Q3 2019 Earnings Call
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[laughter] therapies can cold and sometimes people toxicities, such as European you and thrombocytopenia.
Unfortunately, the management <unk> therapeutic toxicity currently inadequate and finding better ways to prevent will manage chemotherapeutic toxicities has been a huge challenge.
An important advancements was recently made with another biotech company you on therapeutics announced that their drug candidate cost fell cycler rest healthy normal bone marrow cells, and thereby read used chemotherapeutic toxicities in patients with small cell lung cancer.
Then you want Therapeutics has also reported a regulatory pathway for the indication of model preservation based on meetings with regulatory authorities.
That ends were important for us because our nonclinical data shows that 604 has excellent sales cycle the rest of using properties.
All these factors encouraged us to commence our model preservation program and the cornerstone of our program with the creation of a strong nonclinical data set that informs and supports our clinical trials in monetization.
As presented at the you RTC Triple Conference on October 29. This year, we showed that low doses of six nine to four triggered reversible cell cycle. The rest in human bone marrow cells ex vivo and in mouse bone marrow cells in vivo two limits toxicities cost.
Hi chemotherapy.
We believe that our findings can translate to the clinic as an improvement in hematological side effects of chemotherapy and as a result with advanced our program into a phase one lease slash two clinical trial evaluating six centre for as a mild preservation Ting agent in patients with P 53 mutant small cell lung.
On cancers.
The ongoing phase one will be portion of this trial will enroll up to 40 patients and is designed to identify a recommended phase two dose for six nine to four.
This trial in future model preservation trials will will use existing standard June tests to select patients with 53 mutant cancers.
We're very excited about the possibility to optimize the effects of our drug by applying a precision medicine approach and this biomarker based selection of our patients that six nine to four apart from the approach the G. One therapeutics staking.
Based on our compelling Nonclinical data, we recently decided to reallocate capital from our early drug discovery program to our Marler preservation program, adding plans for two additional cohorts without shortening our cash runway.
We added an expansion cohort of approximately 20 randomized patients with small cell lung cancer. This new cohort would use the recommended phase two dose from our ongoing dose optimization phase, one trial and treat patients and alternating cycles with chemotherapy alone and with chemotherapy plus 6%.
Before with the intent to create a more definitive proof of concept.
Secondly, adding and expansion cohort of approximately 20 patients with non small cell lung cancer. This new cohort is designed to evaluate the breadth of the approach we are taking with six centre for as a model preservation agent.
Our current plans to start enrolling patients into these two additional cohorts in the second quarter of 2020 . After we have identified a recommended phase two dose and contingent on resource availability, we expect twins start enrolling patients into the phase two portion of the phase one these last two trial.
Mid 2020 .
Before I hand over to Rick Let me tell you how excited we are about the potential of six cents before.
Given the results we have shared to date, we're fully committed to bring in six nine to four forward as efficiently and expeditiously as possible.
We anticipate several milestones in just the next six to seven months from our two ongoing clinical development programs, including the final data presentation from our combination therapy with Paul the cycle in the second quarter of 2020 as well as the dose optimization data or six centre for as model.
The preservation agent also in the second quarter of 2020 .
With this overview of our operations in R&D strategy I'll now turn the call over to rig to provide an overview of our financials for the quarter rig floor is yours.
Thank you minimal and thank you everyone for joining us today.
Third quarter 2019, we reported R&D expense of 4.5 million compared to 4.3 million in the third quarter of 2018.
The increase in R&D expense, primarily reflects higher clinical development costs of 694 that are partially offset by lower employee costs.
Clinical development of six nine to four during the third quarter of 2019, primarily reflects cost associated with the phase two a expansion cohort of the combination of six nine to four account recycler.
And costs incurred in the preparation of our mild pepper preservation trial.
Clinical development of six nine Q4 during the third quarter of 2018, primarily reflected costs incurred in connection with our PTCL trial, which we completed in our and now Mds trial, which we discontinued in early 2019.
For the third quarter of 2019, the company reported general and administrative expense of 3.4 million compared to 3.2 million for third quarter of 2018.
Net loss was 7.7 million or 28 cents per share for the three months ended September Thirtyth 2019.
Compared to a net loss of 7.4 million or 50 cents per share for the same period in 2018.
As of September Thirtyth 2019, there were 27.8 million shares of common stock outstanding.
Cash cash equivalents in investments as of September Thirtyth, 2019 were 24.6 million compared to 20.7 million as of December 30, Onest 2018.
The company believes that its cash cash equivalents and investments as of September Thirtyth 2019 will enable it to fund operations into the fourth quarter of 2020.
And with that I'll now turn the call over for your questions operator.
At this time, if you would like to ask a question. Please press star one now on your Touchtone telephone to withdraw yourself from the Q you May press the pound once again to ask a question. Please press star one now on your Touchtone telephone one moment, while we Q.
And once again that is star one to ask a question, we'll take a question from Matt fits of William Blair. Your line is open.
Good morning, guys. This is Rob Andrew.
Thanks for taking the questions.
So thinking about a mile preservation city, one of the saw timelines.
Right now.
Moving forward for an FDA approaching the indication.
In light of the recent updates from.
She wants therapeutics is Barlow preservation agent.
And then secondly, how do you think about the potential survival benefit that you guys showed in the preclinical models Triple me in.
I think that this was kind of the more notable data as shown by competitors that.
As much detail.
Thanks.
Thank you very much I will ask our chief Medical Officer, Dr. vocalist to take the special corporate.
Excellent at all and thanks for the question.
The survival benefit.
Next we potentially can see in the clinic.
Can be derived in our opinion by two different means one by optimizing and minimizing toxicity of chemotherapy, we will be able to achieve the optimize deliveries at full dose at full length of chemotherapy, which can translate it to survival benefit.
When you look at GNC books as data presented at ESMO, the able to deliver approximately twice as many cycles of the chemotherapy in patients who were assuming the truck so thats one mechanism.
The other mechanism, which is probably so typically more intriguing.
Is the non effect that activation of 53 exhibit on the immune system.
This effect is very well known and very well described in the literature.
And.
With our collaborators and with our internal data were able to show Preclinically clear effect.
Of our drug six nine to four on the immune system and we have also limited amount of translational data from patients with pick to a biopsies that clearly show.
The effect of the drug in terms of increase secretion of cytokine and setting and traded for example, the city foresee the eight.
T cell ratio.
So this clearly to potential effects, one is optimizing chemotherapy and the other is the effect of the immune system.
Does that answer your question Rob.
And maybe what I think.
Meanwhile, performed on the regulatory strategy that you had mentioned I mean like you. We know only so much as to the regulatory strategy that is being pursued by GE. One therapeutics based on what is publicly available out there, but based on what is publicly available out there. We think that it's a regulatory pathway that is a great precedent for us that's.
We intend to follow.
Okay, great. Thanks, So just maybe one more on so many looks forward to move forward and in like micro sarcoma. I know you mentioned, there's a clinical collaboration that with which we size or are there any plans for kind of partnership and not in that program.
Particularly given that combination with ibrance, thanks very much.
Yep.
We have obviously working closely together with Pfizer the our together with us on a joint development Committee and there are as excited as we are about this combination but at this point in time, we haven't disclosed further steps as it relates to the form of this collaboration and its future.
Okay, great. Thanks very much.
And once again, if you would like to ask a question. Please press star one on your touch tone telephone we'll move next to John Newman of Canaccord. Your line is open.
Mr. Newman Your line is open please check your mute switch.
Hi, Good morning, sorry about that this is justin's Allen on for John Newman.
First I just had a question if you could talk about.
Just how six nine to four is differentiated versus other.
Competitor and the M agents and I've asked some follow ups.
I would ask my head of research elements to take US question Alan Please.
Thanks, I want to adjust and thanks for joining the call. This morning.
And thank you for your question. So few very important differentiating features for your on six nine to four compared to the other MDM two inhibitor. So first of all our 694 is the only peptide drug is addressing the 53 reactivation all the other immune to inhibitors are small molecules and partly as a consequence of using a pet.
I would approach our drug recapitulates the buying properties of P. 53, so both MD, one two and MDM mix over different about chemical profile for binding of our drug to the natural inhibitors of the 53, well that allows us to do and what we're seeing very robustly in the clinic.
We have a much improved safety profile three or six not do for add doses that give meaningful anti cancer activity, specifically, we see far less thrombocytopenia for our drug in all commerce phase one trial the reported for us and for other into inhibitors are much better thrombocytopenia profile, which is an important difference.
I didn't factor for our drugs are not only for combining with Pablo cycle for example, and having a better safety profile. There would also important for our model preservation study. So this is a very important differentiating features for our drug.
Great. Thanks.
Great.
In one area.
And.
Just a few follow ups.
Is the strategy to continue the the Ibrance combination trial and liposuction sarcoma or will you also be looking at other cancer types if the trial.
At this at this point in time, we haven't.
Disclosed plans for additional combination therapies.
Certainly the the pipe the rationale behind such a combination is very obvious as we all know there are plenty of anti cancer drugs that require downstream the effectiveness of a 53 signaling pathway.
And we in the past have disclosed preclinical data that serves as evidence for that to be a promising proposition, but at this current point in time for focusing on these two programs with although combo as well as model preservation program and as such they are currently no other imminent combination therapy programs.
Break on it and then on the Milo preservation trial.
Slide from.
Primary endpoints being.
Reduction in future periods, and I mean, yes.
Are there any other kind of exploratory endpoints such as some biomarkers that you'll look at to kind of.
Increase your confidence of the efficacy of mechanism of action.
Thanks.
Yes, absolutely. Thanks for the question we are.
Our deploying a biomarker driven strategy in our.
Model Protection program.
Not only be use biomarkers to select patients, which I think is a key differentiating feature but we also will be collecting data to explore two biomarkers that directly related to the pharmacodynamic effect of the job. So we'll be looking at proteins that are activated.
By 53 transcription.
And that will be collected multiple times in patients. So we'll be having a very clear understanding between the pharmacokinetic and pharmacodynamic effects of our drug in every single patient.
Excellent. Thanks for taking my question guys appreciate.
And congrats on the progress.
Thank you.
And once again, please press star one to ask a question, we'll move next to Jacques via fraud.
Lifecycle.
Hi, guys. Thank you for taking my questions and congrats on the progress this quarter.
On on my end could you walk us through the rationale for going after mild preservation.
And what the mechanism is there.
It's exciting to fourth.
Sure happy to take that question.
53 release.
He is known to induce a cell cycle arrest.
And.
That can happen itself, but it P 53 protein and its signaling pathways impact, which is the case in all normal healthy cells.
As you know in tumors.
Approximately half of cancers have mutations in 53.
And there's probably also other deficits and problems in the 50 signaling pathway so tumors really.
Most of the time don't have a functioning 53 pathway and that's the key difference due to try to explore it with this rational strategy, we want our dropped to work in normal cells.
In the new cell cycle arrest and not touch the cancer cell. So chemotherapy can do its job.
And so for that reason, we're selecting patients upfront with a genetic profile.
Which corresponds to Pfifty three mutations in the cancer.
And we expecting that our approach will result in a selective cell cycle unrest and selective protection of normal tissues against chemotherapy induced toxicities.
Got it. Thanks, Thanks for that and then just a follow up on so as you mentioned G. One therapeutics has a program Ela preservation.
It is probably set the bar in your first in your for setting CLC can you help us put their data into context, and what would be a win for you.
In the phase one portion of your study.
Sure happy to do that thanks for the question.
Obviously, we can compare our data that will emerge from our small cell lung cancer trial to that are presented by if you want therapeutics.
But we don't have to and the reason is simply because the two drugs their son hours there exploiting different pathways to achieve the same objective cell cycle arrest.
And.
And it that's that's quite different different molecules different pathways. So the results will be.
Not always directly compare comparable.
But.
We are looking at the small cell lung cancer trial is simply as a proof of concept.
The trial.
And as Manuel has limited previously and Alan mentioned also we can really go after almost half of all cancers irrespective of the tumor type and in respect of the chemotherapy the receiving.
And that.
Well basically set us apart in as a differentiating factor against G. One therapeutics.
I hope that answers your questions.
Yes, yes, thanks and.
One more on on on my end here.
Could you give us more color on the synergies between the CDK for six inhibition MDM to inhibition in your and your combo study.
Hi, Good morning, sorry. This is Alan as the unhappy to take that question. Thanks again for joining the call. This morning. Yeah. So this is very well known CDK before and this is a good for pathway through RV, one and Pcs pathway converge on cell cycle rest and anti cancer activity and sell some very well established a signal transduction pathways.
For that so weve shown non clinically as well as are many other folks that there is there is good synergy and non clinical models for combining the two inhibitors RPC reactor six not due for a with palace argument, obviously, the Q4 or six inhibitor, so very well established.
In Nonclinical studies and one other features important was not often recognizes that our CDK for indium to those two anchor Jane's happens to exist or very close by in space on a chromosome 12 and in fact on over 90% of cases, where im going to was amplified as the population we're addressing in our trial.
Over 90% of those have a CD free CDK for co amplification and so in fact, when we're a when we're addressing patients with I agree to application.
Bring a couple of cycle along as they CDK for inhibitor I just makes it makes a lot of sense because of that cut that frequent co amplification.
Scott It's got it thanks for that and yes. Thanks, guys. Thanks for answering my questions and congrats on the quarter.
Thank you.
And once again press star one to ask a question.
At this time I'd be happy to return the call to Dr. either for closing remarks.
Thank you very much.
So to summarize as we look ahead, we are very excited about the opportunities that lay before us six nine to four is a unique agent with important milestones coming up in the first half of 2020 in the second quarter of next year, we plan to release the final data from our phase two combo study of 604 with all the cycle.
And Jim to amplify cancers and in the same quarter, we look forward to delivering the results from the first part of our ongoing model preservation program.
Once we have identified a recommended phase two dose for our model preservation program, we plan to commence enrollment of both aforementioned lung cancer extension cords and we're working diligently to ensure that these studies are successful and look forward to keeping you apprised of our progress.
Thank you for your time and this concludes todays call.
Thank you. This does conclude todays aileron therapeutics third quarter 2019 financial and operational update you may now disconnect. Your lines, everyone have a great day.
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