Alder Biopharmaceuticals Inc. (NASDAQ:ALDR)
Q2 2016 Earnings Conference Call
July 26, 2016 17:00 ET
David Walsey - Vice President, Corporate Communications
Randy Schatzman - President and Chief Executive Officer
Larry Benedict - Senior Vice President, Finance
Mark Litton - Chief Business Officer
Joseph Schwartz - Leerink Partners
Nick Agarwal - Wells Fargo Securities
Brian Abrahams - Jefferies
Vamil Divan - Credit Suisse
Good afternoon and welcome to the Alder Biopharmaceuticals Second Quarter 2016 Financial Results Conference Call. At this time, all participants are in a listen-only mode. Following the formal remarks, we will open the call up to your questions. Please be advised that the call is being recorded at the company’s request.
At this time, I would like to turn the call over to Mr. David Walsey, Alder’s Vice President, Corporate Communications. Please proceed, sir.
Thank you, Christy. Good afternoon and welcome to Alder’s second quarter 2016 financial results conference call. Just after market closed today, we filed our quarterly Form 10-Q with the Securities and Exchange Commission and issued our financial results, corporate highlights press release, both of which are available at www.alderbio.com.
Today in our call, Randy Schatzman, President and CEO will provide an overview and update of the company’s business; Larry Benedict, Senior VP of Finance will review the financial results; and then we will open the call for your questions. Mark Litton, our Chief Business Officer is also with us today for the Q&A.
Before we begin, I would like to caution you that during today’s conference call, we will be making forward-looking statements regarding future events or the future performance of the company, including statements about possible future developments regarding clinical, regulatory, commercial, financial and strategic matters. Actual events or results of course could differ materially. We refer you to the documents that Alder files from time-to-time with the SEC and in particular, the company’s quarterly report on Form 10-Q for the quarter ended June 30, 2016, which was filed with the Securities and Exchange Commission today, July 26, 2016. These documents, which are available on the SEC’s website, contain and identify under the heading Risk Factors important factors that could cause actual results to differ materially from those contained in any forward-looking statements, including without limitation, risks and uncertainties related to the initiation, conduct and results of clinical trials, the availability of data at the expected times, risks and uncertainties related to regulatory application, review and approval processes and compliance with applicable regulatory requirements; the sufficiency of Alder’s capital and other resources; and market competition.
With that, I will pass the call over to Randy.
Thank you, David and welcome everyone. Thank you for joining us today. During the second quarter, we continued executing successfully against our plan to advance ALD403 toward the submission of a biologics license application and the goal of marketing a best-in-class migraine prevention antibody therapy which meets the needs of millions of people living with this debilitating disease.
As many of you know, ALD403 is our wholly-owned development stage novel monoclonal antibody that inhibits the calcitonin gene-related peptide or CGRP. CGRP is a small protein involved in the transmission of and heightened sensitivity to the pain experienced in migraine. This is now a well validated mechanism of action as demonstrated by multiple agents which targets CGRP biology. In March of this year, we reported that our Phase 2b clinical trial in chronic migraine patients met both the primary efficacy endpoints, which was the 75% reduction in migraine days over 12 weeks and the secondary efficacy endpoint of mean reduction in migraine days from baseline after a single ALD403 infusion. Recall that this Phase 2b study is a double-blind placebo-controlled randomized single IV infusion dose ranging study in approximately 600 patients with chronic migraine. Patients were randomized to receive a single intravenous infusion of 10, 30, 100, or 300 milligrams of ALD403 or placebo. Patients averaged about 16 migraine days per month at baseline.
Specifically, the data demonstrated that the 300 milligram and 100 milligram dose levels of ALD403 provided a significant reduction in migraine days versus placebo as measured by the 75% responder rate over the entire 12-week study period in 33% and 31% of patients respectively. In addition, a single administration of ALD403 also met the key secondary 12-week endpoint demonstrating a significant mean reduction in migraine days from baseline throughout the 12 weeks at the 300, the 100, and the 30 milligram dose levels. The 10 milligram dose level was not significantly different from placebo establishing an important sub-therapeutic dose level.
Now, yesterday, we announced positive top line 24-week results from this Phase 2b clinical trial. The data demonstrated a persistent migraine prevention effect through the 24-week period both confirming and extending the previously reported 12-week data described above. More specifically, the 75% responder rate for the entire 24 weeks at the 300, the 100 and the 30 milligram dose levels was 31%, 29% and 30% respectively compared to a placebo rate of 20%. ALD403 also demonstrated a persistent mean reduction in migraine days from baseline throughout the 24-week period similar to the reduction reported previously for the initial 12 weeks of the trial. Further, the 10 milligram dose continued to be sub-therapeutic. The 10 milligram 75% responder rate for the entire 24-week period was 26% compared to the placebo rate of 20%.
The safety profile was consistent with the 12-week Phase 2b data reported previously and earlier ALD403 clinical trials. There were no new safety findings. These data will help us finalize the dose selection and design of PROMISE 2, our second planned pivotal trial. PROMISE 2 scheduled to start later this year will evaluate patients living with chronic migraine with two dose levels of ALD403 administered via IV infusion that will be selected based on our continuing review of the Phase 2b data, other data from our ALD403 development program and consultation with the FDA. The data also validates the dose selection for the ongoing PROMISE 1 study and further demonstrate ALD403’s best-in-class potential as evidenced by prolonged migraine prevention after a single infusion.
Finally, based on the data from the Phase 2b study, we are addressing the target enrollment for PROMISE 1 of 600 patients to 800 patients. PROMISE 1 was initially powered based off the data from our earlier Phase 2 proof-of-concept study in patients living with frequent episodic migraine. We believe that the new target size better reflects the effect size that we may expect in a much larger pivotal study such as PROMISE 1. This change does not alter our guidance for the top line PROMISE 1 data in the first half of next year, because we are taking advantage of the large number of currently opened study sites and the effectiveness of ongoing recruiting.
Our focus remains on advancing ALD403 and building a foundation to support its continued successful development regulatory approval and ultimately commercialization of a best-in-class migraine prevention therapy. As many of you are well aware, current therapies for migraine prevention are challenged by safety, tolerability and efficacy limitations. And until now, there has never been a drug specifically developed for migraine prevention despite the critical need for new migraine treatments. Approximately, 33 million American adults live with migraine with approximately 13 million of those being candidates for preventive therapy. Of this set of prevention candidates, approximately 3 million have chronic migraine representing the most serious segment of the migraine patient population. The scale of the problem can better be understood when you consider that the number of patients in the United States living with rheumatoid arthritis is about 2.5 million or less than one-fifth the 13 million potential migraine prevention candidates. To best optimize our efforts to commercialize ALD403 if approved, Alder plans to focus initial commercialization efforts on United States neurologists by building a specialty sales force of 75 to 100 detailers. Roughly, 43% of candidates for migraine prevention are treated by neurologists. We view this as the initial beachhead for our commercial focus.
Our commitment to develop both an infrequent IV infusion and an alternate formulation such as sub-Q or IM, also to be dosed infrequently fits this focus. IV medications are very commonly used by neurologists. Our own proprietary research found that 93% of neurologists report prescribing IV therapies for their patients and of that number, 73% report prescribing IV medications for migraine. Beyond neurologists, there exists a significant need among patients that are visiting primary care or other physicians. It is here where we see an additional important role for the alternate formulation of ALD403, specifically via sub-Q or IM administration to provide further patient convenience. To maximize the potential commercial opportunity of ALD403 while we focus on the U.S. specialty market, Alder may explore strategic arrangements that provide additional capabilities, infrastructure and improve the potential return on our investments, while improving access for physicians and patients.
In an effort to expand our focus on migraine, we have decided to double our efforts to meet the needs of the millions of people living with migraine by bringing forward a second therapeutic candidate which we call ALD1910, also aimed at migraine prevention. ALD1910 is a monoclonal antibody that inhibits PACAP-38 which we believe has the potential to further benefit patients beyond those outstanding benefits provided by ALD403. PACAP-38 or pituitary adenylate cyclase-activating peptide-38 is understood to be a key factor active in the initiation of migraine. PACAP-38 and CGRP do not employ overlapping pathways. We believe that we are the first to document the differential pharmacology of PACAP-38 and CGRP via in vivo models that establish that these ligands drive different pathways leading to migraine.
As such, we believe targeting PACAP-38 holds significant potential, especially in people living with migraine who have an inadequate response to agents targeting CGRP or its receptor. ALD1910 has favorable characteristics with respect to binding affinity, formulation, viscosity, stability and other key factors critical to a streamline development path. We are very excited to move this candidate forward into our development pipeline. The nomination of ALD1910 as our next development candidate reinforces our strategy and commitment to ALD403 with a program that complements a growing neurology focus and leverages a planned specialty sales force capable of marketing multiple agents in the CNS arena, thereby increasing shareholder value.
Next, we are discontinuing the development of ALD1613. This candidate was being developed for the treatment of congenital adrenal hyperplasia and Cushing’s disease. ALD1613 targets adrenocorticotropic hormone or ACTH and during our preclinical IND enabling toxicology studies, we identified novel target specific toxicology that we will believe – that we believe will limit its human clinical utility. More specifically, we uncovered novel observations in the mechanism of action of ACTH for which there is no published precedent. Our plan is to publish our results to inform the field of these observations, which impact this access as the target for therapeutic development and ensure that the potential safety concerns are widely known.
Overall, the decision to discontinue ALD1613 has the benefit of focusing our efforts on the needs of migraine patients, leveraging our growing expertise in migraine and broadening our CNS portfolio through the addition of ALD1910. In addition, our preclinical pipeline contains several other programs that we are eager to move forward in the future. These are programs that would also be complementary to our focus on migraine and neurology. We are committed to balancing our efforts to bolster our pipeline against our primary focus, while successfully moving ALD403 to BLA submission and ultimately commercialization.
With the continued successful advancement of ALD403 and now the addition of ALD1910 to our pipeline we have expanded the Alder team to support these efforts. An important addition to the Alder team for moving forward is our new Chief Medical Officer. Last month, we were pleased to announce the appointment of Dr. Tim Whitaker to that role. Tim joins us from Shire where he was the global clinical therapeutic area head for neuroscience and responsible for late stage product development and numerous successful regulatory approvals, including buybacks [ph]. With decades of experience, Tim is charged with providing strategic oversight of Alder’s clinical development pipeline and will also be responsible for clinical operations in medical and regulatory affairs. He will play a fundamental role in the clinical development of ALD403 for migraine prevention as it advances through pivotal trials [Technical Difficulty].
Tim is joined by another recent addition to the Alder team, Dr. Roger Cady, Vice President of Neurology. Roger is the leading treating physician, a key opinion leader and a fellow in the American Headache Society with 30 years of experience devoted to treating patients living with migraine including participating as an investigator in over 300 clinical trials evaluating various migraine therapies. Other additions and promotions to the Alder team include Dr. Iqbal Husain as Vice President of Program and Portfolio Management, Dauphine Barone as Vice President of Manufacturing Logistics and Barbara Schaeffler as Vice President of Clinical Operations.
And then on other fronts, in April we bolstered our cash position through a follow-on offering raising approximately $135 million in net proceeds. Our strengthened cash position enables us to execute our pivotal trial program through critical data read outs and to appropriately invest in manufacturing and commercialization preparedness activities. In May, we licensed exclusive worldwide clazakizumab rights to Vitaeris. Clazakizumab is our clinical stage monoclonal antibody candidate designed to block interleukin-6. In exchange for the rights to clazakizumab, Alder received an equity stake in Vitaeris and is eligible to receive royalties and certain other payments. Vitaeris will pursue undisclosed innovative therapeutic indications and chronic inflammatory diseases. And then in June at the American Headache Society 58th Annual Scientific Meeting, we presented the positive top line data for the 12-week primary end point from our Phase 2b study evaluating ALD403 in patients with chronic migraine as well as a poster with favorable data from our Phase 1 study of ALD403 demonstrating that the pharmacodynamics and pharmacokinetics of ALD403 support a self administered quarterly single injection dosing strategy.
As we move towards the ends of 2016 and into 2017, we expect to continue to demonstrate continued strong execution against our business plan. We are on track to initiate PROMISE 2 later this year and look forward to sharing more details on the design and choice of dose levels as we continue analyzing the data from our development program and consult with the FDA. Our objective is also to initiate a study that will further evaluate a formulation of ALD403 suitable for self administration either as a single quarterly sub-Q or intramuscular injection following consultation with the FDA. We will continue to expand our management team to support the late stages of development and commercial preparedness for ALD403. We are also excited to advance ALD1910 into IND enabling studies and we will keep you apprised of its progress. Finally, in the first half of 2017, we plan to announce top line data from PROMISE 1, the first of our two planned pivotal studies.
With that, I will now turn the call over to Larry to review our financials. Larry?
Thanks Randy. Today, I will focus on highlighting our financial results for the second quarter of 2016 and then review the financial outlook for the remainder of 2016. Please refer to this afternoon’s press release and 10-Q filed with the SEC for further details. In April, we completed a successful public offering of 6,182,795 shares of common stock at a public offering price of $22.25 per share which added $134.9 million of net proceeds to our cash and cash equivalents and short-term investments balances. We continue to invest heavily in our ALD403 drug development activities and we ended the quarter with $450.1 million in cash and investments.
Research and development expenses for the second quarter totaled $33.8 million compared to $14.1 million for the same period in 2015. The increase in spending was primarily due to the ALD403 development program and consistent of cash related to the PROMISE 1 and other ongoing clinical trials and manufacturing costs of drug supplies in support of existing and planned pivotal clinical trials. In addition, Alder incurred increased compensation costs to an increase in Alder’s research and development headcount to support our pivotal trial program for ALD403.
General and administrative expenses totaled $6.5 million compared to $3.9 million for the same period in 2015. The increase was primarily due to compensation costs as a result of an increase in stock based compensation and general and administrative headcount as well as increases in the market research and other administrative costs. Alder also recognized a gain of $1.1 million on licensing clazakizumab to Vitaeris in the second quarter ended June 30, 2016. Since clazakizumab was developed internally by Alder, all previous expenditures to develop the compound were recognized as expense and therefore was no carrying value on Alder’s balance sheet. Therefore, Alder recognized a gain on the license agreement which was determined as the fair value of the company's equity stake in Vitaeris and is also the initial carrying value of the company's investment in Vitaeris. Alder will utilize the equity method of accounting for recording investment activity in Vitaeris and will record its results as results of operation in its shares of income and loss in Vitaeris.
Turning to net loss for the second quarter ending June 30, it totaled $38.9 million or $0.79 per share compared to a net loss of $17.7 million or $0.46 per share on a fully diluted basis for the same period in 2015. 2016 operating expenses are estimated to increase approximately twofold over the $86.3 million reported in 2015. However, as we noted in last quarter, we may see period-to-period fluctuations in quarterly results as we continue to invest heavily in our drug development activities, particularly for ALD403. We are currently in a strong financial position that allows us to invest in our critical activities and get some important inflection points in the ALD403 program. As we continue reviewing plans on how to optimize development path and commercialization preparations for ALD403, we may determine to adjust certain investments.
With that, we will now open up your calls for questions. Operator?
Thank you. [Operator Instructions] Our first question comes from the line of Joseph Schwartz of Leerink Partners. Your line is open.
Thanks very much and congrats on all the progress. I was first of all wondering how you are thinking about dose and formulation selection now for PROMISE 2 and the late stage study or studies for a self-administered formulation of ALD403? Thanks.
Thanks, Joe. Appreciate those questions. So I am making a note here. So, in terms of PROMISE 2, as we alluded to in the discussion, we are still working through the data that we have obviously we released both the 12-week and the 24-week top line data as of this date. And what you noted in that data is that the primary endpoint which was 75% reduction responder rate and the key secondary which was the median change in migraine days from baseline are actually fairly blunt instruments and don’t distinguish well amongst the doses in the study other than the 10 mg dose, which was very similar to placebo. So what we are doing today is looking closer at the other measures that we took from these patients to better understand whether they help us tease out the differences between the doses going forward, so that we can choose the best doses that both obviously get us to the regulatory endpoints that we need for approval could benefit patients in a maximal effects and we’ve got some more work to do on that front before we ultimately choose the specific doses to go forward and some discussions to have with the FDA.
Okay, the same question or the same answer for the second question about how will be move forward with our alternate formulation for administration. Again, what we are aiming for is a quarterly injection that we can do as a single injection with this and that will all be related to the dose level that is chosen to move forward in terms of delivering the best efficacy and the best safety profile to patients and some further discussion with the FDA on that front.
Okay, great. So, then the 24-week data make you more or less likely to pursue a sub-Q formulation versus an IM formulation? I know you are looking at a lot of different attributes and a lot of different data, but maybe you can give us some insight into your process there and then also just highlight for us what would IM administration do for you that sub-Q did not?
So, the question really again boils down to what are the other benefits that different dose levels provide to patients when we look at that data? And let me just give you an example and that is if for example the higher doses provided better more durable benefit for relief from maybe severe migraine or improved quality of life that had a longer durability to it than the lower doses did then we may choose to lean toward those. If on the other hand the lower doses provide the same level of those benefits, again I think we would lean towards the lower doses and the least amount of exposure to our patients. And again, I think the jury is out yet as the team work through the analysis of those various datasets. I think as we have talked in the past one of the beauties of you know thinking about a couple of different modes that we could use for self administration is that there are a couple of benefits in particular while the sub-Q is one that I think physicians and patients maybe likely to be the most used to.
On the other hand, an intramuscular injection is something very similar to what we get each year with our flu shot. It’s simply administered in our hands, at least our experience is its painless and it has the opportunity to allow us to deliver a higher dose of drug via a larger volume. As you know, the sub-Q injection route is restricted and sort of overall volume amount to about a mIL to a mIL in the quarter. So, as we think about the dose and how we formulate the drug and our ability to administer it and which way is the best we will take those things into account. What’s interesting is that regardless of how we choose, the drug itself has a very low viscosity to it and again either way we choose it will be using a 27-gauge needle as we move forward.
Okay, great. Thanks for taking my questions.
Thank you, Joe.
Thank you. Our next question is from Jim Birchenough of Wells Fargo Securities. Your line is open.
Hello, afternoon. It’s Nick in for Jim. Jim is on a plane. So the first question, I just want to try and get some clarity in my mind between the 24-week data for episodic and chronic, because the rate more or less say that the waning of efficacy we saw in the episodic has not been repeated in the chronic and is that what’s sort of leading to more perhaps I guess discussion about selection of dose for the PROMISE 2 trial? And I have a follow-up.
So, let me just clarify to make sure I understand the question that you are asking, so in the frequent episodic studies that you are referring to our proof-of-concept study.
Where we administered a gram total of the IV infusion.
Okay. So, let’s go back to that data when we compare the 12-week data and the 24-week data in terms of the responder analysis and look at the integration of that data over either the 12-week period or the 24-week, the results actually across the 50% to 75% and the 100% responder levels are very similar. I think the differences that you are referring to are the change at least at the 100% level from 16% to 11%, 16% at 12 weeks, 11% at 24 weeks and that actually isn’t a weaning of the drug effect. Moreover, it was actually a loss of data. In this case, one of the interesting phenomena that we find with this drug is that typically what you see in a clinical trial is that patients dropout for lack of efficacy. In this case, we are finding just the opposite. In fact, the drug is so effective and we are asking them to report their migraine response on a daily basis that by the time that hit four and five months and they have had no migraines despite the fact that they started the study having you know maybe 15 or 16 migraines per month, they in essence stop reporting, because they feel like they have been cured and it’s one of the things that we have had to get on top of with nurses calling the patients to make sure that we complete those datasets.
Okay, thanks for reminding of that. I guess then are you still convinced then that once a quarter is the right dosing frequency for that drug?
Yes, it is. And we are convinced of that on two fronts. Obviously, the data so far confirms that with very low doses of drug we can achieve that prolonged efficacy. I think it’s in our interest and in the patient’s interest to expose them to the least amount of drug that we can. And in addition when we do our commercial work and we talked to patients about what they would like for convenience. If you stack up a drug treatment that’s once a month, sub-Q whether it’s a single injection or multiple injections versus a drug that’s given just four times per year in every case, they choose the less frequent administration strategy.
Okay. And then maybe moving to 1910, obviously you had some encouraging data, does the properties of 1910 look like 403 I mean should we expect that you will be able to doing this as infrequently as 403 and then do you have any data comparing it to the Amgen antibody?
So, the answer to your first question is yes, by and large, it’s very similar to ALD403 and its properties. In fact, as we did it when we went from clazakizumab, the ALD403, we used the same backbone sequence for 1910 as we used for ALD403. We present the sequence in a similar way in terms of being aglycosylated format. And overall, the affinity is high, the off rate is slow, has a long half life. We expect it and in fact it does formulate well and behaves well at least in the animal models at this point. We will find out in non-human primates and humans in the near future. In comparing it with the Amgen antibody, Amgen is actually taking a different approach than what we are similar to us going after the ligand CGRP in this case and Amgen going after the CGRP receptor. We are choosing to go after the PACAP-38 ligand itself and Amgen has chosen to go after PAC1, which is the primary receptor for PACAP-38.
Great, thank you very much and congrats on the progress.
Thank you. Our next question is from Brian Abrahams of Jefferies. Your line is open.
Hi, thanks for taking my questions and congrats on all the progress. My first question is on PROMISE 1, it sounds like the expansion of that study is really doing hands-powering in the primary endpoint without much downside, but I am curious to what degree the expanded study could enhance your ability to discern other ancillary endpoints like patient reported outcomes that perhaps could play a role in competitive reimbursement and commercial landscape?
That’s boy, you put your thumb right on it, Brian and that is on, I mean, obviously first and foremost, our concern is delivering the best safety profile and the best efficacy profile we can to patients, but as you know Phase 3 studies, while pivotal in nature, are still exploratory in the sense that we are trying to understand what the maximum benefits that can be derived from them are. And I think the insights from dosing more patients at our various dose levels are going to give us those insights.
Got it. And then do you have any updates on the potential timetable for when we might see anti-drug antibody data from the Phase 2b chronic study and are there elements of the production system that might give you a potential advantage in terms of ADAs versus some of the other antibodies in development?
So, as you know, when we measure ADAs here, we wait for an extended period of time following the last dose of drug so that we can washout the endogenous drug which can interfere with any ADA assay that we would perform so that we get an accurate result. The results that we reported this week were 6 months following the last patient getting that last dose of drug. We tend to wait 7 half lives. The half life of ALD403 is about a month. So, we are still actually anticipating getting the last serum samples from these patients. Ultimately that will go to the labs where we have validated assays for performing those ADA assays. So, it will be later in the year before we get those results and obviously we want to get those validate them and then we will review them with the investment community on that. In terms of our production system, as many know, I think first and foremost, we have been expressing clazakizumab ALD403 in a yeast based host system. For that we have been making our antibodies glycosylated. We take off the end link to glycosylation on the heavy chain and in that sense we derive some important clinical benefits from that. We see few to no serious infusion reactions in our experience. We see prolonged half lives as a result of that. We see improved formulation characteristics meaning that we can go to high concentration and retain low viscosity so that we can go through 27 gauge needles at high concentration. And at least so far with the data that we have in hand and most of that – most extensively is from clazakizumab we see low rates of ADAs as a result of presenting an antibody in that format. Obviously it’s still early days with ALD403 but we are anticipating similar results by and large because of the same presentation and by and large because the backbone that we use with ALD403 is exactly the same one that we use for clazakizumab.
Got it. And then one last maybe a big picture question, you are seeing consistent benefits with this new six months data and with prior data beyond several half lives for 403, you presented some data at recent conference on the binding properties for the antibody. What’s your latest hypothesis as to why you have such durable effect and your level of confidence that this is a distinguishing characteristic of the antibody itself that others might not be able to replicate?
Well, that’s a great question. So, the one set of data or one of the sets of data that we don’t have yet Brian from the Phase 2b study is the pharmacokinetic analysis and that will be important to compare drug levels still on board in these patients at the various dose levels and whether those drug levels match what we would expect commensurate response to be for the respective drug levels. One of things that we are still learning about today, and one of the reasons why Alder is taking the development strategy with the studies that we how is this is a new axis of biology and I think it's incumbent upon us to really understand as much as we can about that biology, so we understand the best way to deliver efficacy to our patients and do so with the safest mode of administration or drug levels and ultimately, what we would like to do is expose patients to the least amount of drug to get the efficacy that that we would like to deliver that overall than have them benefit from the safest sort of profile that we can deliver as well. And that's what the studies are aimed at doing. So the – for example the Phase 2b study that we are running where patients got different dose levels of drug that received only a single dose of drug and we’ve now followed them for six months and we will continue to follow them to see how long the drug itself lasts is really an eye toward administering the minimum exposure to these patients to promote the greatest amount of safety while we understand that efficacy along the way.
I think the other thing that we are trying to understand here with respect to the biology is that we know that CGRP while it's involved in a heightened sensitivity to pain and the triggers that are experienced in migraine, there's also some data that suggest there is some neuro-inflammation that goes along with this. And the question really is once we treat as for these various aspects of CGRP biology, what is the outcome? And in fact it could be that the duration of effect outlasts the concentration of antibody on board and if that's the case again we want to understand that to make sure that we are optimizing our dosing strategy accordingly.
Thanks so much, Randy.
Thank you, Brian.
Thank you. [Operator Instructions] Our next question is from Vamil Divan of Credit Suisse. Your line is open.
Hi, good afternoon. Thanks so much for taking my question. So, I just had a couple related to the 24-week data from yesterday and I guess it is you know positive that it seem the duration – durability of your response, I guess we are sort of surprised that the placebo response are sort of holding in pretty well through from weeks 12 to 24. Also I am wondering if you just have any sort of comments on that? And second one related again to the data from yesterday, are you surprised that there is not a bigger sort of dose response between what you see with 30 milligram dose going up to 100 milligram and going up to the 300 milligrams really not that much of a difference between the three, I am just a little surprised or just curious and that’s surprising to you? Thanks.
Yes. So those are both great questions and one we have much discussion over here at Alder. I think the thing to think in terms of the placebo and it’s durability is really twofold and that is that this is a group of patients that by and large has left medical care because they have been frustrated by not having effective therapies to treat the many migraines that they are having and now we have invited them in to get continual oversight and care from physicians and that has a profound effect in terms of the placebo response that we see. Also remember that we are asking these patients to respond to an electronic diary at the end of each day to record their daily experience. And our belief is that continues to contribute to this feeling of well being that they got that they are being taken care of by their physicians, so that at least contributes to that.
In terms of the dose responses I alluded to earlier what our take is that the way we measure migraine today for regulatory approval is in essence counting the number of migraine days that these patients have whether we measure that by the responder analysis or whether we measure that by the change in median migraine days from baseline on a monthly basis. It seems like it’s a fairly blunt instrument in that sense in terms of not really allowing us to distinguish between specific dose levels of drug. I think the other thing that we are watching here though is also a drug, the drug properties of ALD403 in that they are very favorable. The team here at Alder discovered an antibody and actually discovers antibodies overall with very special properties in terms of their ability to rapidly bind to a disease antigen, tie up that antigen and not let go of it until that antibody antigen complexes are actually circulated out of the system. And as such we think that it actually takes fairly low doses of drug to tie up these disease ligands and keep them out of play for a long duration of time. To be honest, we saw a very similar effect with clazakizumab and if you think back to the studies that we and BMS did with clazakizumab with rheumatoid arthritis it looked like the go forward dose for monthly dose for clazakizumab in RA patients who is going to be as low as 25 milligrams per month or a total of about of 300 milligrams per year, which is an incredibly potent drug. ALD403 is very similar to that and you will see as we move ALD1910 forward similar set of properties associated with that as well.
Okay, alright. Thanks so much.
Thank you. And that does conclude our Q&A session for today. I would now like to turn the call back over to Mr. Randy Schatzman for any further remarks.
Thank you, Operator. ALD403 therapeutic profile today presents us with a true opportunity to transform the way migraines are prevented and significantly improve the lives of patients living with migraine. With the exceptional team here at Alder, our strong cash position and a clear path for development, we believe that we can rapidly advance ALD403 to commercialization and continue to add superior candidates to our pipeline as we seek to build long-term value for our shareholders. Thanks everyone for your time today. We appreciate you joining us.
Ladies and gentlemen, thank you for participating in today’s conference. This does conclude today’s program, you may all disconnect. Everyone have a good day.
Copyright policy: All transcripts on this site are the copyright of Seeking Alpha. However, we view them as an important resource for bloggers and journalists, and are excited to contribute to the democratization of financial information on the Internet. (Until now investors have had to pay thousands of dollars in subscription fees for transcripts.) So our reproduction policy is as follows: You may quote up to 400 words of any transcript on the condition that you attribute the transcript to Seeking Alpha and either link to the original transcript or to www.SeekingAlpha.com. All other use is prohibited.
THE INFORMATION CONTAINED HERE IS A TEXTUAL REPRESENTATION OF THE APPLICABLE COMPANY'S CONFERENCE CALL, CONFERENCE PRESENTATION OR OTHER AUDIO PRESENTATION, AND WHILE EFFORTS ARE MADE TO PROVIDE AN ACCURATE TRANSCRIPTION, THERE MAY BE MATERIAL ERRORS, OMISSIONS, OR INACCURACIES IN THE REPORTING OF THE SUBSTANCE OF THE AUDIO PRESENTATIONS. IN NO WAY DOES SEEKING ALPHA ASSUME ANY RESPONSIBILITY FOR ANY INVESTMENT OR OTHER DECISIONS MADE BASED UPON THE INFORMATION PROVIDED ON THIS WEB SITE OR IN ANY TRANSCRIPT. USERS ARE ADVISED TO REVIEW THE APPLICABLE COMPANY'S AUDIO PRESENTATION ITSELF AND THE APPLICABLE COMPANY'S SEC FILINGS BEFORE MAKING ANY INVESTMENT OR OTHER DECISIONS.
If you have any additional questions about our online transcripts, please contact us at: email@example.com. Thank you!