Tango Therapeutics, Inc. (TNGX) Earnings Call Transcript & Summary

Okay. Let's get underway. Good afternoon, everybody. Welcome to our day 2 of the Goldman Sachs Healthcare Conference. My name is Chris Shibutani. I'm a member of the research team. We are pleased once again to have Tango Therapeutics join us. Barbara, you and I get to sit down here and go through the background of the company, et cetera. But let's remind people a little bit about you. I remember the first time I met, there were all sorts of people across generations in kind of the Boston ecosystem, PhDs, there are a lot of sort of MIT, [ homies ] who were sitting there saying it's like, "Oh, Barbara's incredible". So you actually had an interesting journey through academia, through commercial, familiar large-cap pharma stuff and you're in the CEO role, I think it really helps to get that understanding of who is in the C-suite of focused [indiscernible], tell us a little bit about yourself just to start.

Sure. Well, thanks for asking. Actually I am, by training, a medical oncologist. I spent the first half of my career in Academic Medicine, trained at Dana Farber and then on the faculty first at the University of Michigan and then University of Pennsylvania. Where my real focus was on breast cancer, breast cancer genetics and worked on the BRCA1 and BRCA2 projects. And that's really what led to my interest in thinking about how to drug tumor suppressor genes, which led to Tango. In the interim, I left Pan in 2005, first I went to GSK and then ultimately, in 2009 to Novartis to lead the early development oncology group for David Epstein and then [indiscernible] at Novartis. So I do think though it was completely unplanned that it's -- that what I have done throughout my now pretty long career because I'm old, is makes me somewhat uniquely suited for this job that I have now.

You are seasoned. We are a fine wine.

Tango , how did the company get it's name?

Oh, it was named by a Third Rock associate as we were putting together the company it takes 2 to Tango. So the idea of the target and the genetic abnormality.

Yes, exactly. And then there's sort of kinship with the synthetic lethality, but there are so many metaphors that reflect this duality aspect of it, it makes sense. Going back still to ancient history, you guys SPAC-ed, you didn't IPO, you SPAC-ed. So post SPAC, how you're feeling about having that heritage? And what does that make you think about, particularly in terms of your shareholder base and stuff like that?

Well, we had a very unique SPAC, which is why we did it. So we were in the process of preparing for an IPO. We had done an one-deal roadshow looking at the whole list of biotech investors that we would like to get into an IPO and Aaron Davis, who was already on our Board and had led our Series B had a SPAC and he said, "What do you think instead about using the SPAC? " And his SPAC, unlike all others SPACs at that time and subsequently was actually built on the same list of biotech investors that we wanted an IPO. So that's why we did it. And I think there's a couple of things. One, the shareholder base remains largely unchanged. Our redemption rate was somewhere around 2%, which is not the usual number for a SPAC. And I think maybe the bigger issue is that 80% of the company is still held by our top 10 investors, which makes it somewhat illiquid.

Okay. Yes. So there's some consequences to sticky money, I suppose, but it's actually...

Do they like that? They believe in us?

Yes, no. And we've had opportunities to engage and it's very smart, sticky money, too. So smart patient people who...

Absolutely.

Because this is a journey for a longer period of time because you're taking certain degrees of innovative scientific and clinical risk here. And so when the company came public in the journey that you're at now, we're very much approaching a prime time moment for the company, really over the next 6 to 18 months in the clinic. PRMT5 is no longer just a random channel. It actually generates some eyebrow lifting buzz. There's other folks in the industry here. Tell us about that as a target and maybe frame the opportunity just broadly epidemiologically, et cetera, before we zero in and what you guys have?

Yes, thanks. And I would say, again, for just a few minutes of ancient history. PRMT5, which is a methyltransferase, therefore, an epigenetic target was initially being developed as an epigenetic modulator. No patient selection, just maybe this will work in cancer sort of a chemotherapy type of approach. But the Novartis Broad collaboration discovered and published back in 2015, that MTAP deletion and PRMT5, actually, it wasn't knocked out, it was knocked down. We're strongly synthetic lethal. And we picked up on that and developed a PRMT5 inhibitor that actually they speculated in this paper had the mechanism you needed to make a PRMT5 be synthetic lethal with MTAP. That's what we have in the clinic now. That's what Amgen and Mirati, now BMS have in the clinic, and that's what all the ones coming behind that path.

Okay. And I want to remind a little bit, because synthetic lethality, such a cool phrase, documented success all the way to the commercial level, PARP inhibitors were essentially the poster child for having made it there. More recently, it continues to be a recognized sort of landscape to interrogate, but there are challenges. And there hasn't necessarily been son of PARP or there hasn't been this cascading subsequent graduating classes. Talk to me about some of the challenges with synthetic lethality and what's happening to address those?

I think there's 2 major categories. The first was being able to find the really strong synthetic lethal interactions. Really until that there was CRISPR, be able to do large genome scale functional genomic screens. It was really hard to do anything, but sort of hypothesis generating work. And the likelihood you're going to guess, right, was low. So I think that's the first thing. I think the second thing in Chris Lord at CRUK articulated this maybe the best, which is oncogenic drivers have a very specific effect and inhibiting them is often produces pretty dramatic effects, right? The synthetic lethal interactions have a wide range of what he calls penetrants, a genetic term, but in any case, we'll say effect size. And may also be more difficult to predict preclinically. So for example, the PARP inhibitors, preclinical data doesn't actually look very good. They're very strong in the clinic. The PRMT5 preclinical data looks strong and from the data that have been released so far by Amgen and Mirati, I think, is strong, but it's in the 30-ish percent ORR range as opposed to the 70%, 80%, you could see with ALK or EGFR. So yes, it's a different kind of an animal. It's not a key driver in a cancer. It's often employing some other approach to getting at cancer biology.

Yes. It almost feels as if the history reflects some sort of teleologic journey we found out after words by looking and there's all these pulling of wings from dragonflies, it's a metaphors to stools from legs of tools, et cetera. So it's kind of interesting to figure out how to get full momentum going forward. You guys and a couple of other companies. We had Lloyd at repair as well. Everyone sort of taking this avenue to try and figure out with some of these really challenging targets. So it's as if the opportunity is there, the journey is one, which is -- requires real tenacity with science. So...

That's right.

PRMT5, just give us a little bit of a lesson in MTA cooperative.

So it's a complicated story, but this sort of short assertion I can give you is that MTAP deletion results in the accumulation of a molecule in the cell called MTA, which itself is an inhibitor of PRMT5. And what you need is an inhibitor of PRMT5 that takes advantage of high levels of MTA so that it preferentially inhibits PRMT5 in cells that have that MTAP deletion and therefore, high, MTA. So what you want is a PRMT5 inhibitor that binds better to PRMT5 when MTA is present than when it's not. And that's what we and the other MTA cooperative [indiscernible] inhibitors have.

Well done. Well, then usually, this involves all sorts of arrows that are curves and then sequencing diagrams that we've all been with textbooks too late at night. So -- but that certainly makes sense. You have 2 assets here. The genealogy is kind of interesting. I think 908 and 462, one is more brain penetrant, which is a characteristic sort of that we would expect to see the opportunity to explore maybe in those logical GBM type opportunities. But talk about these 2 assets, because I remember the discussion about these immediately, we on Wall Street love horse races and there's going to be a winner and a loser, you're actually intentionally nurturing a path that is completely sort of interrogating the opportunity set that could make sense for both. Talk about the ultimate endgame kind of strategy? Is there a possibility that one will take the lead? And what's interesting to happen is, I think, 462 is kind of like skipped junior high and is almost coming to the same point. So here we are, and a lot of cards are going to turn for both relatively simultaneously, right?

That's right. So 908 is the first one. It is, as you said, brain penetrant, but it's less potent and selective than 908 a year later with some additional med chem work, we put 462 into the clinic, not brain penetrant, but much more potent and much more MTAP selective and for several well-defined reasons, 462 actually caught up in terms of the clinical trial to the same point. So based on our earnings release recently, we announced that we were in dose expansion with 908, and then we would be in dose expansion with 462 by the end of the quarter. We updated that this morning to say we're actually now in expansion with 462 as well. So the clinical update for the second half of this year will be both of them simultaneously.

Okay. That's very exciting, especially for Adam. Keeping him full time, and it's probably good for Daniella as well, your CFO, who has always been very elegant about keeping his great face as I'm trying to pressure test around time lines, et cetera. So we're finally at that moment and thinking about the second half. Let's drill down a little deeper into 908, the brain penetrant version. Just go through a little bit of the data that you shared so far, what do we know? We had some proof-of-concept biopsy data last year. And there was a biomarker SDMA we're trying to reduce that. Talk about how that biomarker correlates with possibly a read-through into clinical success?

Well, as you pointed out earlier, all things, PRMT5 and synthetic lethal are sort of vaguer than one might like. And it turns out that SDMA is the immediate downstream PD marker for the methyltransferase activity of PRMT5. But it also turns out that the assay is not very sensitive. So you can ablate the signal of the SDMA signal way before you get full inhibition of the enzyme. So it's necessary, but not sufficient. And I think that's what everybody has seen at this point. So we have full SDMA suppression with both molecules, but that alone does not guarantee clinical activity.

Acronyms like GBM, glioblastoma multiform to be respected, to be feared to be admired. It takes a certain degree of courage to get there. So maybe you get a bit of a permission slip in terms of what the hurdle rate is in terms of what defines good data and how many patients we need to see. So help us make sure we're in the correct ZIP code with both of those. How many patients will we see when we have the data? And what do you think is fair to say this is good data, this program in this indication is going to continue to move forward?

Yes. So those are a lot of questions at once. I'll start by saying, I think GBM is like every other hard tumor and several of them have already fallen. You get the right drug and enough of it and I think that will be true of GBM also. We will have, I believe, enough data to answer the question in the second half of this year, whether that's going to be with 908 or that isn't going to be with 908. But I think it's really all a matter of getting the right drug in.

Skillfully done. So I didn't hear an end.

So I can tell you about escalation cohorts, those numbers I can tell you.

Leave me with something.

Yes. So for 908, escalation is finished. We actually have approximately 60, 6-0, patients that have enrolled on the dose escalation portion of the study. The dose ranges are from 25 milligrams twice a day to 900 milligrams twice a day, which explains why the study took so long. And remember also that the FDA mandated a 50% increase instead of the usual dose doubling. So to get from 25 milligrams twice a day to 900 milligrams twice a day with 50% dose increases takes a while. We are expanding at 600 milligrams twice a day. And at that dose, there are 14 patients from dose escalation that have been enrolled. That includes both the actual dose escalation cohort itself and the backfill.

Okay. Perfect.

Well, that's a lot of numbers.

Healthy denominators, that's actually very pragmatic. I think one the treasury moments are the initial unveiling of clinical data or people are doing math on very small denominators and that can become kind of problematic because if you push one patient to response in one direction versus the other, the Street loves to jump to a very dramatic conclusion.

So that's absolutely true.

Jumping dramatically 462, a lot seems as if the catch-up pace of the enrollment there. I always like to as many do infer that this has to do with the reflection of some enthusiasm here.

Yes. For sure. And there were a couple of different reasons. One, being a more selective molecule, we were able to start closer to the active dose range with 462. We were able to dose double. And with a year later, so to your point, people were starting to get pretty excited about these molecules. And very importantly, they had gotten used to looking for patients with MTAP deletion. So 462 -- I would say, going back 908, we struggled with enrollment for sort of the first 6 months. 462 open to a wait list and literally still has one.

908 had a little bit of unfairness of the immediate post-COVID, oh, my god, nobody is doing early oncology clinical trials, handicap clearly, right? By the way, how are we doing just for the whole ecosystem, early-stage oncology clinical trials? Do we have a better sort of panoply of people, who are staffing these trials and things like that, have things gotten a little better? Is it back to normal pre-COVID or not quite?

I think so on both sides, I can tell you better on the biotech side, it's certainly much easier for us to hire clinical people to Tango. In fact, Adam sent me an e-mail over the week and said it's raining CMOs. I said, "Well, that's a good thing. " On the academic side, I also hear from our operations team that has gotten better. It's not perfect, but it's definitely gotten considerably better.

Okay. No, that's very helpful. With 462 as well, it seems as if there's potential for a wider therapeutic window. So we're looking at that efficacy profile, safety as well. Comment about what would be the fair way to compare 908 and 462 from that safety and therapeutic window perspective?

I think all of the PRMT5 inhibitors are pretty well tolerated. I will say, I think 462 stands out in that regard. And one particular measure that I think is fair is that based on the publicly disclosed data from the competitors, and what we know about 908 and 462. 462 is the only one that's actually hit true on-target talks with thrombocytopenia and anemia and very good tolerability profiles up to that point. I think Amgen, Mirati and 908, the DLTs have all been something else. So I think that speaks, first of all, being able to take full advantage of that 45x window with very good other tolerability. Beyond that, they're all pretty well tolerated.

Yes, I think it's been interesting for Tango as a stock. The performance in the [indiscernible].

I try not to look at that.

Well, okay. Excellent. Yes. No, I always find it worrisome when I walk into a biotech company and the CEO has got the ticker running every minute on the stage. It's like okay, now this is in the right direction here. But the performance of the stock actually enjoyed or maybe didn't enjoy, but there was a fair amount of volatility, but uplift as we saw competitive data here. So contextualize for us, because we all love to just say blah, blah, blah, caveat across trial comparisons, it's real, right? And so give us the Barbara Weber contextualization of as we look at other data, how we should frame? Bear in mind this when Amgen speaks or bear in mind this when Mirati Bristol speaks.

Yes. Well, going maybe with the stock price, I'd say we did get a significant bump last summer when Amgen announced that they had activity and Mirati showed their data, because up until at that point, people were unconvinced it was going to work at all. So that was the first big thing. We don't know anything else about the Mirati molecule, except preclinically. And I think preclinically, it looks pretty good. They [indiscernible] may have some bioavailability issues. They have to dose pretty high for activity. And that comes along with the price of a lot of GI intolerability. We've not seen that.

There's always an X, Y and Z access. And so X being sort of response, Y being safety, and Z always crops up durability and duration of response. How are you feeling about what we've seen. It's been pretty limited so far, but what could we see? We think about the challenge of what's happening biologically with these tumors, but what's the right framing of expectations with these patients?

Yes. I mean, obviously, I have to be careful not to talk about our own data, but I think what we've seen publicly and heard unofficially is that the durability in people who respond to these molecules, including stable disease is pretty significant.

Can you put some months range-ish around that significant? And again, respectfully, it's this question of many times when we're thinking about these innovations, we're talking about pretty advanced patients, who've been through many lines of therapy. So significant can mean different things in different sets of settings.

I think at this point, I can only talk anecdotally, but I can say, for example, in the Amgen data, there's a pancreatic cancer patient that had a near CR that was on for almost a year.

Okay. That moves the needle absolutely. These are some very tough situations here. There's very rarely, if ever, a single bullet, combinations often is the approach, because biology is just stand it's often 1, 2 and then some punches here. Talk to us about how you're thinking about possible combination approaches? And when might we be able to get a peek under the hood of what your playbook is like?

Yes. And I believe that very strongly. I don't think any solid tumor is ever going to really cave without critical combinations, Bob Weinberg said this 30 years ago. We're going to have to hit at least 2 or 3 and sometimes 4 nodes in a tumor to really kill that tumor. So it doesn't come back. And I think that that's true. I think what we're looking at is orthogonal combinations of 2 different flavors. One is with oncogenic drivers and our current favorites are those in pancreatic cancer that are relevant to RAS. Because almost all pancreatic cancer is RAS driven. So that means that a pan-RAS inhibitor like Rev Med or a G12D inhibitor, like Rev Med and others could be really interesting in combination with an MTAP. You could also -- I mean, a PRMT5 inhibitor, you could also imagine that you get 2 different things from those, one with oncogenic driver inhibitors, you get fast responses, but you get sometimes shorter duration responses. If what we're seeing and hearing about PRMT5 inhibitors, you may get slower to responses, but longer duration, the combination of the 2 could be quite nice. The other combination we're interested in and it's slightly more speculative, but I think it's real, and we really want to do this, is combination with CDK4/6 inhibitors, because basically all MTAP-deleted tumors also have a CDKN2A deletion, which hasn't in the past resulted in strong single-agent activity across tumors with CDK4/6 inhibitors, but I think maybe something to really consider in combination with a PRMT5 inhibitor. So we're working on those 2 approaches. I think Amgen is going more down the chemo combination. We have no idea what BMS is doing, and we're sort of more interested in orthogonal driver combination.

We think of combinations and there tends to be a need for some gentleness, because of potential for overlapping toxicities. Whenever someone said CDK4/6, I think about resting that bone marrow. So how should we think about the potential for overlapping talks with PRMT5?

Well, it's a good question, because I just told you with 462, we are heading on target talks. It's predominantly thrombocytopenia, a little bit of anemia. I think with those drivers, we're talking about neutropenia. So we could end up with like you could say, well, it's not overlapping, but you could also say we can knock out 2 or 3 lines at once at the bone marrow. It is something we'll have to be careful with.

Anytime there's combination and it's been fascinating coming from ASCO thinking about just 2 targets. But even the modality of the sequencing, whether it's in some form of a bispecific somehow synergy might be too broad a word, but there's some element of benefit that can happen in that instance there. So when you think about how you're going to tactically approach this and simply because I think of you guys as having such sophisticated chemistry, talk about your capabilities and rather than just sort of saying, "Hey, you guys have a CDK4/6, let's jam them together and put them on a date". You're actually going to have to be thinking much more specifically about how to develop a nuanced profile in order to succeed through, right?

Yes, once again, you're dead on. And I mean you have to have, I think, deep pockets in the fortitude to do this, but it's very important. Sequencing even alternating of regimens could turn out to be really important. And that means that if you look -- I mean, leukemias, lymphomas, testicular cancer, breast cancers, all those regimens that have turned out in the end to be very impactful are just exactly that to be able to deal with overlapping toxicities. So let's take it a step at a time and first see what kind of efficacy we get and then think about how we move those into longer-term combinations that really make a big difference for patients.

Okay. I introduce you to my brilliant associate in my team, Darwin and he was digging up all sorts of different realms of combinations across the landscape, including from Amgen, a molecule that they're combining with IDEAYA's MAT2A inhibitor, thoughts?

Yes. I mean that's not an orthogonal combination. Those are 2 inhibitors that hit the same pathway, the way to try and get better PRMT5 inhibition with the combination and with a single agent. I think we spent a lot of time in the last 5 years thinking about that and ultimately came to our conclusion that if you have a really good PRMT5 inhibitor and can fully inhibit the enzyme with a signal agent, you won't get any additional -- or we won't get any additional benefit out of the combination, and we'll add all the complexity that we were just talking about. I think there's also a reason -- good reason to think and some rumors that it did happen that with the synergistic activity that you get with a PRMT5 and a MAT2A combination, you also get synergistic toxicity. And you get -- because the MAT2A inhibitors act the same in wild type cells as they do in MTAP-deleted cells. So for us, that's not a big priority. We're more interested in orthogonal pathway inhibition.

Got it. Okay. That's helpful perspective. That's period paragraph, turn the page to having another asset, which is terrific at this stage of maturity for the company. We always start to say, what else you got for me, TNG260 CoREST inhibitor, STK11-mutant tumors. Tell us a little bit about this molecule and where you're at with it?

Yes, I think this is another really interesting program, completely different, and it's a very novel idea, the brainchild of our founder and CEO, Alan Huang, the idea that you could actually find sort of immunomodulatory synthetic lethality, if you will. And so in this case, we showed preclinically and others have shown with retrospective clinical analysis that STK11 mutations in tumors create an environment that makes those tumors largely resistant to checkpoint inhibition. And that by using a CoREST inhibitor that we've developed, TNG260, you reverse those genetic changes and enable those tumors preclinically to become from being strongly PD-1, anti-PD-1 resistant to sensitive. That's what that trial is about. And I think it's generated a lot of investigator enthusiasm. I think that trial is going really well, and we should have an update later this year on what's going to -- what the guidance on that program will be.

Yes, you made reference to sort of the preclinical work that you've done has been in combination with an anti-PD-1 here.

And it was -- I should say it was designed that way. We actually made it to be in combination with no expectation that it would work otherwise.

Got it. If we think about these mutations, there's been other therapies that have been tried before LSD1, pan-HDAC inhibitors. Maybe just reflect upon sort of what the journey and the challenges have been there.

I think with the pan-HDAC inhibitors, if you squint, there may be a bit of a signal there, but it's always something that's been impossible to sort out, because there's not been complete information on STK11 mutations in those tumors. And in a way, they've been selected against in those studies. So hard to note. Maybe the most interesting thing at the moment is from Jubilant that have an LSD1 HDAC6 inhibitor that they reported 1 PR in an STK11 mutant patient. They call it a CoREST inhibitor. To us it doesn't function that way, but we don't know enough about their molecule to be sure, but the idea is similar in combination with the PD-1 reversing immune evasion.

I think it's very generous and terrific that you're commenting about. I always find with these novel targets in these early stages that success begets broader interest. It's like the tide comes in lifts all boats, and we can talk about sort of the competitive framework ultimately based upon clinical profiles and how that -- the rubber will meet the road. And as we look in that direction, in particular for CoREST inhibitors and STK11 mutants, can you give me a little bit of epidemiologic sense for how prevalent and what are we talking about? I think there's actually some very attractive opportunities here in lung, if I'm not mistaken.

Absolutely. About 15% of non-small cell lung are STK11 mutant. So that's a big number. And that accounts for about 60%, about 2/3 of STK11 mutations are in lung cancer. The other 1/3 are in a smattering of breast, cervix, pancreas and unknown primary, which is usually breast or lung.

Dose escalation ongoing. What can you share with us about where you're at with that and how that's going and when we might ultimately be able to get a peek of some data?

Yes. We started with very good and way better than expected PK for that molecule. So I would say the first dose was -- first dose range was pretty close to the active dose range as predicted preclinically. So I think we're already exploring a couple of different doses, and we'll have an update on what that trial is going to look like soon.

Okay. Darwin has unearthed also some work, the STK11 and KRAS mutations, which he observes looking at the literature, not infrequent. Could you see this as a potential combination strategy that you would contemplate? Maybe talk about that. I would have potentially involve the G2C inhibitor, et cetera, or a pan-KRAS inhibitor in something that we histology agnostic. Another broad avenue to consider? Where is that in your mind?

That's right. So about half of STK11 mutant tumors are also RAS mutant. And there's varying data on the effect of the RAS mutant in that setting. So we've got about half RAS mutant, half not RAS-mutant STK11 mutants enrolled. It does lead to interesting speculation about combinations. The issue right now that has to be solved first, though, is with the existing commercially available RAS inhibitors, the G12Cs, combining them with a checkpoint inhibitor can be challenging, right? So this has to be checkpoint, CoREST, RAS. So that's just the one complicating factor.

Let's talk about Tango as a corporate entity and strategy, et cetera, because simply the PRMT5 has really just taken the centerpiece here, we don't hear about it as often, but you do have some partnerships, Gilead in particular, talk to us about how that's worked out over the years? And is there anything that has been part of your experience that shapes your thoughts about, let's do more of this business development type stuff? Or you're fine where you're your own knitting that you're trying to focus on. Talk about Gilead, talk about that approach as a corporate entity.

Sure. So the Gilead collaboration we've had for a long time, and it's been a very fruitful, very scientifically based collaboration. It's really about target discovery for them in the space of immune evasion. And so they periodically select targets and they license them and take them to Gilead and do the work on them. I think we decided early on that -- and that was a pretty big platform deal that, that was enough. We would do one platform deal. It turned out to be with Gilead, and we have not been interested in another one. What we're more focused on now is a development, partnership and very likely with our PRMT5 program. I mean, you and I have talked about this, that the PRMT5 development path is a huge one. Pancreas, non-small cell lung and a whole range of other opportunities. And I think for us, at 150 people based in the U.S. to be competitive with BMS and Amgen, we're going to need a global development partner. So I think that's what you'll hopefully see from us next.

Right. And plus you guys are based in Boston and the whole Boston Cambridge ecosystem makes you very well aware of the big shoulder presence of some players there. Obviously, a very important source for you to draw some talent as well.

It's also what they're the best at, right? Big Phase III studies and commercialization is their sweet spot.

Right. Exactly. Let's talk to numbers, financials, cash, I think, at the last reporting $344 million, takes you runway. And here's where I always joke with Daniella, the vocabulary is very specific, into through, what are you saying about...

We said -- we were saying through 2026, now we're saying into 2027.

Okay. Excellent. And that actually then encompasses certain key sort of proof-of-concept readouts across now...

Yes, for our entire disclosed reprogram.

Reprograms, exactly. I did want to ask you a little bit, so Alan, who had been part of the initial core team, he sort of butted off, but still sheltered within the same sort of roof in laboratory, et cetera. Plus you probably didn't want to resign his -- like Ping pong tournament champions.

He still plays in our ping pong tournament.

Exactly as kind of like a visitor or whatever. But just curious to know how that's been, because I think there hasn't been distinction in terms of complete break off. Remind us the ties there and how he's going.

So it is his company. A lot of the investors are the same. He is in our space. Alexis and I are on his board, but it's a completely different scientific approach. It is, however, based on this idea of a kind of vulnerability that comes from changes that are different between normal cells and cancer cells. And he hasn't disclosed a lot of that publicly, so I'll leave that to him. But the 2 spaces are completely different in terms of development.

Yes. No, but I think it speaks to sort of how generative and productive the core science can be that it could actually legitimately contemplate establishing a whole other entity and taking it its own specific direction and then help and maturity of what you have going on at Tango as well.

Also Alan's brain, it's a very clever idea.

Excellent. Okay. That totally makes sense. I think we've covered a lot here, looking forward to the second half of this year. I think it would be very exciting, and we'll see some clinical cards turn. And I think this is definitely a name that, especially as people recover from the summer thinking about catalyst opportunities. TNGX folks, watch that ticker. Thank you, Barbara. Appreciate it.

Thanks Chris. Thanks very much.