Acceleron Pharma's CEO Discusses Q4 2013 Results - Earnings Call Transcript

 |  About: Acceleron Pharma Inc. (XLRN)
by: SA Transcripts

Acceleron Pharma Inc. (NASDAQ:XLRN)

Q4 2013 Earnings Conference Call

February 26, 2014 09:00 AM ET


Stephanie Ascher - IR

John Knopf - President and CEO

Kevin McLaughlin - SVP and CFO

Steve Ertel - SVP an CBO

Matthew Sherman - CMO


Ted Tenthoff - Piper Jaffray

Mike King - JMP Securities


Good morning and welcome to Acceleron’s Fourth Quarter 2013 Conference Call. At this time all participants are in a listen-only mode. There will be a question-and-answer session at the end. Please be advised that this call is being recorded at Acceleron’s request. I would now like to turn the call over to Acceleron. Please proceed.

Stephanie Ascher

Good morning this is Stephanie Ascher with Stern Investor Relations. And welcome to Acceleron’s fourth quarter and year-ended 2013 conference call. You can listen to a live webcast or a replay of today’s call by going to the Investors and Media section of the website

The agenda for today’s call is, John Knopf, Acceleron’s Chief Executive Officer will provide an update on the Company’s pipeline, clinical plans and R&D efforts. Then Kevin McLaughlin, CFO will review the Company’s financial results and will open the call for Q&A. Matthew Sherman, CMO and Steve Ertel, Chief Business Officer will also be available for Q&A at the end.

Before we begin I would like to remind you that today’s discussion will include statements about the Company’s future expectations, plans and prospects that constitute forward-looking statements for the purposes of the Safe Harbor provision under the Private Securities Litigation Reform Act of 1995.

I would now like to turn the call over to John Knopf.

John Knopf

Thanks Stephanie. Good morning everyone and thanks for joining us today. The fourth quarter of 2013 was particularly productive for Acceleron. Our three clinical candidates advanced crossed nearly a dozen Phase 2 studies and we intend to bring a new candidate designed to increase muscle mass and strength into the clinic in the second half of this year. 2014 promises to be an exciting year for us as we and our collaborator Celgene expect to present data from multiple Phase 2 studies and then by the end of 2014 or the beginning or 2015 initiate a Phase 3 study in beta-thalassemia.

I'd like to start with a few bullet point highlights of the past quarter and then focus today’s update on sotatercept, ACE-536 and Dalantercept. At ASH in December, our collaboration partner Celgene presented interim data from a Phase 2 study of sotatercept in non-transfusion dependent beta-thalassemia patients demonstrating clinically significant dose dependent increases in hemoglobin.

We also reported that a Celgene led Phase 2a study of sotatercept in end-stage renal disease patients on hemodialysis also showed dose dependent increases in hemoglobin, and that Celgene had initiated a Phase 2b study for which Acceleron received a $7 million milestone payment. In mid-January we reported our interim data from the Phase 2 study of ACE-536 and non-transfusion dependent beta-thalassemia patients demonstrating clinically significant dose dependent increases in hemoglobin. We were certainly pleased with positive data across our Hematology programs and look forward to presenting additional data in the coming months.

I’d like to now turn to Aalantercept and our ongoing renal cell carcinoma study. January we initiated enrollment in the expansion cohort of the Phase 2 trial of Aalantercept in combination with axitinib. Also in January results from the Phase 1 clinical trial of Aalantercept mono-therapy were published in clinical cancer research, showing a safety profile distinct from that of VEGF inhibitors and displaying multiple signs of antitumor activity. And lastly, in our busy January we closed a follow on offering with net proceeds of approximately $130 million providing us with funds to support the Company into the second half of 2017.

So next what I’d like to do is provide a brief update of the first two of our product candidates in our emerging Hematology franchise. To begin, sotatercept and ACE-536 are derived from the receptors ActR2A and ActR2B respectively. Both products promote the increased production of red blood cells by stimulating the production of late stage red blood cell precursors. This is in contrast with erythropoietin which stimulates the production of early stage red blood cell precursors. Importantly as you’ll hear later, sotatercept has additional capacity to stimulate bone formation. We’re studying both sotatercept and ACE-536 in beta-thalassemia and MDS syndromes because the anemias in these diseases are characterized by the impairment of late stage red blood cell maturation, which is precisely the stage of red blood cell development positively affected by sotatercept and ACE-536.

So before I go and summarize our recently presented data and because we have so many ongoing studies with product candidates in multiple indications, I would like to first get us all on common ground by taking a few moments to discuss thalassemia and how the disease is currently treated. Beta-thalassemia is a hereditary hematologic disease in which patients' red blood cells fail to mature into healthy functional cells and consequently patients are anemic. This particular type of anemia also causes these patients to experience significant co-morbidity.

There are about 40,000 patients in the U.S. and EU with beta-thalassemia and approximately 300,000 worldwide with no approved or effective drug therapy. The underlying defect in this disease is typically due to decreased production of beta globin protein, one of the two globin proteins that comprise hemoglobin. Decreased production of beta globin leads to a relative excess of the unpaired alpha globin gene which accumulates in red cells and impairs red cell maturation, resulting in cells with abnormal shake that can lead to thrombosis, leg ulcers and the need for splenectomy. These are some of the co-morbidities as I mentioned earlier.

Importantly we have shown in preclinical model the ACE-536 treatment prevents the accumulation of alpha globin, stimulates the maturation of red cells and dramatically improves red cell shape. Indeed it was this data that first garnered the attention of KOLs.

Now individual beta-thalassemia patients produce various amounts of beta globin. The most anemic patients produce the lowest amounts of beta globin and require regularly scheduled transfusions for survival. Typically these patients are transfused every two to three weeks with two units of blood. Transfusion takes several hours at least to an increase in hemoglobin of about 2 grams per deciliter. These patients are referred to as transfusion dependent patients. About half of all thalassemia patients are transfusion dependent. While the transfusion control their anemia and some of the complications caused by this anemia, the transfused red cells contain high amounts of iron which leads to iron overloading, following 10 transfusions or 20 units of blood, typically in just one to two years.

So iron overload is the key driver of mortality in these patients and to treat this iron overload, patients receive an iron chelation therapy which can cost from $24,000 to $40,000 per year. And the most widely used iron chelator is EXJADE with 2013 sales of nearly $1 billion.

Now, with our products we expect to improve the anemia without inducing the iron overload, providing a major advantage for these transfusion dependent patients. Now, patients with higher levels of beta globin expression require infrequent or no transfusions and are referred to as non-transfusion dependent patients and constitute the other half of all thalassemia patients. So it’s important to note while these patients do not require regular transfusions for survival, they typically have hemoglobin levels in the range of 6 grams to 8 grams per deciliter or about half the hemoglobin level of normal individuals.

Nevertheless many of these patients in the physicians choose not to subject patients to the burden of regular transfusion therapy, which can rapidly lead to iron overload and the need for iron chelation therapy. Without any correction of their anemia, these patients typically develop numerous comorbidities, including enlarged spleen, thrombosis, leg ulcers and pulmonary hypertension. And these often present sicker patients than those who are transfusion dependent. So, despite few or no transfusions, these patients develop iron overload in their late 20s due to dis-regulation of iron uptake induced by the failure of their red blood cells to mature. So for all these reasons, I think you can see there is a clear and significant unmet medical need in these non-transfusion dependent patients.

And importantly, we expect our product candidates to improve both the anemia and the comorbidities caused by this ineffective erythropoiesis of late stage red blood cells without inducing iron overload, thereby providing a major advantage for these transfusion dependent patients.

Now, I would like to remind you that our ongoing beta-thalassemia studies have included transfusion dependent and non-transfusion dependent patients. So for today I'll provide a summary of our interim data from the non-transfusion dependent patients.

But at EHA in June, we expect to present data from transfusion dependent beta-thalassemia patients showing a decrease in the frequency of red blood cell transfusion. At ASH this past December, we and Celgene reported data from the Phase 2 clinical trial of sotatercept in non-transfusion dependent beta-thalassemia patients. The study is an open label dose finding study to determine the safety and efficacy of sotatercept. Patients received one of three dose levels, 0.1, 0.3 or 0.5 mg/kg administered subcutaneously once every three weeks.

Celgene presented interim data demonstrating dose dependent increases in hemoglobin across the three dose levels. Sotatercept is well tolerated by all dose groups. Indeed data from the 0.3 mg/kg cohort was available out through the first nine months and showed sustained increase in hemoglobin, with no adverse events greater than grade one.

Furthermore increases of hemoglobin of at least 1 gram to 2 grams per deciliter were observed in nearly all the patients at the 0.3 and 0.5 dose levels. The goal in these non-transfusion dependent patients is to achieve clinically significant increases in hemoglobin of 1.5 to 2 grams per deciliter. These data from the lower dose groups indicate that we are approaching our goal. The plan is to continue to dose escalate until patients experience true rapid decline in hemoglobin or dose-limiting side effect. So to this end Celgene has begun enrolling patients in the fourth cohort of patients dosed at 0.75 mg/kg.

This approach will provide us an effective dose range to use in the next part of our study which we refer to as the expansion phase. In the expansion phase, we begin treating patients with the lowest effective dose level and as needed for each patient, escalate their dose level to achieve the target hemoglobin increase.

In other words, each patient’s dose level will be titrated as we treat to a therapeutic effect. We expect to have two to three dose levels and start this dose expansion phase of the study by mid-year. I remind you in addition of sotatercept, we are also studying ACE-536 in patients with beta-thalassemia in a similar study.

We've completed enrollment of the first three cohorts and reported preliminary data at 0.2, 0.4 and 0.6 mg/kg, which demonstrate dose dependent increase in hemoglobin levels in non-transfusion dependent patients. At the 0.6 mg/kg dose level we observed a hemoglobin increase of 1.5 grams per deciliter after only three doses or nine weeks of treatment.

We recently completed enrollment of patients and the next dose cohort of 0.8 mg/kg and we have begun enrolling patients in the 1.0 mg/kg dose group. The study is ongoing and we plan to report an interim data with ACE-536 at EHA in June. We expect to present additional interim data from the non-transfusion dependent patients as well as data from the transfusion dependent patients. Importantly, in transfusion dependent patients enrolled to-date, preliminary data show an increase to a decrease in the frequency of red blood cell transfusions. We’ll provide additional detail on these patients at EHA in June. As I mentioned previously we and Celgene have a goal to initiate Phase 3 study in beta-thalassemia by the end of this year or early next year.

Let me briefly now turn to our studies in MDS patients. Phase 2 clinical trials for ACE-536 are ongoing in low to intermediate risk MDS patients. Interim data indicates that there is a positive effect on hemoglobin levels in these patients and we look forward to presenting data from both transfusion dependent and non-transfusion dependent MDS patients at EHA in June.

Now I’d like to turn back again to sotatercept to discuss our ongoing study in patients with end-stage renal disease. Now these patients experience both anemia and significant bone loss. Because of its demonstrated effects on red blood cell production and bone formations, sotatercept is well positioned to correct both the red cell and bone deficits in these patients. Because I haven’t talked about the study in the past I'd like take a few moments to summarize the disease.

Chronic kidney disease or CKD is a serious condition with over 400,000 patients in the U.S., characterized by the progressive loss of kidney function. End-stage renal disease or ESRD is the most advanced stage of CKD in which patients require either kidney transplant or dialysis for survival. Indeed the one year mortality rate exceeds 20%.

Anemia is a common secondary disorder in CKD patients and worsens with progression of the disease. A disturbance in mineral bone metabolism known as chronic kidney disease, mineral and bone disorder or CKDMBD effects almost all patients who are on dialysis. CKDMBD can lead to bone abnormalities and or calcification of blood vessels and is associated with increased morbidity and mortality in CKD patients.

We’ve previously shown that sotatercept treatment in healthy volunteers associated with increases in a bone formation biomarker. Serum levels of the bone formation biomarker bone specific alkaline phosphates or BSAP has exhibited rapid and sustained increases after sotatercept administration. Conversely the mean levels of the bone absorption marker C-terminal telopeptide or CTX decreased in subjects treated with sotatercept.

Sotatercept also dosed dependently increased bone mineral density or BMD of the total hip compared with a decrease in the placebo group. So for these reasons Celgene decided to conduct a Phase 2a study with sotatercept, designed the randomized placebo controlled dose escalation study to examine the PK/PD safety and efficacy of sotatercept for the correction of anemia in patients with ESRD and hemodialysis.

Early data from this trial are encouraging and interim analysis indicates that sotatercept produces dose dependent increases in hemoglobin and ESRD patients on hemodialysis. The data will be presented at the National Kidney Foundation Meeting in April. Based on the positive data from the Phase 2a study Celgene initiated a Phase 2b study in December designed as a two part study to assess sotatercept as a therapy to treat anemia and to potentially control the adverse amount of patients of CKDMBD.

The first part of the Phase 2b trial is a dose escalation study of intravenous and subcutaneous roots of administration of sotatercept and approximately 60 patients to evaluate the PK safety tolerability and effects on hemoglobin levels and bone biomarkers. The second part of the Phase 2b study is a randomized control study of approximately 230 patients to evaluate the efficacy and safety as sotatercept versus erythropoietin to increase and maintain hemoglobin levels, Measures the vascular calcification as well as bone biomarkers would also be studied in the second part of this study.

So now I'd like to turn to our third product candidate in Phase 2 clinical trials Dalantercept, which is a novel anti-angiogenesis product candidate designed to inhibit blood vessel formation in tumors by blocking signaling of the Activin Receptor-like Kinase 1 or ALK 1.

We focused on blocking signaling of this receptor because patients with the single defective ALK1 gene, known as Hereditary Hemorrhagic Telangiectasia or HHT2 have reduced the ability to regenerate the capillary bed following an injury. The results from our Phase 1 clinical trial of Aalantercept in adults with solid tumors were published in January in clinical cancer, research showing that Aalantercept exhibited a safety profile distinct from that of VEGF inhibitors and displayed multiple signs of anti-tumor activity.

We’re developing Aalantercept to treat cancer primarily for the use in combination with VEGF pathway inhibitors, where there remains a significant unmet need to more fully inhibit angiogenesis and produce better outcomes for these cancer patients. Support for this idea is found in our preclinical studies where we've demonstrated an additive and potentially synergistic effect of combining inhibitors of these two pathways.

We are currently testing Aalantercept in a Phase 2 study with the VEGF inhibitor, axitinib in patients with renal cell carcinoma who have failed the prior anti-VEGF therapy. In part one of this two part trial, we have completed enrollment of the dose escalation groups and now enrolling patients in the expansion cohort at our selected doses. We expect to provide an update on our interim data on the dose escalation stage of this ongoing trial at ASCO in early June.

Part two of the study will be a randomized comparison of Dalantercept, in combination with axitinib versus axitinib alone. The primary endpoint of Part 2 of the trial will be progression free survival. At the end of Q1, we expect to initiate part two of the study and provide an update on the dose escalation phase of the study. We also plan to initiate an ascending dose study of Aalantercept in combination with sorafenib in patients with first line hepatocellular carcinoma in the first half of 2014.

The primary endpoint of this trial will be safety and tolerability; secondary endpoints include time to progression, progression free survival, disease control rate and overall survival. So, as you can see the remainder of 2014 will be important for us as we expect to share Phase 2 data from all our clinical candidates in the first half of this year.

Now, I'd like to turn the call over to Kevin McLaughlin, our CFO.

Kevin McLaughlin

Thanks, John. I am pleased to report that Acceleron is in a very strong financial position with enough cash to fund our planned clinical programs and operations into the second half of 2017. Our reported cash balance at the end of the year was $113 million. This cash balance includes a $96 million in net proceeds from our September initial public offering and a December payment from Celgene of $7 million for the initiation of a Phase II clinical trial with sotatercept in end stage renal disease patients. Including the net proceeds of our $129 million offering in January 2014, Acceleron's pro-forma cash balance at the end December 2013 would have been $242 million.

Before we open up the all for Q&A, I'd like to remind you again that the Phase 2 data that we expect to present over the next four to five months, end-stage renal disease in April at the National Kidney Foundation Meetings, beta-thalassemia and MDS at the June EHA Meeting, renal cell carcinoma in June at ASCO; and in the second half of this year, we plan to initiate a Phase 1 clinical trial with ACE-083, a locally acting agent designed to increase muscle mass and strength. Lastly, we are very excited to begin the Phase 3 clinical trial in beta-thalassemia patients by the end of the year or the beginning of next year.

We will now open up the call for Q&A. Operator?

Question-and-Answer Session


Thank you. We will now begin the question-and-answer session. [Operator Instructions] Our first question comes from Yaron Werber of Citi. Your line is now open.

Unidentified Analyst

This is Chris in for Yaron. I had a couple of questions. One on beta-thalassemia, I know you touched on this earlier in the call. Can you comment over your assumptions for the transfusion dependent market and what percentage of patients you think you might be able to get? You mentioned that the preliminary data showed a decrease in the frequency of red blood cell transfusions. What do you think you need to show there to actually treat those patients and do you think there is certain transfusion dependent patients that don’t produce enough beta globin that would not be eligible? And then second question was, can you comment on the status of the sickle cell and Diamond-Blackfan anemia programs? Are those still something you're interested in pursuing?

John Knopf

So, Steve take the first part of the question and then Matt can take the second part of the first question and I will address the sickle cell and DBA. Steve, could you go ahead?

Steven Ertel

Sure. This is Steve Ertel. So, we believe there are roughly 40,000 beta-thalassemia patients in the U.S. and Europe. About half of all those patients are transfusion dependent patients. And roughly speaking, about half of those patients, we believe would produce levels of beta globin that would be an appropriate sub-population for us to target in the transfusion dependent sub-segment. Now, in terms of degree of an effect that we would like to see in the transfusion dependent patients, why don’t I let our Chief Medical Officer, Matt Sherman answer that part of the question.

Matt Sherman

Chris, this is Matt. So, in terms of the patients that are transfusion dependent, we are very excited about the data that we have so far. We see decreases in the frequency of transfusions. And we look forward to designing Phase 3 trials that will be able to demonstrate the effect that will be meaningful for patients.

John Knopf

And we will update you little bit more on the study in the transfusion dependent patients at EHA but we did want to give you a sense of where we’re headed on the type of data we are seeing. In terms of the last part of the study, the DBA study is ongoing. Again it is a very rare disease with perhaps as few as a thousand patients in – of the patient population but nevertheless it’s ongoing. In terms of sickle cell, we are interested in pursuing in sickle cell because – I think I may have mentioned this earlier that we are able to demonstrate with ACE-536 that we are able to aid the cell’s ability to get rid of mis-folded alpha-globin protein which is unstable in these beta-thalassemia patients. And with that in mind, our thought is that perhaps we would also be able to red cells and getting rid of the mis-folded sickle protein as well. And so for those reasons, we initiated some preclinical studies. There is an excellent preclinical model that really recapitulates many of the aspects of the human disease. Those preclinical studies are ongoing and we expect to present data from the sickle cell study at EHA in June.


Thank you. Our next question comes from Marko Kozul of Leerink Partners. Your line is now open.

Unidentified Analyst

This is Irene in for Marko. First sotatercept, in the end-stage renal disease patient, can you talk a little bit about qualitatively what we could expect from the National Kidney Foundation presentation in April on Part A of the study and maybe a little bit about biomarkers that you are exploring in the second part of the study? Thank you.

Matt Sherman

This is Matt Sherman. So In terms of data that will be presented at the National Kidney Foundation, what we have said is that we've seen dose dependent increases in the hemoglobin. And that's what -- we'll be elaborating that actually at the meeting itself in the poster that will be presented.

In terms of biomarkers that we also are considering in these studies, these are biomarkers both on the bone metabolism and ultimately on vascular calcifications. So, importantly as we've demonstrated previously in our studies with sotatercept, we can show increases in bone formation marker, bone-specific alkaline phosphatase as well as a decrease in the bone resorption marker CTX. And so that delta between those two lead to increased bone formation and indeed we have shown increases in bone density previously by DEXA scan. So these will be some of the bone biomarkers that will be incorporated in the ongoing trials as well as additional markers on vascular calcification.


Thank you. Our next question comes from Ted Tenthoff of Piper Jaffray. Your line is now open.

Ted Tenthoff - Piper Jaffray

I just wanted to clarify and I apologize if this has been answered. The data that you're going to be showing in April that Jim will be reporting in CKD, that’s the Phase 2A data and they have already started a larger Phase II study, is that correct?

Matt Sherman

This is Matt. Yes, that’s correct. So, the data that will be presented at the National Kidney Foundation meeting is from the ongoing Phase 2a study and that initiates a dose ranging study. The study that has been initiated -- that was initiated in December as a Phase 2b study and that is a larger study that is ongoing.

Ted Tenthoff - Piper Jaffray

And when do you think we might get data from that study?

Matt Sherman

Yes, that’s really a vast, very robust study. So it could be a couple of years. That’s for these two parts initially a dose ranging part, which is looking at both IV and subcutaneous dosing and that’s going to comprise approximately 60 patients. And following that there will be a selection of two of those cohorts to move into a randomized active control study comparing it to EFA and that is nearly 230 patients. So, part two will follow part one. So, data from this study overall, might be a year or two.

John Knopf

This is John Knopf. There is a possibility certainly of presenting some interim data from the 2a part of the study. We'll have to see how rapidly this study accrues and again it’s up to Celgene as to what meeting they would like to present this data. But at this point we don’t really have any immediate plans.


Thank you. And our next question comes from Mike King of JMP Securities. Your line is now open.

Mike King - JMP Securities

A couple of questions. I wanted, JK you didn’t mention anything about the study of Aalantercept with bevacizumab. So, I was wondering is that a 2014 item?

Matt Sherman

Hi Mike, this is Matt, I will take that question. Yes, so we do also plan to initiate a study of Aalantercept in combination with bevacizumab in patients with glioblastoma. And this could be a study in a previously untreated – of bev-naïve patients I should say, combining Aalantercept with bev [ph] in those patient populations. And we expect that we will initiate that study by the end of 2014.

Mike King - JMP Securities

And then on coming back to sotatercept in the transfusion dependent population, I'm just trying to look back at my notes here but correct me again if I am wrong; but you did say that data in that population would be expected at EHA?

John Knopf

Yes, so Celgene representing on sotatercept at EHA, that’s correct.

Mike King - JMP Securities

In the beta-thal transfusion dependent?

John Knopf

Yes, in both the dependent and independent, yes.

Mike King - JMP Securities

Right. So, specifically about transfusion dependent, can we get a little bit of color on where you are dose wise and can you say at least qualitatively. You said you are seeing but I just wonder if you can say to qualitatively, where you are, relative to the independent patients as far as transfusion is concerned.

John Knopf

Sure, actually today the focus was of the presentation was on ACE-536 and on ACE-536 again we talked about showing a decrease in the transfusion frequency, with ACE-536 in the transfusion dependent patients. And Mike as you know, on ASCO we really have to -- we don’t want to jeopardize -- the ETA. I'm sorry, EHA, we don’t want to jeopardize our opportunity to present this data. So we’re only summarizing in this way. But you’ll get much more detail in June and again we’re excited to be able to report that we’re seeing decreases in transfusion frequency.

The other one I could add to this Mike as again, remember we reported data on the 0.6 mg/kg group, where we showed [indiscernible] deciliter increase. We have since gone on and completed the enrollment of the next cohort at 0.8 mg/kg. And then lastly we have just initiated dosing now in the 1.0 mg/kg dose group. So we've gone two cohorts further than the 0.6, where we saw the 1.5 gm per deciliter increase. So I hope that gives you some sense as to where we are from a dosing perspective.

Mike King - JMP Securities

And then just on with regards to sotatercept in CKD, is there any contemplation for trials in pre-dialysis patients at all?

John Knopf

Matt you want to take that?

Matt Sherman

At this time no. At this time the study that is on-going nearly 300 patient study and patients that are on hemodialysis.

Mike King - JMP Securities

And then just as far as the hemodialysis end-point is concerned Matt, the approvable end-point is what; increasing hemoglobin or reduction in transfusion or some combination?

Matt Sherman

We just don’t know yet what the approval end-point will be for Phase 3 study. This Phase two study will give us an estimate of the treatment effect. So from here we’ll move on to planning a Phase 3 study.

Mike King - JMP Securities

And you are measuring the quality of life at all in Phase 2b?

Matt Sherman

Yes we are.


Thank you. [Operator Instructions]. I'm showing no further questions at this time.

John Knopf

Great. Well thank you everyone for your attention today and listening to our update.


Thank you sir. Ladies and gentlemen thank you for participating in today’s conference. This does conclude today’s program. You may all disconnect. Everyone have a wonderful day.

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