Aptose Biosciences Inc. (NASDAQ:APTO)
Q3 2016 Earnings Conference Call
November 15, 2016 05:00 PM ET
Susan Pietropaolo - IR, SMP Communications
William Rice - Chairman, President and Chief Executive Officer
Gregory Chow - SVP and Chief Financial Officer
Avanish Vellanki - SVP and Chief Business Officer
Adnan Butt - RBC Capital Markets
Joe Pantginis - Roth Capital Partners
Good morning. My name is Karen and I’ll be your conference operator today. I would like to welcome everyone to the Aptose Biosciences Conference Call for the Third Quarter Ended September 30, 2016. At this time, all participants are in listen-only mode. After the speaker’s remarks, there will be a question-and-answer session. [Operator Instructions] Thank you. As a reminder, this conference call may be recorded.
I would like to introduce Ms. Susan Pietropaolo. Please go ahead.
Thank you, Karen. Good afternoon and welcome to the Aptose Biosciences conference call to discuss financial and operational results for the third quarter ended September 30, 2016. My name is Susan Pietropaolo with SMP Communications, the Investor Relations representative for Aptose Biosciences. Joining me on the call today are Dr. William G. Rice, Chairman, President and CEO; Mr. Gregory Chow, Senior Vice President and Chief Financial Officer; and Mr. Avanish Vellanki, Senior Vice President and Chief Business Officer.
Before we proceed, I would like to remind everyone that certain statements made during this call will include forward-looking statements within the meaning of U.S. and Canadian securities laws. Forward-looking statements reflect Aptose’s current expectations regarding future events, but are not guarantees of performance. And it is possible that actual results and performance could differ materially from these stated expectations. They involve known and unknown risks, uncertainties and assumptions that may cause actual results, performance and achievement to differ materially from those expressed.
To learn more about these risks and uncertainties, please read the Risk Factors set forth in Aptose’s most recent Annual Report on Form 20-F and SEC and SEDAR filings. All forward-looking statements made during this call speak only as of the date they are made. Aptose undertakes no obligation to revise or update the statements to reflect events or circumstances after the date of this call, except as required by law.
I will now turn the call over to Dr. Rice, Chairman, President and CEO of Aptose Biosciences. Dr. Rice?
Thank you, Susan. I’d like to welcome everyone to our call for the third quarter ended September 30, 2016. We held our last conference call only a month ago when we brought you an update on the status of our clinical hold on APTO-253. We announced that day that the FDA had informed us that they will be requiring the standard Chemistry, Manufacturing and Control or CMC information for the final GMP drug substance and clinical supply before deciding whether or not to remove the clinical hold of Aptose’s Phase 1b clinical trial in patients with hematologic cancers.
We spoke about that that might mean for our timelines and the expectation that initiation of patient screening would likely be in the first quarter of the year. So on today’s call, we plan to further update you on the status of APTO-253 or just 253 as I’ll call it and getting our clinical trial back on track. Following, we will review our business developments, our quarterly financials and then open the call for your questions.
So first, 253, as a quick reminder for some of you, 253 our lead compound is a first-in-class inducer of the Kruppel-Like Factor 4 or KLF4 tumor suppressor gene. It’s the only clinical stage compound targeted for patients with suppressed KLF4 levels which have been reported in the scientific literature as a key transforming event in the onset and progression of AML and high risk MDS. Importantly, 253 recently has shown another compelling activity in our mechanistic studies, specifically its ability to inhibit the expression of the c-Myc oncogene, a major driver of cancer cell proliferation but without the typical toxicity to normal cells caused by other c-Myc inhibitors such as Bromodomain or BET inhibitors. The ability of 253 to potent inhibit c-Myc oncogene expression is a major finding and speaks to why we observed potency against a multitude of hematologic cancers and even certain solid tumors.
253 also has demonstrated a very favorable safety profile with no evidence of bone marrow suppression in animal models or in humans which not only differentiates our candidate from other AML and most cancer therapies but underscores the absolute importance of its clinical development. I would like to again emphasize that the clinical trial hold was based on the clogging of an inline filter, a chemistry and manufacturing issue only and not a safety issue that is so often the reason for a clinical hold. And so we have remained absolutely focused towards resolving the clinical hold issue of the 253 clinical trial and addressing such a major cancer need.
After a month of disciplined work conducting a root cause analysis, evaluating multiple formulation and production methodologies, performing multiple mock infusion studies on drug product prototypes and more, on September 12 we provided a complete response to all the questions that the FDA had cited in the clinical hold letter to us. In that response to the FDA, we also proposed corrective actions based on the prototype drug product that we have manufactured and tested to our satisfaction. As the drug substance or API was changed from a salt to a free base and the proportions of the original excipients were modified in the drug product formulation, the FDA came back to us and asked to review the CMC information for the final drug product that we intend to take to the clinic, in other words, the clinical supply.
Indeed the FDA’s response focused exclusively on the request to provide the agency with complete CMC information on the intended clinical supply and did not request further studies to be performed. As I mentioned on our October call, while we would like to have had the clinical hold lifted, we were encouraged by the fact that all of our hard work with the prototype drug product has allowed us to proceed with manufacturing of the clinical drug supply. So where are we now? Well, I try not to be too granular here but rather as straightforward as possible and answer some of the questions that some of you have articulated.
Recently, we produced a 40 leader engineering batch of the drug product using the GMP drug substance and all the excipients that will go on to the final drug product, and we leverage this engineering run to optimize multiple parameters of the process and to perform suitability methods development for sterility, endotoxin, container and closure integrity and stability studies. We also now have manufactured a 40-liter GMP batch of the drug product for the clinical supply. So let me repeat that. We now have manufactured a GMP batch of drug product for the clinical supply and the vials have been placed on accelerated stability testing for one month and on long term stability testing.
The batch records and release specifications along with the stability and sterility data will comprise much of the CMC package that we plan to provide to the FDA in order to have the hold lifted and reinitiate the clinical trial. Despite some of the delays caused by the hurricane which we mentioned on our last call, we worked closely with our contracting manufacturing organization to expedite the manufacturing process. Again, while we’ve learned that anything can happen, we expect to deliver the package to the FDA as soon as one month stability data can be verified and reported, and the full CMC package can be assembled. If all proceed smoothly, we should be able to deliver that package to the FDA by the end of this year or the first half of January.
After the FDA review and assuming the clinical hold is lifted, we also will be submitting that information to the Institutional Review Boards or IRBs for all of our clinical sites. We already have provided them with all of our data to date, the protocol amendment has been submitted and budgets have been negotiated, but they also wish to see and review the information related to the final clinical supply. While we have been focused on the 253 formulation work, our clinical team has put a tremendous amount of effort into expanding the number of clinical sites to be prepared when 253 enters the clinic. You may recall that originally we had four clinical sites enrolling patients. Over the next few months, we expect to have up to 15 sites ready to go. This has been another focused effort to ensure we have rapid recruitment of patients into the future. While there are no guarantees that the hold will be lifted, upon such notification we are well prepared to move quickly and we look forward to sharing that news with all of you.
Again, as a quick refresher on the 253 clinical study, the study is an ongoing open label single agent dose escalating Phase 1b clinical trial in patients with relapsed or refractory hematologic malignancies including AML and high risk MDS. The study is designed to assist safety, tolerability, pharmacokinetic and pharmacodynamic responses and efficacy of 253 as a single agent. Two following single agent expansion cohorts are planned as well as two Phase 2 cohorts for drug combination studies.
Assuming we can reenter the clinic at the dose of 100 milligrams per meter squared, where we left off, we will have completed about half of the dose escalation and we would estimate that the remaining dose escalation portion of the trial would take approximately six to nine months depending on the number of dose levels evaluated. One silver lining arising from the difficulties with the prior drug product is that we identified a formulation that we perceive to be superior and to have the potential to gain additional intellectual property for 253.
While we have remained intensely focused on the clinical supply of 253, we did not take our eye off other essential activities, for instance research. In parallel with the formulation studies, we continue to study the mechanistic activities of 253. Our research group has made significant strides in understanding the mechanism of action of the drug in different kind of cancers. As we recently mentioned, we identified key signaling pathways that lead to the modulation of KLF4, p21 and c-Myc gene regulation. This deeper understanding of the mechanism of action of 253 may also bring us new intellectual property for the molecule. Some of this research will be highlighted at the upcoming American Society of Hematology or ASH Meeting this December in San Diego.
I like to now provide an update on our activities related to our second product, CG’806. In June, we announced an exclusive global option and license agreement with South Korea based CrystalGenomics focused on the development of its exciting new candidate CG’806. CG’806 or 806 as I will call it is a highly potent, non-covalent small molecule therapeutic agent. This first-in-class multi-kinase inhibitor exhibits a picomolar IC50 towards the FLT3-ITD receptor tyrosine kinase and potency against the wild type FLT3 and a host of new performance of FLT3. 806 also demonstrates single-digit nanomolar IC50’s against the BTK kinase [Bruton's tyrosine kinase] and its C481S mutant known as BTK C481S.
As a potent inhibitor of FLT3-ITD, 806 may become an effective therapy in this subset of AML patients as the FLT3-ITD mutation occurs in approximately 30% of patients with AML. Importantly, 806 targets other oncogenic kinases, which may also be operative in the FLT3-ITD AML including Aurora kinases and Src family kinases thereby potentially allowing the agent to become an important therapeutic for this difficult to treat patient population.
Regarding 806s ability to target BTK, the C41S mutation of BTK arises from therapy with covalent irreversible BTK inhibitors that target the active Cysteine or Cys as a result of an effort of BTK, thereby resistance to other covalent BTK inhibitors. Of note, following mutation of Cysteine residue at 41 position, the Cys target of most covalent irreversible inhibitors no longer exist in the BTK enzyme. However, as a non-covalent reversible inhibitor, 806 does not rely on the Cysteine 41 residue for the BTK enzyme. Consequently, patients relapsed refractory are intolerant with other commercially approved or development stage BTK inhibitors with chronic lymphocytic leukemia CLL or mantle cell lymphoma MCL may continue to be sensitive to 806 therapy.
806 is currently in studies to select an appropriate synthetic pathway to manufacture the molecule and formulation development studies, and in various preclinical biological pathway in animal efficacy studies. Provided the studies continue on the anticipated timeline, Aptose expects to initiate first-in-human clinical trial in the second half of 2017. For clarity, 806 is being developed as a once daily oral therapeutic and we plan for initial IND to focus on AML patients.
As mentioned, we were impressed with the early profile of 806. During our due diligence process and evaluation, we were able to reproduce CrystalGenomics compelling preclinical data. Our scientific advisory board members all agreed that the in vivo potency of 806 “shows unprecedented potential”. Finally, the combination of 806s potency with a very robust safety profile gives us enthusiasm for 806 as a therapeutic option for patients with AML, CLL, MCL and other malignancies. The potential option exercise would occur prior to submission of an IND application in the U.S. Upon exercising the option, Aptose would own global rights to develop and commercialize the program outside of Korea and China.
So now as a final thought, over the past year, we’ve been in a bit of a dark tunnel as we solved the product manufacturing issues with 253 and as we literally initiated development of CG’806. Now we are emerging with a new drug product for 253 and with highly compelling data for 806. So we are now beginning to see the light and we are very optimistic about the future of Aptose.
I’d now like to turn the call over to our Chief Business Officer, Avanish Vellanki, who will provide an update on activities related to our third program. Avanish?
Thank you, Bill, and good afternoon everyone. About a year ago, we entered into a collaboration with Moffitt Cancer Center for exclusive global rights to potent, multi-targeting, single-agent inhibitors for the treatment of hematologic and solid tumor cancers. These small molecule agents are highly differentiated inhibitors of the Bromodomain and Extra-Terminal motif or BET protein family members, which simultaneously target specific kinase enzymes. The collaboration with Moffitt brought access to intellectual property reset would be helpful to a new therapeutic candidate.
At that time, we also announced an exclusive drug discovery partnership with Laxai Avanti Life Sciences or LALS of India for epigenetic-based therapies. In the 12 months of work for this program, LALS has produced numerous structures that overcame many of the limitations of initial parent structures from Moffitt. Such structures present us an inventory activity against Bromodomain and specific kinase, and Aptose will file intellectual property protecting those novel structures that were synthesized at LALS. However, Aptose will halt all further efforts on the Bromodomain / kinase program at the current time and focus all efforts on the APTO-253 and CG’806 programs. Nevertheless the IP generated by the program will be valuable in the event after chooses to resume efforts in the future.
With that said, I would like to turn it over to Aptose’s Chief Financial Officer, Mr. Greg Chow. Greg?
Thank you, Avanish, and good morning everyone. Just a quick reminder that our reporting currency is in Canadian dollars, we ended the quarter with $10.3 million in cash and cash equivalents compared to $12.6 million at June 30, 2016. During the quarter, we utilized approximately $3.3 million of cash in our operating activities compared with $2.6 million during three months ended September 30, 2015. For the nine months ended September 30, 2016 we utilized $4.4 million compared to $9 million for the nine months ended September 30, 2015. We currently believe we have capital resources efficient to fund our research and development and operations into early 2017.
Moving on to the income statement, we had no revenues in the three months ended September 30, 2016 as September 30, 2015. Research and development expenses were $2.2 million for the quarter compared to $1.7 million for the three months ended September 30, 2015. This increase was due to costs associated with the LALS market collaboration, increased research and clinical outpatient headcount, and increased formulation and manufacturing costs associated with 253 and the root cause analyses.
General and administrative expenses for the quarter were $1.9 million compared to $2.2 million for the three months ended September 30, 2015. The decrease over the comparable quarter is due to lower stock-based compensation, travel, legal and consulting cost associated with projects completed in the prior year offset by higher cost in the current year due to new programs acquired in late 2015 and the current year. We reported interest income of $12,000 and a foreign exchange gain of $67,000 for the quarter compared to interest income of $56,000 and a foreign exchange gain of $661,000 for the three months ended September 30, 2015.
Finally, our net loss for the quarter was $4 million or $0.31 per share compared to a loss of $3.3 million or $0.27 per share in the three months ended September 30, 2015.
I will now turn the call back over to Dr. Rice. Bill?
Thank you, Greg. I’d now like to open the call for questions. Operator, if you could please introduce the first question.
Thank you. [Operator Instructions] Our first question comes from the line of Adnan Butt from RBC Capital Markets.
Hey, good morning everyone. A couple of questions. First, Bill, in terms of the FDA, is the FDA at this time okay with the root cause analysis that the company presented?
So the answer to that one is, yes, they are very recipient of the root cause as well as our corrective action plan of transitioning to the free base and modifying the proportion of the excipients. So that was not in question at all. They just wanted to make sure that since our earlier studies, what we presented to them, all of those studies were performed with a prototype. They wanted to see the full CMC package of the final clinical supply that we are taking to the clinic, that’s all they ask for, but they were fine with the root cause analysis and the corrective action plan, yes.
And in terms of submitting the package back to the FDA, is the only thing remaining at this time the stability testing or is there anything else?
Well, it’s not only stability. So as soon as you manufacture a batch, you have to meet all the release specifications. And so that is ongoing, you have to have certificate of analysis, the evaluation of stability, sterility, endotoxin test, all of those. It’s the standard package for every clinical supply. So all of those are ongoing now and those typically take about a month or so to complete especially the accelerators to build these studies for one month.
Also in parallel, we have told the FDA that we were – the plan all along was also to look at the pharmacokinetics of this new formulation. So what we’ve done is we are doing rat studies now, those are ongoing and we are dosing the rats with either the prior drug product which had the HCL salt versus the new drug product which has the free base. Those studies are ongoing and thus far that looks good.
The other thing that’s required is just blood compatibility study where you dilute the drug in the blood and look at any potential haemolysis. Those studies are also – those are just in vitro studies, those are ongoing. So all of those comprise the package that we’ll submit to the FDA and all of that should be there in time to submit and collect all the reports by the end of December or the first half of January.
And once the package is submitted, how long does the FDA have before they can get back to you either or before you can decide that you can restart the Phase 1b and at what dose?
We have Orphan Drug Designation, so they are typically expected or if anticipated they would come back to us within 30 days to give you the expedited review and responses from the FDA. So we would expect to hear from them within the 30 day window. They could come back and say, you are good to go or they could ask us to do additional studies. They could change the dose at which we have to enter. Those the FDA can do whatever they wish there. We believe we’ve made compelling arguments for all of these. We’ve really spent the time and effort to get at what we believe is a very compelling drug product that meets all the requirements. We will put the package together. We want to make sure that it is a quality package and have all the data there but they could come back and say we want you to do additional studies or start at a different dose. We don’t expect that but they could, the FDA, or they could say do additional studies and that’s going to take longer and we have to assess that at that time.
Okay, Bill. Let me ask a pipeline question as well. On 806, there are a number of agents targeting BTK resistance FLT3 et cetera and in development, is there something that differentiates 806 at least at this stage, is it potential potency, safety, what would make it different?
It’s a combination of all of those. I mean to have a small molecule with picomolar potency, so it’s most potent inhibitor that’s been described in development against the FLT3-ITD. But not only does it hit the FLT3-ITD, it hits the wild type as well as many of those receptor tyrosine kinase domain mutation. So it inhibits - and let’s just talk about the FLT3 aspect and the AML for a moment. So it inhibits all of those various [inaudible] that we are talking about for the FLT3 and the various mutations there, very potently. It also has a – it inhibits other kinases that are operative in AML. We talk about that some of the RET, the SRC and Aurora kinases. So those are operative and so you’re able to hit the cells in multiple pathways.
But the remarkable part is, when you have a multi-targeting kinase, you think of Sorafenib or a Sunitinib as a good example. And it will hit certain clusters of kinases, so does ours. But as it turns out we are able to hit that FLT3 cluster kinases but without hitting other clusters that caused the toxicity. So it’s this very wide therapeutic window that we’ve seen in the animal models, where we literally wipe out and eradicate the tumors in the animals with no observed toxicity.
The other aspect is we have seen known inhibition of the CYP450 there and the hERG channel. So if you have a clean CYP450 profile and a hERG profile, that allows you to dose escalate further and to get a better therapeutic window. You may be familiar with quizartinib and it had more of a narrow therapeutic window, couldn’t dose escalate higher because of the hERG toxicity. And so we do not have that limitation. So that’s the AML.
When it comes to the BTK, yes, there are other non-covalent reversible inhibitors out there. We believe ours is as potent or potent as any of the other non-covalent inhibitors that are able to inhibit this [C401S] [ph] mutant, that’s the one we really want to go after. We are not going to head-to-head with ibrutinib or acalabrutinib, those are going after wild type BTK. So we are looking at the [C401S] [ph] mutant; we’re very potent against it. We have no activity against the EGF receptor which is what causes some of the toxicities associated with ibrutinib, yet we still hit ITK very potently.
And we’ve had some of the key opinion leaders contact us because they are so interested in this molecule; it not only inhibits BTK and the [C401S] [ph], it inhibits this ITK which is very important for the activity against MCL, CLL but also in potential inflammatory disease and again with that wide therapeutic margin. So we think this could be best-in-class both for AML, the FLT3-ITD targeting patients as well as the patients that are driven - the B cell malignancy is driven by the [C041S] [ph], patients who are resistant, refractory and intolerant to the other covalent inhibitors. So it’s the combination of all the parameters. So that’s why we are so excited about it.
So last question here, then I’ll get back in line. The 806 program obviously 253 is the focus, but 806 is still a program you will continue investing in to get this into the clinic perhaps next year.
Yes. In fact we’ve had those strategic discussions internally. Do we want to just move forward with 253 or do we want to continue with both of them? We believe that data are sufficiently compelling on both programs that we wish and our Board has also voted that we want to move forward with both of those programs, invest in them but which also means we have to raise the capital to do so, but we find both of them to be very compelling and to have the potential to demonstrate responses in Phase 1 trials. So that’s why we want to continue moving forward to both of them.
Okay. Thank you.
Thank you. [Operator Instructions] Our next question comes from the line of Joe Pantginis from Roth Capital Partners.
Hey guys, good morning. Thanks for taking the question. Bill, I wanted to make sure I understood or a little more color on the accelerated stability testing. You are able to submit the package on the one month stability testing and/or do you need the long term as well or with the long term be more of a supplement later on.
Typically, especially for instance if you’re going to file clinical supply for your IND or CMC package, you will always want to have at least one month accelerated stability, pass those stability test and that gives you confidence that your drug is stable for at least three to six months under ambient conditions. So hopefully it will go well. We’ll be able to take those accelerated one month data and be able to file on that. But I also should say we have other batches that we’ve made with these same materials that have been stability studies already for more than three to four months. So we will be able to provide the FDA with data showing ambient conditions with earlier batches for instance a prototype batch, engineering batch, those have been put on stability studies, so we will have multiple batches showing stability data that are more than one month plus the one month accelerated stability on the clinical supply, and that typically is plenty to be able to submit to the FDA. But we also have to show them that we have the drug on long term stability both under accelerated conditions as well as ambient conditions. And when we say accelerated, that just doesn’t mean in time, it just means to show everybody that higher temperatures and higher humidity, that typically accelerates degradation of a molecule, that’s why it’s called accelerated to building studies. So if your drug is stable under those intense conditions for a month, that gives you confidence under ambient or normal conditions that it’s going to be stable for a much longer time in the future. Does that answer your question?
Great. It certainly does, very helpful. Thank you. And then just staying on 253 for a second, you mentioned the potential to have what I guess I would consider to be significant IP, not only in the new formulation but as you mentioned mechanism data as well. Are those patents in prep? Are they ready to be submitted? Where should we consider them in the process?
We are in the process of preparation. Literally we have to get through this process where we manufacture the formulation because now that you have to develop the formulations, you also have to reduce it to practice. So you need to make sure that you come up with the various excipients, the conditions you are able to manufacture you show that the drug is active in the various systems not just in necessary clinical trial but also in vitro. So we are collecting all of those data, and all of the various types of studies showing that what we developed was it was not intuitive and it was not expected. So we should be able to get intellectual property on this but it is in the process of preparation now, collecting all the data around it, that’s for the formulation. With the IP, that’s something we are also preparing but we are collecting a lot of mechanistic data right now. So we have our labs here at Aptose working on it as well as Steve Howell’s laboratory, working on these various studies, collecting it and again we are seeing some very unexpected data coming for mechanistic studies and hopefully that will bring us IP. But again that was also in the realm of preparation. Nothing has been filed on that yet.
Certainly look forward to seeing that update at ASH. And then just lastly on 806, in targeting the clinic for second half of 2017, all of the preclinical studies that are ongoing, what would you consider to be the gating factor time wise, the one that’s going to take the longest with regard to the preclinical studies.
The one – there are actually two elements that we want to make sure that we get correct upfront. It’s the census and the formulation, so that’s why putting all of our effort right now because we all know that if you don’t repair the appropriate form of the molecule in formulation, we’ve learned that you pay a heavy price and I think all the companies are larger than that. So what we are focusing right now is develop this synthetic pathway to make sure that we can manufacture it, have robust level of manufacturing, so that we can manufacture at the levels that we need. And secondly then works flow in multiple different formulation whether it be from different types of dispersion to milling and [indiscernible] you name it. So we are exploring a variety of formulations that we hope will give us - a formulation that gives us appropriate poor availability but also the ease of manufacturer and the low cost. So those are the studies we are putting most of our time right now. In parallel, we are doing all the studies in the laboratory looking at the pathways showing that do we inhibit the FLT3 and BITK pathways and sales, yes we do. But we need to be able to show all of those data. Those are ongoing and parallel, but you key question was, what the gaining activities. It’s really the manufacturing and the formulation right now delivering the molecule so that we can initiate them, the true animal studies, the GLP talks and drive it to the clinic.
Got it. Thank you very much guys.
Thank you, Joe. Appreciate it.
Thank you. And I’m currently seeing no further questions. I would now like to turn the call back over to Dr. Rice for closing remarks.
All right, well, I’m going to say it to everyone. Thank you for joining us today. We do thank you for your support, your patience especially as we take all of these necessary steps to reinitiate the patient direction with the 253 in clinical trial at the current and new clinical sites with high quality stable clinical supply. We remain confident in the potential of our lead therapeutic agent as an important option for patients with AML B cell malignancies and also look forward to reporting on our progress on this program and on the continued advancement of 806. Please note our recent webcasts and presentations can be found the website at www.aptose.com. We thank you again and everyone have a great day. Thank you. Operator?
Thank you, ladies and gentlemen. That concludes today’s conference. You may all disconnect and have a wonderful day.
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