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Ladies and gentlemen welcome to the Arrowhead Pharmaceuticals' Conference Call. Throughout today's recorded presentation, all participants will be in a listen-only mode. After the presentation, there will be an opportunity to ask questions.
I will now hand the conference call over to Vincent Anzalone, Vice President of Investor Relations for Arrowhead. Please go ahead Vince.
Thanks Lauren. Good afternoon everyone. Thank you for joining us today to discuss Arrowhead's Results for its Fiscal 2019 First Quarter ended December 31, 2018.
With us today from management are President and CEO, Dr. Christopher Anzalone, who will provide an overview of the year; Dr. Bruce Given, our Chief Operating Officer and Head of R&D, who will discuss our clinical programs; and Ken Myszkowski, our Chief Financial Officer, who will give a review of the financials. We will then open up the call to your questions.
Before we begin, I would like to remind you that comments made during today's call contain certain forward-looking statements within the meaning of Section 27A of the Securities Act of 1933 and Section 21E of the Securities Exchange Act of 1934.
All statements other than statements of historical fact, including without limitation, those with respect to Arrowhead's goals, plans, and strategies are forward-looking statements. These include statements regarding our expectations around the development, safety and efficacy of our drug candidates, projected cash runway, and expected future development activities.
These statements represent management's current expectations and are inherently uncertain, thus actual results may differ materially. Arrowhead disclaims any intent and undertakes no duty to update any of the forward-looking statements discussed on today's call.
You should refer to the discussions under Risk Factors in Arrowhead's annual report on Form 10-K and the company's subsequent quarterly reports on Form 10-Q for additional matters to be considered in this regard, including risks and other considerations that could cause actual results to vary from the presently expected results expressed in today's call.
With that said, I'd like to turn the call over to Christopher Anzalone, President and CEO of the company. Chris?
Thanks Vince. Good afternoon everyone and thank you for joining us today. 2018 was a very productive year for us, a year ago we were preparing to start first-in-human clinical studies for the first two candidates built on the TRiM platform, and today there are five candidates either in or approaching the clinic. ARO-HPV against chronic hepatitis B infection is in a phase 1-2 study and is partnered with Janssen. ARO-HPV will now be referred to as JNJ 3989. The second candidate is ARO-AAT against a rare genetic liver disease associated with alpha-1 antitrypsin or AAT deficiency, which has completed the phase 1 study.
We are actively working with the FDA to get feedback on potential endpoints and design of our next study. The third candidate is AMG 890 against cardiovascular disease and is partnered with Amgen. Amgen is evaluating AMG 890 in a phase 1 study to assess safety, tolerability, pharmacokinetics and pharmacodynamic effects. The fourth candidate is ARO-ANG3 against dyslipidemia in the phase 1 study in healthy adult volunteers, and dyslipidemic patients. And the fifth candidate is ARO-APOC3 against hypertriglyceridemia. I am pleased to announce that we have received ethics approval and now we wait for regulatory feedback on our planned first-in-human phase 1 study of ARO-APOC3. We are preparing to begin the trial rapidly, once all necessary approvals have been received.
That is impressive progress to go from 0 to 5 clinical programs all built on the TRiM platform in just 12 months. In fact we have exceeded virtually all the aggressive development goals that we set in 2018, and I believe that we are fastest and most innovative company in the RNAi field. As productive as 2018 was, 2019 has the potential to be even more so.
Let’s talk about some of our goals and expectations for calendar 2019, they are one, complete dosing and report data from the phase 1 study of the ARO-ANG3; two, complete dosing and report data from the phase 1 study ARO-APOC3; three, present additional phase 1-2 data from JNJ 3989 formally ARO-HPV. To that end, we already have accepted presentation at the Asian Pacific Association for the Study of the Liver Meeting in February and the EASL International Liver Congress in April, and we expect additional abstracts to be submitted throughout the year. Note that the abstracts use the name of the compound JNJ 3989 rather than the older name ARO-HPV. Four, begin a phase 2 study or studies of ARO-AAT and we hope to provide clarity on the potential path commercialization. Five, file a CTA for our first inhaled pulmonary program ARO-ENaC against cystic fibrosis. Six, file a CTA for our first solid tumor program ARO-HIF2 against renal cell carcinoma. Seven, discuss additional programs we’re developing using the TRiM platform. And eight, we also anticipate that Amgen may share initial clinical data on AMG 890 later this year or in early 2020.
This is a lot in a short amount of time, but Arrowhead has a proven track record of accomplishing what we set out to do. It also speaks to the growing maturity of the TRiM platform. To review the TRiM platform is built around structurally simple conjugates that utilize ligand-mediated delivery and stringent bioinformatics. The TRiM platform also offers several potential competitive advantages including a sophisticated RNAi trigger selection in screening process that identifies potent sequences rapidly and locations that RNAi competitors may miss.
Multiple routes of administration, including subcutaneous, intravenous, and inhaled, potentially faster time to clinical candidates, optimized pharmacologic activity, and long duration of effect allowing infrequent dosing, potentially wide safety margins, simplified manufacturing at reduced cost, and the promise of taking RNAi to tissues beyond the liver, which will represent a big leap forward for the field and substantial competitive advantage for Arrowhead. The data that we presented at the AASLD Liver Meeting in November 2018 for our first two TRiM enabled candidates ARO-AAT and ARO-HBV have been very encouraging. They are both proving to be potent molecules with a long duration of affect. For example, three monthly doses of 300 milligrams of ARO-AAT led to reductions in serum alpha-1 antitrypsin to below the level of quantitation in 100% of subjects. These reductions were sustained for greater than 14 weeks, indicating that quarterly or less frequent dosing appears feasible.
ARO-HBV achieved a mean reduction in S antigen of 1.9 logs or 98.7%, with a range of 1.3 logs or 95% to 3.8 logs or 99.98%. In addition, ARO-AAT and ARO-HBV appear to be well tolerated at all doses tested. This bodes well for these candidates and potentially for the rest of our TRiM enabled pipeline.
With that overview, I’d now like to turn the call over to Bruce Given. Bruce?
Thank you, Chris. Good afternoon everyone. Since we are just starting the clinical program for ARO-ANG3 and ARO-APOC3, I want to spend some time describing these candidates and the current clinical studies. Despite all of the progress with cardiovascular drugs over the past years and decades, atherosclerotic cardiovascular disease remains a major cause of death. While the current standard of care is effective at lowering LDL cholesterol in the vast majority of patients, large well run trials continue to show substantial unmet medical needs for risk modifying therapies with novel mechanisms of action.
Hypertriglyceridemia and elevations in triglyceride bridge lipoproteins have been shown to be important cause of risk for otosclerosis independent of LDL cholesterol. Elevated triglycerides can lead to highly dangerous pancreatitis, may participate in hepatic steatosis that are seen in metabolic syndrome. Metabolic syndrome is a complex and inter-related risk factors for cardiovascular disease in type II diabetes mellitus.
Let’s start with ARO-ANG3, ARO-ANG3 is subcutaneously administered RNAi therapeutic targeting angio poietin-like protein 3 or ANGPTL3, being developed as a potential treatment for patients with dyslipidemia as in metabolic diseases. ANGPTL3 has emerged as an important regulator of plasma lipoprotein levels including triglycerides, LDL cholesterol, high density in lipoprotein cholesterol and very low density lipoprotein cholesterol by inhibitions of enzymes including lipoprotein lipase and endothelial lipase. ANGPTL3 may also be involved in regulating apolipoprotein B particle containing synthesis and hepatocyte clearance of LDL cholesterol and this important through mechanisms independent of low density lipoprotein receptor. This feature of LDL receptor independence is potentially very important and makes ANGPTL3 inhibition potentially novel and interesting as a therapeutic on the LDL receptor deficient hypercholesterolemic patients.
Intrahepatic targeting of ANGPTL3 may also improve hepatic steatosis, which can progress to nonalcoholic steatohepatitis or NASH. Human genetic studies indicate that ANGPTL3-deficient homozygotes show lower serum insulin, lower serum glucose, and improved measures of insulin resistance compared to non-carriers. Given how often atherosclerotic cardiovascular disease and diabetes intersect, these effects have seen with ARO-ANG3 will be welcome.
Our first-in-human study, ARO-ANG1001 is a phase 1 single and multiple dose study to evaluate the safety, tolerability, pharmacokinetic and pharmacodynamics effects of ARO-ANG3 in up to 70 adult healthy volunteers with elevated triglycerides and various types of dyslipidemic patients. The single-ascending dose portion of the study is designed to include up to four cohorts of 10 adult healthy volunteers per cohort. Each SAD subject will receive a single-dose administration of either placebo or ARO-ANG3 at dose levels of 35, 100, 200, or 300 mg. The multiple-dose portion is designed to include up to four patient cohorts, including patients with non-alcoholic fatty liver disease or NAFLD, patients on a stable statin treatment regimen with elevated LDL cholesterol and triglycerides, patients with heterozygous or homozygous familial hypercholesterolemia, and patients with severe hypertriglyceridemia.
The MAD cohorts will receive two monthly doses of ARO-ANG3. ARO-APOC3 is Arrowhead’s subcutaneous administered RNAi therapeutic targeting Apolipoprotein C-III, better known as apoC-III being developed as a potential treatment for patients with hypertriglyceridemia. APOC3 has emerged as a therapeutic target for triglyceride reduction. APOC3 is a regulator of triglyceride rich lipoproteins or TRLs and is presents in TRLs. APOC3 is a known inhibitor of lipoprotein lipase or LTL and LDL mediator lipolysis of these TRLs. APOC3 also delays clearance of lipoproteins remnants by the liver by inhibiting hepatocytes receptive mediated uptick.
Inside gains from transgenic mice over expressing APOC3 and APOC3 knockout mice has shown that APOC3 delays very low density in lipoprotein cholesterol hydrolysis in vivo and may delay the removal of TRL remnants. Human genetic studies indicate that APOC3 deficient heterozygous show reduction in plasma triglycerides and LDL cholesterol levels. Risk for cardiovascular disease in these carriers was reduced as well. APOC3 deficient individuals or homozygous do not demonstrate a significant hepatic steatosis and appear to be phenotypically normal. Familial chylomicronemia syndrome or FCS is a severe rare genetic disease with a prevalence of one in a million often caused by various monogenic mutations leading to extremely high triglyceride levels typically over 900 mg/dL representing the top 0.1% of the population. Such severe elevations lead to various signs and symptoms including acute pancreatitis which could be fatal, chronic daily abdominal pain, type II diabetes mellitus, hepatic steatosis and cognitive issues.
There is no currently available therapy that could be adequately used to treat FCS. Our first-in-human study of ARO-APOC3 is quite similar in design to that of ARO-ANG3. ARO-APOC3 1001 is a phase 1 single and multiple dose study to evaluate the safety and tolerability pharmacokinetics and pharmacodynamics of ARO-APOC3 up to 63 adult healthy volunteers with elevated triglycerides in patients with severe triglyceridemia and FCS. The single ascending dose portion of the study has decided to included up to four cohorts of 10 adult healthy volunteers per cohort, each (inaudible) to receive a single dose administration of either placebo or ARO-APOC3 at doses of 25, 50, 100, or 200 mg.
The multiple dose portions is designed to include up to three cohorts of patients with severe hypertriglyceridemia and one cohort in patients with FCS. The MAD cohorts will receive two monthly doses of ARO-APOC3. Consistent with our first-in-human studies we’ve designed ARO-ANG1001 and ARO-APOC3 1001 to give us readout on safety and tolerability as well as a robust look at the pharmacologic activity and duration of effect. We are planning to measure ANGPTL3 and APOC3 levels as well as LDL cholesterol, total cholesterol, non-HDL cholesterol, HDL cholesterol, BLDL cholesterol, triglycerides, liver fat content using magnetic MRI PDFF in one H3 cohort and other measures of drug activity.
I also want to touch briefly on the status of ARO-AAT, ARO had second generation subcutaneously administered RNAi therapeutic been developed as a treatment for a rare genetic liver disease associated with alpha-1 antitrypsin or AAT deficiency. We are currently interacting with the FDA on that program. Keep in mind that to our knowledge there has never been a drug to treat AAT related liver disease in front of the FDA, so they’ve never had the opportunity to considering a proof of pathway. We had a pre-IND meeting with them in October and our discussion since then have been helpful and productive. We’ve discussed ideas on potential designs and end points which they are considering. We have completed the required long term toxicology studies and the study reports necessary for submission are now available as well. So our intention is to move forward with a phase 2 clinical study or studies as soon as we have clarity on the FDA’s thinking around end points. Our hope is that the next study or studies maybe able to become pivotal and provide a path to potential commercialization but we do not have clarity on that yet.
With that brief review of our clinical programs, I’d like to turn the call over to Ken Myszkowski, Arrowhead’s Chief Financial Officer. Ken?
Thank you Bruce and good afternoon everyone. As we reported today our net income for the quarter ended December 31, 2018 was $12 million or $0.13 per share, based on 95.6 million fully diluted weighted average shares outstanding. This compares with a net loss of 13.2 million or $0.18 per share based on 74.8 million weighted average shares outstanding for the quarter ended December 31, 2017. Revenue for the quarter ended December 312. 2018 was 34.7 million compared to 33.5 million for the quarter ended December 31, 2017. Revenue in the current period relates to the recognition of a portion of the upfront payments received from our license and cooperation agreements with Janssen, while revenue in the prior period related to the recognition of a portion of the upfront payments received from our license and collaboration agreement with Amgen.
Revenue from the Janssen agreement will be recognized based on our estimate of the proportion of efforts expanded towards fulfilling our performance obligations, primarily overseeing the completion of the current phase 1-2 HBV clinical trial. We expect a majority of the revenue to be recognized in this fiscal year, while we also expect revenue in fiscal 2020, as we will continue to perform certain follow-up activities through 2020.
Total operating expenses for the quarter ended December 31, 2018 were 23.7 million compared to 17.3 million for the quarter ended December 31, 2017, this increase is primarily due to increased drug manufacturing and political trial cost as a pipeline of clinical candidates has increased. Net cash provided by operating activities during the quarter ended December 31, 2018 was a 168.3 million compared with net cash used in operating activities of 14.7 million, during the quarter ended December 31, 2017. The key driver of this change was the 175 million upfront payments from Janssen during the quarter.
Excluding cash inflow, our cash burn for the quarter was higher than in previous recent quarters as we paid off a note payable in the amount of 2.3 million during the quarter. We estimate our near-term cash burn to average 20 million per quarter. Turning to our balance sheet, our cash and investments totaled 303.3 million at December 31, 2018, compared to a 76.5 million at September 30, 2018. The increase in our cash and investment was primarily due to the cash received from Janssen. Our common shares outstanding at December 31, 2018 were 92.6 million.
With that brief over view, I will now turn the call back to Chris.
Thanks Ken. I mentioned at the beginning of the call that 2019 could be even more productive than 2018, and I view a few primary areas driving that. First, we expect the ARO-ANG3 and ARO-APOC3 to create a lot of value this year. These are attractive targets that address a number of high value unmet medical needs and we are the first to use RNAi against them. Importantly, we expect to generate a substantial amount of data across several patient groups this year, and I believe that we will have a good idea if ARO-ANG3 and ARO-APOC3 can become drugs by the third or fourth quarter.
I expect this year the current studies will generate the type of data that people are used to seeing from small molecule candidates at the end of phase 2b studies. These will be important readouts and as we did with ARO-AHC and ARO-HBV last year, we will look to report data at appropriate conferences. ARO-AAT and ARO-HBV were value drivers for us in 2018 and I hope to see ARO-ANG3 and ARO-APOC3 producing similarly for us this year. Depending upon what patient population we chose to focus on, we could have a rapid (inaudible) to pivotal studies.
Second, we are not finished generating and reporting data from the ARO-HBV 1001 clinical study. Patients will continue to be monitored for one year post last dose. ARO-HBV was very active in all patient study and we look forward to seeing that even short term dosing can have longer term beneficial effects. I expect that we’ll continue to report data throughout 2019.
Third, we expect to begin phase 2 studies in ARO-AAT this quarter and are hopeful that these may become pivotal. As we discussed, we are in active discussions with the regulators and beginning studies with agreed upon design and end point could be a substantial value driver.
Fourth, we expect to file CGA’s for ARO-ENaC and ARO-HIF2 this year, representing what we believe to be the first commercially viable efforts to use RNAi outside the liver. This is a large leap forward for the field and an important strategic step for Arrowhead. And finally you can never discount Arrowhead’s great view potential. We have consistently shown breakthrough speed and innovation that we believe is best in the field and I expect this to continue.
We disclosed our analyst day in the fall that we can now target muscle cells and I believe that unexpected breakthroughs will continue to be our hallmark and continue to build value for our shareholders. As I said, I expect 2019 to be a big year for us. We are well on our way towards achieving our long term goals to file two to three new CTAs every year, target a new cell type with the TRiM platform every 18 months and have 10 TRiM enabled candidate in clinical studies by the end of 2020.
Thanks again for joining us today and I would now like to open the call to your questions. Operator?
[Operator Instructions] our first question comes from Maury Raycroft with Jefferies. Your line is open.
I’ll start with ANG3 and APOC3, I may have missed this, but are you saying how many patients you are going to include in both of those studies and are you going to start dosing the patient simultaneously or are you going to start with the healthiest first and then move in to the patients?
Hi Maury, this is Bruce. As far as when we’ll start, I mean we’ll run through the normal volunteers first, especially for ANG-PCO3 world. We want to figure out the dose range before we move in to the patient groups. My recollection is that those cohorts are generally about 8 to 10 in number, I think may be 8 for (inaudible) or 10, again the 10 signal there. So it’s hard to keep all of these trials clear, but yes 10 per cohort.
And so you’ll include about 10 patients in each one of the study.
In each of those separate cohorts that we described.
And then as far as the timing goes, you mentioned even though whether you had to drive by 3Q or 4Q, but presumably you’re going to show us some sort of an update before then on the dose escalation. And so, is it going to be similar to with AAT and HBV disclosures where that could come at a medical conference or do you plan on top lining that for press release.
So we’ll see Maury. It is our hope that we can report data at American Hearts Association meeting in November of this year. So it our hope that we can submit our facts to that, but as you pointed out with AAT and HBV, we found some other smaller conferences before in those cases AASLD where we could give a little bit of an update on what we’re seeing. My hope is that we can those as well. I don’t know that we can, I don’t know the time of the workout, but it is my hope that we can do that similar to what we did with AAT and HBV.
And for the AAT study, looking forward to seeing that design, I guess for the end point discussion can you talk about what the considerations are or the options that are on the table that you’re discussing with the FDA?
I don’t really think I can. We continue to believe and I don’t see any reason not to believe that this is an indication that is going to require biopsies. But outside of that I think it’s premature really to say much anything else.
And I think we are - relatively speaking we are close to the point where we can talk about this in a more granular way. It is our hope that we will be filing an IND this quarter. So we’re not asking you to wait too long, but I think we can have better clarity later this quarter.
Our next question comes from Ted Tenthoff with Piper Jaffray. Your line is open.
Could you give an idea for a key study, how large will be the phase 2-3 and how soon do you anticipate we could get data from that study?
Ted this is Bruce. We don’t know the size yet, because it really depends quite a bit on the end points and some of the design parameters that we’re discussing. It’s one of those where the devil is in the detail if you will. So it won’t be a small study. Now AAT as orphans go is a large enough orphans disease to have a reasonable size study. So it will I think actually a landmark study in the field in all likelihood. But we’ll have to see where things in the end, end up to be – for me to be clear on that.
And is your goal still to start that in the first quarter and sorry Bruce didn’t mean to cut you off.
Yes, the goal is to – sorry about my first quarter, I was going to say your other question was about data timing. As Bruce says we’re still a little bit influx on end points and design and number of (inaudible). So we’re not ready to give guidance on data. But I can tell you this, it is highly unlikely that we will have any data this year; I don’t think that’s in the cards. But again we can give you better guidance once we have a set design. Obviously one of the things on the size of the trial and on our dosing or on enrollment. This is our second generation drug against AAT disease and so we have a good relationship with PIs here and in Europe. So I think that – I think that’s going to bode well for us when we look in general to study. We’ll also have a good relation with the Alpha-1 Foundation and they’re going to be I think a good help for us as we enroll the study.
And then just a quick kind of housekeeping on the revenue side, I know you had – from a balance sheet and cash position, a lot of money that came in from the JNJ partnership congrats on that. How do you anticipate recognizing revenues in the March and June quarter?
We’re recognizing a 197.8 million in total from the initial upfront payment which includes also the premium that we calculated on the stock as well as the drug supplies. So we’re estimating that the majority of this will be recognized over the rest of this fiscal year, but it definitely will go in to next year as well. And it will depend on our efforts as we monitor them throughout the next couple of quarters compared to our budgeted efforts on that and exactly how we’ll calculate the revenue --.
And that’s separate from the 50 million from – 50 million milestone.
That’s separate from that.
Our next question comes from Katherine Xu with William Blair. Your line is open.
I am just looking for the MAD for both Asia and the cardiovascular, why you’re doing just two monthly versus the three that you did before, and with just the two months dosing with Kinetics you can figure out real dosing or proposed dosing for the future. I’m curious about that. And then also another general question is on the RNAi agent in the US, so you guys including a lot of other people are doing the phase 1 outside the US and then kind of come back and open the IND’s here. Is it a practice that we’re going to continue to see or do you think that FDA would be more receptive for early stage RNAi study?
Well let me take the second one first, I wouldn’t characterize the FDA as unreceptive. I could really only speak for ourselves, but we have found Australia, New Zealand to be an excellent place to do these studies. It’s just a very clear sort of regulatory path that has been pretty consistent and predictable. So that has really worked well for us, and we have liked it. But others may have – I know that others have for instance tended to go to the UK, I don’t really know what their reasons are, you’d have to ask them, but for us it’s been a very straight forward path.
There are also frankly incentives that are offered in Australia that have been useful for us as well, especially early in our life cycle when having significant rebates on clinical costs were meaningful for us.
And Katherine let me add one thing to that, as you know , we have always followed the science in these clinical programs and the flexibility that we’ve seen in New Zealand and Australia and actually for HBV in Hong Kong has enabled us to follow that science quite rapidly. We’ve had a number of protocol changes with our studies just because we learned something new along the way and we’ve been able to get those things through quite quickly like in the order of one or two weeks. And if we are in United States, it takes substantially a little long than that. So that’s made a lot of sense for us and it’s been good for us then to generate all those data and then you go to the FDA for these discussions around AAT, because we go with an awful lot of data that we can talk about, and so I think that has facilitated really productive discussions because we have a substantial amount of data to talk about.
Let me Katherine go ahead and answer your first though. So we had initially designed the programs to be three doses, just like we had done for AAT and HPV and then as we really had a chance to collect all this data in the AAT program and live with that data, we recognized that we would actually had been better off to do two doses and be able to follow that second dose out for a really good shot at understanding duration of effect and dosing frequency.
It’s becoming impaired to us that it’s likely that for most indications we’re going to be looking at quarterly dose scene or may be the less frequent than that. And by giving three monthly doses, it was obscuring the picture of what’s really happening. So with the single dose data and normal volunteers, we’ll get a good idea of what the depth and duration of the knockout with a single dose is. By doing the two monthly doses that second dose – if the first dose doesn’t get you all the way to complete suppression of whatever is achievable, the second dose certainly does, and then we get to follow the kinetics of recovery all the way out.
So we actually surprised ourselves when we were sitting there one day talking about, say G we should be doing three doses here we should be doing two. Our task was designed to let us do three, we could have done three, we did three we AAT and HBV and we actually looked in the mirror and said geez, well we only did two. So that’s why we did it, that’s why we submitted the protocols to do that, and it feels to me like it’s going to be really helpful for us in figuring out what we think that the right sort of dosing frequency will be moving forward from here. That makes sense Katherine? May be you’re on mute, but --.
[Operator Instructions] and our next question comes from Keay Nakae with Chardan. Your line is now open.
Getting just back to AAT, if for whatever reason couldn’t get agreement with the FDA about the next study being a possible registration study, what would you look to prove in the next phase 2 study that you might then do?
Always hard to deal with hypothetical case. I think that one things for sure, if we don’t come to an agreement on a sort of phase 2-3 design, we at least will have good clarity with the agency on sort of what the right next step is. So I think one way or another we come out of these discussions with pretty good idea of sort of where the program is likely to be going, whether we are able to seamless phase 2-3 or whether it rewinds up being a classical phase 2 leading to a phase 3. I think we will have a good sense, but today I couldn’t play that scenario for you, we’re really still talking each other and thinking about this.
We have to remember it’s a frontier, they’d never been here before, no company has ever been here before. Any time you’re on a frontier, it takes a little bit of thought and planning to figure out what the route is. So this is quite normal and it feels to me quite normal. So we’re just working our way through in a sort of conjugal and positive way.
Would you characterize if there is generally a strong consensus on what the appropriate end points should be?
I never characterize the agency until they speak for themselves. So, I think at this point we’re not done yet. I think we sort of said that, that we’re still talking and we’re still thinking and I guess bouncing ideas off of each other, you might almost say. So at this point, we’d never want to characterize what they may or may not be thinking or where we’re going to wind up.
I think the type of message here that these are truly productive discussions. They are receptive, they appreciate the problem that we are looking to solve and so I think we are working at this truly collaboratively.
And I’m not showing any further questions at this time. I would now like to turn the call back over to Chris Anzalone for any closing remarks.
Thanks everyone for tuning today and we’ll talk to you soon.
Ladies and gentlemen, thank you for participating in today’s conference. This does conclude todays’ conference and you may all disconnect. Everyone have a wonderful day.