Q2 2020 Cue Biopharma Inc Earnings Call
[music].
Thank you for standing by that's just a conference operator welcome to the Q Biopharm <unk> second quarter Twentytwenty earnings call.
As a reminder, all participants are in listen only mode and the conference is being recorded.
After the presentation, there will be an opportunity to ask questions.
The joined a question Q you May proceed Star then one telephone keypad.
She didn't need assistance during the conference call you may signal on up I read it by pressing star and say well.
I'd now like to tend to come friends over to George Zavoico, Vice President Investor Relations and corporate development. Please go ahead.
Thank you and good afternoon, everyone. Thank you for joining us on today's Investor and analyst update call. Joining me on the call today are dentists area do you buy pharmacy O Dr. Ornish, Siri, President and Chief Scientific Officer, Dr. can't be into acting <unk>, Chief Medical officer, and carry until our Chief Financial Officer.
Before we begin I'd like to remind you that during today's call. The company would be making forward looking statements various remarks or the company makes during this call about the company's future expectations plans and prospects constitute forward looking statements for purposes of the private Securities Litigation Reform Act of 1995 actual results may differ materially from those indicated by the forward looking.
Statements are the result of 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 20 to 2020 and the most recent quarterly report on form 10-Q filed with the FCC on August seven.
Well, it's other filings made by the company to they have to see from time to time, which can be accessed on the Edgar database at Www Dot FCC Dot Dot. In addition, any forward looking statements and any forward looking statement represents the company's views only as of today August 31st that should not be relied upon as representing the company.
He is views as of any subsequent date.
Well 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 should not be relied upon as representing the companies use of any day subsequent to today.
Please be advised on today's call is being recorded webcast slides were presenting today and a record any more color will be available on our website for the next 90 days. We will also be available via email provided on our website for questions not addressed during the call I'd now like to turn the call over the Q CEO Dan.
Yeah. Thanks Judge a good afternoon, everyone and thanks for joining us today for a review of our ongoing progress and second quarter financial results, which are available in more detail in our form 10-Q filed with the FCC on.
I guess seven also I to remind everyone on the call a as we proceed through the through the called out the slides maybe advanced directly from your computer.
So the next slide on slide three shows our agenda for todays call I'll provide a brief synopsis an overview of our pipeline a emphasizing the importance of data. This emerging from our lead program Q1 O. One representative of our breakthrough approach for the selective modulation of disease relevant T cells directly.
In the patient spotty.
Emphasize breakthrough because we believe were on the cost spoke demonstrating that Q1 or one is it which is representative of our Q1 hundred series is capable of presenting a tumor associated antigens directly to the targeted T cell receptor or TCR together with a costimulatory.
I'd kind in this case.
I want to specifically and selectively to selectively activate not to safely activate only disease relevant T cells directly and a patient to elicit a clinically meaningful response without dose limiting off target adverse events.
I'll be followed by Dr., Ken P. after who will provide further details on our most recent observations from our ongoing phase one Q1 on one monotherapy dose escalation and expansion trial and HPV positive head neck cancer patients.
Then dr. any sure eight will describe our continued innovation and additional progress that we've made and advancing our differentiated and meter stat and associated Neo stat platforms. I Nish will also highlight our expanding immuno oncology pipeline, including the continuing progress with our Q.
300 program in collaboration with Merck.
The progress we've made with our ongoing phase one trial with Q1 on one and additional programs, particularly throughout the challenges of the ongoing covert 19 pandemic demonstrates focused execution towards platform validation to this point I'd like to just take the time to thank our dedicated employees for their.
Wavering commitment and focus and diligently working under these difficult stressful conditions.
All the way to nieces update carry N. Miller, who.
Has recently been promoted to Q Biopharmas Chief Financial Officer will review, our current financial status. I'll, then provide concluding remarks and followed by a question and answer session.
Okay on a the next slide and overview of our core strategic objectives in progress in the second quarter is shown here on slide four.
Our primary objectives through focused deployment of resources continue to be first.
Increasing shareholder value through validation and systematic risk reduction of our in munis that platform through continual generation of data from our phase one Q1 on one dose escalation clinical trial furthering confidence that our approach represents the potential to be up.
Major disruptive breakthrough for safe and selective immune modulation.
Near term goal is to de risk Q1, O one by demonstrating safety and tolerability, thereby reducing the uncertainty in risk profile associated with the Q1 hundred series, which is aisle to based.
As well as our follow on Q3 hundred series and biologics from our Neo Stat platform.
In addition, we believe the clinical data generated with Q1 on one is likely to be predictive of the entire Q1 hundred series.
As the underlying molecular framework is largely preserved.
And all biologics up this series. The primary difference is the tumor associated peptide epitope presented by the molecule, which determines the cancer indication being targeted.
In this regard and our ongoing Q1, all one phase one trial and so far through the first four cohorts, we continue to observe dose proportional pharmacokinetics, our PK early signals, a relevant pharmacodynamics or Pee dee Ann activity and encouraging evidence that the drug appears.
To be clinically active as a single agent.
Moreover, since our last earnings call, we've advanced through cohorts for in five and following authorization from our Safety Review Committee last week, we're now enrolling cohorts six.
Which is at a four makes broking.
Secondly, broaden our pipeline by initiating a Q1 on one trial in combination with anti PD. One antibody pembro are true as it's known in October as well as the Neoadjuvant trial.
It was he added this year our early next year, both in the frontline setting.
We're also expanding our protein engineering and platform applications for developing therapeutics to address other cancers, specifically, one or two and willms tumor one our WT, one expressing cancers as well as expanding into auto immune and infectious diseases.
Moreover were incorporating additional HQLA illegals into our biologics to further broaden patient coverage.
And third acceleration and enhancements of our productivity through further development of our newest that platform, which is already demonstrated significant promising preclinical studies. In addition to cancer immunotherapy. We're also assessing the potential applications of Nia stat, and infectious diseases, particularly against novel.
Virgins, such as Sars, koby, too where immediate T cell responses could provide protective immunity to those infected with Sars koby too.
In each will elaborate upon this in his update on Nia stat.
I'm now going to turn the call over to Ken who will provide further details regarding the progress of clinical development for Q1 on one which is our first clinical drug candidate representing the Q1 hundred series Ken.
Thanks to the end and I'm excited to be cocky debt.
And.
I talk to you.
But.
We have three to participate in clinical centers and associated oncologist shown here on slide five.
Ralph Jacoby 19 pandemic. This group of highly respected in dedicated oncologist and remain focused upon screening and enrolling HPV 16 positive head and neck cancer patients to participate in our trial.
Evidenced by the full enrollment cohort five and towards cord for import five since our last earnings call in May of this year.
Through our pre screening process, we continued to identify patients for our travel future cohorts slide six shows that high level sounded a bit design for ongoing phase one trial Q1 to one.
As a reminder, we are holding second line and beyond patience with recurrent or metastatic had next squamous cell carcinoma driven by HPV.
Typically HPV 16.
This represents approximately 70% of all had net cancers occurring in the world Barron's Your region accounting for an estimated 13500 patients annually in the U.S. alone.
Dr. Rescission medicine approach. This phase one trial find molecular inclusion criteria to include head and neck cancer cancer patients that are easily able to a one costs in tumors are confirmed to be driven by HPV 16.
Through these specific inclusion criteria, we're ensuring that only patients with the potential for clinical benefit are enrolled and treated. This trial is designed with the primary endpoints of safety and Tolerability, while concurrently defining the PK parameters from Q on the secondary endpoints of PV evidencing the drugs.
Mechanistic activity on T cell activation.
Gration as well as the testing signed the clinical activity activity be via periodic patients scans.
The trial is a standard two part trial with it the first part AIDS designs as a typical three to three monotherapy dose escalation patients receive Q1 or one once every three weeks the IB infusion.
However, the trial protocol also provides the opportunity the doses 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 build supporting data prudent and most appropriate so scared the part b expansion.
After the.
35.
Cats break it down.
And they have enrolled to seven patients at this time.
Based on the Greg safety, PK, PD and efficacy data from the dose escalation part a we will accrue additional patients at the appropriate dose level.
I heard the expansion phase <unk> from the recommended phase two dose.
20 patients.
Therefore in summary.
It's a via the trial.
The safety.
Well evaluate safety and Tolerability, if you want to one expansion cohort is designed to confirm the safety biologic activity and anti tumor activity at the effective dose and additional patients to provide further support.
In confidence as we move into later phases with more patients.
As we show on slide seven we initiated dosing cohort one in late September last year, and then move forward to cohort two in December cohort three in March and cohort four in May.
One of the first three patients in cohort for experienced a grade three indeed, yeah that was designated as a dose limiting toxicity or D. L. T that was possibly drug related.
We therefore neural three more patients in cohort four in July per protocol design.
After these three patients were observed through a 21 day safety period without any additional D. L. Keys, we were authorized fire Safety Review Committee to proceed with enrolling three patients in cohort five.
Two milligrams per kilogram during the month of August we have completed the enrollment in safety period for all three piece you said this dose level and the data from these three cohorts five patients reviewed by or Src last week and I'm pleased to report that we've been authorized to commence treating patients in cohort six.
As for makes for kick over the coming weeks.
To date 19 patients in cohort one through five have received.
Total.
Sorry.
A total of 54 doses.
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Of 54 doses of Q1 on one three weeks apart with the what appears to be an attractive safety profile with limited toxicity.
We've been able to administer doses of Q1 on wanting cohorts five that deliver about 60, you called higher amounts of an eye out to varying on a mall weren't basis, then I'll to delivered by the approved dose of Proleukin.
With this data we are confident that we can deliver high doses of an Io variant on target safely. We continue to be highly encouraged by early progress an observation.
We continue to observe encouraging early signs of biologically clinical activity in its heavily pre treated patient population.
It's worth pointing out that the average pacing in this trial has received for prior lines of therapy, they've been exposed to at least six different anti cancer agents, while getting those therapies.
Previously reported in cohort one a patient inadvertently received five times the prescribed dose if you want to one word dose between the doses intended for cohorts two and three this patient demonstrated tumor regression on scan after receiving this does but also developed worsening of a pre existing bullous pemphigoid.
Brash as a result of the bullous Pemphigoid grass Q1, or one was discontinued but the pace. It remained with stable disease off therapy for nine weeks before eventually progressing.
[laughter] heavily pre treated patient from cohort two and who had previously progressed line therapy with a checkpoint inhibitor has confirmed stable disease with tumor reduction of the target lesion. This patient was on trial for 19 weeks a patient in core three and a patient cohort for demonstrated to stable disease. After.
Two cycles of therapy, but manifested disease progression at three months.
Three patients in cohort four and three patients in cohort five remain on trial with the first part patient cohort five having received their third does so ready.
The latest PK data with patients in cohort for as shown in slide eight continues to demonstrate dose dependent increases exposure.
In patients that received multiple cycles. If you want to one we see no evidence of a decrease in exposure or you want to one we suggest lack of the immunogenicity of drug clearing anti drug antibodies are 88.
And as I just mentioned, we continue to see a high highly favorable safety and Tolerability profile, even with about 60 times, a moment content of our aisle to variant in cohort five.
Two milligrams per kilogram compared to the approved dose of Proleukin.
Therefore.
We really want to emphasize as we've already established that we have a safe vehicle for delivering unprecedented doses of aisle to the patients.
As shown in slide nine we continue to generate and evaluate PD biomarker data, including detectable expansion of targeted H.P.B. seven.
Specific T cells from peripheral blood.
Early cohorts with an emerging trend that appears to support a correlation at T cell expansion and duration on trial.
The veracity of this correlates who will be further studies in the ongoing analysis of patient samples from higher dose cohort dose cohorts that is cohorts for and higher.
An example of early PB analysis from cohort for shown here, where in H.B.B. specific T cells were not evident in the credo sample or at the first sampling at day 21. After the first cycle. However, it day 42 after the second treatment cycle, and then burgeon population.
<unk> HPV specific T cells as detected by peptide. It's your late Tetramerous was noted.
We continued to be encouraged we remain highly optimistic.
Ongoing data generation and analysis and look forward to providing further details as they become available.
The totality of the current metrics are strongly supported by then and emerging synopsis of safety Tolerability as well as biological clinical activity.
I also want to emphasize and point out that the totality of our data already in the early with our early monotherapy study has given us the confidence to move forward with our combination trial with Keytruda.
Slide 10 shows our culture, our collaboration with Merck to initiate this parallel trial in frontline therapy to evaluate Q1 or one in combination with pembrolizumab or keytruda for patients with HPV positive.
Head neck cancer, who also each delay until one positive our intention is to continue to advance the monotherapy trial for stuck in second line in later HPV positive tumors.
And patience and enhance our patient reach by expanding into frontline patients in combination with great Keytruda, which is the current standard of care in this trial referred to as keynote <unk> 70, and we intend to translate our preclinical findings demonstrating highly significant synergistic anti tumor activity.
With Q1 on one combined with an anti PD one antibody. In addition, the safety and Tolerability data from our current ongoing monotherapy trial enables us to start the combination trial at a higher starting dose of Q1 or one which is a significant step forward in terms of timelines for generation of clinical data.
As we noted we've already been approved at multiple sites in this trial will commence in October of this year at our monotherapy sites, we're using the same sites.
We also plan on initiating a neoadjuvant trial in patients that newly diagnosed with respectable and localized head and neck cancer.
Cancer patients in the coming months the trial designed to provide us with further evidence and insights into Q1 on ones mechanism of action by directly studying the tumor tissue post resection test that's infiltration proliferation of HBV specific tumor infiltrating infiltrating lymphocytes hotels.
This latter point as an important one respect with respect to the mechanism of action in Q1 on one and then these will further elaborate upon this with some recent data that underscores our excitement for the Neoadjuvant trial and finally once we've established clinical proof of concept for Q1 to one hadn't next squamous cell carcinoma.
We may expand opportunistically into other HPV driven cancers for example, cervical cancer I'll now hand, the call overdue in east to discuss the other advances in our pipeline and platform Nish.
Thanks, Ken and thank you everyone listening in and I Hope all of you and your families continue to be safe and well.
I'd like to underscore on slide 11, a scientific vision to fully exploit the exquisitely selectivity and specificity of the immune system, while not compromising patient safety. We believe this approach for selective modulation of T cell directly into patient is distinct and differentiated from other approaches wedding.
Broad immune modulation or global systemic activation often present, what's significant challenges associated with compromise safety compromised efficacy and tolerability. They munis that framework as exemplified by the Q1 hundred series as shown in slide 11 contains the two key signals.
Signal, one and signal to the tumor specific T cell activation Q1 to one I'll need to clinical candidate is our first drug from the Q1 hundred series signal one hit on the Q1 hundred series consists of stabilized peptide MFC molecules to engage tumor specific T cells via the T cell receptor.
TCR, thereby locking in the specificity combined with rationally engineered two molecules serving as a costumed literally signal to the selectively act upon those T cells to control their activation directly in the patients. There are two modifications to our I'll do vary in molecules that are important for its specificity.
And selectivity the first as abrogation of binding to while do receptor Alpha sub unit in order to avoid T Reg engagement, which labels it as a nod alpha IR tube area and the second is attenuated binding to the I'll do receptor beta sub units such that the IMO two activities biased to those tea.
So that adult to the specific peptide Asia leg called blacks via that T cell receptor as perhaps best shown at the top down view of the Q1 hundred see these framework here.
Now we've invested considerable time and effort to define this molecular framework and spatial organization, thereby enabling selective activation of tumor specific T cells, while mitigating or eliminating effects on the vast majority of the it relevant non tumor specific T cell repertoire, and thereby minimizing safety liabilities such as vascular leak.
Central These features of the Q1 hundred Cnis is what distinguishes it from all the Io to modalities, either why antibiotic to order not out file to variance wherein the Io too broadly acts upon many T cells without preferential bias well specificity east was the desired top.
But diesel repertoire.
We are highly encouraged with the emerging metrics and clinical data associated with you want to one and by implication the eyes to base Q1 hundred series. In addition, the initial BD data continue to demonstrate early evidence of T cell expansion in blood, which will be further bolstered with continued sampling and analysis from cohorts.
Four and five and beyond the measure of T cells in the periphery. As you can appreciate it is a several good for mechanism of action with the understanding that the ultimate gold standard for successful immunotherapy is the measure of diesel activity and function within the tumor lesion to that and it is important to highlight key observations was it with respect to the.
The Immunostatus framework and its potential for direct activity within the human tissue I'll address this more in detail in the following slides. So the next slide slide 12 shows the data from our recent paper and clinical cancer research wherein we made the observation that the murine Q1 on one treatment.
Resulted in a highly enriched presence of tumor antigen specific T cells in the tumor tissue when compared to the presence of the same T cells and the peripheral compartments like not horse lean as we show here post treatment with most Q1 or one of approximately about half a percent of C.D.A.T. cells measured in blood us means.
<unk> was specific to the tumor antigen in contrast, and the tumor tissue. The same T cells, what enriched by almost two orders of magnitude nearly 50% of all CDH was specific to the tumor complementing our published data in clinical cancer research and the data emerging from the climate current clinical trial.
I wanted to share with you and equally important data center, an observation, which is presently impressed and as such details a embargoed or what I can share is that this preclinical work highlights that the targeting peptide amici moiety of the Q1 hundred scout for penetrates and localized as two solid tumor tissue and directly and.
Gauges antitumor T cells in the human tissue, there's observation could have very important implications for the differentiated mechanism of action of the Q1 hundred series in other words, the ability to localizing directly engaged tales within the tumor tissue to activate the effect of killing responds maybe a unique.
And highly promising property off the immuno stopped platform in light of these important datasets, we believe that expediting neoadjuvant clinical trial in respectable localize head and neck cancer, but provide convincing translational and biomarker clinical data that further strengthening the case for Q1 no one's Mac.
As of action.
Slide 13.
Yeah. It provides an update on Q1, though to a second asset in the Q1 hundred series, which targets a unique epitope from when steel mill, one or WT, one a well characterized at an attractive on coffee Atlanta Gen for many hematological and solid cancers. We've continued to make significant progress with this program what.
He is being prosecuted with both actually able to an h. and a 24 deals. We're pleased to inform you that an eye Andy filing for the able to Q1 or two program is projected for laid in the second half of Twentytwenty. One data recently presented at the A.C.R. and the New York Academy of Sciences virtual meetings.
So with that Q1 or two selectively expand primary human T cells from blood. These expanded T cells out poly functional as measured by cytokine production as they mediate killing of targets expressing the WT. One antigen. An example of each of these functional attributes as shown in this slide as predicted.
By the platform similarity across the Q1 hundred series of compounds. The preclinical safety assessment of Q1 or two has mirrored what was noted with Q1 or one that is the rational engineering awhile to prevented and minimize or eliminate it affects on T regs and irrelevant T cells. This observation underscores my previous.
Point that the current clinical experience with Q1, no. One has an enormous net positive effect and de risking the platform and the Q1 hundred based pipeline. Let me briefly comment on the recent developments and exciting prospects with a next generation Neo stopped platform, which is which is expected to.
Greatly accelerate us capability and enhanced our productivities and efficiencies both from a time and cost perspective. So the next slide slide 14 is a schematic of the neo start platform a p. step forward and platform enhancement was to reproduce the key components of the Q1 hundred Sealy Scott board, but without it.
Any specific peptide attached to the H. and a molecule to remind you. The peptide epidural is an integral part of the munis dot, meaning it's incorporated into the molecule as the fusion protein at the time of synthesis and contrast, neo stuff that synthesize without a peptide epitopes that as with an empty amaechi pocket instead, the peptide epitope is attached.
Subsequently using an advanced attachment chemistry as shown in the carbon figo via the examples of three different peptides bound to the neo stat scaffold. The versatility afforded by this approach is expected to significantly expand out region to divert antigens for applications in cancer immunotherapy and more reason interest in emerging.
Infectious diseases, including the SaaS Corona virus.
From an ambition to perspective, the neo stopped platform allows us to generate a core generic scaffold for any agent and lead the a single cell line and then use the scaffold conjugate various peptides of interest based on the disease to generate therapeutic candidate molecules. The fact that only a single its capital needs to be generate.
Did let's say it was a no. It was let's say of a significant resources in both time and cost the generation of clinical good grade material in a prior presentation. We shed proof of concept data supporting the biological activity of molecules generated via the neo start platform shown in slide 15 odd representative examples of T cell expansion to a bottle epitope.
Namely from the cytomegalovirus or CMV or T cell expansion against a tumor antigen, namely from an epitope from marked one as shown here the neo start platform could be effectively deployed using to call I'll do based Q1 hundred series to generate molecules that enhanced pathogen specific T cells or tumor specific T cell.
The anti CMV T cell response as shown on the left about what end the CMV Neo stats shown in Dalton lateral red lines expand T cells with the same efficiency as conventional CMV immunostatus shown in in solid Red lights. The marked one neo start here is a negative control.
Similarly, the anti Modwen T cell expansions from primary human blood as shown in the right behind them here again, Mark one Neal starts in daughter Blue lines demonstrate T cell expansion that is very comparable to what we're seeing what mark one immuno stats shown in solid new lines.
As shown on slide 16 based on these promising proof of concept studies, we've now initiated preliminary studies to determine the application of the neo stopped platform to generated robust T cells against Sars will be too we believed that the neo stopped platform, maybe uniquely positioned to selectively induce and expand antibiotic.
He says, especially in instances, where pre existing immunity is non existant or inadequate. Numerous recent studies have highlighted a key role for T cells and beneficial outcomes and Sars Gobi to infections. Furthermore, while most vaccines are focused on generation of protective neutralizing antibodies as a prophylactic measure.
Induction and expansion of anti Saar scobey to tease out maybe a unique determinant of therapeutic immunity, especially in circumstances, where the virus is present in the intra cellular compartment in infected cells and is largely invisible to antibodies in the extra selling them and do we are very excited about that.
Aspect of deploying our science and innovation to help with the source Corona virus global endemic and look forward to providing updates on the progress in this new direction in the near future lost any additional data underscoring the protein engineering design and manufacture ability of Neossance what disclosed at a recent presentation of the pegs virtual.
The meeting this past week more details with regard to this presentation are available on our website. Let me move on to slide 17 that highlights our pipeline progress. We've made significant progress with you want to one in the phase one dose escalation monotherapy trial as you heard and are well positioned for the combination trial with Pembrolizumab.
Scheduled to start next month Q1, or two would WT, one and two different agent and he is able to in a 24 continues to make strong progress with the planned R&D submission for Lake Twentytwenty. One as mentioned before we've also made promising progress without K Ross program within the Q1 hundred series and applying to share those data at an appropriate for.
I'm in the near future, we continue to extend the application of a platform with the Q2 hundred communities, where we have early datasets without surface receptors, such a CD 80 and for wouldn't be liken to that end. We'd recently quoted a paper published in loss in June Twentytwenty, but dr., Steve automotive cofounder of Q Biopharma. This study deploy.
All right structure bays rational protein engineering dissent, the molecular interface between BT, Laggan, C.D.A.D. and Cdtwenty Etsy teleflora interactions to enable the choice of modules for future immuno stats such as the few 200 series and finally as disclosed recently, we continue to make progress in autoimmunity with the Q3 hundred series.
And we've successfully generated immunostatus, incorporating clos to actually a means to selectively targeting merchandise auto reactive cdfour T cells as weve underscored in prior presentations day munis that and by extension the Neo step platform address a fundamental immunological challenge, which is how does one maintain selectivity and specificity.
We have a desirable immune response without reaching patient safety appreciating toxicities, we've been able to approach builds upon rational protein engineering, which is now bolstered by the supporting datasets offers a highly promising solution to patients suffering from gallons sold immune diseases and and threats from pathogenic infections with that I'll now turn the call.
All over to carry to review our financial results.
Alright, Thank you Anish, turning now to slide 18, I'd like to provide a brief update on our financial results for the second quarter ending June Thirtyth 2020, we finished the quarter with approximately 84.9 million in cash cash equivalents and working capital of approximately 73.5 million.
During the second quarter 2020, we extended our cash runway with 42.4 million.
The market equity offerings.
The company acted AD sales agent cash received from the ATM equity offering.
And a solid financial position support the development of RMBS that platform, including clinical development at Q Auto line into 2022.
What is collaboration revenue of 1.1 million from a collaboration with Merck and LG Chem during the second quarter 2020, which is consistent with the 1.1 million we recorded for the same period and 29.
Research and development expenses were 8.1 million for the quarter ended June 30, 2020, as compared to 6.9 million for the same period and 29.
This increase in R&D expenses was due primarily to an increase in laboratory and drug manufacturing costs that stock based compensation and clinical expense.
These increases were offset in part by decrease in travel expenses due to the cold 19, pandemic, which hampered travel throughout the second quarter.
General and administrative expenses were 3.9 million for the quarter ended June 30, 2020, as compared to 3.4 million for the same carried in 20 banks.
This increase in general and administrative expenses is primarily due to the increase in stock based compensation expenses and legal and accounting fees incurred during the second quarter 2020.
I'm pleased to say that despite the challenges presented from the cobot 19 pandemic, we've been able to money on team on them.
The clinic and of our pipeline, while strengthening our financial position through a combination of aftermarket equity offerings and disciplined spending we continue to be well positioned to execute against our 2020 objective I'll now turn the call back over to Dan for closing remarks, Dan.
Thanks, Gary since our last update call and despite these ongoing challenges that we're all confronting due to the covert 19 pandemic.
We continue to make significant progress across our platform and associated programs as a I'm showing here in slide 19.
Our key accomplishments include the ongoing timely enrollment through cohorts, one to five and now into cohort six which is at four milligrams per kilogram and our Q1 on one monotherapy trial.
And the demonstration of favorable safety and Tolerability through cohort five add two milligrams per kilogram.
Dose proportional exposure, which is has been in line with our preclinical projections and emerging evidence of PD activity in early signs of monotherapy clinical activity.
Having raised additional capital this past quarter, and having enrolled and treated patients into cohort five in our phase one trial of 101, our lead program, we're very well positioned to continue building a meaningful body of data, including safety Tolerability, PK and PD bio market activity.
As well as ongoing scans from patients to assess clinical activity.
We're also advancing closer to determining a recommended phase two.
Dose for Q auto one as a monotherapy and to initiate a combination trial.
With Keytruda in October and a Neoadjuvant trial.
Beginning end of year or a few one of 2021, both and a newly.
Diagnosed and previously untreated patients in head and neck cancer.
These data was significantly de risk and validate our approach, allowing us to then further build our pipeline based on the same foundational principles upon which we brought Q1 on one forward into established Q biopharma as a differentiated leader in the immunotherapy space with a potentially transformative and disruptive.
Breakthrough therapeutic platform.
Our guidance for the second half of 2020 milestones as shown in a slide 19.
And they are largely unchanged from our last call are reporting PK PD results from cohorts, four or five and perhaps cohorts six from our phase one one on one clinical trial by year end.
The potential for reporting clinical responses in phase one.
Q1 on one via resist criteria by year end initiating a Q1 on one combination trial with Keytruda in frontline HPV positive head neck cancer in October.
And by year end, we also expect to initiate and extend I, Andy enabling activities for Q1 out to select the target for Q1 O three.
Demonstrate needless that manufacturability and further efficiencies.
Identify potential clinical candidates in auto immune disease.
And finally to perform initial feasibility assessments of the nearest that platform for activating and enhancing T cells against cope with 19.
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 also like to thank our shareholders and our board of directors for continued support enabling us to advanced skew Biopharmas platform.
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 obviously, our Q1 on one phase one trial.
Most importantly, we are grateful to all all who have enabled us to pursue our noble vision to serve patients in need and with that I'd like to open the line for questions operator.
Absolutely we will now begin the question and answer session joined the question Q You May Press Star then one on your telephone keypad.
You will hear a tone I know alleging your request.
If you are using his speakerphone. Please pick up you headsets before pressing any key.
To withdraw your question. Please press Star then too.
So amendment as colors join the queue.
The first question comes from Steph Stephen Willey from Stifel. Please go ahead.
Yeah. Good afternoon, thanks for taking the questions and congratulations on the progress.
Oh, the six stations that you talked about remaining on therapy I think three cycles for three cycles five are you able to to say.
I guess, how many cycles on average those those patients have seen our they'd be on cycle. Two are they in cycles. Three I guess any color on on that front with respect to just kinda treatment intensity would be helpful.
Yeah can do you I know.
Yeah.
The patients are.
Still relatively early there you know passed a the the cycle.
Cohort for folks are beyond a cycle to and just and one of ours cohort five patients is beyond cycle or beyond cycle too.
At this point so it's still relatively early.
In the process for these guys.
For these patients got it.
And then just with respect on.
So with respect to the expansion of the peripheral T cells that you're seeing I know, it's it's maybe not the best of surrogates and it sounds like you may have some.
Data coming out to suggest that perhaps the real impact is happening within the tumor microenvironment itself with respect to direct engagement of tells but.
Is is that day 42 metric of T cell expansion that is being shown is that is that a pre dose or is that a post dose level.
And I guess, if it's the latter is there any interest and trying to do a little bit more refined.
Peripheral blood draws between doses just in an effort to may be better understand what the persistency about expansion in the periphery might look like.
Yeah, that's that's a great.
Go ahead and you go ahead.
No I was just got are just going to jump in here.
Go ahead please.
Sorry, just as Steve just to clarify that was Whos Ddos analysis, and rightfully and I think a this is what Ken was getting too as well that one of the sample type points is the challenging because these are all 21 days apart so what.
Happens after you get the drug.
In the interim time, and if that is extravesated into the peripheral lesion tumor tissues is exactly what's not measurable here.
And to what Ken alluded to the Neoadjuvant study becomes very important to study that mechanistically. So one of.
The limitations of course here is that limited availability of tumor tissue to be able to quantitate that I think the bay, but.
That we presented from a clinical cancer research and this publication that's in press I'm, making a very important point, which is that what ultimately matters and immunotherapies what happens locally.
Referral is a is it is a good several good for the for the mechanism as you alluded to Steve, but ultimately whats been missing here.
Is that final piece and the positive, which I think the Neoadjuvant gets as there I'd, let can comment on on frequency into the sampling frequency and again you know in the current times due to a how best weve navigate to that.
Yeah, I was just <unk> it can add that we work as we learn more and more about you know the PD and sampling.
We have thought about expanding out quite a to be quite honestly, you know where right now we're limited by co bid.
In that most of the sites in the hospitals don't even want to patients coming in for any extra blood grants.
But we're constantly monitoring how do you know potentially get more data for example were exploring using mobile slow bother me to try and fill in some of those future data points.
Especially where thinking hard about that and in as we start the combo trial in October.
You know that if could cope with its still going to be a problem, which is likely that it is going to be we really feel that we need to be able to be as nimble as possible in collecting.
Samples that you know I think you you you all have notice that we.
We have done what I'm continued to be as a medical oncologist amazed by is our ability to recruit patients on time.
Through this cobot, a crisis and I'm I'm humbled by the fact that my <unk> medical oncology colleagues have you considered it's so important to that to administer Q1 I want to these patients that they no. Good managed to keep our trial opening.
And accruing.
It is a challenge though.
You know the once again, a man to get those extra blood draws that we'd all like to see a again to decrease exposure of the patients to the risk of co that and that's why we're you know exploring other options to help us filling those.
Data points in the future. So that was up mid to long winded answer, but I hope that helped.
Yeah, I know that was very helpful commentary, Thank you and and I guess, just lastly from me you.
You talked about now being able to start at a higher dose of Q1 and one in the Keytruda combo study are you able to say what that target starting dose will be.
Well, what I'm wondering I can say is its on where I'm going to analyze where we'd actually like to start. Initially for example, we were I think you we'd have to start a cohort three at point in time for mix for keurig, but really.
What we're planning on doing you started yet and safe does minus one so currently that or you know what started to make her kids.
And and we May or May not go to to mix for kick depending on where we are with accruing cohorts six and at that time. So.
Yeah right now we're at a big project.
Great. Thanks for taking the questions.
Thanks next question comes from my do Kumar from Baird. Please go ahead.
Let me dairy.
Oh.
Hey, Joe first questions on.
I mean, do your breaking up a bit difficult to understand.
Operator may be a getting worse could.
Yeah, we're not able to a catch you.
Operator, maybe we can take another question.
In sequence and then put Madu Bakken.
Our next question comes from Tom Shrader from <unk>. Please go ahead.
Good afternoon, and not surprisingly have almost the same questions as Steve.
Can you, let us know your longest stable diseases. So far I guess these are from cohort three what are the longest couple you've seen.
Sure can you want to take that.
Yes, so our longest couple they have been and 19 weeks and.
We hit the one patient that had the braking therapy with it the BP and that was about a total of 12 weeks.
And our they both still on therapy.
No.
Okay, and then kind of a question for a nish. This this patient.
Can I assume that's a pretty good responses is that consistent with the memory response to you. The time course can you dig any quantitative data out of there between what happens between day 21, and they 42 or is this somebody building kind of a response from naive T cells is that something.
Can dig out a data like those.
Yeah, I think Tom look firstly these the only metrics. So the data looks promising we need to build this out a bit more if you would have compare this to an established chronic a sort of a memory repertoire against a viral determinants like CMV already BV this would not be as robust as Doug and.
Fact is even with.
You know if you look at the stealing pre though is you don't really see much of a population. So you could say, maybe there was something bad, but I'd really rather frequency and it took a couple aside because the treatment for it to present itself.
Or the likelihood is that it's a being pride from a naive baseline repertoire, hence you need the additional sort of time on therapy for it to manifest and present itself I think that's how we interpreted as this being either at a rat hole from an unpriced simply because of the fact that.
Based on you don't see that population if you go into the view in contrast, if you look at.
For example, the data with Q1 or two in that examples that we presented Tom I mean, there you could see a little bit of.
Pre those.
The population that's present that baseline in blood, which then further expanded out. So this is these are rare T cells frequencies, we know that they are usually not.
Easily detectable inpatients and the fact that we've started to see them is whats very encouraging and promising and that's exactly the building out on.
Going up in the Ddos, an escalation and and exposure to see if we can further solidify these metrics.
And then maybe of Ken could just comment on does that change the way you think about a trial like this if you are really going to need.
Eight weeks to see a response.
Yes, So I you know I think where we all recognize.
That these patients are our our SEC right I mean, they got rapidly progressive disease safe had multiple lines of therapy.
And you know ideally we will move to you know earlier treatment I think that's what makes the combo study so important because those patients where were have you know be first line therapy patients and that gives me.
Let me optimistic that we'll see even a better responses and they have more time to see those responses.
And then it also makes me think about whether you know in the future as we think about other diseases. Certainly you know again, the last heavily pre treated patients the better and so I really am optimistic and continued to be optimistic about.
The first line therapy patients in as well as even the Neoadjuvant. So you know as you well now in these phase one study so first in human studies.
First and foremost its safety safety safety and anything we can see clinically is is that your is a huge win.
Got it thank you for the details.
Hey, Tom just to clarify.
Just an add on again I wouldn't look at it that it takes eight weeks, where response because one of the things coming back to the point, but discussed when but Steve with the fact, that's in the tumor lesion is something that is not being quantitative so while these up peripheral signals if you've got a presence that extravesated localized to the human drug is getting the which is why this important pay but coming out.
That's very important then that effect may well be a very central to the response, but not being fully appreciated by just a blood analysis I always want to put that caveat, which is why I come back and what can articulate a very nicely the importance of the Neoadjuvant study to get this to Greeley delved deep into that Mechanistically.
Yeah got it kind of thank you.
Our next question comes from Reni Benjamin from GMP Securities. Please go ahead.
Hey, good afternoon, guys. Thanks for taking the questions and Bob Watson, all the progress I guess.
Maybe just to start off with a question for for a nish hopefully you can hear me, okay. How selective we keep focusing on the selective population at T cells, expanding out I'm kind of curious what other metrics outside of be selective T cell should we be I'm looking at all or you know be measuring.
For example, maybe cytokine levels or a CD eight and see for you know T cell ratios, what all or you are you gathering that might be able to help kind of complete the picture of of what's happening here.
Yeah, Randy intentions.
In parallel to look at immuno phenotype in for other subsets like you pointed to.
One of the cell types from a preclinical models.
Is the activation and possible effects, and then kase, which could be something that could be favorable they're highly sensitive to aisle to even attenuated versions.
We've not seen any consistent movement on T. Regs, a you know with with sort of a.
Consistent data and that's in line.
Other global Upregulation of T cell subsets should not really happened by the molecular design show a and that is.
At least in these early data says that seems to be consistent, but but I think I think overall immuno phenotype being an understanding other I'll do from the periphery. It's something we will continue to look at and that date and.
We'll continue to be strengthened a we haven't looked at a cytokine sweep of course bangle samples would come back to that as you know as we said accumulate enough sampling and decide on time points.
The other than being overlapped metrics off just a.
Immune recognition and FX a mechanism again coming back the human tissue becomes a very important composite up really what I referred to as early as a so some of the gold standard metrics and that it in the monotherapy, where the biopsies have been optional is going to be limited and again, if we can garner some of that through the Neoadjuvant study that can do.
Described I think that further add on it and that modality, one could focus not only on the antigen specific localized but also the repertoire diversity, including affects another immune subsets, which would be very telling to the mechanism of action.
Got it and then.
When we think about you know the kind of cohorts six that they're going to be starting to enrol well have started to enroll there. It's a sick theres a significant amount of.
You know those kind of relative to the.
Proleukin dose right and and of course, you continue to have a really good side effect profile and I'm trying to maybe you can help me reconcile it.
This is this a true reflection of the side effect profile of the drug or are the <unk> are the patients immune status.
And that we can do means that status since they I think Ken mentioned had four prior lines of therapy, because that does that potentially impact what the side effect profile.
It's actually looked like in a in effect or we masking the side effect profile the true side effect profile, given the patients and you in Oh system status.
Yeah can do you want to take that one.
Yeah. Thanks.
That's a really interesting question I think the the best way to think about answering that and thinking it through is that if you look at the aisle to data for the Proleukin data in similarly.
Groups of patients.
You saw you didn't see in attenuation of the side effect profile.
The toxicities that all of Iowa.
Proleukin I mean, not even in heavily pretreated sick patients like like we're dealing where the toxicity profile of Proleukin was was very very evident. So I don't personally believe that that's the car. The reason why where were not see you know.
A lot of great Green grade four toxicities I think it's because we really do have selective on target.
We have a selective on target treatment.
And I, so I really again pro the Proleukin patients really did have a you know a lot of side effects. You also saw that in the checkpoint inhibitors or when they when you go into early trials.
Given the very advanced patients you saw them have tremendous toxicities.
No I don't I don't think that are bad idea hold up.
Got it right and just one final one for me.
All this data that that you know is being accumulated when do you think.
We might be able to us to see this in a in a scientific or publication called.
So when we have the clinical.
Bill had good Ken if you want to comment on the clinical data presentations late in the area.
Well I think you know we would typically not publish certain only a manuscript on their side until we got through the phase one and one be where we had no total data clinical PK PD did on you know Oliver.
Our patience that went forward to establishing the RP to de you know I think we'll start putting out some you know abstracts and things for example to add Sissy and and.
Ask go next year in between but that but the totality of the data, we'll wait till the trials kind of complete.
But we are and we do have an abstract we'll be.
Presenting at Citi.
Great. Thanks, taking my questions.
Extra thank you Ryan.
Our next question comes from Mark Breidenbach from Oppenheimer. Please go ahead.
Hey, good afternoon, and congrats on all the progress with guests escalation and also carried congrats on the promotion two quick ones for me.
Maybe maybe.
Revisiting one of the questions from Tom on the kinetics of T cell expansion, you're seeing in patient 10.
Obviously 42 days seems.
Maybe a bit longer than I would've expected based on.
What we saw in some of the preclinical models and I just want to be absolutely clear and you start Ken if you're attributing the discrepancy in kinetics between preclinical and clinical data to to the fact that we're looking at peripheral T cells, only and maybe in the preclinical models you where you were looking.
I I add tumor biopsies as that did not the right way of thinking about it.
Yeah, I think I think mark.
A couple of things into preclinical models, you're not facing the headwinds all fade compromised immune performance status. So these are all extremely sick patients as you realized.
And so you you are starting baseline is a healthy <unk> diverse repertory can tap into where they whereas here you know obviously have the spectrum of spaces that have been through multiple lines and that's hard to decipher I think you're not own instances that would be in cases, where we've seen it after the first cycle and then in cases like this where you know it needs a bit.
Well in that comes out of the question well the patient really didn't have enough that you had to prime and boost and that's what you're seeing here that's what it's indicative.
Or did they have something in a peripheral leaves no side that you're not able to quantify and I just put that out as a variable because we you know through through much of the work in cancer immunotherapy reading things out in the blood. That's the one variable that is very hard to pin coin doing again coming back.
To the preclinical model, but the reason I showed you. The data is if you look at it and blood and the preclinical motors is again fraction of <unk> percent in the same animals. The way you had the responds and when you look to the tumor lesions that relative presidents off a piece of repertoire that was enriched enormously that we are obviously blind to here in this and.
We're always but a preferred present that we're using out again in fractions of a percent without knowing what's happening centrally and that's again comes back to the importance office study like a neoadjuvant way you have the pre and post.
Moss with you to be able to really quantify and establish that relationship once for all.
Okay Fair enough and I guess me tell your question.
In relation to how you'll know one to stop the Scott escalation.
So you go through cohort seven it makes per gig and you still are not seeing deal to use.
How do you really decide when to declare a recommended phase two dose you know what why not consider going higher and it makes for Kate.
Yeah can do want to take that one.
Yeah. Thanks, So I think that's.
We built this trial and again put on the Basie in approach over the top of the three bikes redesign.
Specifically, so that we could expand a dose cohorts.
No.
Now up to nine patients so that we could explore clinical response as well as as PD.
Because if we don't yet any maximally tolerated tolerated dose we have to choose not to what our biologically effective doses. There's there's no reason why we can't go to higher cohorts at all due to higher doses and we may consider that.
As we move forward, but again that whole approach to really see if we can define a biologically effective dose by not just relying on three patients per dose level and actually going up to nine will give us confidence that potentially that we can that define a b E D.
When we don't see and T.D., So we really.
I'm just so thrilled with this design because it gives us this opportunity <unk> to find that effective dose as we anticipated that we may be so safe that we can't find an MTD, but that's the longer answer the shorter answer is we may decide to go to higher doses.
As.
We just <unk>, we'll we'll just see what happens.
Okay got it thanks for clarifying and congrats again, thanks for taking your questions.
Thanks box, where.
Our next question comes from Mad Kumar from Baird. Please go ahead.
Yes, I hopefully this is better in terms of being able to hear me.
Yes.
Okay, great. So.
Let me kind of coming back to my other questions that have been coming out during this call. If you put it all together and think about.
The absolute so far a resist responses with one on one monotherapy.
What is the all believe that's due to intervention dose of <unk> drug.
Kind of refractory nature, the patient population or the absence of PD L. PD, one PDL, one blockade or any kind of mixture of.
How would you kind of rank those three in terms of kind of like the reasons why you haven't seen resist responses so far.
Yeah. So this is Dan <unk>, probably the least qualified to answer that question I'll give it sort of broad overview and I'm going to turn it over to Ken and a niche. So the do it. Good question Great question, and it's probably all of the above in various aspects is a heterogeneous patient population.
You know very poor health condition compromised immune system.
Immune system has been basically circumvented by the tumor in various ways. So I think.
All of the above is probably at play in various degrees with this patient population.
So the objective with a monotherapy as obviously primarily to show that the drug is well tolerated and safe showing the drug like properties pertaining to its a dose proportional exposure with PK PD effect and as this conversation is obviously focusing on.
In a series of questions is tying all that into what's going on at the tumor level, we appear to be seen metrics of clinical benefit. So the monotherapy, it's really dose escalating to the point, where we see in a subset of patients clinical activity and just to remind everyone. In this patient population, if we see one patient out of 10.
On average.
With a resist criteria partial response, that's extremely encouraging just based on history historic performance with this patient population. So you know we're going to be following this data clearly going into upstream into the frontline with Pembro I think bodes very well for.
The compilation of data, we've already seen but even with a monotherapy we just continue to.
Move forward with optimism based on the metrics that we've seen emerged to date so on that I'll turn it over to the clinician, who obviously oncologist knows a lot more about this and I do can do you want to elaborate.
Well you did a great job answering I think I would turn it around and go I'm amazed we've seen the amount of activity. We've already seen in fact, you know I think we worry as I mentioned on.
On the call.
We've already seen enough data to be confident to move forward into that into the combo study.
Because of the amount of activity, we see and I think it's just too early you know to expect more you know that's.
It's just amazing to me that we've seen as much as we have already and I'm. So highly encouraged by that that we I said you know we've got a pull the trigger on the on the combo.
And and as well as the Neoadjuvant to get us even more more data I mean, those are things, we do unless we're really confident we have a an active dry dock so I'm not at all.
Discouraged or somehow surprise that we haven't seen more I'm.
Actually surprised we've seen as much as we have.
Okay.
Following from that if you see kind of better then P. One and they get see when you combine one on one with PD, one and in front line HPV 16 positive head and neck cancer would you revisit one on one monotherapy and they kind of more early line crocs of all kind of right after PD.
One line of therapy that kind of.
To address this issue of these super lay line patients not really be immunologically ups for a new experimental agent like would you be only poppel to revisit kind of a secondary second third line therapy post PD, one rather than you had a really lay line patients.
[laughter].
Yes, absolutely I went off you know I would point out by the FDIC that we were you know constrained that you know our albeit the patients in the monotherapy trial had also had that the platinum.
Based chemo and that's why you know we have an average of four lines previous therapy on all of these patients I also think we'll be seeing the.
You know will be see what effect, we have as a single agent.
You know in there in the Neoadjuvant study. So so I think we'll get started to get more hints about that as we move forward, but absolutely again short answer absolutely yes.
Okay, great. Thanks for taking my question.
Thank you.
Our next question comes from Q Bloom from Needham and company. Please go ahead.
Hello, everyone and thanks for squeezing me in there and congratulations on all the progress. So just a couple exco questions first on.
There's some Q1 on one of the combo study it was.
Maybe you can clarify something related to think that Pembroke combination with chemo at a higher response rate done just pembro by itself is there a reason to go with just number by itself.
Maybe due to the immuno suppressive effect of the chemo.
Can you want to take that so.
Yeah. So so there is.
There is some day that unit the data with.
Chemo plus Pembro, we wanted to you know again as we move forward and try and understand how our drug works best we thought it would be better.
And cleaner to and were expecting great activities. So.
We thought it would be cleaner and as did Merck together with us think it would be cleaner.
Maybe the most sense just to do the dual agent combo.
And not mixed in with the chemo.
I find that next doesn't make sense.
Maybe a bit of different question on the Q2 hundred series. So these are some tumor necrosis factor agonized is there any challenges associated with the the structures and the primary station that's required from from these signals.
Yes, so we do a systematic I'm sort of derivative position, where we look at the.
Sort of spatial relationship of the molecule house, all sort of tenant together.
And then we do a systematic extension contraction of the various linker lanes et cetera, we try to optimize the failing sees of where these receptors are on the t. cell. So we're not just putting these molecules together and seeing what happens. It's a very systematic study trying to sort of optimize the combination in terms of spatial relationship.
Yep.
And how they engage with these this sort of <unk> collection of receptors. So that we don't have stark hindrance and we have sort of optimal.
Sort of residents so available above the valence c. so that the signals are.
And able to sort of align with each other based on that combination of factors.
And all of that obviously plays into our intellectual property.
Right and that makes sense I mean, you definitely have the potential of using more than one by again.
On each antibodies, so there might be assessed credibility there.
Yep Alright, that's it for me everyone else because although we do see your questions early on [laughter]. Thank you all right. Thanks, Joe really appreciate it.
This concludes the question and answer session I would like to turn the conference back over to Dan theory for any closing remarks.
Okay. Thank you operator, I again want to thank everyone for our your ongoing interest listening in.
We look forward to providing continual updates were obviously entering a very exciting period for the company going forward and everyone stay safe and stay well. Thank you very much.
This concludes today's conference call you may disconnect. Your lines. Thank you for participating and have a pleasant day.
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