Q4 2020 aTyr Pharma Inc Earnings Call
Yeah.
Good afternoon, ladies and gentlemen, and welcome to the API of pharma fourth quarter.
Full year 2020 and conference call.
At this time all participants are in a listen only mode. Later, we will conduct a question answer session and instructions will be given at that time.
As a reminder of this conference is being recorded for replay purposes and is now my pleasure to hand, the conference call over to actually Dunson and.
And at times director of Investor Relations and corporate Communications. Mr. Johnson, you may begin.
Thank you operator and good afternoon.
And everyone. Thank you for joining us today to discuss eight kind of sports quarter on full year.
2020 operating results and corporate update we are joined today by Dr. Sanjay Shukla, our president and COO.
Yeah and nice.
Jill Broadfoot, our CFO on the call Sanjay will provide an update on our corporate strategy, including our clinical program for E. T Y on 1923 preclinical program for a T Y R 28, com and our research programs and marathon to or and a P Q and trna synthetase.
Biology, gentlemen, let me give you the financial.
Results and our current financial positioning beforehand, and get back to Sanjay to open the call up for any questions. Before we begin I would like to remind everyone that except for statements such historical facts. The statements made by management and responses to questions on this conference call on forward looking statements under the safe.
And if harbor provision of the pilot private Securities Litigation Reform Act of 1995 of these statements involve risks and uncertainties that can cause actual results to differ materially from those and such forward looking statements.
Please see the forward looking statement disclaimer and the company's press release issued this afternoon as one of the.
The risk factors on the company and SEC filings and included in our most recent annual report on form 10-K, and quarterly reports on form 10-Q and.
Do you rely and should not be placed on forward looking statements, which speak only as of the date. They are made of.
And circumstances underlying these forward looking statements may change.
Except as required by law the tire pharma disclaims any obligation to update these forward looking statements to reflect future information events or circumstances, I will now turn the call over to Sanjay.
Thank you Ashley.
Good afternoon, everyone and thank you for joining us for our fourth quarter and full year 2020.
The results conference call.
Amidst the backdrop of the COVID-19 pandemic.
2020 was a highly productive period for a tire.
Which included significant clinical research and discovery advancements that we expect the yield value for the company throughout 2021.
We remain focused on our clinical program for our lead therapeutic candidate AG wire and 1923 or 19 and 23.
And we of advanced and expanded this program of great deal and the past year.
We're tracking towards the readout for a proof of concept study for our lead interstitial lung disease of ILD indication.
Pulmonary sarcoidosis and the third quarter of this year.
We anticipate these readouts, having recently gained key mechanistic insights regarding $19 23, and anti inflammatory effects in patients from biomarker data obtained from the study, we completed and patients with COVID-19.
We advanced the preclinical.
For them in cancer for our lead anti <unk> two antibody a T Y R 28 and 10.
For 2008 of them and we initiated discovery programs for two trna synthetase.
We're highly encouraged by our progress and look forward to build building upon our clinical and preclinical programs.
And discovery pipeline.
And from our novel Biology platform as we move forward this year.
Since we last spoke in November we achieved several critical milestones for our lead therapeutic candidate and 1923.
We completed enrollment and our phase <unk> trial of 19, and 23 and patients with pulmonary sarcoidosis and we expect to report data from this proof of concept.
And the third quarter.
We released positive results from our phase two trial of 19, and 23 and COVID-19 patients.
With severe respiratory complications.
The study met its primary safety endpoint and moderate to severe hospitalized COVID-19 patients and demonstrated a signal of activity through clinical improvement.
And the three milligram per kilogram cohort compared to placebo.
We also reported positive biomarker data from our study and COVID-19.
Patients treated with 19, and 23 demonstrated a trim of overall improvement and key biomarkers analyzed compared to placebo.
19, and 23 reduced several.
Inflammatory cytokines, and chemokines, including including those that are implicated and circuit doses and other ILD.
Which is consistent with findings from our animal models.
The data provides the first inpatient mechanistic proof of concept for $19 23.
Joe and.
Suite of Golar partner for the development and commercialization of $19 23 for ILD and Japan completed the last subject visit for its phase one trial of $19 23, and help the Japanese volunteers, which triggered a milestone payment for a time.
In addition, let me review recent highlights from our research and discovery program.
We presented preclinical findings and a poster at the Keystone symposia entitled tumor metabolism and microenvironment.
At that conference this poster demonstrated that and our P. Two of express on key immune suppressive cells further validating and RP two of the potential regulator of solid tumor progression.
We.
And the poster at the Society for laboratory automation and screening International Conference and exhibition.
Or SLS.
Describing our novel approach to identify receptor targets for two extra cellular trna synthetase fragments and.
All of Neil trna synthetase for ours.
And as per <unk> trna synthetase.
Page four doors.
Further validating the company's biology platform.
We announced two trna synthetase discovery programs from our pipeline to investigate the functionality of selected fragments of ours and doors and cancer fibrosis and inflammation with.
And with the programs initially focusing on natural killer.
Or NK cell biology.
We recently appointed leading cancer researcher.
And Dr. Judith Varner Professor and the departments of pathology and medicine at the Moores Cancer Center here of the University of California, and San Diego as the scientific adviser to the company for.
Her research on myeloid cell biology.
Tumor macro funds signal transaction will lend support to the development of our and our <unk> antibody programs.
And finally, we have.
And two upcoming posters from our preclinical program for our anti and RP two antibody 28, 10 and accepted for presentation.
And at the upcoming American Association for cancer.
The research or ACR annual meeting.
So we're very pleased with what we've accomplished and the passenger and we're already off to a great start thus far and 2021.
Today I'll provide an update on our clinical program with our lead therapeutic candidate in 19 and 23.
Our preclinical program 28 and 10.
And research and development efforts for our programs and <unk>, two and trna synthetase biology.
Joe will conclude with a review of our financial position.
Let's begin with our clinical bone growth.
We are developing 19 and 23 of the potential treatment for severe inflammatory lung diseases.
19, and 23 of the potential first in class.
Class of immuno modulator, the downregulates aberrant immune responses and inflammatory disease states.
19, and 23 has been shown pre clinically to down regulate inflammatory cytokine and chemokine signaling and reduce inflammation and fibrosis.
And our <unk> is up regulated on king of immune cells known.
And to play a role and inflammation.
And as particularly enriched and inflamed lung tissue.
But we believe 19 and 23 bind selectively to the MLP to and therefore has the potential to normalize the immune system serving to resolve inflammation prevent progressive fibrosis.
Thereby stabilizing lung function and.
And alleviate morbidity and mortality for these patients.
Our lead program is focused on the ILD of group of rare immune mediated disorders.
The cost progressive fibrosis of the alone.
Our initial ILD indication of pulmonary sarcoidosis, the most inflammatory form of IOP.
Which is characterized by the formulation.
And the formation of Granulomas or clumps of immune cells and the lungs.
Left untreated it can lead to irreversible scarring and diminished lung function.
And current treatment options are limited.
Often include treating the inflammation with corticosteroids or other immunosuppressive therapies.
But these have limited efficacy.
Could be serious long term toxicity.
And many patients and our response.
Our trial and employee sarcoidosis, and the phase <unk> randomized double blind placebo controlled multiple ascending dose clinical trial and 37 pulmonary sarcoidosis patients the.
The trial consists of three cohorts testing doses of one.
One three and five milligrams per kilogram of 19, and 23 or placebo.
<unk> intravenously every month for six months the <unk>.
Primary objective of the studies to evaluate safety and Tolerability of multiple ascending doses of 19 and 23.
Secondary objectives include assessment of the potential steroid sparing effects.
FX of 19 and 23.
In addition to other exploratory assessments, such as lung imaging lung function of assessed by pulling of function tests and relevant serum biomarker.
And we recently recently complete enrollment and the strong data is expected for the third quarter.
This year.
But.
While we work to complete enrollment in our trial and soccer doses, we observed that many COVID-19 patients with severe disease experience of form of interstitial pneumonia caused by an excess of inflammatory response, and the law, which can lead to serious sometimes fatal respiratory complications.
Medical literature reported that lung tissue analyzed from patients.
And die from COVID-19.
As shown on expression of <unk> to.
The very same receptor the 1923 binds to <unk>.
Based on the strong scientific rationale and 1920 three's mechanism of action and overlap and disease pathology, we initiated the trial to investigate and $19 23, and and acutely inflamed.
Patients patient population.
Of this trial also provided an opportunity.
For us too.
Mechanistically test the ability of 19, 2019, and 23 to down regulate inflammatory cytokines in patients.
Patients with Covid, 19, and become hospitalized of systemically and flame serum biomarkers.
And pay assayed and compared to placebo.
This phase II trial was the randomized double blind placebo controlled study and hospitalized COVID-19 positive patients with severe respiratory complications who did not require mechanical ventilation.
And it's enrolling the trial of a randomize to a single intravenous dose of either one or three.
And that can be or placebo.
One of the three milligrams of mics, and 23 or placebo and were followed.
For 60 days post treatment of <unk>.
Study was not powered for statistical significance and was designed to evaluate safety and identified preliminary signals of activity of 19, and 23 as compared to placebo.
And January.
But its positive topline results from the study.
The trial met its primary endpoint of safety demonstrating that single that a single intravenous dose of 19 to 23 was generally safe and well tolerated and both the one and three milligram per kilogram per kilogram treatment groups with no drug related serious adverse events.
In addition.
The report study demonstrating the signal of activity and clinical improvement and the high dose cohort of three milligrams per kilogram.
For the assessment of two determinants of recovery time to recovery and.
And the proportion of patients achieving recovery within a week.
Patients who received a single three milligram per kilogram dose of 1920.
<unk> the experienced a median time to recovery of five five days compared to six days and the placebo group.
Also 83% of these patients receive who received the three milligram per kilogram dose of <unk> 19, and 23 achieve recovery by day six.
Compared to 56% of patients and the placebo group.
Patients of the one milligram.
23 of them between the group had a medium type of recovery of seven days.
All patients receive standard of care.
Treatment at the time of enrollment which included from desert for your <unk> dexamethasone.
Today, we will add that we have completed an analysis of the 60 day follow up from the study and see no disability of long term limitation of activity.
African and patients treated with <unk> three milligrams per kilogram of 19 and 23.
As compared to placebo and where we still observe disability at day 60.
This is further evidence of activity for the three milligram per kilogram dose.
Demographic and baseline characteristics, where most of the balance of the study. However, we did.
<unk> and important imbalances and our randomization, including.
More patients for the 1923 treatment groups over the age of 65.
Or more patients with severe hypoxia.
Or more patients with multiple based on Comorbidities compared to placebo. These factors are associated with the greater risk of Coke.
Notice of and complications and worse outcomes.
And suggests that randomization and our treatment groups yielded a cyclical horn of patients compared to a placebo population.
While we were encouraged by the modest benefit and clinical improvement reported for the three milligram per kilogram cohort.
We were also very interested.
For the nine clinical biomarker data collected during the study.
The patients these patients were acutely and flame.
In order to see if 19 and 23 may provide additional benefit and insight into COVID-19 disease pathology.
And its effects on key inflammatory biomarkers, including inflammatory cytokines.
Last week, we reported positive biomarker results from this study.
Which showed that patients treated with 19 and 23 demonstrated a trend of overall improvement in several key biomarkers analyzed.
Compared to placebo.
Today, we want to provide some additional details regarding these findings.
The data we analyze <unk>.
<unk> 17, Biomarkers that were both detectable and elevated and patient serum samples.
The 17 Biomarkers.
Those were patient serum levels had significant elevations compared to normal healthy volunteer data that the ITAR has and its repository.
Upon the analysis, we saw that.
14 of.
The 17 elevated biomarkers at a greater numerical reduction for the 19 and 23 treatment groups compared to placebo.
Thus, indicating that patients treated with 19 and 23.
And an overall trend of improvement and 82% of these biomarkers of these elevated biomarkers compared simple.
The placebo.
In particular patients treated with 19 and 23 at.
The greatest reductions and levels of several of inflammatory cytokines, and chemokines, including interferon gamma interleukin six and monocyte chemoattractant protein number one.
Furthermore, patients treated with 19 and 23 also had a.
Typically significant reduction and levels of serum amyloid.
Or SAA and marker of inflammation and fibrosis that has implications and sarcoidosis.
We're very pleased with these findings, which provide the first mechanistic proof of concept for 19, and 23 and patients and.
And demonstrate.
In 'twenty three is impacting inflammation and patients consistent with what we've seen pre clinically.
Notably the cytokines that we saw reduced to the greatest extent as a result of 19th 2000, and pretreatment and the COVID-19 patients are the very same cytokines and <unk>.
19, and 23 Downregulates and.
And the impact in our animal models.
These findings further support and potentially validate and 1920 threes and anti inflammatory mechanism of action.
As we mentioned demographic and baseline disease characteristics from the study showed that the 19 and 23 treatment groups had more patients with factors associated with the greater.
The ninth.
Over the 19 complications and worse outcomes.
<unk> marker data confirms this at baseline patients.
Patients enrolled and the 19 and 23 treatment arms compared to placebo had higher levels of inflammatory cytokines and known COVID-19, biomarkers, including Ferritin D dimer and C reactive.
The risks, indicating a more inflamed patient population and the 1923 treatment arms.
Overall, we're very pleased with the full results from the study, which continued to demonstrate and $19 23, and its favorable safety profile and inflammatory lung diseases.
As well as encouraged by the relatively faster time to recovery.
Protein, adding just a single dose of three milligrams per kilogram 1923 to standard of care compared to placebo.
While this was a small study overall trend showing a reduction of inflammatory biomarkers.
Combined with the higher baseline levels observed in the 1923 treatment groups and.
And the benefits seen.
Seen by and the recovery suggests the clinical correlation.
But we of drug activity in the 19 and 23 appears to provide an added anti inflammatory benefit even when given on top of steroids.
These findings further demonstrate the potential of $19 23 as of therapeutic for severe inflammatory lung diseases, including pulmonary sarcoidosis.
And for Us and other Iot.
We continue to focus on our upcoming readout for our lead study and plenty of sarcoidosis, where we believe 19 and 23 is the greatest opportunity and near term of ability to generate value.
We are on leader and the development of potential new treatments for the multi inflammatory forms of ILD.
We strategically chose this therapeutic area based on the limitations of currently available treatments and the need for novel therapies for progressive disease, with better efficacy and side effect profile.
Our trial and COVID-19 allowed us to test and validate on mechanistic hypothesis for 1923.
Sorry for those that we of full results of the phase II trial future development plans and COVID-19 are being assessed relative to the trajectory of the pandemic the.
And the administration of vaccine.
And the assessment of a evolving treatment landscape.
Against this backdrop of the constantly evolving pandemic.
Now we remain laser focused on the upcoming readout and sarcoidosis.
As we think about the findings the results of the study and COVID-19, we want to highlight some of the main clinical and biomarker findings and takeaways as they relate to our lead program and the ILD, including our current trial and pulmonary sarcoidosis.
From a clinical perspective, we want to note that the trial and pulmonary sarcoidosis administers six monthly doses of <unk> 19, and 20 compared to a single dose administered and the COVID-19 study.
Throughout the COVID-19 studies standard of care evolved to include dexamethasone, a powerful steroid.
We reported that the three milligram per kilogram dose.
But he showed a signal of the colonic activity on top of the steroid.
By trial design, the study and pulmonary sarcoidosis reduces steroid use tapering patients through a sub therapeutic dose of steroids and if possible, we're moving steroid altogether, while evaluating the one three and five milligram doses.
And that's the 19 and 23 compared to placebo.
When it comes to the Biomarkers, we are highly encourage the $19 23 downregulates. The same cytokines that we have seen of Downregulates and our animal models.
Which was the fundamental translational work and mechanistic hypothesis upon which the ILD program was established.
All of you also reiterate that patients with 19, and 23 had a statistically significant reduction and levels of hey of rather excellent finding from the small study.
The medical literature supports the growing importance of SAE is a marker of sarcoidosis, including a recent paper published by leading researchers at the interstitial lung disease.
The center of excellence in the Netherlands, suggesting that SAA has implications not just and sarcoidosis, but also and other fibrosis ILD.
We look forward to the results of the study that evaluates <unk> 19, and 23 and police sarcoidosis, which we expect to report and the third quarter of this year.
Now, let's turn on of our research pipeline, starting with our <unk> antibody program, which continues to advance the we're producing.
It's first potential Iot and ERP too as a compelling therapeutic target.
Many areas of oncology and inflammation.
And cancer <unk> is up regulated on various solid tumors such as <unk>.
<unk> lung and renal to name a few.
Hi, and RP to expression is linked to worse and patient outcomes and many cancers, which in some cases may include drug resistance to current therapies antibodies that can selectively block different and our P. Two signaling pathways may of therapeutic potential and the aggressive cancers, where <unk>.
<unk>.
Two of implicated.
As we continue to explore the role of <unk>, two and the progression of certain aggressive tumors. We wanted to determine the expression of <unk> on a variety of the immune cells and the tumor microenvironment.
And its role on each of the cells.
A recent poster presented at the virtual Keystone symposia.
Demonstrated that <unk> is highly expressed on immune cells implicated and regulating cancer progression.
These included myeloid derived suppressor cells or <unk>.
Tumor associated macrophages or <unk> generated from triple negative breast cancer cell lines.
And mature.
<unk> sales.
Further research showed that MTS even terms.
The press T cell proliferation and activation.
So we're very pleased to have demonstrated for the first time that <unk> is highly expressed.
On key immune suppressive cells of the tumor microenvironment.
Important cells that.
George the implicated and regulating the progression of tumors and the metastasis.
These findings provide further validation of <unk> two of the regulator of solid tumor progression and support the potential of and RP to as a.
Potent target for cancer therapeutics, possibly through the immune regulation of the tumor microenvironment.
As we look at the panel of antibodies that we develop develop to selectively target distinct domains of the <unk> 28 tenders on the IND candidate.
This is a fully humanized monoclonal antibody that specifically and functionally blocks the interaction between <unk> and veg F. One of its primary ligand.
The role of <unk>.
Of signaling in the tumor microenvironment and its importance and.
And the progression of certain aggressive cancers is becoming increasingly validated.
We selected the candidate to advance the IND, enabling activities based on data that we have generated and various tumor models and compelling preclinical data presented last year at the <unk>.
And <unk> annual meeting from our collaboration with Dr. Arthur material one.
One of our scientific advisers and his lab at the University of Massachusetts Medical School.
This data showed that 28 and 10 demonstrated tumor inhibitory effects.
And increased sensitivity and the chemotherapy and human derived organoid and other in vitro.
The models of triple negative breast cancer, and extremely aggressive cancer, where <unk> have been shown to be highly expressed and many patients are not responsive to currently available treatments.
Since then and we have continued to explore the potential of 28% and breast cancer and other solid tumor models work on RPT was.
The trauma.
And next month, we will present two posters at this years ACR annual meeting.
One of these posters builds upon the research that we presented.
At ACR last year and breast cancer.
And while the second poster presented new preclinical findings from our research in lung cancer.
And we're looking forward of presenting these posters and providing additional deep.
Details regarding these findings at ACR.
Finally, I wish to update.
Our trna synthetase discovery program, which has recently yielded some transformative findings, most notably rediscovered new receptor targets.
For two trna synthetase us from our pipeline.
Ours and ours were.
And we presented these findings and a poster at Sn layoffs and January.
And the receptor targets for these two trna synthetase may have utility.
And the development of new therapeutics to treat cancer of fibrosis and inflammation.
In particular, the synthetase fragments demonstrate binding to NK cells important immune cells that play.
And mate immune responses and maybe.
Key therapeutic targets in oncology.
Based on these findings of <unk> pursuing research activities related to selected fragments of.
And we have announced new discovery vertical that will initially focus on NK cell biology.
We look forward to exploring these receptors and biologic pathways to determine their potential roles and immune mediated disease, we expect to.
To provide more information regarding these findings and the future.
These.
Ours, and finding that presented and SMA as further validate the relevance of our trna synthetase biology platform.
Two important disease pathways and demonstrated its ability to generate new drug targets.
We now have receptor targets identified for three trna synthetase.
Ours ours and ours.
As far as a reminder, <unk> tires intellectual property portfolio consists of and covers protein derivatives from all 20 trna synthetase gene families with over 300 protein compositions patented.
We believe we are only at the beginning of unlocking the potential and promise of.
Of this novel.
Algae platform.
So with that I'd like to turn it over to our Chief Financial Officer, Jill Broadfoot to review our financial results.
Thank you Sanjay we're proud to report $10 5 million and total revenues for 2020, our revenue for 2020 consisted primarily.
But of license and collaboration agreement revenue.
Which we received from Kieran Pharmaceuticals.
As Youre aware and January 2020, we entered into a collaboration and license agreement with Kieran and the development and commercialization of $19 23 for ILD and Japan for which we received an 8 million of.
Hang on.
In addition, we received a 10 million milestone payment in January 2021 for a phase one milestone that was achieved by Ken and Japan and December 2020.
On the expense side, our research and development expenses for $17 3 million and 14.
And for the years ended December 31, 2020, and 2019, respectively.
The increase was due primarily to the progression of $19 23 clinical activities and both pulmonary sarcoidosis and COVID-19 patients with severe respiratory complications.
General and administrative expenses.
And were consistent between periods at $9 1 million and $9 4 million for the years ended December 31, 2020, and 2019, respectively.
From a balance sheet perspective, we are now well positioned for the further development of our lead programs.
With previous guidance in November.
For 2020, we repaid all long term loans.
And exceeding our previous guidance of ending the year with greater than $20 million and cash we ended the year with $31 7 million and cash cash equivalents and investments and.
In addition, since year end, we've raised over $25 million and cash in addition.
November and giving the $2 million Kieran milestone payments.
We raised approximately $9 9 million and gross proceeds from our aftermarket offering program before deducting commissions and operating expenses.
And raised of perhaps approximately $15 3 million and gross proceeds from a purchase agreement with aspire capital Fund.
On to results.
While we won't be giving specific guidance this year for ending cash we do expect our research and development expenses to increase as we continue to develop 19, and 23 and 28 10 and move forward and our discovery programs.
Now I'd like to turn the call back over to.
All of it before we open it up to Q&A.
Thanks Jill.
Overall, we're very pleased with what we achieved in 2020 and are proud of our significant progress.
We have of potential proof of concept readout for 19, and 23 and pulmonary sarcoidosis and site.
And now supported by a mechanistic proof of concept.
From our biomarker results from our trial and COVID-19 patients.
We have a preclinical program for our lead anti <unk> antibody of 28 10 on.
Undergoing IND, enabling studies and cancer.
And we have two trna synthetase discovery programs.
<unk> receptors identified and ready to be explored.
We started the year with a major license deal for 19, and 23 for Iot and Japan with current.
The partnership that has already brought and $10 million and payments.
We had and onerous debt structure of that that we've been able to eliminate.
We exceeded.
With target EBITDA guidance for our 2020 year end cash the cash position and.
Through milestone payments and use of available equity vehicles, we've raised over $25 million and the first quarter of this year.
We're already off to a great start in 2021, and we look for that momentum to continue and the year to come.
And we appreciate your interest your continued support look forward to providing updates in the future at this time and Joe and I will be happy to take your questions.
And as a reminder, ladies and gentlemen ask the question you will need to press star one on your telephone.
To withdraw your question press the pound key police.
And by all of the compile the Q&A roster.
Our first question will come from the line of <unk> from Oppenheimer you may begin.
Great. Thank you for the questions and the updates on J Jill.
One question on 28 10.
Which.
From what stage of sort of IMD, enabling is it on Sunday.
And then as you are going to be presenting the state on breast cancer and follow up on non small cell lung cancer.
And you had a pretty heavy duty addition to your board of scientific Advisory Board as you indicated.
And the oncology area, where do you think you'd see the initial.
Which is on.
You said of 2010 on the breast cancer non small cell lung cancer will be more monotherapy or combination therapy.
Once your R&D, enabling work is done and I just got a quick follow up on that too.
Yeah, Hi touch for.
And so for 28 10th of this year, we were very much part and that Stu.
The stage of looking.
King at <unk>.
In vivo efficacy models, so testing different solid tumor models, where in Europe, Poland is implicated.
And as you pointed out we've already seen good data and triple negative breast cancer the year.
On the year now with additional data coming out of the ACR and now new data in lung cancer.
No.
We're continuing to look at a few other tumor models, but towards the second half of this year, we'll take a look of that is state of of animal efficacy data and determine really which which tumor environment will be the best indication for us to move into once we get into patients.
And we'll also learn along the way as you point out.
And all of our therapy is best positioned as the monotherapy.
On top of another therapy to unlock more of efficacy.
Or even be able to be used.
In conjunction with chemotherapy. So all of those those answers will be laid out here over the course of this year, which is also why we really want to bring in.
Whether the expertise.
And in the oncology space and someone like Dr. Maura foreigner, and even Dr material previous previously added last year, they're experts with regards to this biology and.
And they serve as great guidance for us in the meantime, there is also quite of bit of work on the talk side that we have to complete.
<unk> and.
Submission.
I would say stay tuned we continue to demonstrate and learned more about where 28 and 10.
Can be best use which tumor environment and then from that standpoint, we will also learn whether or not it's best use of monotherapy or is the combination.
Prior to testing it.
Both ways.
And then Sanjay.
And I think you've made the point that.
And the 1923 designed as chronic therapy, right, which is maybe one of the rate limiting steps for the COVID-19 trial, where you can only get at once.
For 2010.
I assume.
And that that antibody would be designed and such where SB, given kind of and as acute cancer setting correct.
Yes, I think thats, that's yet to be determined but in general that is and.
In general how you think about biologics here.
And the antibodies that are targeted so it's led to be of targeted therapy.
<unk>.
The the relative manner in which we dose and the PK of that.
Yet to be worked out, but we will certainly have that.
Mapped out here before we move into a clinical indication.
Great and then my last question is just on the CSL Behring collaboration can you just give us an update as to.
When we could see sort of next steps there and then also.
What kind of kind of milestones could be at and maybe this year and next year.
Thank you for all the cash.
Yes, so that's the collaboration where.
Of our findings that we have we've been able to.
And really bring back over and over the fence.
Around the odds of doors.
Each of that work came out of that collaboration.
And he tire owns.
The the areas of oncology from from from those findings. So we are we really were excited to have them sort of on our side of the fence here.
With regards to.
For your further work with CSL.
I think right now we're really focusing on internally moving these forward as they fall within.
Of therapeutics.
And sort of the area of expertise.
CSL doesn't and does it really have.
And so as it turns out these findings of really.
For the US and we now are moving forward with some of those NK cell activities internally here.
Great. Thank you Sanjay Thanks, Joe.
Our next question will come from the line of gel and to Guinness from H C. Wainwright.
And Ben if you may begin.
Everyone and good afternoon. Thanks for taking the question Sanjay of my questions are going to focus right now on just continuing to continuing to build the profile for 1923, so as we look towards the third quarter update for sarcoidosis.
Are we going to have the ability to see.
And the marker data is it built into the.
Sort of the clinical trial protocols based on what you guys just announced especially for S. A a and then sort of related when do you think we might be able to get visibility for additional I L DS as well, especially since you mentioned.
The buy on SCA has implications towards other ILD.
Yes, Hi, Joe So one thing to remember that's unique about what we've been able to take advantage of if you will from the COVID-19 studies.
Readily saleable serum biomarkers these patients are coming and not only severely inflamed.
Mentioned and their lungs, but they're also presenting a lot of and in the case of our studies and 17 highly elevated biomarkers and we can assets just by by pulling blood.
And in ILD patients they tend to be severely and flame locally there and the lung lessor systemically so from a biomarker perspective.
And in the.
We would.
The best way to do this is to do a bronchoscopy, the bronchoscopy and and really try to grab tissue from the lungs, which is patients really don't don't like that as much.
And so on the ILD.
And this mechanistic proof of concept that we were able to demonstrate and COVID-19, we think carries.
<unk> over <unk>.
Let's also understand that assaying systemic biomarkers is a little trickier in ILD patients Nonetheless, looking at the literature and looking at.
And it'll be a L fluid and bronchoscopy, what's there and the literature, the sensitive cytokines and we impact.
The result, very same ones that we already know.
From the literature are highly elevated right, there and the lungs of ILD patients. So.
We rely on the experts and Europe of course, there's a little bit more of a tendency to the assay.
And lung and biopsy and bronchoscopy and not so much here and.
All of us.
But with these findings I think it gives us really really good confidence that we've got of anti inflammatory that directly impacts some of the most important cytokines and chemokines that.
And that are involved and the pathology of ILD and.
And I think and I think when we think about R. R.
And the UL, that's reading out here, we will be looking at serum biomarkers.
But I think the the greater sensitivity here is probably being able to see clinical change.
Mainly through the reduction of steroids.
And in that study I think that's the real activity and point of pay attention to.
Got it.
Try it out and that clarification as well.
So keeping with this indication and I was just curious if you obviously I know you'd say, we should ask them, but any updates around the QR and study.
Yeah.
And we just say that.
Things are progressing as planned.
Thanks for the acute.
Sure and has their own.
IR and PR group that reduce a hit and I can't speak to what they will put out of won't put out but I will say that we are on track to have pure and join our next trial, which will be of worldwide Registrational trial, we expect the and sarcoidosis.
Number.
Experts and centers are teed up.
To get started and we do not anticipate any delays.
And any of any any hiccups there with the clinical development plan that would be on working on with them.
Got it got it and then my last question I think is pretty quick because with.
With regard.
To your comments about COVID-19, and potential next steps and obviously, it's an ever changing landscape that you alluded to but maybe can you take a stab.
Stab at sort of what the low hanging fruit is regarding your decision tree, especially as a therapeutic landscape evolves to.
And to decide whether you want and moving forward.
Well.
I think the key thing here is we have seen them, even recently, the dexamethasone and it's having an even greater utility not only and patients that are hospitalized on the event, but also those are not on the bed and we experienced that and our trial there was a potentially.
You know of potential confounding to a lot of our data as it turns out.
<unk>.
We've shown and we've.
Talked about today that the additional benefit of 19 and 23 is very apparent to you and when you look at the clinical and the biomarker readouts that we've presented above and beyond dexamethasone.
The our drug is showing utilities.
Our view is that if theres, a sensitive or a pop.
And that might be resistant the dexamethasone and COVID-19 that could be of low hanging fruit, but we just don't know the epidemiology of that cohort yet is it is the tens of millions of patients millions of patients 10000 patients. We don't know what I do know is that there is potentially 100000 pulmonary sarcoidosis patients.
Populate our of sensitive population with pathology that we know our drug.
Can impact looking at our preclinical data and also now from the COVID-19 data. So I think what that Albert of evolving landscape and the fact that we have this very very near term readout coming we're squarely focused on on thinking about circuit.
But and are excited to potentially make an impact here as we are really the leader in ILD work and any compared to any worldwide biopharma.
Understood. Thank you very much.
Thanks, Joe.
And again Thats on style on for questions.
Our.
And also the question on and kind of fine of just like the.
And <unk> from Roth capital you may begin.
Hey, guys. Thanks for the very.
Very helpful. I think I'll just have a couple of the phone questions at day. The first of all of this kind of piggy back off of.
Because of question and I know like you said Sanjay you're trying to kind of see have the.
And I can ask them involved and buying a lot of that more of that those patients that might be and you know.
Unable to be treated with that's the methods and I felt like the Vista.
And so.
I think of it would just be interesting at the of our pulmonary sarcoidosis data and having pegging do you think that actually influence your decision to move.
Click on the Covid study as well.
So your question correctly, if we saw good data and sarcoidosis does that.
Does that change our mind for for Covid.
Is that right yes.
Especially you think youre going to have five milligram data as well and you know be able to better.
Following the point of that heightened and so that's a very good point, we're testing the highest dose and sarcoidosis. So certainly.
If we see a dose dependent sort of improvement and the sarcoidosis patients.
I think we all understand that as a small company, we would love to you know.
You know we.
Steve English the run five phase II trials, and I say this before but if we were large pharma and theres a number of indications we could move into we try to be very careful about how we manage our cash and we also try to move into programs that we think and grid generate value and the near term right now with Covid.
And there's there's there isn't the solid.
We have been and gaped out there give it given a lot of the movement. There we've shown three milligrams could be potentially useful in and acute indication frankly, I think our our drug could be used and any acute interstitial pneumonia and I think it and we've demonstrated that could be useful whether you.
Viral pneumonia of Covid etiology.
Lance you or other etiology of the drug is really built really really well as a chronic treatment of treatment that can be used and chronic conditions like ILD and we see the Iot market as the.
And our eyes a multi.
And several billion dollar market, where there is a green space of a commercial.
D all of the opportunity, but a dearth of really good treatments. Good safe treatments and then the last thing I'll add here is the.
This is the environment ILD, where patients when they get off steroids, where and in the acute ICU setting you're throwing steroids that these patients because you're just trying to keep them alive. So we.
Commercial and on the ILD side of the defense here.
The competition and we won't have the compete with steroids because of the pie of the patients everyone wants to get off steroids. There I think it's I think it's a huge opportunity for us and now with some of the biomarker data, we can really see some daylight here.
On the phone growth.
In total for the backbone.
Our growth.
On the positive.
Positive on the rule it out and so regarding the law just wanted to know of.
And from Donlin and all of that.
On the left the bottom line and are there.
And something that's kind of the last thing just at the hub that the.
And what the impact of them.
Yes, I think.
You can look at certain things, where you may have some impacts of good.
And patients every center is a little bit different and they want to keep patients safe.
There can be missing.
Data points here and there we try to minimize that as much as possible I would say the key things here are.
Because of your own some COVID-19 restrictions certain sort.
And.
For example visits where you have pulmonary function testing kind of centrally there at the hospital.
Some hospitals don't want patients kind of blowing a lot of sort of aspiration of lot of error. There. So we are trying to basically use local.
The ftes to sort of cover these sort.
The things that might be an area, where we don't think it's going to be a problem, but we you might see a slight replacement there of around how we report pulling the function testing pet scans are another thing where the.
Model institutions.
No.
Are the prioritizing pet scans right now.
It's not.
It's a it's an exploratory endpoint for us so it could be some there could be some patients there we also.
Missing data there too, but I think the key thing here is that from a safety and from a steroid sparing perspective, we have.
And really really the ability to preserve most of the data from this.
Yeah.
Amazon Zone, and then another point you made was with Karen and their participation and perhaps in the large global study a phase III study and so I was just wondering.
When might you move into your next study you know after this data readout.
Yeah.
Travel will be moving into that study after the readout you know assuming this readout is good and we feel good about moving forward, we will sit down with regulators and we'd like to start the trial next year.
We feel as though we already have.
Good alignment on.
And the rationale of our drug the relative nature.
And what the trial should look like based on the trials that have been run previously and the Iot space.
And we also know that as probably the day, leading Iot development company right now.
There's a real need for for a phase III trial and these.
The patients right now so we.
And we would be looking to move.
Moving to that trial next year and I can't give you guidance just yet on fourth quarter, we would look to start that because I think it's up.
Little premature for that but we.
We would be looking to move into this trial and.
And do it with cure and and potentially other partners of next year.
For the island's Dennis Green Bay on the.
And the quarter specific quarter, but.
But we've guided and partners of you just mentioned and actually had it on my list of questions to ask 2010, and it sounds like you.
And you are working on the preclinical Tox studies, where the and you said it sounds like you can execute on that independently or perhaps you might want to do.
But I think I'm more worried about the early stage work and you talked about you know that came out of your collaboration we'll see S. L. A is that something that you will want to partner early just looking at your cash balance and you know how you're allocating capital.
Yes, I mean compared to about a year ago, where we really just had one program.
And now we have three we have a clinical program that's about to have Readouts. We have a preclinical program. That's in the IND, enabling work and then we've got discovery programs not only on the MRP two antibody side, but now with these two exciting new.
Fragments that we've found a balance of natural killer cells. So we have to we have to.
We have to really look at.
All we can accomplish kind of on our own the.
The great thing is now we have more opportunities to have those sort of business development conversations it's something I don't guide to with regards to.
And if and when they take partnership can happen cure and came in quite early I think that was.
The rather transformative deal we did at the beginning of 2020 now we have more opportunities for our BD team to reach out and more options.
And if partners are interested in and.
Interesting.
Oncology data around and.
Exciting new targets like normal and two we will have datasets to present to them.
And if theyre interested in growing and a little bit earlier with discovery programs and now are our anchor to potentially natural killer cells. I think this is also.
The more options. So certainly a lot more options this year than we've ever had.
Really really previously and a tire.
We have a pipeline here.
Here, the three clear verticals clinical preclinical and discovery all of which we will look to.
Potentially engage partners if it's the right thing for us to do.
For for ourselves and shareholders.
On the Sanjay and congrats on all of the progress.
Thank.
And as clinics for the question.
Thank you and I'm not showing any finished the questions from the queue and I just don't turn it over to Sanjay for any closing remarks.
And I, thank everyone for their interest certainly had a lot of information and go through this year.
I think that's reflective of around the number.
We are going on very important year for us we're excited and particular for these phase of these readouts here and our circuit doses trial, thank everyone for their interest and.
We will keep you up to date and speak to you and the future. Thanks again.
Ladies and gentlemen, this concludes today's conference.
For a sale. Thank you for participating you may now disconnect.
[music].
And from Cowen.
[music].