Q3 2023 MiNK Therapeutics Inc Earnings Call
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Good morning, and welcome to make Therapeutics third quarter 2023 conference call and webcast all participants will be in a listen only mode until the question and answer session.
Please note this event is being recorded.
If anyone has any objections you may now.
Connect at this time.
I will now turn the call over to stop Army head of Investor Relations.
Thank you operator, and thank you all for joining US today today's call is being webcast and will be available on our web site for replay.
I'd like to remind you that this call will contain forward looking statements, including statements regarding our clinical development regulatory and commercial plans as well as timelines for data release and partnership opportunities.
These statements are subject to risks and uncertainties and we refer you to our SEC filings for more details on these risks.
Joining me today on the call are Dr. Jennifer Buell, President and Chief Executive Officer, Dr. Mark Vendetti, Chief Scientific Officer, and Christine <unk>.
All financial and accounting officer, now I'd like to turn the call over to Dr. Buell highlight our progress in 2023 and plans for the year ahead.
Thank you Sir.
Good to have you all with us for late third quarter earnings call turning to slide three.
Im excited to report on the excellent headway, we've made this quarter, particularly with our proprietary IMTT.
Knowledge and pipeline program.
This progress was presenting compelling new data on our flagship product Hs 797 at the recent society for immunotherapy of cancer annual meeting that took place last week.
To reiterate 770, <unk> Allogeneic T.
T cell therapy.
Same with scalability robust immune modulus, great properties and its administration without the need for toxic pre conditioning regimen.
Estimates of the versatility and promise of the cell.
So finally being reported.
Included first of kind of data highlighting many of these unique benefits of IMTT is particularly related to the lengthy persistence of the cells without the put in place in our top six pre conditioning <unk> tell you a bit more about that shortly.
So last Friday, we reported an update on that.
On the durable clinical benefit of <unk> 797 across a diverse set of tumor types in patients who have exhausted all other treatment options.
Notably in late stage metastatic cancer.
We observed long term durable disease stabilization and biomarker responses and more than 30% of the patients treated and these are patients with non small cell lung cancer refractory to prior therapy testicular cancer Appendiceal cancer that were refractory to prior chemo prior chemo.
And or commonly used immune therapies like anti PD one.
Additionally, the durable responses in a pace and a third with second line metastatic gastric cancer continues. This patient was on this concept of prior chemotherapy as well as prior chemotherapy combined with anti PD one therapy.
This is an exciting continued finding for us and these data provide continued evidence of the potential that agents 70, 97 holes in patients with solid tumor cancers.
Our data presentations also underscore the benefits of <unk> J T cells beyond cancer, including in infections inflammatory diseases and auto immunity.
Just earlier this year at the end of May we presented data at the American Thoracic Society meeting the international low meeting and we showed an improved survival.
More than 75% when patients were treated with <unk> 797, compared to in hospital controls that range anywhere from 10% to 30% and survival rates and these include patients who were on the most severe form.
Life support patients on Vv, Ecmo, where theres lots of being oxygenated externally that the step past mechanical ventilation and we had reported earlier and patients with viral Rds on mechanical ventilation also showed a survival exceeding 75% compared to in hospital controls it.
10% to 22% at that same time points.
We continued plans to expand this program through externally finance platform.
These data along with the others presented earlier this year at ACR continued to demonstrate that <unk> 797 is well tolerated up to 1 billion cells alone as well as in combination with some of the most widely used immune therapy.
And these cells also promote clinical benefit in a range of solid tumor cancers.
Another important finding from these data are the new translational insights that we've generated into iron K T cell immune modulating mechanisms and Theyre long term persistent.
Our data demonstrated that 787 facility to persist amplify and accelerate immune responses and promote tumor infiltration beyond what has been observed with any other cell therapy today I am going to turn the call over to Dr. Marc <unk>, our Chief Scientific officer.
To discuss more about these discoveries.
Thank you Joe.
Because we continue to deepen our understanding of the <unk> T cells unique mechanisms in the clinic for more and more encouraged by the potential of what they can do for patients with cancer. He was alone or in combination with other agents.
Curable responses in cancer patients required access to vigilance immune system to prevent the tumor from escaping in going back again, the key finding in our cancer trial is that we have observed clear signatures and activation of the patient's immune system upon infusion patients 787.
The clear signals of this car the systemic immune activation or changes in cytokine levels.
We see these changes both systemically in the blood as well as locally within the tumors and the patients we treated in this trial.
One such signal is interferon gamma.
This is a key immune activations hydrocarbon and a hallmark of ITT expectation.
Interferon gamma spikes in the blood of patients 24 hours post infusion of <unk> 707, potentially indicative of tumor <unk> activation.
Despite his Jeremy interferon gamma correlates with dose and interestingly patients treated in combination with empty PD, one demonstrate elevated baseline levels of interferon gamma and show an enhanced post infusion spike of interferon gamma.
You're indicating elevated immune system actually set the UN combining anti PD, one with agents have been nine seven.
Now to retain control of the tumor the patient's immune system needs to remain vigilant.
In that respect it's important that the anticancer activation state of the patients immune system is persistent.
Data showed first of accounting persistence of allogeneic <unk> T.
T cell therapy in cancer.
Could we use a very specific independent method based on high sensitivity donor specific SNP analysis by duplex sequencing of peripheral blood mononuclear cells.
So we found that agents have been nine seven persist for at least six months.
And in addition to showing such low persistence. We also sold a patient centered on several seven levels and blood of patients just to correlate with response. So you pay a higher in patients with partial response and stable disease four intelligently sell product to stay around for six months is remarkable even more so when it is administered with LIFO depletion, which is toxic.
Pre treatment used for the majority of cell therapies in clinical use today even.
Even more remarkable.
Finding that agents have been 97 persistence was apparently independent of HLA matching.
Additional knowledge has is that the highest degree of actually I mentioned is between donor tissue and the patient the longer the donor tissue will be tolerated and stay functional.
Finding that allogeneic T cells persist and are responding gastric cancer patients for at least six months, even when there was only one out of 12 HOA. Much provides further support for the unique nature of it very killer natural various natural killer T cells.
Underpins a great potential for therapeutic use in cancer.
And other immune mediated disorders.
To you John.
Mark. Thank you. This is this is really profound work and unique set of finding that are quite different than what we observed with the other available.
Cell types and witnessing observing the theoretical advantages of ion K T cells actually come to fruition in clinical practice as well as in translational data observations as a true Testament to your teams.
His dedication and innovation appreciate your overview Mark.
As we reflect on our scientific advancements. It's also really important to acknowledge our attention and financial Prudence that is truly underpinned our journey.
Our disciplined demonstrated by our contained cash flow.
Our clinical progress in which we've launched preclinical program we.
Studies J T cells allogeneic off the shelf cells in patients with virally induced acute respiratory distress and presented those data for different conferences, we launched the trial or buying J T cells alone and in combination with commercially approved anti PD, one therapy, <unk> and Pam Melissa.
Mt.
And we've presented those data most recently now at 50, but also earlier this year at ACR and also last year as well.
Announced observations were the findings of long term durable clinical benefit co correlating with the translational insights that Mark just presented.
And we've done this with a contained cash a cash outflow and its been carefully managed to support the completion of these program and internalization of our manufacturing process and scale.
Looking ahead, we anticipate a meaningful reduction in our quarterly cash burn rate will be by the external financing of our clinical programs and importantly, the progress that we've made in manufacturing has included our ability Devin FCA.
<unk> process that is now automated closed and fully internalize highly scalable now beyond 5000 doses per donor and beyond thousands of doses per year. So we have the processes to support the development needs going forward.
Now importantly, advancing our clinical program has been critical for us and we're continuing to do so in a few different ways first our phase II clinical trial in second line gastric cancer led by Dr. <unk> <unk> chief of gastrointestinal oncology at Memorial Sloan Kettering cancer.
Center is on track to launch this quarter.
This trial will include the combination of the cells on top of standard of care chemotherapy.
As well as the combination of cells on top of standard of care chemotherapy and combination with built in film App and <unk> done that this is an optimized multi functional T cell engaging technology that also volumes anti <unk> four from our collaborators at agenda.
<unk> <unk>, an anti PD, one therapy from agenda as well.
Next we are advancing our <unk> 787, an opportunistic disease settings, and infectious respiratory distress and autoimmunity, specifically gvhd. These externally funded trials will be designed to build on the exciting survival data, we reported in patients with viral induced respiratory.
Tori distress.
This is an unmet need where there are currently no approved therapies.
And finally acute gvhd remains a severe and often fatal complication and more than half of the patients undergoing hematopoietic stem cell transplantation.
Imtt's have demonstrated a natural capability to not only improve in grassman success in these patients, but also to mitigate gvhd.
Given our robust tolerability data.
We are advancing external and externally funded trial to address this important unmet need.
We believe that small and effective trial and generate data to support this opportunistic indication where rapid development pathway are available.
You'll hear more on all three of these programs later this year.
In parallel to our clinical endeavors, our team is advancing our GMP manufacturing capabilities and continuing to scale, our ion K T cell production as I mentioned earlier.
We're continuing to ensure that we can meet the therapeutic needs of patients battling cancer and other immune related diseases.
Our progress as events with effective financial Prudence, we are judiciously allocated resources emphasize data generation scalability and advance our innovative platform.
Our existing infrastructure has been leveraged to astellas, allowing for this full internalization of our manufacturing process, which underscores our commitment to cost effectiveness and operational efficiency.
Additionally to strengthen our balance sheet, we are in discussions with strategic partners and regional partnerships research and development collaborations and manufacturing services all of which are focused on accelerating our development be advancing our innovation more rapidly and leveraging our core capabilities and non dilutive ways to continue.
To fund our business effectively.
I will now turn the call over to Christine to go over our financials.
Thank you Jen.
We ended the third quarter with a cash balance of $6 4 million as compared to $10 6 million at June 32023, and $19 6 million at December 31 2022.
Cash used in operations for the three and nine months ended September 32023 was $4 2 million and $12 $7 million respectively.
This is a decrease when compared to $5 6 million and $14 $4 million for the same periods in 2022, reflecting our financial Prudence that John just described.
Net loss for the nine months ended September 32023, but $17 million or <unk> 50 per share compared to net loss for the same period in 2022 of $22 million or <unk> 60 per share.
I will now turn the call back to the operator for questions.
The floor is now open for your questions. So I'll ask the question. This time. Please press Star then the number one on your telephone keypad.
Well pause for just a moment to compile the Q&A roster.
Okay.
Your first question comes from Emily <unk> from H C Wainwright.
Hi, good morning, and thanks for taking my question.
If you can put it into context.
The data that you presented at <unk>.
I know you talked about the six month persistence, maybe you can discuss what's the typical persistence.
Cell therapy is an autologous southern and you also had a median PFS of six months in combination. So maybe just discuss what you would expect the PFS to be what.
Use of checkpoint inhibitors alone.
Similar patient population. Thank you.
Thank you so much for the question.
And I'll come back with me I'm going to have him give you an overview of the translational data presented at <unk> and I would say with respect to the median PFS, which as you pointed out is really quite compelling. This is a patient population who had failed all prior lines of therapy in their disease Senate and then they were really quite sick hetero.
Phase one population we observed that.
In some cases, we've had patients of course with a.
Refractory cervical cancer non small cell lung cancer, who had failed prior chemo.
<unk>, we had patients with testicular cancer, who had failed or prior lines of therapy. The median prior lines of therapy exceeded four for this population at their typical PFS as you can imagine in this particular setting.
On the currently available therapy would have been far less than that closer to about.
One eight to two months, depending on the tumor the tumor type. So thats just for framing we're seeing and we're continuing to follow patients now.
Now for progression free and disease free survival as well as overall survival. The translational data I'll turn it over to Mark to give you a sense of the reference.
What we would expect what we have seen as we've gone through the data over time, what we've seen in comparative cell types and what we believe that this may lead to the development of that Mark.
Okay.
Okay.
Okay.
I think we may have a little technical glitch.
Mark can you here can you hear him Emily.
No I just hear you.
Okay.
Thank Mark is now on music.
Okay.
Is this better.
Yes perfect.
Okay. Good.
So it would be well on my way to answering the question. So the fact that we.
We see six months persistence in an allogeneic non HLA matched therapy without any reconditioning.
I haven't seen that anywhere yes.
In autologous car T cell trials patients are heavily pretreated with LIFO depletion to make room for the new T cells coming in and then those T cells from the patients itself, which is a full HLA match and they are the spike and then they go away and in some cases like pediatric cases.
T cells have been detected for decades, but thats full HLA matched setting or by the patient's own T cells in any other allogeneic setting that ive seen reported all I haven't seen any persistence reported go longer than a month and.
And that's also with patients that have received quite toxic heavily pre conditioning LIFO depletion to.
Total down the immune system of the patient and expense persistence that way, we don't do that so we have no pretreatment and we have no actually mesh and we still see six months persistence and I haven't seen that reported anyone else or any other cell types in the setting. So that's what we think fairly unique and we think a special property of these T cells.
Alright very helpful. And then maybe if you could just provide an update on your car on Q T cell therapies in that first though.
Bouncing builds toward the clinic.
Great question. This is we absolutely are we thought our stock car <unk> and RP CMA car <unk> K T. Both armored the first second of which the <unk> car <unk>. We highlighted in prior calls we've shown potential best in class activity with this pre clinically and we completed.
Effectively the IND, enabling package.
<unk> mentioned that as we have.
Contemplated advancing our programs forward. The CMA is something that we have been in deep discussions with partnerships and seize opportunistic as the next generation therapy for companies, who are actively developing this program with a broader footprint than mix. So that is something that continue.
To be advancing that car <unk> K T was most recently presented updated preclinical data this year and I'll have Marc highlight some of the key features of that program. We are planning our IND. We are still on track for our 2020 for submission.
Yes, just on the data we actually quite excited about this whole our car T program because it has even more impactful the tumor microenvironment that we've seen with the native T cells, specifically for high resistance across solid tumors. We think that that is a benefit we see that it really potential.
The immune system to go in and change the market environment from cold to Hot and we think that that's going to really help extend the reach of native language T cells in cancer.
One of the fundamental mechanisms to tackle tumor suppression is by attaching the sort of immune suppressive stroma and Thats Whatsapp call entities have shown to do very very well both in vivo systems that we've actually reported on the company in a couple of conferences this year as well as all in vitro data that we hope to actually publish pretty soon.
So full speed ahead for this program for us.
Yeah.
Awesome. Thanks, so much.
Thank you.
Your next question comes from Jack Allen from Baird.
Great. Thanks, so much for taking the questions. Congratulations on the progress made throughout the quarter.
My first one on the on the translational data Mark you spoke a bit about the persistence, but could you elaborate a little bit more on the expansion of these cells and what youre seeing in the acute dosing as it relates to translational data from the 707 program.
Yes. So that's a good question. So what we see is typically when you when the moment. We infuse. These cells. They are quite rare in the normal blood would be infused 1 billion cells at the time of dosing, which at the time of infusion is about 15% to 20% of your total white blood cell count, which is a bolus.
We think is one of the reasons why you got the systemic effects of the reactivation on that on the whole immune system beyond that what we see is that these cells are continued to be detected in blood for over six months no. We don't have definitely evidenced that which part of the tissues that go from clinical data pre clinically they go to lung liver.
Bone marrow. So we expect that in patients themselves. This would also be the case and we expect them to go to tumor send some evidence of that we do see.
We can't currently say how much of that is driven by expansion in active division of <unk> T cells, Doug detection level in blood over six months remains relatively stable, although in responding patients, we see sort of cycling and the cycling maybe two things one they are actually actively dividing two directly trafficking between department the.
Compartments in the body can be called clearly distinguish between those two but they do stay around for much longer than we had thought they would be able to stay around given that they are not HLA matched.
Got it got it great and then you made some comments on the call as it relates to partnership discussions.
Operate a little bit more about what kind of partnerships, you're contemplating would you be indication specific or product specific how are you thinking about that path moving forward.
Thanks, so much Jeff.
Such an important part of our strategy and maybe just as a reminder, mark and I have.
Have both together shared leadership roles that are our parent company <unk>, where we were incredibly <unk>.
Successful and prolific at establishing partnerships that not only expand our discovery engine and capability, but also.
Speed the development of agents. So our discovery capability is incredibly prolific here at <unk> with Mark and his team producing discovery targets and particularly in engineering them all in house and I'm going to have mark speak a little bit about about the unique capability to support our team that make to.
Being able to not only isolate novel targets, but then engineer them into Imtt's for cars for TCR or engaged in those activities are very actively underway in order for us to fully leverage that engine.
We are in active discussions at this time.
With companies, who need innovation and two are very interested with with quite a large appetite to be able to take on some of our discovery items. So could we help a partner in that regard and those are one of the types of discussions we are talking to partners about wood.
Supporting the discovery engine through our research and development collaboration in addition.
The opportunity for us to take 787, and the clinical data that's been generated to date and fully exploit its benefit and that is an optimal combinations and expanding benefit and we've seen in our own hands that these cells can be incredibly powerful in the clinic in combination of course with widely used chemotherapy as well as.
Most commonly used immunotherapies like anti PD, one keytruda Opdivo. In addition to that we've demonstrated pre clinically that these cells can expand the benefit of what we observe with engages in the clinic as well as some other more novel technologies.
So we are also contemplating the strategic collaborations that would enable us to provide access to 787 to expand the benefit incumbent and optimal combinations for patients with cancer and those are both global discussions as well as regional partnership discussions that are actively underway there is sub parts.
Of the World, where make does not have a footprint and being able to leverage experts regionally will also help us to expand our footprint and Jason our development speed and ease in different parts of the world. So certainly that research and development capabilities, leveraging those capabilities and supporting that the acceleration of <unk>.
Some of these technologies to the clinic more rapidly as well as leveraging the clinical data from 797 to support expanded benefits for patients with cancer through really optimal combinations.
As soon as the start of course would be our combination in the clinic with second line gastric cancer.
J T cells will be in a randomized study the sales on top of standard of care.
<unk> therapy, and then the sales on top of standard of care chemotherapy plus.
<unk> really exciting products.
<unk> and valve filler map from agenda.
That trial as I've mentioned earlier during the call will be run through you Elena <unk> and externally finance trials like that are being actively pursued in our discussions through collaborators at this time.
Got it great and if I may just a couple more on the auto immune diseases, it's great to see that on the <unk>.
<unk> here as it relates to the pipeline.
As I read the slide I mentioned that 2023 and essentially in a phase one study initiation should we expect that in the coming months here and then just briefly.
Its innovative programs I assume that you've added a premium programs here early discovery aspect of your pipeline would love to hear any thoughts you have around the frame targeting and its potential across multiple solid tumors.
Excellent on the first on the first question with respect with respect to advancing our clinical program with <unk> 707 in patients with acute graft versus host disease that is something that we plan to launch this year with with into the clinic effectively amending the IND with our new study program.
That's very close to getting into the clinic at this time, so where we believe we will be announcing that this year. We're on track to do so we're certainly planning to do so with respect to the print PCR I'll have mark to say a few words about that.
Yes.
Signing program for us actually because we've actually been working on <unk> for quite a long time now we have several of them generated including what we believe is a very very good tissue or frame.
Jim as you know has actually already started to show some really good benefit in solid tumors.
A T cell approach to this and given the.
Just to the properties of <unk> T cells can actually getting into difficult places into tumor suppressive tumor microenvironment.
And then enhancing that with the TCR, we believe will be extent or has the potential to the extent clinical benefit beyond what T cells could do it and that's what we're hoping to exemplify <unk>. Currently is in preclinical stage and this will be one of the programs that we will progress following the fab car program that we are currently speaking to two in R&D.
Quite excited about that and also the specific thing of this these T cells now express <unk>, the <unk> as well as be in variance TCR T cells and they are both useful and they're both active in the tumor microenvironment.
I think the unique aspects of combining TCR expression with Ikea diesels, and then specific to frame program as a front runner.
It's a very very valuable program for us.
Great. Thanks, so much for taking all my questions and congratulations again on the progress.
Thanks, so much.
Your next question comes from Ryan common Tommy from B Riley.
Hi, This is Brian calling on for myeloma.
Thanks for taking our questions.
Just I guess first regarding the landscape in gastric cancer, we saw Doctor Jones again give a presentation on Tuesday, and I think there was another presentation on.
Or that was on the.
I think there was another presentation on our non agency <unk>.
Gastric and I was just wondering how you think the cells in an emergency.
In the emerging landscape.
Given the.
Thank you Susan.
Yes.
Absolutely so.
Im familiar with that presentation, and and we agree we actually have discussed this with you Elena and right now as you can see there's a very significant and relatively urgent need for patients in the second line setting after rent tax failure.
And being able to expand the benefit of what's currently being available to patients that are in a rapid way is quite opportunistic and in addition to that.
We believe that based on the observations we have seen in Gi cancers overall.
But until 11 <unk> and this is in patients now over 741 patients treated.
In which the products are quite active both in.
In the in the disease setting in CRC, but also more broadly outside of CRC.
Lung cancer ovarian endometrial and we see activity not only at the disease sites, but also in metastatic sites that have largely escaped.
Attack by other available therapies like <unk>.
Metastatic lesions of the bone the peritoneum and liver.
Given the preponderance of evidence that we've seen here in the data observations, we do believe that there the cells in combination not only will expand benefit with what what's currently available which is quite a rapid path for us with the sales on top of chemo, but also the sales on top of chemo with expanded benefit from <unk>.
<unk> combination, we believe can be immensely beneficial to patients and quite.
Potentially a potential best in <unk>.
Class approach for patients with gastric cancer. In addition to that we've also had some preclinical observations and observations from others.
But the sales combined really quite effectively and tolerably with other agents in those including gateways as well as ADC technology. So I think that when we look at these cells and I'll have Mark say, a few words, specifically immunologically about what's happening when we administer these cells. So not only were administering with.
HLA matching without lymphoid depletion no toxic reconditioning the cells are tolerable to up to over 1 billion cells now per dose.
We see that these cells appear to modulate the tumor microenvironment in ways that eliminate tumor escape mechanisms that we do observe with technologies approved therapies today as well as some of the developing technologies that are not yet approved.
And therefore, I see a place in which these cells just like I mentioned earlier with the expansion of benefit from our observations with engage errors.
We also see expansion of benefit with some of these other more novel technologies in March to give you a little bit of additional insights expanding on the observations we presented it to see today in that regard.
Yes, I think I mean.
So a lot of the Io failures that we see today, we think are due to at least in large part resistance within the tumor microenvironment than big.
Part of that for instance is myeloid cells macrophages.
Myeloid derived suppressor cells and <unk>.
One of the unique features of <unk> T cells with the <unk> and Varian TCR, they target <unk>, which is universally expressed on myeloid cells and we've also seen that they can actually modulate and two macrophages.
Macrophages, specifically for instance, so that's an additive effect beyond what is possible with checkpoints or we think that together with checkpoints.
Can start to really changing the microenvironment in a way that potentially with a much better renewal sponsored the tumor. So that's why we think on Q T cells on top off for instance, port filing the gastric cancer or <unk>.
T Mo or standard of care the changes.
The way to tumor sort of operates.
<unk> helps augment the overall clinical response that we think is possible because it starts to address non overlapping immune suppressive mechanisms in the tumor itself. So that's what we and also of course, the fact that we do.
T cells to patients without LIFO depletion, we don't attack their immune system. If you link for the.
Patients you actually diminish their immune system quite significantly we don't do that we don't do that because we don't need it but we also don't do that because we think it diminishes. The overall effect of the infusion of our NK T cells on conjunction with for instance, while checkpoints can be.
Can achieve.
Clinical setting.
That's the key reason why we think our eqt's with our great additive to pretty much all the IL therapies out there at the moment.
Did I answer your question Scott.
Yeah, Yeah, no that's helpful.
And I guess, maybe just to follow up on the trend that you mentioned between.
Our responses and critical levels of southern So then I was just wondering if you think there's enough data there right now to give you confidence in that trend and what we would see.
We can expect to see from that going forward.
You may all the participants yet we continue to follow that actually quite accurately because to be honest it surprises us and also in light of our thinking about how to re dose.
Should we does and when to re dose. This is key data for us to help us decide when it makes sense to re dose and why we would do just wondering what patients for instance, so we'll be collecting a lot more data on this.
Phenomenal more persistence and also how it relates to responses in patients because we have some early indications that the levels of Banca T cells. We detect are higher in patients that have either stable disease or partial response, and we're just trying to understand why that is and what's happening.
Okay.
Got it got it and then lastly, I guess.
Had to ask on the particular patient that dropped out just wondering if you could give us any details on the reason behind that.
If there is any update on the other particular cancer patient.
Was presented at ACR and also I think that the <unk> poster.
Poster mentioned an expansion cohort for statistics testicular can you give us any details on that.
Absolutely so.
What we're looking at here is in patients who actually have.
Refractory testicular cancer is currently nothing available for them and the observations that we've seen now are are somewhat early but really quite compelling and the patient would continue to see the durable response that durable disease stabilization in the patient who is continuing in the trial and we're continuing to follow those patients and we also.
To follow everyone for survival, even if they've made choices to come off the trial.
In order to.
Now in this current trial, if we get enough information from the patients now biologically from the from the paired biopsy samples as well as.
Peripheral samples that we collect so that patient who.
Did discontinue just the follow up period of the study is still accessible to us and.
And available to us.
The other patient as a continued durable disease stabilization and it's really quite intriguing. So we will expand.
The trial in our own hands.
Our phase one trial going into phase one beam.
Adding a dose and additional dose to patients and specifying some are deepening our understanding and some specific disease areas, where we have seen some very provocative signals of activity activity in patients who are not responsive to other therapies and that includes gastric and includes non small cell lung cancer and it includes <unk>.
A lot of refractory testicular cancer.
And so.
Those data will continue to develop over time and we'll be sharing updates.
At upcoming meetings of course.
Great. Thanks for taking our questions.
Thank you.
Your next question comes from Matt Phipps from William Blair.
Yeah.
Hi, Ed.
For taking my question here.
Just outsized effect and that gets her cancer patient do you think there's any reason to specifically look at MSI high cancers.
Well, that's a very intriguing question more broadly.
There is Alan first I'll have maybe mark for the broader group just highlight a couple of the observations that we've seen.
With respect to microsatellite MSI high as well as MSS some of our patients.
Our stable or microsatellite stable, but there is there may be a biological rationale to your point, Matt about expanding our observations more broadly in a tumor and a pathologic agnostic way, but using MSI high, particularly in some of the combinations given the observations were seeing as well as some germline tumors.
Where we have seen some continued evidence of activity maybe mark.
So Amazon is an interesting tumor time, because you could expect there is more new epitopes, there. So theres more intrinsic T cell priming in the in the in the patients and one of the indications where <unk> is approved we sort of capitalize on that existing T cell response against those tumors are not entirely cold, but this particular patient.
Progressing on Levo was progressing on Perm row. So clearly that was not enough. There was still some resistance in the tumor microenvironment that prevented the full response, even though there aren't we detected specific cancer. So new antigen specific T cells in the tumor prior to treatment with <unk> T cells. So he was progressing given in that state.
Let me out of the IQ T cells. It appears that some of the brokerage that prevented the T cells to activate was removed or diminished because of the T cells in the tumor which started to expand dramatically. So we feel a lot more CDA T cells in the tumor post infusion of <unk> T cells, and that's sort of to me speaks.
Speaks to what we think is happening in the tumor microenvironment is that T cells are able to reduce some of the local suppression in a way that the intruder potentiation of already existing T cell response, but that was blocked so that's what I alluded to earlier, we think there is overlapping.
Additional benefits of <unk> T cells by reducing suppression that is not tackled by standard I O therapies in the gastric cancer patients is currently the Best example, we have of that particular mechanism there.
Do we see this also in our choice I think it helps if you have an existing T cell response and of course, having been pre treated with PD. One and then progressing will be has led to a change in the activation state of T cells and in many cases. This is still not enough and kind of like a T cell.
A further response gastric cancer patient indicates that that potentially as possible. So we hope to see more of that.
Okay.
Sorry, if I missed it but given.
Have you said how frequently you are going to test more re dosing or multi dosing given the persistent.
That's it.
Again, like I said I could ask you to give some insight. This I'll tell you what we're thinking currently our clinical team is thinking at this time is the most important component for US right. Now is as we continue to separate out the debt.
And the administration and the trafficking and a persistence based on where the cells are localizing peripherally locally at the site of the tumor.
Does give us a sense that we could dose.
<unk>, we don't need to dose any less than six weeks. So it gives us an opportunity to dose at around the six week, Mark which enables us to combine really well and favorably with widely used standard of care therapies. At this time, particularly in some of the tumor types that we're seeing are most pronounced benefit and in <unk>.
That.
We may and this will be something that we're going to explore more deeply in our expansion cohorts.
Can we push that persistence out, which we're still monitoring in the patients who are on the trial does it change the dynamics within the tumor microenvironment based on the localization and should we explore delaying that do possibly 12 weeks and we don't know the answer to that at this at this time.
Based on the fact that we have seen a very transient allo antibodies, which we presented at the <unk> two years ago.
We know we've already established that we believe we can dose safely without any rejection and six weeks appears to be the time point that is in the sweet spot.
We may optimize the benefit and optimize the convenience for patients undergoing current standard of care.
Great. Thank you.
That was your final question.
I'll now turn it over to Dr. Bill for closing remarks.
Thank you very much operator, and thank you all for your time and attention and continued support to make I. Appreciate your time.
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