of our programs were picked specifically with combination potentials in mind. So an example would be our mesothelin program. Mesothelin is co-expressed with folate receptor alpha. There's an approved folate receptor alpha ADC that AbbVie acquired from ImmunoGen, called Elahere, that would be a very nice combination product for us to develop. Also, a lot of our competition isn't using high-affinity CD3. They're using weaker payloads. And we think that will ultimately leave efficacy on the table.
The reason those companies who've used weaker payloads is they're worried about the primary side effect with this class, which is cytokine release syndrome. But it turns out clinicians have gotten very good at managing CRS over the last couple of years. They do that in a very cost-efficient manner, with step dosing. They give a priming dose to warm up the immune system before the full dose. And then they actually just give prednisone. So it's a commonly used generic steroid. They give 16 milligrams, the first and/or second dose. And that blunts the immune response, but it doesn't have a huge impact on activated T-cells. And so through that, clinician ingenuity, the main dose-limiting side effect has been mitigated, to a large extent. And so our competition is really using weaker payloads. And the analogy I always give is in the ADC space, people always talk about drug-antibody ratio. How much chemo can you attach to an antibody?
And if for an equivalent ADC target, if you have manageable side effect profile, you'd always want a DAR of eight versus a DAR of two. You'd want more drug per antibody to maximize the effect. And we think the same thing here with high-affinity CD3.
Makes sense. So you discussed some of the techniques and strategies for addressing the CRS issue. What are you doing regarding durability and potentially clinical activity?
That's the $64,000 question, the T-cell engager space. Where we are today, T-cell engagers, generally speaking, have slightly better durability than ADCs, typically on the range of 10%-30%. The reason being ADCs are debulking agents. And so they'll decrease the tumor size initially, but then have poor durability. T-cell engagers struggle with T-cell exhaustion in some cases. And so you can shrink the tumors, but over time, the actual fitness of the T-cell decreases, which is what's engendering your therapeutic effect. And so what we've seen recently is monotherapy activity with these drugs. You have the most recent approval, Amgen's DLL3 targeting CD3, tarlatamab, which is now branded as Imdelltra. That was the first ever approval in second-line small cell lung cancer.
That had about a 40% response rate in its registration trial and a 4.9-month median PFS, which is quite good in that indication. But to answer your question, how do you improve on that? And there's really two ways of doing it. So historically, with T-cell engagers, companies would run into CRS. And so they wouldn't actually get into real dose optimization 'cause they were optimizing for the safety, not for the efficacy. So I think what you're gonna see, Eric, in the coming year is companies, 'cause they don't have to worry about that side effect much, doing true dose optimization. And so durability may just be enhanced by playing with how often you're giving the dose and how much dose you're giving. A higher dose with a T-cell engager may not actually be better versus a lower one.
The second thing is how do you functionally improve the fitness of the T cells? There's a variety of approaches people are doing. One is in combination with checkpoint inhibitors. So the attraction there is pembrolizumab or Keytruda is gonna go generic shortly, and so the cost to do those combinations decrease. What we've seen from preliminary, primarily academic data, is that combinations with pembro tend to improve T-cell fitness and improve T-cell persistence, and so you can improve durability with that combination. The other is through the use of what's referred to as multi-specific antibodies. So combining a CD3 with a co-stim like CD28, 4-1BB, or CD2. I think our preference would be CD28.
And there's some interesting data initially, again, very early, primarily academic, looking at combinations there where you would actually give a lower dose of a CD3 potentially to combine with a weaker co-stim to improve that, that persistence. So I think that's, that's sort of an interesting area of science. I would say it's, it's science versus data right now. But that's certainly what we're looking forward to over the next year or two.
Got it. Turning to CTIM-76, this is your Claudin 6 CD3 bispecific.
Yeah.
Could you explain the biological rationale for targeting these two combinations of receptors? And, I guess any data you have to support this at this point?
Yeah. So fortunately, we just presented data on Saturday, at SITC, in Houston, talking about our first dose selection for CTIM-76. CTIM-76 targets Claudin 6 on cancer cells. And I think what a lot of oncology companies are searching for is targets that are wholly restricted to cancer cells. The idea being that you could then use a very potent cytotoxic to kill the cancer cells and spare all the numerous normal cells. There aren't a lot of targets like that out there, to be honest, probably about a handful. Most are what's referred to as oncofetal proteins. So these are proteins required for the development of the fetus and then post-birth, often shut down through epigenetic silencing. Claudin 6 happens to be one of those five oncofetal proteins. Interestingly enough, it was discovered in the 1990s during the Human Genome Project.
A little individual named Uğur Şahin , who then would go on to found BioNTech, discovered it with his wife, and then really spent the next 20 years trying to iron out how one developed an antibody against the target. The beauty of Claudin 6 is it is found only on cancer cells and a wide range of cancer cells. The challenge is our body has about two dozen different types of these Claudins. Claudins serve as tight junction proteins. So they help cells attach to one another to maintain cell permeability and barrier function. The Claudin 6 history, if you look at the phylogenetic tree, most recently diverged with Claudin 3, 4, and 9. Or say it differently, 3, 4, and 9 look very similar to Claudin 6. 3, 4, and 9 are found in your liver, pancreas, ear, and gut.
The challenge for the field is developing an antibody that is selective for Claudin 6. In that antibody-binding region, 6 versus 9 are different by one amino acid. So it took a lot of, I would love to say, ingenuity science to develop that antibody. It was like years of trial and error. You know, you bang one mole in the Whack-A-Mole game and another pops up. And that's really what happened. And ultimately, people finally cracked that nut. When they developed those antibodies and put it in animals, they were very toxic and they didn't know why. And it turns out Claudin 3 and Claudin 4 also share very similar homology. They differ by three amino acids. And so it was just very hard to develop an antibody that was just 6 selective versus the others. And so that's really what we bring to the table.
It's not a fancy antibody that we have. There's no real bells and whistles. We're using high-affinity CD3. But I think that reflects the sort of provenance of the target, that it's a pretty simple target. It's restricted to the tumor. And therefore, our antibody reflects that. Very different than our other programs, which have much more logic gating associated with them given the challenges of those particular targets.
And so what tumor types are you targeting, at least based on what you have so far?
Yeah, so as you may know, I'm a recovering venture capitalist, and so one of the things I never had much favor for as a VC were basket trials. For our companies. The reason being, you know, you would get the data from the trial and it'd be like eight lung cancer patients, six ovarian, and I would never know how to underwrite the next investment. And so I think one of the things that we feel very strongly as a company is, we really want to avoid basket trials as much as possible and give ourselves, let alone investors, data that we can use in an actionable sense. And so Claudin 6 is expressed in a wide range of tumor types. It has a very high prevalence in gynecologic cancers. And so about 50% of ovarian and endometrial patients will have Claudin 6. And they have it at pretty high levels. And so our feeling was, let's focus on those patients for the phase I. I think it's pretty reasonably well appreciated that for ovarian right now.
Anything north of a 35% response rate isn't interesting to investors, therapeutic doses. And then for endometrial, about 25%. And so for us, focusing on those tumor types also creates tremendous economies of scale for the clinical trial. You just need good oncs. You can do it U.S. only. You only need about a dozen sites.
Got it. And I guess with that, could you give us some more detail on the study design for the phase I/II that your phase 1a, 1b study that you have upcoming?
Absolutely. So one of the questions we get a lot from investors, particularly those who had invested in T-cell engagers 10 years ago, was, well, isn't your phase I trial gonna take years? Isn't there gonna be a lot of trial error? Well, to be fair, there's always trial and error. But we've learned a lot from our predecessors. And there's two companies that really come to mind, Amgen and Harpoon, that learned a lot in their clinical trials that we're adopting and that, frankly, the FDA is advising. And so what people do now is they do step dosing. So you don't give just one dose. You start at a low dose, prime the immune system, and then give a higher dose. You co-medicate with prednisone as well. And so those two levers that people use to manage CRS should make clinical trials much more efficient.
And so for our trial, it will be a phase 1a/b trial, dose escalation expansion in the 1a. The first two cohorts are single patient. So the FDA requires you to start at a very low dose. It's referred to as the MABEL dose, which is typically your EC20 and your most sensitive in vitro assay. But then they enable you to scale quickly from there. So we're going in half-log increments from that point. And then, from those two single patient cohorts, you move into a 3x3 with a traditional design, ultimately in the Project Optimus in the 1b, which is evaluating two doses. You're minimally biologically active, and then your recommended phase II dose.
Got it, and what criteria are you using to figure out how to move forward with your phase II dose? What are your main selection points?
So, that I'd love to say we could tell you right now, that's a discussion with the FDA. Project Optimus is still very new, and so what the company tries to articulate, particularly through PK/PD modeling, is. This is our recommended phase II dose. This is our MABEL biologic reactive . This is why we think Y for each. And you move forward, and the hope is we'll be able to get to that really quickly and then start the 1b while the 1a is still going and backfill in the 1a.
Got it. I guess with that, could you give us a bit more of the timeline of the next 12-18 months on this trial, what to expect and any potential data flow?
Yeah. We're pretty conservative in our guidance 'cause weird things happen in clinical trials all the time, so our guidance right now is initial data the first half of 2026 for that program. That trial just started getting up and running.
Got it. Let's turn to CT95. This is your Mesothelin CD3 bispecific. Could you explain how you came to this construct and what data guided you there?
Yeah, so this, this was an interesting one 'cause mesothelin for me was a blast from the past. I remember when I was at venture capital looking at companies like Aduro, Atara, Harpoon, TCR2, and remembering that this target failed for all those companies. And so when we initially looked at this asset, I said, "Oh, you know, no. I don't wanna fail," and, you know, a number of our scientific advisors said, "You know, the science has changed. We should really, really look at it." And so while we were looking at the target, we came to find that there was a key paper in 2020 that came out about mesothelin.
It may explain why some of those historical failures occurred. It turns out mesothelin is a GPI anchor protein, much like Nectin-4, that is cleaved. It was always thought that mesothelin saw one enzyme. It was cleaved into two pieces, one that stayed anchored via GPI to the tumor, and then the other sort of floated away. But that cleavage process was inefficient. So it really didn't matter where on the protein you bound. What the 2020 paper said was actually the protein sees six different enzymes. It's a very efficient cleavage process, and there are sites all over the protein.
And so you really wanna bind as close to possible to the cell membrane. And so that was interesting. That would explain a lot because if you're binding to the portion that's floating away from the tumor, you're not gonna have good data. The other thing that became apparent is all those companies were giving very high doses of drug that normally for a T-cell engager would be very toxic. And so it would make sense. You're giving a lot of drug because it's all being absorbed by these fragments. There's not a whole lot of free drug available. While this was all going on, there were deals happening. And so we saw Pfizer buy a mesothelin ADC for $53 million upfront from Harbour BioMed . RemeGen, on June 3rd had really exciting data.
Mesothelin high patients in the phase I trial where they had 45% response rate in ovarian, which is quite strong, and then about a 33% response rate in non-small cell lung, as well as cervical. That really caught our attention. And then in August, Outpace Bio, which is a private biotech, raised $144 million financing led by RA Capital to predominantly fund their lead mesothelin CAR-T program. And so we were seeing all the tea leaves that the science was coming together, that pharma and investors were starting to believe. And so we jumped all over the asset and the opportunity. Mesothelin's found in 30% of all cancers. It's just a massive, massive market opportunity, and one that we really couldn't pass up on.
And, I guess in your avoidance of basket trials, how do you plan on moving forward with this construct to figure out which tumor types you'd be most successful in?
Yeah. So we're gonna, and I always like to frame this. It's not that we're all into ovarian. Ovarian's a very logical starting place for mesothelin because almost all the patients are mesothelin positive and at a high level, so you don't need to screen. We did buy this asset. The prior company did not have a mesothelin diagnostic, so we're wrapping up development of that. And then we would increasingly add cohorts, particularly around pancreatic and mesothelioma, which is a rare cancer that's associated with asbestos exposure, but still about 1,500 people die per year in the U.S. And so that would be a nice rare cancer opportunity for us as well.
Could you elaborate a bit more on the phase I study design?
So that is very similar to our Claudin 6 design. With the only difference being instead of a 3x3, it's a Bayesian adaptive design.
Got it. And would you consider potential combos with this asset?
Over time. So for all of ours, I think what would make sense is combinations with an ADC or a radioligand that view both as DNA damaging agents. And so the nice thing, if you look historically at the pembrolizumab combinations with chemotherapy, the idea again is pembro is very good at tumor or is very good at activating T-cells. In the case of chemotherapy, it is very good at debulking the tumor, releasing a bunch of neoantigens, warming the tumor microenvironment. So it is a strategy that makes sense. For us, for mesothelin, it is co-expressed with folate receptor alpha. And I just think if you look at folate receptor alpha, it is expressed in over a dozen different tumor types.
Ovarian just happens to have a very high level of folate receptor, and that's where the approval is. But I think we could potentially, through that combination, greatly expand the use case of folate receptor alpha ADCs.
Got it. And what's the timeline look like for this trial over the next 12 to 18 months?
So that's moving forward quickly. So we acquired the asset July 15th. We're targeting first patient, early 2025, and then initial data, you know, somewhere in the first half of 2026. So it's cooking.
Yeah. It's going quick.
Yeah.
Excited to see you at that time.
It was. It helped. We bought the asset. It had. It was IND cleared. They had drug manufactured, so really it was a blocking and tackling exercise to set up the clinical sites.
Turning to the Nectin-4 asset you mentioned earlier, CT-202, this is a Nectin-4 x CD3 bispecific. I know you briefly touched on it, but could you elaborate a bit more on how you plan to, I guess, establish a market presence here, how you differentiate from other potential competitors?
Yeah. So there's the question we always get is, how are you gonna compete with the dozen or so clinical stage or approved Nectin-4 ADCs? And we love that. That's actually part of the reason and our underwriting of this acquisition. We have an approved Nectin-4 ADC right now from Pfizer via their acquisition of Seagen. That drug's called PADCEV. You have a variety of late-stage programs from Bicycle and others. You have two phase ones ongoing from Lilly. And so the idea being here is these drugs will get approved. They're right now just approved in bladder and urothelial cancer.
There are many other cancers where we would love to take these drugs into colorectal cancer, particularly microsatellite stable, which is about 65% of the market, triple negative breast. So these are large underserved markets that, I think a combination with a Nectin-4 ADC would make a lot of sense. So for us, but initially we're focused on Nectin-4 resistance. All of these drugs that are in development are gonna suffer from durability issues. It's just on mechanism for ADCs, right? They debulk tumors. They provide selective pressure on the low and medium cell populations. Those clones propagate, and that's the new tumor.
For us, Nectin-4 is, of our three programs, actually the largest market. You know, our bottoms-up analysis directly put it at about 125,000 treatment-eligible patients in the U.S. right now. That's substantial for a cancer opportunity. If you look at PADCEV, the approved ADC in Nectin-4, right now it's at about a $3.5 billion -$4 billion run rate just in bladder cancer. This is a tremendous market opportunity.
One we're super excited about. The asset itself is fascinating, so Nectin-4, the challenge from a drug development standpoint is it's not untargeted. It's not perfectly selective for the tumor. You have it in your skin, your hair follicles, sweat glands, and so driving selectivity is key, and so our antibody has a couple of components to it that help potentially overcome that normal expression. The first is it's avidity-enhanced, meaning it is not a high affinity binder to Nectin-4. It's actually a very moderate to even weak binder to Nectin-4, and so when we see a Nectin-4 monomer, our drug has a very high on-and-off rate. You tend to have a lot more Nectin-4 in the tumor versus your skin, and so there, where there's more substrate for the antibody to bind to, you can have bivalent binding.
And so there are those two weak bonds when both, both bind to the tumor associated antigen. That's when the avidity kicks in. The drug becomes very, very tightly bound to the tumor cell surface. It's a thermodynamically stable bond with a high on-rate. And so it's stuck. And then we have monovalent binding of the CD3 to the T-cell. So you need a lot of these constructs that we have, our CT-202 drug, in the tumor microenvironment to sufficiently activate the T-cell through TCR cross-linking. The last part is, and pretty nifty, we licensed the drug from a company out of San Diego called BioAtla. BioAtla has a pH-dependent platform. So cancer cells are different than normal cells. Normal cells rely on oxidative metabolism. They make ATP. ATP is the universal currency of how our cells work.
Cancer cells prefer to burn sugar in glycolysis. It's a very inefficient energetic process, but that's what they do. They create a lot of lactic acid. That creates a lot of protons in the tumor microenvironment, so you get an acidic tumor microenvironment, or, to say it bluntly, a normal cell has a pH of about 7.2 to 7.4, a cancer cell about 6.5, and so what BioAtla did very painstakingly, these are hard assays to run, so they found that they could tune the affinity to be tighter in an acidic microenvironment, and so for us, I don't know how much that matters for Nectin-4, but for CD3, where you really want to drive the inflammatory response to the tumor, I think that's huge.
They have sixfold higher binding with CD3 in the tumor microenvironment than they do in normal cells. You know, considering the expression in skin, the side effect would predominantly be rash or itching, which is inflammatory. So you wouldn't want to drive any excess inflammation there. And so I think it's a really elegant approach that they gave. Again, it's a three-part approach here with pH dependence, avidity enhancement, and CD3 cross-linking to drive that activity in the tumor.
Got it. And, you, you touched on it briefly as well, but could you give a little more detail on targeting the low and medium Nectin expressors and where that puts you in the landscape and how you think about that going forward?
Yeah. It's fascinating. So we don't, and we talked about this earlier offline, we don't develop drugs. Context is essentially a roll-up strategy. Kind of think about us as a traditional, almost like private equity play where we don't have any in-house research. We use investors' capital to identify interesting assets. We acquire them and develop them. If you looked at the spectrum of targets that were in our purview, so there's about 20 clinically validated ADC targets. And we would've thought, you know, competitive density would be correlated with how restricted those targets are to the tumor, meaning the more restricted, the easier it would be to target and the size of the market.
And so for Nectin-4, it's pretty restricted to the tumor, and the market size is like three or four times prostate cancer. And so we thought it would be super competitively dense. And it's not. There's two competitors predominantly right now, Bicycle Therapeutics, which is using a very weak immune activator. So in their phase I trial, they only had two out of 33 patients respond. So they weren't hitting low expressors, they weren't hitting much of anything. And then there's another company, Rondo Therapeutics, that's using CD28. CD28's a co-stim. It's also rather weak. So in our view, okay, PADCEV is approved. That's an ADC that's gonna kill the high expressors. Rondo's strategy is to avoid the low expressors 'cause that way they can avoid hitting native Nectin-4 in the skin. So they're only targeting the mediums.
I don't know how you run that clinical trial, Eric, to just hit that one population and how one would underwrite your probability of success. So where I think we're different is we can hit the spectrum of low through high. I don't know how many high expressors there really would be if you're used after an ADC. And so the question is, can we hit low and mediums and do it to a sufficient level to not only impact the tumor but also not create untoward toxicity? And based on the preclinical data thus far, it looks to be that way.
And so we're really excited about that program.
That's great. And as you plan for this phase one, what are some of the major, I guess, strategic points of differentiation you wanna show, and how would you do that with the trial?
So not sure yet. It's still early days. I think where we are quite interested again, I think colorectal and triple-negative breast are underdeveloped. PADCEV is approved in bladder. I think there's a rationale to be used in combination with PADCEV. To bump up its activity. Even though it's improved in bladder, you know, it's PFS was about five months. You know, you can improve on that.
And then it's a drug that, in the case of PADCEV, is not approved everywhere for first-line use. And so going into PADCEV-naïve patients, particularly ex-U.S., I think would make a lot of sense. I think there's some clear use cases. We've got some time though, and I'm sure our approach will be tailored based upon the competitive landscape over. The next 18 months.
Nice. And I guess, turning quickly to some final questions, between all these various trials you discussed today and potentially whatever else you might have in the pipeline, what should we most look forward to in the next 12-18?
That's like asking which of my sons is the better baseball player, and I always say they're both great depending on the day. We have three great assets. In the case of Claudin 6 and Nectin-4, Claudin 6 just entered the clinic. Mesothelin's gonna enter the clinic shortly. I don't think it's a stretch to think within the next quarter or two they're neck and neck as far as stage.
Claudin 6 is a very cool new target. Mesothelin's a target that people are looking at once again. The reality is mesothelin's 2X the market size, and so from an NPV basis, that fundamentally should be a bigger driver for the company. Nectin-4 is much earlier. We're not gonna be in the clinic for about a year and a half. There's always risk that weird things can happen prior to entering the clinic, but that's bigger. You know, the Nectin-4 market's almost the same size as our mesothelin plus Claudin 6 programs, and so I think that all has to be taken account over time, but the important thing is I think each of our products can stand on their own two legs. Each has very strong rationale to be used as a monotherapy and then has a clear rationale to be used as a lifecycle management product with a cognate ADC.
We talked about mesothelin with folate receptor alpha. Claudin 6 is a very interesting target to combine with a Claudin 6 ADC. Merck just put their CDH-6 in phase three. They bought it for $1.5 billion last year from Daiichi. And so I think each are fantastic. They're each my favorite kids.
That's great. Could you give us an overview on your cash runway and over the next few quarters how you plan to allocate your resources between all these trials?
Yeah. So we just reported Q3 earnings. We had cash of approximately $85 million. That funds us into 2027. We were fortunate to do a PIPE in May, led by a strong syndicate of institutional investors. So we raised $100 million then. That really was transformative for us. That current capital gets us through both of the dose escalation portions of our Claudin 6 and mesothelin trials as well as the IND filing for our Nectin-4 with runway on the back end. We haven't divvied up how the cash is being allocated per program. And we don't give guidance to specific yearly spend.
Will you be considering partnerships for these various assets and?
I hope not. It's my duty as CEO is to our shareholders, so we're gonna do whatever is right to optimize their returns. On the flip side, one works their whole career to get to the point where the company's on a clear upward trajectory. I think we absolutely feel like the wind is at our backs here. We have three great drugs. T-cell engagers have made huge progress over the last year. You had Harpoon acquired for $680 million on phase I data.
You had Janux with 30 patients' worth of phase I data, had their stock go up by $1.6 billion. And you had the first ever approval in small cell lung cancer with Imdelltra from Amgen. So I think now's the time to really develop these drugs. I think the way you maximize shareholder value is to retain ownership in your assets as long as you can raise money at sequentially higher valuations so that the capital raising is not so dilutive that the equity and the assets become a wash. And I think we're in a place where we can do that right now.
Great. I think we're coming up on time here, but thank you so much for giving us your overview of Context, and glad we got to speak with you.
Appreciate it.
Thanks.
Thanks so much.