Q1 2020 Earnings Call
[music].
Greetings and welcome to Q bio pharma first quarter 2020 earnings call.
At this time, all participants are in listen only mode.
Question and answer session will follow the formal presentation.
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As a reminder, this conference is being recorded.
It's now my pleasure to introduce your host actually Robinson Investor Relations. Thank you you may now be yet.
Thank you Doug and good afternoon, everyone. This is actually from lifestyle advisers and thank you for joining us on today's investor and analysts update call. Joining me on the call today or Dan Siri, Q, Biopharmas, CEO, Dr., and new Siri, President and Chief <unk>, a scientific officer, Dr., Ken Piavitsa acting Chief Medical Officer.
Im carry anvil, our vice president of financing principal financial and accounting officer.
Before we begin I'd like to remind you that during today's call. The company will be making forward looking statements various remarks that the company makes during this call about the company's future expectations plans and prospects constitute forward looking statements for the purposes. The private Securities Litigation Reform Act of 1995.
Actual resorts results may differ materially from those indicated by these forward looking statements as a result, various important factors, including those discussed in the risk factor section of the company's annual report on form 10-K filed with the FCC on March 12, 2020, I'm quarterly report on form 10-Q filed with yes, you see on May 7th.
2020, as well as other filings made by the company to the FCC from time to time, which can be accessed on Edgar database at Www Dot actually see dot Gov. In addition, any forward looking statement represents the company's views only as of today may 19th 2020 and should not be.
Be relied upon as representing the company's views as of any subsequent date, while the company may elect to update these forward looking statements at some future point the company specifically disclaims any obligation to do so even if the companies use change. These forward looking statements it should not be relied upon as representing the company's views as of any date subsequent.
Today. Please be advised of today's call is being recorded and webcast I would like I would now like to turn the call over to Q Biopharmas CEO, Dan sorry, Dan.
Yeah, Thanks, Ashley and good afternoon, everyone and thank you for joining us today for a review of our ongoing progress at first quarter financial results, which are available in more detail at our form 10-Q, two as filed with the yes, we see on May seven.
As a reminder of the slides were presenting today.
As well as a recording of our call will be available on our website for the next 90 days also as a reminder, those of you I. Loosening then you can advance the slides from your computer and will notify you and what slide were addressing at that time.
We will also be available.
Via the.
Email provided on our website for questions that may not be addressed a <unk> during today's call. When you may want ask subsequently.
I'll beginning with slide three.
Which shows our agenda for todays call I'll provide a brief overview and update of our pipeline.
With an emphasis on our lead program Q1 O one.
It will be followed by Dr., Ken P. after our acting Chief Medical Officer, who will provide further details on our most recent observations from our ongoing phase one Q1, or one monotherapy dose escalation and expansion study.
Following a doctor he had his update talked a knee surgery, our president and Chief Scientific Officer will further describe our continued innovation and additional progress that we've made and advancing our immuno stat and neo stat platforms.
Hello, underscore how our rationally engineered I L. Two based Q1 hundred series is differentiated and finally highlight the rest of our expanding pipeline that now includes Q1 or two.
Okay rash neo stat as well as the Q2 hundred in Q3 hundred programs. The latter I've been in a collaborative partnership with Merck.
Our progress with all of these programs demonstrates focused execution towards platform validation, especially through the ongoing phase one trial with Q1 on one and further pipeline and platform developments.
Following a knishes update a carry n. Miller Q bio pharma as principal financial and accounting Officer will review, our current financial status and I'll, then provide concluding remarks, followed by a Q1 day session.
To begin I'd like to thank our dedicated employees for their focus and consummate professionalism and diligently working under these challenging and stressful conditions from the covert 19 pandemic.
Through their efforts, we have been able to keep our lead drug candidate Q1 O. One on track in our first in human monotherapy dose escalation phase, one trial and H.P. Vought positive head and neck cancer.
Now moving on to slide four which shows an overview of our core strategic objectives in progress and the first quarter.
In summary, our core objectives have been to a one.
That would date, our immuno stat platform through the ongoing generation of data from our Q1, all one clinical dose escalation study.
To.
Expand our pipeline by selecting additional epitopes with the Q1 hundred series and developing other disease applications include including auto immune diseases. That's for the Q3 hundred series.
And three to accelerate and enhance our productivity through further development of our newest that platform.
To date, we have dose escalated through the first four cohorts and continue to generate translational data and corresponding clinical data essential in providing proof of concept of our aisle to based Q1 hundred series of Immunostatus.
And as as a reminder, Q1 or one represents the first of what we believe will become a broad set of biologic drug candidates from the Q1 hundred series targeting tumor associated antigens linked to a variety of Kansas.
To this point, our near term goal is to de risk, one or one by demonstrating safety tolerability and clinical activity, which will [laughter], thereby reduce the risk profile associated with the Q1 hundred series per se as well as our follow on Q2.
203 hundred series of Biologics as a reminder.
We have also been developing our neo stat platform to significantly enhance our productivities and.
Provide cost efficiencies to fully exploited the potential de risking in validation of the immune a stat platform, which we are in the process of generating data to demonstrate that.
And this is going to elaborate upon neo stat later on in the call.
Importantly, and the ongoing Q1 O one phase one clinical dose escalation study favorable characteristics in drug properties, including dose proportional PK early signs of relevant P.D. activity and growing evidence supporting that the drug appears to be clinically active have.
Emerged to date for my first three cohorts I want to emphasize that we are conducting the dose escalation study of Q1 on one end a monotherapy trial in second line and beyond resistant metastatic HPV positive head and neck cancer patients.
And this highly challenging stepped up setting.
Well still quite early in our clinical study of the drug we have observed data supporting an apparent increasing the level or the levels of HPV reactive effector T cells and the peripheral circulation in several patients.
Moreover, we have observed preliminary evidence of single agent clinical activity of Q1 O. One.
As we continue to build data with the objective of demonstrating single agent activity in this challenging patient population. It is our hope that we maybe able to define a clinical and regulatory path forward for monotherapy, providing benefit to patients who currently have no effective alternative.
[noise] taken together, we interpret these highly encouraging, albeit early results as evidenced supporting the prospects of Q1 or one single agent activity that needs to be further confirmed in additional patients.
We also recently announced the establishment of a clinical collaboration agreement with Merck for a combination study with Keytruda, which is an anti PD one biologic agent as a first line therapy in patients with advanced HPV 16 positive head and neck cancer.
And a planned dose escalation phase one study to be called the key note a 78.
This collaboration allows us to expand our patient coverage by moving Q1 O. One upstream into the first line therapy, where Keytruda is approved as a standard of care.
The rationale to combine Q1 on one with an anti PD one agent.
As based on our robust preclinical data, which demonstrated that are promising monotherapy activity with Q1 on one was further enhanced when combined with an anti PD one agent.
The progress we've made in the clinic to date with Q1 on one with early emerging monotherapy data.
Gives us bolstered confidence in moving forward with our current ongoing monotherapy trial as well as the planned phase one trial in combination with Keytruda.
That has the potential of expanding the application of Q1 or one into the frontline therapy setting for recurrent or metastatic HPV 16 positive head and neck cancer patients.
Additionally, we continue to make solid progress on the development of our pipeline of drug candidates advancing through the modularity of the platform.
With Q1 zero to targeting WT, one our willms tumor at one.
In Q1 O three which is presently being reviewed with our Asia partner LG Chem.
We also have generated supportive preclinical data for our K Ras Q1 hundred drug candidate and Aneesh will follow a kens one or one update.
With a review of the progress made in these various programs as well as an overview of the core competitive features of our platform.
To remind everyone.
And for those of you are first listening in Ken will now provide a further details regarding the progress of our clinical development for Q1 on one which is our first clinical drug candidate a I'll now turn the call over to Ken Ken.
Thanks, Dan and good afternoon, everyone I'd like to first remind you about the tremendous commitment we have from but participating clinical centers and associated oncologist.
I'm here on slide five.
Throughout the cope with 19 endemic this group of highly respected and dedicated oncologist and remain focused upon screening and enrolling HPV 16 positive head and neck cancer patient to participate in our study.
Our investigators enthusiasm for the Q1 on one program reflected that in the fact that today, we have been very successful in our precisely.
The screening process to determine eligibility for the trial.
Recognizing that current therapies are not or rarely curative, we put into place it system whereby patients on first line or second line therapy for HPV direct head and neck cancer, our prescreen by each delay type and confirmatory HPV status.
You determine eligibility for future Q1 on one therapy.
The demonstrated demand to patients for pre screening underscores the significant unmet medical needs in this indication.
No.
Slide six we show a high level summary of the design for our ongoing phase one trial in Q1 to one.
As Dan mentioned, we're very pleased with our progress of dosing patients <unk> trial, and our highly encouraged by observation the date.
As a reminder, we are enrolling well post first line patients with recurrent or metastatic hadn't next squamous cell carcinoma, driven by HVB, specifically HPV 16. This represents approximately 70% of all head neck cancer is occurring in the oropharyngeal region accounting for an estimated 13000.
500 patients annually in the U.S. alone.
This phase one trial is defined molecular inclusion criteria to include had not cancer patients that are each elio to a one positive and whose tumors are confirmed to be driven by HPV 16.
Through the specific inclusion criteria, we are ensuring that only patients with the potential for clinical benefit our role enrolled and treated.
Really a translational precision medicine approach whereby each of our immuno stat drug candidate is intended for patients with specific molecular fingerprint.
This trial is designed to provide insights into safety mechanistic activity and potential antitumor efficacy.
The trial is the standard two parts study with the first part eight designed as a typical screen plus three monotherapy dose escalation trial patients. We see Q1 on one and once every three weeks via IB engine.
However, we've also provided the opportunity to dose up to nine patients in any given cohort, where we see evidence of clinical activity or PD effect.
This strategy allows us to further explore PK PD effects as well as build supporting data for determining the most appropriate dose for the part B expansion.
Based on the safety TV in efficacy data from the dose escalation part we will secure additional patient that that dose level. During the part B expansion phase two confirmed the recommended phase two dose for in total of 20 patient.
Therefore in summary, both parts, a and b of the trial will evaluate and safety and Tolerability of Q1 on one with biologic activity and anti tumor responses also being followed.
The expansion cohort is designed to confirm the safety biologic activity in anti tumor activity at the effective dose need additional patients to provide further support and confidence as we move into the later phases with more patients.
To evaluate on target activity, we're measuring several translational biomarkers, including T cell expansion in peripheral blood measuring exciting time production by antigen specific T cells for anti tumor activity. We're looking for objective responses by resist criteria six week intervals were after.
The two cycles of Q1 on one [noise].
I'm very pleased to report that after initiating dosing cohort one in late September last year, we successfully moved forward the cohort two in December and cohort three in March.
And we've now enrolled three patients in cohort slower during the first two weeks of Maine.
To reiterate on earlier comments. The fact that we continue on schedule and made such good progress. Despite the cobot 19 pandemic.
Which has shut down multiple clinical trials that are now close to accrual. We view. This is an important metric of the commitment of our clinical collaborators and the enthusiasm there half for our approach to prevent puts a 10 to potentially provide clinical benefit to their patients.
As a reminder, our preclinical modeling, let us to initiate dosing with cohort one and what we believe is the low biologically active dose and then a biologic Lee and clinically active does maybe it seems starting cohorts three or four.
[noise] shown in slide seven are the dosing groups for our patient cohorts. We initiated the trial at 0.0 0.06, Megs per keurig with a threefold expansion up to cohort three and then a twofold increase for subsequent cohorts.
As noted on slide we compared the absolute dose by math as well as moeller content vial to to be approved dose of Proleukin, which is 0.037 makes for cash.
So looking at the Wild type filed a molecule generally known as Aldesleukin in the second cohort on a molnar basis, we were already above the proof approved goes the proleukin and by the third and fourth cohort were approximately four to eight fold and ball or access.
To date, the 12 patients in cohort one through four have received a total of 31 infusions of Q1 on one.
Three weeks apart with what appears to be an attractive safety profile with limited toxicity.
One placement in cohort four at the one big protein does having infusion rate reaction that resolved quickly and recall that we have shown that this dose to is about eight fold higher in terms of administered aisle to.
And the island to delivered by an approved dose of Proleukin.
With this data we are confident that we can deliver high doses of aisle to on target safely.
We continue to be highly encouraged by our early progress in observation.
Including early evidence, suggesting biologic activity.
We have observed preliminary signs of T cell expansion and activation and our initial PK PD results.
That we plan on confirming and extending in future analyses, coupled with the clinical evaluation.
Importantly, we have now observed early signs the biologic in clinical activity.
Cohort one patient inadvertently receive five times, the prescribed dose where Q1 on one dose between the doses intended for cohort two and three.
This kind of placement demonstrated early signs of T cell expansion as well as tumor regression on scan after receiving this dose, but also developed worsening of a pre existing bullous Pemphigoid Ras Q1 on one was discontinued but the patient remained with stable disease off therapy for several months before eventually progressing.
One patient cohort to demonstrate an early signs of T cell expansion and had stable disease that first and but did not the thing that continued response.
Another patient from cohort two has confirmed stable disease with tumor regression of the target lesion.
This is heavily pre treated patient who progressed well on therapy with a checkpoint inhibitor continues on study.
Also a patient in cohort three has demonstrated activation and expansion of T cells and remain on study.
We note that we are still in the dose escalation stage of our phase one trial you continue to monitor the five patients. We're can continue to treat.
We will provide further details as they become available over the course of the study.
Based on the totality. These metrics, we will continue to evaluate report on the emerging data as we prepare to advance to the dose expansion part b of the current study.
In addition to the ongoing immuno therapy trial, if you want to one in HPV positive head and neck cancer. We've shown on slide eight our collaboration with Merck to initiate any have submitted to the FDA a concurrent study to evaluate Q1 on one in combination with ample isn't that or keytruda as frontline therapy.
For the same indication in patients who are also equally to a one positive.
Our intention is to continue moving forward with the model for therapy trials. The second line or later HPV positive refractory and that's the head neck cancer patients and enhance our patient reach by moving into frontline patients in combination with great to that which is the current standard of care.
In this trial referred to as you know a 78, we intend to translate our preclinical findings demonstrating a highly.
Significant synergistic anti tumor activity with Q1 on one combined with an anti PD one antibody.
These data along with the Q1 on one monotherapy activity in the preclinical tumor model recently published in the main script and clinical cancer research last month.
We intend to convince this trial and the second half of this year once we confirm the safety of Q1 on one in the phase one trial.
Furthermore, sliding also shows that we have the option of evaluating Q1 on one in the neoadjuvant setting in patients newly diagnosed with localized head and neck cancer.
And finally once we have established clinical proof of concept in Q1 on one had next squamous cell carcinoma, we may expand opportunistically in the other is BB Durbin cancers. For example, cervical an email cancers I'll now hand, the call over to the needs to discuss the other advances in our pipeline than platform Nish <unk>.
Thanks, Ken and thank you to everyone listening in I hope all of you and your families a safe and well through these times.
I'd like to remind everyone of the scientific vision that has underscored our focus on efforts from the very stop vision that was centered on a singular all important question, which is how does one take advantage of the selectivity and specificity of the immune response was not breaching patient safety, we believe our immuno start framework as exempt.
Defined by the Q1 hundred series as shown in slide nine of which Q1 or one is representative of the rational solution and couldn't sophisticated protein engineering from inelegant perspective, the best map off the landscape is the landscape itself to that end the landscape of T cell modulation and cancer immunotherapy kind of involved.
Many elements however, the key fundamental signals for specificity coupled with controlled activation are what ultimately govern the outcome of the immune reaction. These very core elements are incorporated into the molecular framework of the Q1 hundred series. The two key signals on the 100 series as shown in slide slide.
Nine consist of stabilize peptide age lay molecules to engage the tumor specific T cells via the T cell receptor, thereby locking in the specificity combined with rationally engineered Io two molecules that selectively add to both of those T cells to control their activation. We believe this control mechanism.
It's an obligatory prerequisite for T cells and cats Remunity in other words in absence of the appropriate antitumor T cell repertoire. The application of a T cell modulating approach be it singular cytokine that will be like two or its variance or antibodies targeting checkpoint molecules is likely going to be sub optimal for.
Todd endeavor from the earliest approval of Proleukin aisle to has been a validated target for T cell activation. The challenge for broad application awhile to has pertain to safety liabilities due to cytokine release investment leakage and indiscriminate activation of immune cells and brought to you. So its upset including regulatory T cells for T. Rex.
We evaluated the incorporation of Io too in the Q1 hundred series guided by structure based rational protein engineering solutions from the very beginning we sought to achieve two key objectives, one was to generate inyo to that avoids the safety liabilities and T. Reg engaged.
When properties of wild type bio too and to ensuring that the I'll do with selectively delivered to tumor relevant T cells. The output of these efforts resulted in the generation of the Q1 hundred CBC framework as you see here in slide nine the top down view of the ribbon dive them of the Q1 hundred series as shown here.
Provides a good contextual perspective for this patient engagement of these molecules, but human specific T cells.
No. There are two modifications to the two molecules that are important for us specificity and selectivity. The first is abrogation of binding.
Two of the two receptor Alpha sub unit in order to avoid T. Regs engagement. The second modification is the attenuated binding to the onto receptor beta CW and it such that the two activities biased to those T cells that I've talked to the specific peptide isolate complex via that T cell receptors well TCR.
We believe this engineered biologic framework allows us to maintain specificity and selectivity, while avoiding the systemic toxicities associated with indiscriminate two dependent activation of many different cell types and indeed as you've heard from Canada as you've seen the dose cohorts the initial clinical dataset.
It certainly appears to support this thesis several key point should be emphasize first we have a novel biologic scaffold that demonstrates exposure and dose proportionality inline with projections, which is highly encouraging. Furthermore, we have not seen major safety liabilities at doses were in a more look content a comparison of.
While too we are significantly higher than the approve those are proleukin for example of the other those other than the fourth cohort Q1 to one has approximately eight times the more look on done divided to compared to Proleukin. In addition, the early BD data seems to suggest that we have activity and engaging and expanding the targeted at T cells Basin Tetra.
And at least bought analysis. These are early data at early time points that well be confirmed and extend that as we obtain additional patient samples, but perhaps most encouraging as the composite view from the clinical experience. Thus far with designed a novel biologics platform that appears to possess favorable properties pertaining to drug exposure.
NPD and also appears to be demonstrating monotherapy clinical activity as we continue to obtain further supporting data from Q1 to one we are highly enthusiastic about the broad possible applications off the Q1 hundred series that data generated from Q1 to one clinical experience has the potential to de risk the entire.
And 100 series since the quarter, while two elements coupled to the peptide actually framework remained constant.
Okay I'd like now we want to slide tend to remind you of the key features that we believe underscore the superior differentiation, although I have two based Q1 hundred series over other while two modalities that outfit. The slide has been presented before as a part of a corporate debt and highlights the important facts that the Q1 hundred seen these can selectively deliver I'll too.
To the relevant T cells that is the tumor specific T cells, while minimizing the safety liabilities and brought affects another two cents upsets both the T. Rex and the vast majority of the loan to you might react to effectively so repertoire that that all of US hub. This isn't stark contrast, with a lot Alfonso to variance that that minimize the activity and T. Rex.
It's still act with equal opportunity on all other T cells. The vast majority of them have no relevance to tumor specificity.
Furthermore, the pool frame work of the Q1 hundred communities can priming, the and expand T cells from a naive T cell repertoire as also reported in our recent publication and Cliniqa cancer Research last month.
The not alpha aisle to variants rely upon a pre existing antitumor T cell repertoire that must be present within the patient to derive benefit.
The next slide slide 11 highlights our immuno oncology development strategy to exploit the fullest potential of the Q1 hundred framework. The present clinical trial, what Q1 to one provides us with the foundational proof of concept in an indication of unmet medical need it and as mentioned previously won a one is positioned to potentially de risk the entire.
100 series, we have thus positioned ourselves to maximize success for the Q1 hundred series by exploiting the key strength of immune to start platform, which is modularity and flexibility that allows us to target different tumor antigens, along with distinct HLN neos for global patient populations this strategic growth.
The opportunities is exemplified from a covered ongoing work with Q1 or two and beyond wave, where we have focused on tumor antigens like web zuma, one or WT, one and K RASK and have initiated programs with additional elite. Besides the age related to these include agent a 24.
A 11, both being dominant in Asia, which was the primary reason for our LG Chem partnership for the first three programs. We have made strong progress with our Q1 or two programs and to have generated pilot data demonstrating ex vivo expansion of human T cells, only functionality and they're killing of target cells.
These data were recently presented at an invite to talk at the front is in cancer immunotherapy meeting organized by the new data Sciences on May 12.
We would also look forward to other avenues and photos to disclose these promising datasets, including the upcoming AC Virtual conference on June 22nd where we will be presenting a poster.
Okay. So based upon the foundational date work of our immunoassay platform. We have further developed a next generation platform referred to as neo stuff, which greatly accelerates our scalability in generating new clinical candidates. The neo stopped framework, specifically enhances our productivities inefficiencies.
Both from a timing cost perspective, and builds upon a versatility to talk in multiple tumor antigens, including post translational modifications and personalize neoantigens in the future.
The next slide Slide 12 focus is a bit more on the neo start platform.
A key intellectual leap here was to design a platform enhancements that significantly expanded reach into diverse tumor antigens to remind you that current immunostatus platform incorporates singular primary tumor driver antigens. This is great for examples like the HPV 16, eseven protein as in our lead mall.
You'll Q1 to one or targets like WT, one, okay, Ross and such and these cases, they immune assault to a dominant human driver antigen is likely to provide meaningful clinical benefit indeed with all of the examples mentioned above data from cell therapy based clinical studies utilizing either TCR T cell therapy or tenant base.
Adoptive cell therapy have demonstrated clinical responses. However, looking into the future. We will also be positioned to capture the Boston landscape of available tumor antigens tumor sequencing and profiling data emerging in real time is providing us a continual source of new antigens that can be effectively deployed use.
In Q1 hundred series. This this is the thinking that is what propel the neo step platform wherein we can generate the entire Q1 hundred CV scaffold without any specific peptide attached to the h. and a molecule and again. This is in Stark contrast to the current immunoassay platform, where each diesel epitope isn't interval.
A lot of them either stat, meaning it's incorporated into the molecule as a fusion protein at the time of synthesis Neil status emphasized without a peptide epitope instead the peptide epitope is actually attached subsequently using sophisticated attachment chemistry as shown covenant.
But they examples of three different peptide bound to the neo start scaffold. This advance allows us to generate the core generic scaffold for any actually by a single cell line and then use the same product conjugate a different tumor antigens to expand our reach the fact that only a single scaffold needs to be generated.
Will save us significant resources in both time and cost, but generation of clinical grade material and then doing so.
Provides an essentially with an off the shelf biologic to target T cells directly in the patient we have generated early proof of concept data supporting the biological activity of molecules generated via the Neo SAP platform and an example, one such dataset as shown in the following slide 13 additional data underscoring the protein.
Engineering efforts were disclosed at a talk at the World vaccine and immunotherapy Congress meeting about six months ago in December 2019 in San Francisco, So moving on to slide 13. The top on here shows expansion of CMV specific T cells from three human donors the bottom out on shows expansion of Mark one specific T cells.
From additional three human donors marked one as a known antigen in melanoma in each case, the pbmcs from human from human don't as we expand it with immunostatus, but in the CMV. A marked one diesel apatow is made as a fusion protein or with neo stats, but in the respective diesel antigen is chemically conjugated to the Scott.
As you can know the expansion of relevant T cells specific for CMV OMART one of those very compatible that munis that expanded T cells are shown in solid lines, while the neo sat expanded T cells for each specificity as shown in dotted lines. These data provide enormous confidence that the neo step platform can be done.
Well up for future therapeutic applications and will complement and extend the current application off the immunoassay platform note that the scaffold of the neo start describing the covered slide is essentially the Q1 hundred series without antigenic peptide, but the same cord configuration and valence zeolite two molecules.
The next slide Slide 14 highlights our pipeline progress we've made significant progress with Q1 to one in the monotherapy trial as discussed by Kennen, Dan and up positioned well for the combination study with Pembrolizumab later this year Q1, or two with WT. One continues to make strong progress through to remind you. This program is being.
Prosecuted with two different age layer leos, HM two and actually a 24, which is a dominant Leland Asian population Q1 hundred three is being better at currently with LG Chem, Malaysia partner and will be disclosed in the near future and I've listed here. We've also made meaningful progress with our K rest program for the Q1 hundred.
Series, we have been hopefully find an appropriate for him to share those data in the near future.
We continue to extend the application of our platform at the Q2 hundred series wherein we have early data sets with south of as receptors like CD 80, which as Vseven, one that binds to cdtwenty eight on t. cells and for would be we like and and finally as disclosed recently, we continue to make strong progress in autumn energy in alliance with.
Look using that Q3 hundred series, but until we have successfully generated immunostatus incorporating close to a delay molecules to selectively target or the reactor CD for positive T cells in human patients selective modulation opened a baron immune response in autoimmune diseases with abroad immunosuppression as is the.
Case with current therapies is likely to bring superior clinical benefit to patients. We believe this goal can be achieved with the platform like ours in conclusion and as I've stated in prior presentations the immune those stat and by extension the Neo stop platform address it fundamentally immunological challenge, which is how does.
One maintain selectivity and specificity for desirable immune response without breaching patient safety or creating toxicities. We believe our approach that is built upon rational protein engineering and is bolstered by supporting datasets may offer a unique solution to patients suffering from cancers autoimmune diseases, and then threats from chronic.
Pathogenic and infections, okay with that I'll now turn the call over to Kevin to review our financial results. Kevin. Thank you Manish turning now to slide 15, I'd like to provide a brief update on our financial results for the first quarter ending March 31st Twentytwenty.
We finished the quarter with approximately $48.7 million and cash cash equivalents.
60.6 million in total assets and working capital of approximately 39.1 million.
Revenue generated from a collaborations with American LG Chem, and the first quarter of 2020 or 9.9 million as compared to point 4 million for the same period in 2019.
For the quarter ended March 31st 2020 research and development expenses were 9.9 million at compared to 8.4 million to the same period and 29 for.
The increase in research and development expenses is primarily due to clinical trial costs related to our ongoing Q1 on one monotherapy trial that was initiated in the latter part of the third quarter of 2019 as well as manufacturing cost for Q1 on one to supply our recently announced combination trial of Q1 aligned with Merck's Keytruda.
General and administrative expenses were 3.9 million for the quarter ended March 31, 2020, as compared to 3.4 million for the same period and 29.
This increase in general and administrative expenses is primarily due to an increase in stock based compensation expenses and legal and accounting fees incurred in the first quarter of 2020.
In April 2020, we extended our cash runway truly an aftermarket equity offering sales agreement for aggregate proceeds at 34.3 million net of commissions paid to Stifel, who acted as sales agent.
The successful deployment of the ATM facility in April has enabled us to and strengthen our cash position to further support the development of our immune stuff platform and associated pipeline, including the clinical development of Q1 online as both a mono and combination therapy.
Based upon our current forecasts, which includes the further build out of our ongoing clinical studies. Our current cash position is estimated to take us into the fourth quarter of 2021 with that I'll turn the call back over to Dan for closing remarks, Dan.
Thanks Kerry.
Yes, since our last call and despite the challenges we continue to faced by the covert 19 pandemic, we've made significant progress across our platform and associated programs as I'm showing here in slide 16.
Having raised additional capital in April and having enrolled and treated patients through cohort three and now into cohort four and our Q1 on one phase one trial.
Well better positioned strategically to continue advancing Q1 on one for determining a recommended phase two dose as a monotherapy and into a combination trial with keytruda as well as further advancing our platform and the associated programs.
As just described above our lead program Q1, or one is well positioned to generate a body of data, including PD biomarker activity and patient scans to demonstrate biologic and clinical activity.
And this patient setting these data would significantly de risk and validate our approach, allowing us to further build our pipeline based upon the same foundational principles upon which we brought Q1 O one forward.
With Q O Q1, or one now being dosed at what could be biologically active in clinically relevant levels. We believe we're very well positioned to establish Q biopharma as a differentiated leader in immuno therapy with potentially disruptive breakthrough therapeutic platform.
A couple of our key accomplishments in Q1 include continued and timely enrollment.
Of cohorts one through four in a in the Q1 on one monotherapy trial.
Along with demonstration of favorable safety and Tolerability.
Dose proportional exposure in line with preclinical projections.
And early signs of PV activity in emerging clinical activity.
Our guidance for 2020 milestones as shown on slide 16 are unchanged from our last call and principally they are PK and PD results from the phase one Q1 on one clinical trial in the second quarter of 2020.
And we've demonstrated that is on track today.
Clinical responses in phase one for Q1 hundred one via resist criteria in the second half of this year.
We are already beginning to see what appears to be emerging data supporting that.
Initiate combination trial with Keytruda in first line head and neck squamous cell carcinoma patients in the second half of this year and we're on track with that with the announcement of the consummation of the partnership.
With Keytruda.
Initiate and extend I, Andy enabling activities for Q1 zero two in the second half of this year we're on track.
And then selecting.
Hey, defined target for Q1 O three and the second quarter of.
This year and we are on track for that and discussions with our partner LG Chem.
Demonstrate neo stat Manufacturability inefficiencies in the second half of 2020 and as you heard from Aneesh we've made.
Quite significant progress towards that objective and then finally identify potential clinical clinical candidates in our auto immune collaboration with Merck in the second half of this year.
So with that I'd like to once again, thank our employees for their hard work and commitment to advancing our science forward during these challenging times.
And finally I'd like to thank our shareholders. Our board of during our board of directors for continued support enabling us to advance Q biopharmas platforms towards validation in the clinic, while also moving our preclinical assets closer to I, Andy enabling studies.
We look forward to providing further updates on the validation growth and expansion of our pipeline, including our Q1 on one phase one trial and most importantly, we are grateful to all who enable us to pursue this noble mission to serve patients in need.
I'd like to now open the line for questions operator.
Thank you we will now be conducting a question and answer session.
We'd like to ask your question you May press Star one on your telephone keypad. The confirmation total indicate your line is another question Q.
You May proceed start to if you would like to remove your question from me too.
Core participant Ginnie speaker equipment, and maybe necessarily pick up their handsets for Prosigna Starkey.
Our first question comes from line of Boris Peaker with Cowen. Please proceed with your question.
Congratulations on the progress you guys make amis environment.
Thank you really appreciated force. So my first question asked so in the part a of the study design allows you to expand doses out to nine patients. If you see activities. Just curious if you have expanded any or if you plan to expand any doses by based on the initial activity that you.
Observing.
Sure Hi, Ken why don't you take that [noise].
Yes, hey, thanks for the question Boris.
So, yes, where we are planning to expand.
And based on our Bayes being approach, we have not fair to do expand because we've been focusing on.
Escalation since we have not reached a DLP weve may be a conscious decision and to continue to dose escalate.
Prior to.
Expanding at any given dose level, but we're constantly evaluating that but the short answer is we have not started to expand any of the lowered cohorts as of yet.
Gotcha and my second question in times of the dose escalation I mean, Youre plan has seven cohorts right now estimated or I guess per protocol I'm just curious at some point if you get to the seven cohort and the drug is still tolerated is there any thoughts of going higher or how do you kind of think about the highest.
Those level work testing in dose range you consider you haven't agonist versus most of time, we're used to thinking if antagonist.
Yes, so thats a great question and that's why we really built in that basically an approach to look at two really evaluate what types of responses were having both clinically as well as.
By PB Biomarkers, and we fully expect that.
By dose seven we're going to be see those types of biologic in clinical markers that would allow us even if we haven't seen toxicity to expand out.
At the lower cohorts I am I seriously doubt, we'll have to go higher than dose as seven but we're prepared to but the reason we built in this at this overlying basie an approach over the three by three design was really too because we were concerned that we would not see it.
Limiting toxicity, and we want to be able to pick a rational dose.
For the part B dose expansion, so I think before as long as we're seeing PD and clinical effect, we're likely to use our expansion of being lower cohorts to allow us to pick a phase two what we think it's going to be the recommended phase.
Two dose.
Without doing necessarily higher.
Great. Thank you very much for taking my questions.
Hi source.
Our next question comes on the line Stephen Willey with Stifel. Please proceed with your question.
Yeah. Good afternoon. Thanks for taking the question and congrats on all the progress and the incremental information on some of the early cohorts.
Maybe a couple of question for for trend. So you mentioned I guess, an infusion reactions is happening I think it was maybe cohort three.
Has no scores.
Okay workforce. So can you maybe just talk about the severity of the.
You that was observed there and.
Do you think you might have to pre Medicaid as you as you move higher.
Yes. So it wasn't it was an essay E and not in another deal to be and.
The patients where it would rapidly resolved.
Over the strength of an hour basically and in it required at the patient did get some ibuprofen.
But there was we began investigators of disgusted we've discussed it at this point, we don't believe we're not planning on pre medicating at the next dose level.
And have no indication right now that we would have to do that.
Again this was not a sustained.
Fee.
That leads you to would lead us to.
Change what we're doing at this point.
Okay No that's helpful and then.
Just curious as to when in the.
In the time course of treatment are you evaluating T cell expansion in activation in these patients.
How soon after administration.
So.
So we're lucky as we look at.
I'm not quite sure I understood the question I'm sorry.
So just curious as to when you're assessing these patients for peripheral T cell expansion and elevation.
How soon after administration are you looking.
Right. So maybe I can the Covington that this is a nisha Steve so the first.
As you will remember the the cycle is a three week cycles. So the drugs given and the first analysis of the first couple of weeks than than at each of the cycles before the drug is given we're able to look at the T cells.
So we there's a couple of weeks time lag between the dose of the drug and the time, we get the blood for the analysis and again as Ken pointed out and as I stressed. These are early time points. So we need to build this out with additional time points and additional those as an additional patients. So these are early signals that we.
Started to measure at this point.
Okay, and then you mentioned that you're continuing to treat five patients I think I heard so it sounds like that might be the one cohort two patient that's had a confirmed stable disease.
Can you maybe just kind of.
Directionally point as to where those other patients are in terms of in terms of cohort sure.
Sure. So we have the one patient from cohort two we have another patient from cohort three and then three patients from cohort for.
Okay, and then maybe just lastly.
Can you kind of deal you have enough information at this point just based on where you are dose escalation.
To initiate the PD, one combo dose escalation in parallel or do you want to push those a little bit higher where you get back on.
Well, we really want to push doses a little higher.
Before we get thankfully.
We wanted to be sure that we had enough information.
In in the monotherapy arm to to be able to pick a dose because we would like to pick it does the tying out on that we could start to see early in immediate effect in the combo and so we did offset the combo to start in the second half of our this year.
For a rather than right away.
We did suggest that we would start at least at a minimum of cohort three with the combo, but it means we're hoping that we can potentially you could go higher so.
In our submission to the FDA.
We said at least you know that we that we put in cohort three but where we also have the option of changing that.
Great. That's really helpful. Appreciate the answers and ER Congrats again.
Thanks, Steve Thank you see.
Our next question comes from the line of Mark Breidenbach with Oppenheimer. Please proceed with your question.
Hey, good afternoon, guys and congrats on a forward progress with dose escalation and especially on the early signs of tumor regression in sounds like some of the patients.
Let me ask for the patients who have shown some early indications of tumor regression have they all progressed on prior PD, one therapy or were any of them only up previously treated with chemo.
Yes, Mark Thanks for the question. This is Ken all the patient.
Have been heavily pretreated, including with checkpoint inhibitors, so they've all progressed on checkpoint.
Okay, and so can you comment is there a political mandated PD one washout period and maybe can you can you just.
Give us some color on the interval between the last PD one day, some nice start Q1 on one for these patients.
Yes, so it's a really great question and then there is no mandated a washout period per se.
All we are requiring is that patients are progressing.
The different so every patient has a different length of time.
That they've been off PD, one checkpoint type therapy.
The.
In general that's a bit at least a two to four months of a from their their last dose.
Okay. Okay. That's helpful.
Maybe maybe a quick one for for Dan I'm, just wondering if we can expect the more.
Fleshed out PK PD data to make an appearance at a medical meeting in second quarter or are you thinking this will be delivered by a press release more once you have enough follow up on these patients.
Oh sure I'm, all answer that sort of as an overview and I'll ask a nice to elaborate but look we're going to be opportunistic about it we're not going to hold on data waiting for.
The conference unless we already have at lined up and the timing aligns so and we won't put out a press release, unless we think it's you know is substantively warrants.
That type of release, so our intention is to compiled data as we've been doing obviously, we're using the quarterly calls as a as a venue.
But at various conferences and also we have investor conferences that we have the opportunity to update on an intermittent basis. So in this sort of a covert 19, new new normal that we're dealing with we'll we'll use virtual venues where applicable our web page and and.
A press releases as appropriate I don't know if you want to.
I think thats right Mark I mean, we have.
Ourselves getting equate to the new normal of.
As I mentioned, even with the WT. One for example, we add that at AMC, that's not going to happen in June, but we will certainly be looking for.
Appropriate forums, where we can thoughtfully compile the data and share at these meetings and.
Of course late in the year, we've got opportunities, but said C and such but we'll look at bonds before that too and that's something that we continue to.
Discuss amongst ourselves with Ken will find those opportunities.
Okay, and just a quick follow up on on the a CR presentation on I guess Q1 or two.
We are we going to see any data in.
In that presentation that might give us more of an indication on which types of tumors. You initially intend to focus clinical development on for Q1 or two thanks.
So the AC out presentation, Mark with WT, one is focused on characterization of the molecules and the early data that we've seen with primary human T cells, and the downstream effect to responses, which up very encouraging.
As for the indications. This is something that can and that team are we this is a but sort of one of a core priorities. This year is to align and define those and as you were low in contrast to HBV driven had an accounts of 87 stratify nicely WT, one has a spectrum payments logical unsorted cans.
Says and there's a few of them that stand out and the teams continuing to sort of flesh that out.
And we'll be able to hopefully share with a that's those sort of thoughts.
In the let later half of this years, what I'd imagine we'd have that the plan sorted out for a current thoughts for clinical development strategy and how we apply this molecule also in contrast to want to London, where the allelic variant is able to the WT. One program is being developed with able to for this part.
Of the world, but a 24 for the Asian territories as I mentioned with obviously different T cell epitopes that also provides a breadth of opportunity in different geographies.
Understood. Thanks for taking the questions.
Thank you maam. Thank you.
Our next question comes from the line of Matt who Kumar with Robert W. Baird. Please proceed with your question.
Well, hey, everyone. Thanks for taking my questions. So I think our first one is kind of maybe scientific philosophical certainly per tenant finish. So how long do you think it practically takes to educate T cells activate against HPV E. Seven from Q1 on one.
And then kind of following from that do you think that timeline for T cell activation, the you're observing so far it's consistent with kind of naturally already present HPV directed T cells kind of emerging out of the mill you or representative.
Kind of single they really haven't each kind of train denovo to engage with and going after 18 seven.
Yeah, I'll take a crack out as much of that that's an excellent point, which is the kinetics of the evolution of at T cell response, as a function of the pre existing repertoire. So the point that you brought up isn't very important one.
And it entirely depends on what the baseline composition is if you haven't sensitize and you're going from a naive Virgin repertoire. Then obviously that time to effect is going to be longer than if youre going to be expanding from a pre primed repertoire and that was the case. We also stressed in the paper that we published last.
Month, where you could see new ones as an intensity and presence depending on whether you had a pre prime repertoire or non.
My bias as an immunologist as these first signals that we've seen from the patients. After the first few doses are likely from ones that have some presence in the periphery.
And I think that goes to say the that on the longer run.
There may be patients that.
I need a little bit more time on drug to perhaps exhibit similar peripheral signals. That's just the periphery and again I come back to the central question that this or that they don't we look at the peripheral blood as a surrogate for the lesion of tissue in case, there are scenarios, where you have resident populations that of whole into that.
You might not so much present in the periphery. One may expect a disconnect where you may not see much in the periphery, but you may start to see certain tumor Legion of specific.
Activities and that's something we've got to just keep an open mind, because ultimately what the effect to site as harboring.
Is still an open question ended the you know you could have rest of themselves against the very dominant antigen that up positive that I held back for whatever local resistance mechanisms all that that could be engaged by the drug we know that the molecule can get to the tumor effect aside and our preclinical models. The degree of tumor resident expansion was.
Significantly higher when we measure the a tumor specific T cells as opposed to.
The periphery, but all those when would you bring up a excellent nuances of experimental immunotherapy that were aware off and as the data emerges, we'll be able to sort of hopefully put some solid cohesive ER structures around these thinking.
Okay also following from that question, so think about they're going to Moeller equivalents continued high given have you done the kind of exposure equivalent given that the your drug is much more persistent then co Luke and is kind of in circulation.
So as we just we need to get some more exposure data. These are early points mother, and we'll be able to put that in perspective and that is the intention.
We were very encouraged to see.
That the early exposure looks in line with what was projected but the proleukin exposure is very different than ours and that's a that's a that's a factor that needs to be further.
Fleshed out as we get additional exposure data from the higher dose groups, but thats a very good point.
Yes, we also recognized that.
These doses that we are showing our based on a single dose of Proleukin.
And of course.
Much of the toxicity of Proleukin due to the multiple doses that you need to give to get exposure.
So that's one thing or I should that Ken just yet.
Yes.
Our next question comes from the line of Ren Benjamin with JMP Securities. Please proceed with your question.
Hi, Good afternoon, guys. Thanks for taking the questions and that's on the progress I, either maybe just starting off a question for CAD.
If I just look at cohorts look one through three nine patients. If I heard you right. There were there are two estes and to patients with T cell expansions or or Activations and and if that's right I'm curious why wouldn't.
Why wouldn't the two patients what the T cell inventions also be the ones, who are getting gas fees I'm, just kind of your thoughts on that and what's the longest as the that youve recorded to date.
So.
I think that some of these patients we've seen what we've seen.
Is that you have these patients are all rapidly progressing and.
And the fact that we've seen anything at all.
At the low doses is pretty tantalizing two to me personally.
And to to all of Us and I think what we've seen that.
Ah that we've started to see some TV effect. Some you know what looks to be early managed and activation, but that is just not been enough to overcome.
Patients with basically exponentially growing tumor and deep low doses, we just haven't been able to see a sustained.
Response.
Even in the patients who are starting to show us some biologic activity.
[music].
So the if you look at.
Our longest.
Stable disease.
Pacing.
What we have is exactly Oh, we have one patient.
Who eight.
The is through.
Cycle.
Cycle five on and we have to get to at least to confirm our response, we have to get at least through a fourth cycle for so we've had two patients.
That have made it through our through to cycle five dosing.
Got it and and just.
I know, it's early days, but I'm kind of curious when you when you look at.
The other patients are there any negative selection metrics are biomarkers that maybe are starting to pop out are you guys are starting to evaluate.
You can even something like T cell exhaustion markers right that that you might be able to utilize moving forward or do you kind of feel that.
Once we start moving into less heavily pretreated patients.
Yes.
We think that the the repertoire is going to be healthy enough that that it's not really going to be an issue in terms of patient selection.
Unit locally great question I think.
We just we don't have enough data yet on exhaustion and we're certainly looking into and have plans in the protocol to evaluate those types of biomarkers that to try to understand.
Who is not responding.
I do think moving into earlier groups like we are with the combo study, which will be also a dose escalation study by the way, we'll be able to see patients who don't have exponentially growing tuner and and we'll have a little bit more time.
With those patients to have an effect and I think that's going to be critical but I also think that again choosy why do you were trying to understand why the check we fail.
And in combination with you if we're not happy.
Having a good response I think we are going to see some use the FICO scores et cetera, we're going to be able to start to get to feel for why Q1 or one might not be working.
So.
We're we're thinking hard about that we've done some biomarkers built in and we're looking forward to treating earlier patients.
Yes, just to add onto what Ken said I think one of the parameters of immune fitness in terms of looking at the repertoire. The induction up part of a biomarker panel that we'll we'll get to evaluate its just a point of collecting and having more data I think it a fundamentally was quite remarkable as you've got a novel protein framework going for the first time.
In mine and the fact that it is inducing the appropriate what we think is that right repertoire to us is very encouraging obviously, the fact that aisle two of these high doses.
As being sustained and to tolerate its with the appropriate safety parameters again becomes very important and as you well pointed out whether that also then core merges with other metrics that we've started to see is a component that we are very much. We're looking forward to studying a the relation.
The ship between the PD metric and clinical response in terms of absolute numbers I mean, I just want to be very careful that because ultimately what's going to matter is what is the infiltrate at a tumor leaves no side. What is the phenotype of the infiltrating repertoire, what may be local resistance mechanisms, we may need to come.
I'd say to.
To that end or the combination with pembro.
Makes very good sense.
But I think I think as we gather more data into all of these.
Wonderful lead relevant immunological parameters I think.
We'll we'll hopefully get addressed.
Got it and and just regarding the PK PD results that we're still expecting this this quarter. If I know originally correct me if I'm wrong I thought originally we were thinking about cohorts one into but enrollment seems to be going so well. It is it fair to say that when we're looking at these PK PD results that will likely be cohorts one too.
Yeah, and three or.
I'll be expected.
Yeah, I think so I think our expectations and the way. This is something that's ongoing when we can shed that our exposure data. The early exposure data from cohort three we anticipate to have it oh by the end of this month. So our hope is.
As you pointed out the fact that we've continued to see enrollment and we continue to sort of dose escalate that as we start to gather more of these data and put it out that it should have a composite body that goes beyond one and two we're very excited about that.
I guess despite that.
I was just going through AD and in here that.
We are so grateful again as I mentioned in the call that were so grateful that we've been able to continue to just to enroll.
We are hyper aware that 90% of all cancer trials or not.
In rolling right now across the the academic institutions and again, the fact that we've been able to our investigators have and convince their institutions that we are a critical drug that should be allowed to enroll is a real testament to to the <unk>.
Coordinate think this is and I.
I am just isn't you know as an academic investigator myself I am thrilled that we've been able to enroll through this.
So thanks.
No it makes sense and thanks for that at one last question I want to leave yeah, Dan out of the discussion here, but you've got to a really nice significant cash position and and and you can I guess I can sort of think about it in two ways. One is it could result in an acceleration of the pipeline and.
Things that we were expecting might take a year or two.
Oh coming in a little bit earlier or that you know at this stage in the game there enough kind of rate limiting steps.
Maybe manufacturing where no matter how much cash you put all added it's not necessarily going to speed up you know the timeline, how should we be thinking about kind of the usage of cash and the.
The acceleration of the pipeline.
Yeah, that's a really important question Ren and by the way I. Appreciate your perspective on no matter how much you throw out to be as a lot of companies think by just hiring more people they can.
Increase output skilled requires rigor right and that's what we've been putting in play.
Laying the foundation over the past year, plus and we look at the data emerging from 101 as a validator of what was the 100 series could represent.
So as we continue to date it generate more data such as what you've heard today, but you know on a going forward basis with more patients.
Our intention is to then we can expand out with one on one we have to advance one out too and as a nish described earlier neo stat is meant to be a platform advancement.
To be able to exploit these observations and a let's say more productive cost efficient manner. So it's a hybrid between what you articulated we're not going to be conservative and just continue systematically building data on one or one and wait on everything else.
But we're also not just going to start increasing our burn rate, we're going to do this in a very deliberate purposeful trajectory. The first thing is to generate de risking validating data with one or one.
Which can then justify increasing expenditure on other assets that benefit from that de risking. So that's that's the way where we're basically approaching us.
Great. Thanks for taking the questions and congrats again.
Thanks, Ron really appreciate it.
Our next question comes from the line of Tom Shrader with BTG. Please proceed with your question.
Good afternoon. Thanks for squeezing me in so going back to what was a very interesting line of discussion about the T cells may actually need to be in the periphery for you to have time to work do you measure that you can you get an accurate read on the T. equals zero.
He felt that might respond to your antigen.
Yeah, Tom So whenever these analysis done there always compared to the baseline from the blood pre dose. So you have a sense.
Got it or not.
But can you sort of back extrapolate now that it has to start here to have a chance of being an anti Tau response, given the call that.
That actually is that those sorts of hard numbers can be put it in brett species, an experimental animals, but in the winter when you get too.
The population.
The level of the species of human those those numbers are all over the place simply because you have different levels of sensitization do you have different diversity of the repertoire and don't forget through the treatment regimens that these patients have been through the immune competence and fitness criterias.
Our.
In may maybe quite variable so that you can do it on a per individual basis, but.
It is I think it'd be very difficult of bracketed as a as a group basis.
And then put maybe the same question.
We are people that you treated all over the place in terms of their prior PD. One response and there is there any anything interesting to think about between what they got out of PD, one and what they got out of your approach.
Southern Ken mentioned that almost I think Ken mentioned. This is just have just a few moments ago that almost all of them. Prior checkpoint failures and again can that comes back to the Centrepoint on which is if you are fundamentally don't have the right effector repertoire or the appropriate specificity locked in the application of.
Checkpoint is not very relevant I mean, the checkpoint is working with the assumption that you've got the respiratory as one of the questions for us as we gather more data is to understand those very relationships and.
Hopefully as some of these clinical responses solidify one can perhaps establish those relationships and if thats true then the combination with Keytruda should further build upon that and should have figured out what we think could be quite remarkable outcome in the sense that you've got an Asian doesnt using the right repertoire in a very select.
Active stable manner, coupled with if they should upregulate PD, one they should gain benefit from that angle, but having just repeating went longer in options are the repertoire doesn't do much.
Okay got it. Thank you can I would just and note that.
None of the patient tenets sustained checkpoint response.
Before going on study.
Okay. So they were like primary failures that just blew right through PD one.
Yes.
Pretty much blew right through yet.
Okay.
There are no further questions any queue I'd like to hand, the call back to management for closing remarks.
Okay. Thank you very much I also want to thank everyone for your time and attention.
And.
For your interest in support of our Q Biopharma, we look forward to giving you continue we'll update says it become available and most importantly, we hope by everyone stays.
Safe and healthy during these challenging time, so thank you very much and take care everyone.
Ladies and gentlemen, this does conclude todays teleconference. Thank you for your participation you may disconnect. Your lines at this time and have a wonderful day.