Arrowhead Pharmaceuticals Inc  (NASDAQ: ARWR) Q1 2020 Earnings Call Transcript

Arrowhead Pharmaceuticals Inc  (NASDAQ: ARWR) Q1 2020 Earnings Conference Call

February 05, 2020

Corporate participants:

Vincent Anzalone — Vice President of Investor Relations

Christopher Anzalone — President and Chief Executive Officer

Bruce Given — Chief Operating Officer

Ken Myszkowski — Chief Financial Officer

Javier San Martin — Chief Medical Officer

Analysts:

Edward Tenthoff — Piper Sandler — Analyst

Alethia Young — Cantor Fitzgerald — Analyst

Maurice Raycroft — Jefferies — Analyst

Mayank Mamtani — B. Riley FBR — Analyst

Esther Rajavelu — Oppenheimer — Analyst

Keay Nakae — Chardan Capital Markets, LLC. — Analyst

Presentation:

Operator

Ladies and gentlemen, welcome to the Arrowhead Pharmaceuticals Conference Call. [Operator Instructions] 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.

Vincent Anzalone — Vice President of Investor Relations

Thanks, Annie. Good afternoon, everyone. Thank you for joining us today to discuss Arrowhead’s results for its fiscal first quarter ended December 31, 2019. With us today from management are President and CEO, Dr. Christopher Anzalone, who will provide an overview of the quarter; 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.

In addition, we welcome three new members to the management team, Jim Hassard, our Chief Commercial Officer; Dr. Javier San Martin, our Chief Medical Officer; and Dr. Curt Bradshaw, our Chief Scientific Officer. Dr. San Martin and Mr. Hassard will be available during the Q&A session of today’s call.

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 and commercialization 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 Chris Anzalone, President and CEO of the Company. Chris?

Christopher Anzalone — President and Chief Executive Officer

Thanks, Vince. Good afternoon, everyone. And thank you for joining us today. We made a lot of progress over the last two years as we build clinical validation of our TRiM platform. Early in 2018, we predicted that moving TRiM into the clinic to drive substantial value for us, and that came to pass. We initiated clinical studies with ARO-HBV, now JNJ-3989 and ARO-AAT. That same year, Amgen initiated clinical studies with AMG 890, formerly ARO-LPA. Together, we see these as first clinical proof-of-concept for the TRiM platform and represent what we believe to be promising future drugs. We start to accomplish even more in 2019. We thought we could build shareholder value by continuing development of existing programs and introducing into the clinic two potentially powerful cardiometabolic drug candidates.

As with our goals for 2018, these two are accomplished. We launched a potentially pivotal Phase 2/3 study with ARO-AAT. Janssen launched two large Phase 2 studies with JNJ 3989, and Amgen continued their study with AMG 890. Importantly, we also expanded our clinical pipeline by launching Phase 1/2a studies for cardiometabolic drug candidates ARO-APOC3 and ARO-ANG3, and we reported initial data from these studies at the American Heart Association Scientific Sessions in November. This would represent a very productive year for any company in our industry, but we are not finished.

We also filed to begin clinical studies for our first tumor-targeted drug candidate ARO-HIF2 and the first ever candidate against a highly anticipated NASH target, ARO-HSD. So how do we keep up this productive value creation. What are the growth story for 2020? We think of three broad value drivers. First, 2020 is the year of bringing RNAi outside the liver to address a raft of new unmet medical needs. We are clear leaders in this endeavor, and I believe we will have clinical proof-of-concept to silence target genes in lung and solid tumors by the end of the year.

Just look at what we have done in hepatocytes, and we believe we can do the same in lung and solid tumors. This model of rapidly expanding our pipeline in new cell types could offer powerful new options for countless patients and enable the promise of continued value growth. Second, we are looking to advance multiple liver targeted programs into mid and late-stage studies, including up to three potentially pivotal clinical trials. And third, we expect to continue to expand the reach of the TRiM platform and enable access to an important new cell type, skeletal muscle. It will mean a lot to our business if we are able to execute in these areas.

By the end of the year, we could have 10 TRiM-enabled drug candidates in the clinic, eight of which could be wholly owned, targeting up to four different cell types with up to three candidates and potentially pivotal studies. Let those numbers sink in for a moment. I don’t believe there is a company our size anywhere with this type of reach, and remember that this is all built on a single scalable platform. As you know, however, we are only getting started. I believe those 10 clinical candidates could double to 20 just a few years later.

This pipeline has a healthy mix of early, mid and later stage candidates designed to address both small well-defined rare disease populations as well as high-prevalence diseases. This gives Arrowhead and our shareholders a couple of key features. First, to provide diversification where risk is spread out across the portfolio. Second, and maybe more importantly, it enables a consistent flow of data readouts to help demonstrate that our candidates are on the right path.

But 2020 and beyond is not just a pipeline expansion story for Arrowhead. We are also making an orderly transition from a discovery and early clinical stage company into a late-stage clinical and emerging commercial organization backed by a powerful discovery engine. We want to build this out in a way that value, speed and execution, but also in a way that is efficient and capital conscious. We intend to partner strategically and selectively to manage risk, source capital to develop and commercialize wholly-owned programs and maximize patient access to our drugs worldwide.

We will approach this phase in typical Arrowhead fashion with innovation in mind. This is a big opportunity and a big step for us as a growing platform pharmaceutical company. Let’s now take a closer look at some of our progress during the last quarter and the period since our earnings — our last earnings call and how this is preparing us for this next phase of growth.

As I mentioned, we reported initial clinical results for our two wholly owned cardiometabolic candidates ARO-APOC3 and ARO-ANG3 at the American Heart Association Scientific Sessions in back-to-back plenary presentations. These results were from the single ascending dose portion of first-in-human studies. They demonstrated robust, durable and dose-dependent reductions in APOC3 and ANGPTL3 proteins, leading to impressive changes in triglycerides and various other liver parameters. This is an important accomplishment by virtue of the quality of the data, the remarkable durability of the effect shown and the power of the targets. We are now treating patients in the multiple dose portion of these studies, and while they are still ongoing, I can give you an idea of what we are seeing. In addition, Bruce will provide a bit more detail when he speaks.

At a 50 milligram dose of ARO-APOC3, we are seeing reductions of around 95% in circulating triglycerides in patients with severe hypertriglyceridemia. This is quite frankly astonishing. To put this into perspective, one patient started the study with 4,818 milligrams per deciliter of triglycerides, and this fell to just 231, just 29 days after the first dose of ARO-APOC3. In fact, the mean absolute reduction for the three patients with at least 29 days of data at this — in this cohort was minus 3,183 milligrams per deciliter. We would expect this type of reduction to have substantial clinical and quality of life impacts, particularly in patients with history of pancreatitis.

We’re talking about patients with severe hypertriglyceridemia moving to relatively normal triglyceride levels extremely rapidly. This supports our plan to develop ARO-APOC3 as a focused triglyceride lowering drug and we expect dosing to be every four months or potentially less frequent. While we believe this could be a powerful drug for patients with familial chylomicronemia syndrome or FCS, we plan to develop this more broadly to also treat patients with polygenic hypertriglyceridemia and history of pancreatitis.

This is still a rare indication, but KOL will tell us that the effective population is approximately 100 fold that of FCS, representing about 30,000 potential patients in the US alone. We are also seeing promising data in the ongoing studies with ARO-ANG3. For instance, in patients who already are on statins, but unable to reach their LDL-cholesterol goal, we have seen a further reduction in LDL-cholesterol of around 40% after short exposure to ARO-ANG3 and in patients with triglycerides greater than 300 milligrams per deciliter, we saw a 79% reduction in circulating triglycerides. One of the cohorts still blinded, is also evaluating the effective ARO-ANG3 on insulin sensitivity and liver fat.

As with ARO-APOC3, we expect dosing to be every four months or less frequent, while we view ARO-APOC3 as a rifle shot against severe symptomatic hypertriglyceridemia, we are developing ARO-ANG3 as a broader market drug where genetic studies indicate, it could have a profound impact even in the age of statins and PCSK9 inhibitors. Because we expect it to hit multiple pathways in pathologies, we view this as a potentially important medicine against metabolic syndrome and dyslipidemias, fellow trailers in creating cardiovascular risk.

ARO-ANG3 and ARO-APOC3 appear to be powerful medicines indeed, and there still haven’t been any reports of drug-related AEs rated as serious or severe and no discontinuations due to drug. We expect to present data throughout 2020 at various scientific conferences as the studies readout. These data are providing further clinical validation for the TRiM platform broadly and hepatocyte targeted programs specifically. We believe Arrowhead is achieving benchmark activity, durability and tolerability. So far we have enjoyed very consistent and reliable translation of preclinical results in animals to human clinical studies and this speaks to the scalability and predictability of the platform.

This gives us confidence as we move into the clinic with our latest hepatocyte targeted candidate, ARO-HSD. We expect ARO-HSD to be the first drug candidate of any modality targeting HSD17B13 to reach human testing. Published human genetic data indicate that a loss of function mutation in HSD17B13 provides strong protection against NASH, cirrhosis, and alcoholic hepatitis and cirrhosis with approximately 30% o 50% risk reduction compared to non-carriers. This target has generated a great deal of unsolicited inbound interest from multiple potential partners.

In December, we filed a CTA for this program and I’m happy to report that we now have regulatory and IRB approval to begin clinical studies. I expect the dosing will begin this quarter and it is possible that we could have some data by the end of the year.

I would now like to talk about what to expect with the ARO-AAT program. We are enrolling patients and continue to activate sites in North America and Europe in the potentially pivotal SEQUOIA study. That is a blinded placebo controlled study in which the last patient is to receive approximately two years of treatment. Because of this, it will be some time before there are any data to share, but we believe that SEQUOIA structure provides us with the fastest possible path to registration.

Last month, we began dosing AROAAT2002, an open label Phase 2 study with liver biopsies at baseline and after six months, 12 months, 18 months and 24 months treatment. The first cohort is fully enrolled, so we expect to have the first six months repeat biopsy data by fall and we hope to share at least some aspects of those data publicly by the end of the year.

As we’ve discussed extensively in the past, we believe that for RNAi to truly transform medicine, it needs to be applied in tissues outside the liver. We made important progress over the past months and as I stated earlier, we see 2020 as the year we established clinical proof-of-concept for TRiM-enabled RNAi beyond hepatocytes.

In December, we filed an IND for ARO-HIF2, our first tumor targeted candidate against renal cell carcinoma. HIF2 Alpha is a well-validated target for the clear cell form of RCC. So, we are very excited about ARO-HIF2 and what it can mean for patients. The delivery technology, we are employing is designed to get into other solid tumors as well rather than specifically RCC. As such, establishing clinical proof-of-concept that we are silencing HIF2 Alpha in the current study could represent an important value inflection point.

It could mean that we have a potentially important drug for RCC and a platform that can be used against numerous targets across multiple solid tumor types. Once we achieve clinical proof-of-concept, our model is to rapidly expand our pipeline with additional candidates focused on new tumors against a variety of oncology targets, some of which may be here to for undruggable. This is a potentially powerful and scalable model. So, then the question is, when we could achieve clinical proof-of-concept. I believe this answer is as early as this year. I’m happy to report that we now have clearance from the FDA to begin the Phase 1 study and we hope to begin dosing the patients this quarter.

Let’s now move to the lung, as you know, we have been developing our ability to deliver to pulmonary epithelial cells the inhalation for some time now with an initial focus on silencing the pulmonary epithelial sodium channel or ENaC for the treatment of cystic fibrosis. Last quarter, we presented preclinical data at the North American Cystic Fibrosis Conference on ENaC — on ARO-ENaC. We remain on schedule for a CTA filing in the first half of 2020 for this candidate. As with ARO-HIF2, we view establishing clinical proof of concept as a potentially important value inflection point. ENaC has a well-validated CF target that has been undruggable due to systemic toxicity, so we believe positive data would be a big step for CF patients with potentially any genotype. More broadly it could serve as an important validation for our pulmonary delivery system.

Once we have data demonstrating the relationship of how animal data translate to humans, we will be aggressive in pipeline expansion. There are a large number of potential opportunities in such areas as COPD, asthma, pulmonary fibrosis and others. We are clearly creating a lot of value with our hepatocyte-directed TRiM platform and we believe we can do the same with solid tumor and lung directed TRiM platforms. Needless to say, everything I’ve described will take a tremendous amount of creative and highly integrated work. For instance, during remaining 11 months of 2020, we hope to have up to three end of Phase 2 meetings with FDA and EMA for AROAAT, ARO-ANG3 and ARO-APOC3. Filed two to three new CTAs, have clinical data readouts across most of our existing clinical programs, create our first program targeting skeletal muscle cells, continue working on next-generation undisclosed programs and start to build out a pre-commercial infrastructure.

Toward these ends, we expanded our senior management team with the hiring of seasoned biotech and pharma leaders, Dr. Javier San Martin as Chief Medical Officer; Dr. Curt Bradshaw as Chief Scientific Officer, and Jim Hassard as Chief Commercial Officer. These additions have already been impactful to Arrowhead and give us confidence so we can maintain our innovative culture as we continue to grow. We wanted leaders with proven track records of running effective discovery, development and commercial programs in rare and high prevalent disease areas.

Together, they have been responsible for dozens of INDs, small and large clinical studies, NDAs, commercial launches and product marketing campaigns. Curt joined us from Tollnine, a company he co-founded to develop novel antibody conjugates for immuno-oncology. Prior to that he was with Solstice Biologics, Traversa Therapeutics, CovX Research, Ligand Pharmaceuticals and Abbott Laboratories.

Javier joined us from Ultragenyx where he was Senior Vice President and Head of Global Clinical Development. Prior to that he held clinical development roles at Alder Biopharmaceuticals, Amgen and Eli Lilly after beginning his career at CMEC University Hospital in Buenos Aires as attending Physician in internal medicine. Jim joined us from Coherus BioSciences, where he was Senior Vice President of Marketing and market access. Prior to that he was with Medivation, Amgen and Schering-Plough. We also appointed Dr. Marianne De Backer as a new Independent Director. She is currently Executive Vice President, Head of Global Business Development & Licensing, and a member of the Executive Committee of the Pharmaceuticals Division of Bayer AG.

We got to know Dr. De Backer when she was Global Head of Business Development at Janssen and we were negotiating our partnership with them. Her passion for finding new innovative medicines for patients, broad technical background and deep experience in hundreds of transactions makes her a great fit as part of our Board of Directors.

Of course, in addition to great talent, requires capital. Toward that end, we improved our balance sheet and extended our cash runway with the financing last quarter with gross proceeds of approximately $267 million. Clearly, there is a lot going on at Arrowhead and we had another quarter of impressive execution. Even after much progress made in 2018 and 2019, we feel that we are still in the very early stages of growth for our company and for the RNAi therapeutics field broadly. We view Arrowhead as a clear leader in the field and we intend to keep our foot on the gas to maintain that position.

With that overview, I’d now like to turn the call over to Dr. Bruce Given. Bruce?

Bruce Given — Chief Operating Officer

Thank you, Chris. Good afternoon, everyone. I’ll give a quick update on the status of our clinical development programs. Let’s start with ARO-AAT, our second-generation investigational RNAi therapeutic being developed as a treatment for the rare genetic liver disease associated with alpha-1 antitrypsin deficiency. We are currently conducting two clinical studies, SEQUOIA, which is an adaptive design, potentially pivotal Phase 2/3 study, and AROAAT2002, which is a pilot open label Phase 2 study to assess changes in a novel AATD histological activity scale. For SEQUOIA, we intend to open around 40 sites in the US, Canada and Europe. To review, SEQUOIA is designed to enroll 120 patients with the last patient enrolled receiving approximately two years of treatment.

The primary endpoint is the proportion of ARO-AAT treated patients relative to placebo, achieving a two point improvement in a histological grading scale of AATD liver disease and no worsening of liver fibrosis at end of study biopsy. We are also moving forward quickly with AROAAT2002. The 2002 study is designed to enroll approximately 12 participants in two sequential cohorts. Between the two cohorts, biopsy data will be assessed at baseline and after six months, 12 months, 18 months and 24 months of treatment with ARO-AAT. We have fully enrolled the first sequential cohort and all patients have received at least their first dose.

The second sequential cohort is also moving quickly. We anticipate that it will be fully enrolled this quarter. This will allow us to collect the first repeat biopsy at the six month time point around the middle of this year. This is important because it may be the first view of what happens inside the liver in AATD patients after a therapeutic intervention using any modality. We are eager to see how Z-AAT monomer production is affected and whether the accumulated Z-AAT polymer could start to clear. AAT is a very attractive target for an RNAi-based intervention because it is primarily produced in the liver and the misfolding of the mutant Z-AAT protein is clearly the cause of the progressive liver disease in these patients.

We believe that dramatically reducing the liver production is likely to halt the progression of liver disease and may allow regression of existing liver pathology. It’s also important to point out that we have previously presented clinical data showing that ARO-AAT treatment led to reductions in serum AAT levels to below the level of quantitation with a multi-month duration of effect. This indicates that we may be achieving near complete suppression of the liver production. We think for patients that are already on their way to progressive liver disease that the intervention that achieves this high level of activity has the best chance of showing a clinical benefit.

In my mind, any approach that doesn’t seek to get full suppression of the mutant protein mainly patients with existing liver disease at high ongoing risk. Press releases and presentation materials on ARO-AAT are available on our website, if anybody wants a refresher.

Now let’s turn to our two cardiometabolic candidates, ARO-APOC3 and ARO-ANG3. We presented data on both candidates at the American Heart Association Scientific Sessions in November. These were single dose data from the ongoing first in human studies. We are in the process of generating multiple dose data in various patient populations for both candidates, which we intend to share publicly at various venues this year.

Let’s talk about the status of these studies in more detail and how we’re thinking about the development programs moving forward. I’ll start with ARO-APOC3. Our RNAi therapeutic candidate targeting apolipoprotein C3 being developed as a potential treatment for patients with hypertriglyceridemia. We view this is having the most applicability to rare disease populations specifically, patients with severe hypertriglyceridemia with the history or at a high risk of pancreatitis.

Some of these patients have a single genetic cause for their disease such as familial chylomicronemia syndrome or FCS but a significantly larger population has polygenic causes for their hypertriglyceridemia. Whether it is monogenic or polygenic, their disease has very similar clinical manifestations. So we are exploring various trial designs for what a pivotal study would look like. We intend to have discussions with the FDA and EMA this year and hopefully gain clarity on some key study design considerations.

The current clinical study is called ARO-APOC31001. It is the Phase 1/2a single and multiple dose study to evaluate the safety, tolerability, pharmacokinetics and pharmacodynamic effects of ARO-APOC3. The single dose portion of this study is in healthy volunteers and the multiple dose portion includes patients with both severe hypertriglyceridemia and familial chylomicronemia syndrome.

As I mentioned, we presented single dose data at AHA. We are now enrolling and dosing the multi-dose portion of the study in two primary patient populations. There are four cohorts of patients with elevated triglycerides above 300 milligrams per deciliter to give a detailed view of dose response in a patient population. One of the four cohorts has been enrolled and dosed and we are working on completing the other three cohorts. To accelerate completion of these cohorts, we are now opening Canadian centers where there is a very important founder population.

There is also one cohort of patients with severe hypertriglyceridemia above 880 milligrams per deciliter. This is the patient population I discussed earlier where they may be monogenic such as FCS or polygenic. This cohort has five patients enrolled, three of which are through at least their first month of therapy. Let me give you a flavor of what we are seeing. These three patients have started triglycerides in the thousands and responded to 50 milligrams of ARO-APOC3 with a mean maximum 97% reduction in APOC3. This has resulted in a mean maximum reduction in triglycerides of 95% with an absolute mean fall greater than 3,000 milligrams per deciliter.

We look forward to the opportunity to present these data at a medical meeting this year. Now let’s turn to ARO-ANG3, our RNAi therapeutic targeting angiopoietin-like protein 3 or ANGPTL3 being developed as a potential treatment for patients with dyslipidemias and possibly metabolic diseases. The current study is called AROANG1001. It is a Phase 1/2a single and multiple dose study to evaluate safety, tolerability, pharmacokinetic and pharmacodynamic effects. The single dose portion of the study is in adult healthy volunteers. The single dose data was presented at AHA in November and received a good amount of attention.

We are now conducting the multiple dose portion, which includes patients with various types of dyslipidemia, including patients on a stable statin regimen with persistently elevated LDL cholesterol, patients with heterozygous or homozygous familial hypercholesterolemia, patients with hypertriglyceridemia, and patients with non-alcoholic fatty liver disease. The familial hypercholesterolemia cohorts are almost at full enrollment, and all of the other cohorts are already fully enrolled. To give a sampling of patient data here, at doses of 200 milligrams or 300 milligrams, mean maximum percent reductions in ANGPTL3 approached 90%. Mean maximum triglyceride reductions in the high triglyceride cohort approached 80% and mean maximum reductions in LDL cholesterol in the various LDL cohorts are averaging around 40%.

It is important to note that most of the patients in these cohorts are already on maximal medical care consisting of statins plus or minus acetamide with PCSK9 inhibitors in some. This study will yield data throughout the year and we intend to provide various data readouts at different academic venues. From a safety and tolerability perspective, both ARO-ANG3 and ARO-APOC3 continue to look similar to our other TRiM candidates with the most common AEs being headache, respiratory tract infections and injection site reactions without drug related discontinuations.

We feel very good about the data generated to-date and are eager to share additional data once they are mature enough. The unique challenge for Arrowhead concerning data release is that TRiM-enabled RNAi therapeutics have such long duration. Two doses tend to give us six months or more of activity. So follow up times are much longer than for small molecule drugs or monoclonal antibodies. It’s a good problem to have because that duration gives our RNAi candidates a very attractive product profile. But it does make data release an abstract rating for instance challenging.

I now want to give a brief update on where we are with our newest clinical candidates. ARO-HIF2 is our candidate against the target HIF-2 Alpha being developed to treat clear cell renal cell carcinoma. We filed an IND in December to start a Phase 1 dose range finding study in up to 18 clear cell RCC patients that have been refractory to VEGF targeted or checkpoint inhibitor therapy.

The primary objectives of this study will be determination of a Phase 2 dose and safety. Secondary objectives will include pharmacokinetics and then efficacy based on resist criteria using either CT or MRI imaging. A key exploratory objective for ARO-HIF2 will be gene target knockdown in the tumors using tumor biopsy.

The IND was activated within the normal 30 day clock and we are in the process of initiating sites. Our goal is to have the first patient dosed around the end of the first quarter. ARO-HSD is our new investigational candidate targeting HSD17B13 for the potential treatment of alcohol and/or non-alcohol related liver disease. Published GWAS data have indicated that loss of function mutations in the HSD17B13 enzyme provide the strongest known genetic protection against NASH, cirrhosis and alcoholic hepatitis and cirrhosis.

It has also generated a considerable amount of unsolicited inbound interest from large pharmas that are active in the NASH space. In our view, it is the most sought-after target for NASH at the moment. We filed a CTA in December to begin a Phase 1/2a single and multiple dose escalating study to evaluate safety, tolerability pharmacokinetics and pharmacodynamic effects of ARO-HSD in normal healthy volunteers, as well as in patients with NASH or suspected NASH.

Additional exploratory objectives include assessment of various measures of drug activity using liver biopsy. We now have regulatory and IRB clearance and we are working to dose our first normal volunteers this quarter. As with AAT, HBV, APOC3 and ANGPTL3, we are once again the first RNAi company in the clinic against a very exciting target.

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?

Ken Myszkowski — Chief Financial Officer

Thank you, Bruce, and good afternoon everyone. As we reported today, our net loss for the quarter ended December 31, 2019 was $2.7 million or $0.03 per share based on 97.1 million weighted average shares outstanding. This compares with net income of $12 million or $0.13 per share based on 95.6 million fully diluted weighted average shares outstanding for the quarter ended December 31, 2018.

Revenue for the quarter ended December 31, 2019 was $29.5 million compared to $34.7 million for the quarter ended December 31, 2018. Revenue in both periods relates to the recognition of a portion of the upfront payments and milestones received from our license and collaboration agreements with Janssen as we continue to work towards completing our performance obligation of managing the current Phase 1/2 HBV clinical trial.

Revenue from the Janssen agreement is recognized based on our estimate of the proportion of effort expended toward fulfilling our performance obligations primarily overseeing the completion of the current Phase 1/2 HBV clinical trial. We expect the remaining $54 million of deferred revenue to be recognized in this calendar year. Any additional milestones achieved with Janssen or Amgen would be additive to this projection.

Total operating expenses for the quarter ended December 31, 2019 were $34.3 million compared to $23.7 million for the quarter ended December 31, 2018. This increase is primarily due to increased clinical trial and toxicology costs as our pipeline of clinical candidates has increased. Increased personnel costs in both R&D and G&A also drove the increase as our head count continues to grow.

Net cash used by operating activities during the quarter ended December 31, 2019 was $23.5 million, compared with net cash generated by operating activities of $168.3 million during the quarter ended December 31, 2018. The key driver of this change was the $175 million upfront payment from Janssen last year. We estimate our near-term cash burn to average $25 million to $30 million per quarter.

Turning to our balance sheet, our cash and investments totaled $528.3 million at December 31, 2019, compared to $302.9 million at September 30, 2019. The increase in our cash and investments was primarily due to the December 2019 equity financing we completed, which generated $250.5 million in net cash proceeds for the company. Our common shares outstanding at December 31, 2019 were $101.1 million.

With that brief overview, I will now turn the call back to Chris.

Christopher Anzalone — President and Chief Executive Officer

Thanks, Ken. I’ve talked in the past about this being the beginning of a golden age for RNAi as a therapeutic modality. I believe this. I also see Arrowhead continuing to push the RNAi field forward and developing many important and differentiated medicines that help countless patients without adequate treatment options. This is what drives us every day and keeps us focused on our long-term goals.

We are doing something very important in a way that no other company even in the RNAi field has been able to match. Our drive toward innovation and finding a way even when the way is not clear is a hallmark of the Arrowhead culture. 2020 is another opportunity for us to demonstrate that. We believe we could achieve great — we believed we could achieve great things in 2018 and we did. We believe we could achieve great things in 2019 and we did. We believe we will achieve great things in 2020 and here are some of our goals.

To file two to three new CTAs, initiate two new pivotal pp potentially pivotal studies with ARO-APOC3 and ARO-ANG3, move SEQUOIA into the pivotal portion of that study, initiate our first pulmonary clinical study with ARO-ENaC, establish clinical proof-of-concept for lung delivery, establish clinical proof-of-concept for solid tumor delivery, generate our first clinical candidate targeting skeletal muscle, share clinical data throughout the year from the following programs. ARO-APOC3, ARO-ANG3, the AROAAT2002 open label study, ARO-HIF2, ARO-HSD and ARO-ENaC. We believe these are all substantial value drivers for us and we are excited to go after them.

Thanks again for joining us today, and I would now like to open the call to your questions. Operator?

Questions and Answers:

Operator

Thank you. [Operator Instructions] Our first question comes from the line of Edward Tenthoff with Piper Sandler. Your line is open.

Edward Tenthoff — Piper Sandler — Analyst

Great, thanks. Can you hear me okay?

Christopher Anzalone — President and Chief Executive Officer

Yes.

Edward Tenthoff — Piper Sandler — Analyst

Hey, how are you guys? Congrats on all the progress, really exciting to see as you guys to maybe go deeper and further into the clinic. Question on alpha-1 antitrypsin, I’m curious if with the competitive programs, both small molecule and other RNAi’s whether you’re having any trouble finding patients and whether you’re seeing that impact registration at all, maybe you can just kind of layout out how you see the landscape between RNAi mechanism and the orals? Thanks so much.

Christopher Anzalone — President and Chief Executive Officer

Bruce, you want to take that?

Bruce Given — Chief Operating Officer

Yeah. Thanks, Ted. I don’t know that we’ve seen that really showing up yet in our space. I think with respect to the other RNAi’s they are just in Phase 1 and so they don’t have a very broad footprint at all, I would say. So, at this point, I don’t really see them as creating any meaningful issue for us. We certainly haven’t perceived that. With respect to the oral, I mean I think there is a lot of confusion on the street about that. I don’t think that there is really a whole lot of confusion at least yet in the investigator community that I can see.

We don’t think it’s actually going to be a competitive mechanism because we — we don’t think there’s going to be enough clearance of the monomer from the liver to really allow the livers to heal. That’s of course improving at this point, but we kind of feel like you know judging from what we’ve seen in infectious hepatitis for instance that you really need to remove the insult to allow the livers to heal. That’s our belief. So we think a partial improvement in the amount of monomer in the liver is unlikely to allow livers to heal over any sort of reasonable period of time, maybe over a period of five years or 10 years, an approach like that could be helpful. But we don’t see it in a meaningful clinical trial setting being a very competitive therapy. So we’re not, we don’t really see the orals as likely to, in the end, from a clinical trials perspective of being very successful. But we do recognize that there is a lot of noise out there and a lot of confusion. And I guess it’s incumbent upon us to try to help clear up that confusion.

Christopher Anzalone — President and Chief Executive Officer

And just to put a finer point on that clearance issue, look, the alpha antitrypsin is thought to be the second most abundant protein in the body that it’s thought that the liver is making about two grams of this a day. And so it will take an awful lot of corrector to move that out of the liver. We know from our data that we are probably silencing that almost completely within the liver.

Edward Tenthoff — Piper Sandler — Analyst

Okay, cool. Excellent. Thank you so much guys.

Christopher Anzalone — President and Chief Executive Officer

Thanks, Ed.

Operator

Thank you. And our next question comes from the line of Alethia Young with Cantor Fitzgerald. Your line is now open.

Alethia Young — Cantor Fitzgerald — Analyst

Hey, guys. Thanks for taking my question. Congrats on the progress with the cardiometabolic platform. Maybe a couple from me. One, I was intrigued by your HSD commentary and the partnership interest. I was just curious if this is an asset that you might think about kind of commercializing a little bit further or is it something that you would think about kind of potentially partnering earlier?

And then I have another question on, you were talking to potential non-liver catalyst on data. I just want to make sure I had it right from my own purposes that we could get some data on HSD and which one was the other one, not ENaC right? And I think we had…

Christopher Anzalone — President and Chief Executive Officer

HIF2.

Alethia Young — Cantor Fitzgerald — Analyst

Yeah, HIF2, right. So, you have HIF2. So, that’s the second question. And then the third question is, I just want to talk a little bit more about kind of ENaC in general. Do you guys, I mean, maybe talk a little bit why I know obviously Vertex studied that in the past, and why do you think RNAi is a superior approach there as well? Thanks.

Christopher Anzalone — President and Chief Executive Officer

Okay. So, let’s start with the HSD partner or no partner. So, we’re in a good spot here. We’ve got plenty of capital. We’ve got good experience running early to mid-stage clinical programs, and we’ve got a good track record of conducting those rapidly. So there is no pressure on us to partner that anytime soon and we are happy to move into the clinic on our own on that. Having said that, as with all of our other programs, we are happy to look at the landscape and make a good decision about partner versus no partner.

As we talked about in the past, look, we’ve got the embarrassment of riches here in that we’ve gotten a machine that will churn out clinical candidates quite quickly and no company, much less company our size, but I don’t think any company could commercialize all of the potential drug candidates or potential drug that we’re going to be creating, and so there will be partnering going forward. Absolutely. The question is which one of these assets, we’re going to partner and when we’re going to partner it and how we’re going to partner it.

So we are certainly open over time to partnering some of our programs. We just don’t know at this point, it’s not clear when or if we would partner HSD we’ll just keep our eyes open on that one. We’re excited to start dosing that study shortly as I mentioned, we’ve got, we’ve got clearance to move forward. And so my expectation is we will start dosing that this quarter. And now converging to your second question about data. Look, it’s probably a bit too early to guide to data release this year. We talked about some goals and it’s certainly our goal to have data in our hands from HSD, from ENaC even and certainly from HIF2 Alpha.

Are those data mature enough to present publicly? We’ll just have to see. And we’ll certainly guide when we are in the clinic long enough and we have a good idea about how much data we’re going to have by the end of the year, but we certainly feel good that we’re going to have data internally for all those programs by the end of the year. And we’ll — again, we’ll just see how much we can share by the end of the year. We are certainly motivated to get it out as quickly as we can, we put it that way. And regarding ENaC and prior failures there, Bruce, you want talk about biology there.

Bruce Given — Chief Operating Officer

Yeah, no, that’s great. So Alethia. This has been at a pharma target for a long time and people have been trying to develop small molecule ENaC inhibitors. They have been able to develop small molecule ENaC inhibitors there. It’s not been that difficult to come up with small molecules that can do it. The problem has been that that you know ENaC is also very, very important in the distal tubule of the kidney, and it controls potassium in the blood. So, the goal was always to try to figure out some way to keep the small molecule inhibitor in the lung and keep it out of the bloodstream. And in so doing, try to get the benefits of ENaC inhibition in the lung without creating hyperkalemia, which is potentially fatal.

And every single effort so far has failed. And you’ll remember that Perion developed an inhaled ENaC-inhibitor that GSK licensed and gave up on and failed, gave it back to Perion and Vertex wrote a big check and bought it again and took it into the clinic and they also failed. So which also by the way, there has been a little bit of dialogue of why do you need ENaC inhibitors in the age of correctors. And I would just remind everybody that even Vertex thought that this was a very important mechanism to have their hands on even after it failed in GSK’s hands, they wrote a big check to go and fail again with it. So the small molecule inhaled inhibitors have all failed because you just can’t keep them out of the bloodstream.

Well, so why is RNAi the right approach? Because RNAi does not passively cross cell membranes. The only way you get it into a cell is with Ligand mediated delivery. So we are using a ligand receptor combination that doesn’t exist in the liver and for that reason, even though some of ours gets into the — gets into the bloodstream, it doesn’t get into the distal tubules. And we’ve never been able to — no matter how much we poured in to animals, we’ve never been able to get any knockdown in the kidney and nor do we expect any.

So that’s what makes it so perfect for RNAi. Not to mention the fact that the CF patients are having to nebulize multiple times on a daily basis. And the thought of having an effective agent that they could nebulize once every few weeks, one time every few weeks or something like that or even if it was a couple of three days, and then they didn’t have to do it for another few weeks or a month, that’s also just from a patient convenience and benefit perspective is great as well but the big advantage for ENaC will be, you know that that the therapeutic index around this is concerned about hyperkalemia. So far, we’ve never been able to see a problem, including our toxicology studies. So that’s the reason Alethia, this is probably the only practical way to successfully go after this particular target.

Alethia Young — Cantor Fitzgerald — Analyst

Awesome. Thanks for the color, guys. Keep up the good work.

Christopher Anzalone — President and Chief Executive Officer

You bet.

Operator

Thank you. And our next question comes from Maury Raycroft with Jefferies. Your line is open.

Maurice Raycroft — Jefferies — Analyst

Hi, everyone. Congrats on the progress. And thanks for taking my questions. To start, so the data that we’re looking out in the press release for ANG3 and APOC3 that’s all single dose data, right?

Bruce Given — Chief Operating Officer

Maury, actually some of that data is from the first dose and some would be after the second dose. Remember we’re dosing on day one and then four weeks later, just thinking that that’s probably going to give us maximal knockdown and then we’ll follow that out to understand what our true duration is going to be in chronic dosing. So, some of this data is just from the first of those two doses and some may be in that second dose where we are in the active follow-up phase. So this is just a first look.

Maurice Raycroft — Jefferies — Analyst

Got it. So it’s somewhat of a hodgepodge of data. And then, I guess will you provide more details on this at ACC? And then what other details you plan on providing at the ACC meeting coming up?

Christopher Anzalone — President and Chief Executive Officer

So look, so it’s not clear. So we will not be providing more data at ACC on these. We do expect to provide complete datasets throughout the year at various conferences. We’ll just see when the data are mature and how that corresponds with various conferences. ACC, it looks like — it’s just going to be a bit too early for mature data for these programs.

Maurice Raycroft — Jefferies — Analyst

Got it, okay. And then I know we don’t have a lot of details from the ANG3 program in the topline recently. I guess, what are your views on their lack of liver fat or A1C changes and did you learn anything strategically from their topline update that you can potentially incorporate into your program that could increase chances of detecting liver fat reduction and/or metabolic changes?

Christopher Anzalone — President and Chief Executive Officer

Yeah. So we didn’t learn anything from that because we haven’t seen the data, we’ll just have to wait and see what that looks like when they actually provide data. But I will say broadly speaking, we feel that when you can use RNAi, it is just, it is as a class, a potentially more powerful tool than antisense Oligos. We feel strongly that we should have generally better safety profile in antisense. We feel like we should have a better dosing schedule in antisense. And then we’ll see what the activity looks like with antisense versus RNAi. So far, we look at least competitive than maybe sometimes better.

Maurice Raycroft — Jefferies — Analyst

Got it, okay. And then for the NAFLD patient cohort, are you only dosing those patients twice, so once per month. And then you unblind them or how many months, can you dose them?

Bruce Given — Chief Operating Officer

Right. So it’s two doses. You know the first dose and then a second dose 28 days later. But we are — we are doing MRI-PDFF I think on day 71 and then a second on day — I’m looking at Javier here. 169?

Javier San Martin — Chief Medical Officer

168 yeah.

Bruce Given — Chief Operating Officer

168, 169. So you know that which is just a test again to the incredible durability of RNAi. So we’ll have two shots to take a look here at MRI-PDFF liver fat.

Maurice Raycroft — Jefferies — Analyst

Got it. And last question is just for the patients in the press release. If you can say whether you’re seeing a dose response for ANG3? And is the 50 mg dose for APOC3, is that likely the go-forward dose they are going to use?

Bruce Given — Chief Operating Officer

I think we’re, you know 50 is certainly a good dose whether in the end, it could wind up being as low as 25 we’ll have to wait and see. I think at this point, we don’t have our full dose response data for APOC3 yet. For ANGPTL3 we have more dose response data, and I think it’s fair to say we’re probably seeing a dose response for ANGPTL3 levels. I don’t really think we’re seeing a dose response for other parameters as best I can tell at this point, but, you know I would say that we obviously saw — had enough data that we felt very comfortable doing this preliminary release.

I don’t feel like we have the fullness of the data for full depth and duration and full dose response. And where dose response may really show up may be and duration, not so much in maximum depth for instance. So we have more to learn here, all of which is going to be really interesting and I think fun. But what we have already we thought was frankly of sufficient importance that we should go ahead in topline a few of the key features today just because it really was so impressive. It kind of felt wrong to sit on it.

Maurice Raycroft — Jefferies — Analyst

Got it. Makes sense. Congrats again. And thanks for taking my question.

Christopher Anzalone — President and Chief Executive Officer

Thanks Maury.

Operator

Thank you. And our next question comes from the line of Mayank Mamtani with B. Riley FBR. Your line is open.

Mayank Mamtani — B. Riley FBR — Analyst

Thanks for taking my question and congrats on a productive quarter, and great to have Jim, Javier and Curt joining the team. Quick one for Bruce, on AAT on this end of Phase 2 meeting in fall. Could you maybe talk about the — like from efficacy from a six-month readout and also from a lung safety standpoint, what are some of the considerations you may have from a data review with the agency standpoint?

Bruce Given — Chief Operating Officer

Well, so I think we’ll be wanting to hold that data at that meeting after the Part A is complete and we’ve got the 36 subjects and the DSMB has selected a dose. At that point, we’ll of course have. For us, we will be blinded but we will at least have data on any serious AEs, for instance, whether we’re seeing any sort of pulmonary issues, and the FDA will have the unblinded data. So they will actually have data we don’t have. But I think it’s an opportunity then to check in with them, see how they’re feeling at that point and also to discuss other elements of the program potentially beyond just SEQUOIA. We do have some other ideas of other things that we think would be potentially valuable to discuss with them at that point.

But presumably, the DSMB will have chosen the dose, the final dose that’s going to be used in Part B and the FDA will have been comfortable with that and that’s a good time I think to sit down with them and make sure that we’ve sort through everything else that they might want in an NDA. And expect —

Mayank Mamtani — B. Riley FBR — Analyst

Okay, great. And then on the HIF2, can you remind the dosing and duration that you’re pursuing, and maybe the frequency of scans you’re doing in that cohort?

Bruce Given — Chief Operating Officer

Oh, boy. So it’s —

Javier San Martin — Chief Medical Officer

15.5 weekly.

Bruce Given — Chief Operating Officer

Weekly, right. IV?

Javier San Martin — Chief Medical Officer

Of course.

Christopher Anzalone — President and Chief Executive Officer

Yeah. And what about frequency of scans? I want to say it’s like every six weeks or something. Yeah so the scans are every six weeks and the frequency of dosing is initially weekly at least. There are provisions and thoughts in there that depending on what we see, we may stretch that to less frequent dosing. It’s cancer. So we just want to, we want to be sure to the extent that there is any cell division going on that we’re having a chance to hit those new cells early, which is why we’re doing weekly. I mean, we certainly expect duration longer than that in the cells that have been dosed. But given proliferation in cancer, we are at least starting out with weekly dosing.

Mayank Mamtani — B. Riley FBR — Analyst

Great. And just one final one on HSD. And maybe could you talk in context of alcoholic liver disease. Obviously, I mean NASH, there is a lot to go around for the strategics. Could you maybe talk how the inbound interest is from an alcoholic hepatitis standpoint, which again can be fatal and very costly to the system too?

Christopher Anzalone — President and Chief Executive Officer

Yeah. So thanks and that’s an interesting, it’s certainly an interesting set of patients to go after and the GWAS data are at least as compelling in those groups as they are for NASH, potentially even more compelling. So that, so I appreciate you are, you are bringing up that patient group, it’s one that we’re, that we are thinking about certainly. Beyond that I really, I really don’t want to get into any discussion about what companies may or may not be interested in. It’s still early days. And as I mentioned, we are not, we are not actively looking to partner that at this point.

The take-home message there is that we think it’s a very compelling target and we are the first ones of any modality in the clinic against that target. And so I think we’ve got it. We’ve got a pretty interesting asset. At some point it may be, it may be right to partner, but at this point, we’re happy to go ahead and start those studies.

Bruce Given — Chief Operating Officer

Yeah. And the key thing we’re trying to learn in this study is depth and duration and of course dose for patients. And we don’t really have any reason to believe that any of those would be different in a NASH population versus an alcohol population. So, you know it’s just — we felt that the NASH population was maybe the best population to go ahead and do our biopsies and understand the relations — relationship of dose to depth and duration of knockdown. So we think that would apply equally in alcohol and that’s — so that decision of NASH versus alcohol doesn’t have to be made now. And we just thought this was the best population to do this study in.

Mayank Mamtani — B. Riley FBR — Analyst

Got it. Thanks for taking my questions.

Bruce Given — Chief Operating Officer

Sure. Thank you.

Operator

Our next — thank you. Our next question comes from Esther Rajavelu with Oppenheimer. Your line is open.

Esther Rajavelu — Oppenheimer — Analyst

Thanks for squeezing me in guys. Bruce, can you quickly share any information you have on the respiratory tract infections in these two studies that you press released? And for the ANG3 study have you seen any liver tox signals. I think there was a case of an ALT elevation in the healthy volunteer portion?

Bruce Given — Chief Operating Officer

So let me take the second one first. I don’t think we are perceiving that we have a liver signal. We see transaminase increases in normal volunteers. We see it in placebo. We see it in active. It’s a chronic problem in the industry because normal volunteers tend to occasionally have a — exciting weekend and they can come in with a pop in their transaminases, but we have not received a signal at this point. I would say with any of our drugs that that we are concerned about is a drug related signal. So nothing that’s worrisome yet, that doesn’t mean, of course, that once you have a database, NDA database of 1000 or more patients that’s something may not show up that gets your attention. But so far, we’re not perceiving that we have an LFT issue.

Now could you be a little more specific on your question about infections? Are you talking about in the AAT patient population? Can you be a little more specific about your question?

Esther Rajavelu — Oppenheimer — Analyst

Yeah. The ARO-ANG3 and the APOC3, the press release indicates sort of —

Bruce Given — Chief Operating Officer

Oh you’re talking about the upper respiratory tract infections?

Esther Rajavelu — Oppenheimer — Analyst

Yeah.

Bruce Given — Chief Operating Officer

Yeah, look, I think that those are probably going to turn out to be no different than placebo. So in any clinical trial you know your most common adverse effects and placebo patients tend to be headaches and respiratory infections and you know that’s — this has been true in all of our clinical studies that it’s always been that way, and so far, they’ve never differentiated from placebo and the studies were unblinded. But in a fair balance we’re just seeing what — we’re seeing what the most commonly reported AEs are that we’ve seen, but we don’t know yet whether it’s any different from placebo or not. And if I were a betting man, I would bet that the upper respiratory tract infections will be the same between placebo and drug. But we — I can’t say that with certainty at this point.

Esther Rajavelu — Oppenheimer — Analyst

Got you. And then, in terms of the data readout and the maturing of the data. Can you maybe help us — can you maybe just kind of help us be a little bit more specific on the timing, I mean is that, are you waiting for these particular set of patients? Are you kind of planning to dose more patients before you can release the data? What’s — is it first half, second half?

Bruce Given — Chief Operating Officer

No. So I mean we wrote an abstract for ACC but that abstract was written like a week after or two weeks after the AHA and at that point we had very little. Here now we’re two months later and we have quite a bit more data, so we had enough that we could do this and we could certainly now write abstracts for future meetings and we like to present our data at academic meetings as you know, that has been our tendency generally unless we are sort of in a situation like we are now, where we have really interesting data, but we kind of don’t have a forum in which to present it in the near term.

But I think there are meetings that come up in summer time and late summer and in the fall and we could — we could certainly write very interesting abstracts right now, and will be, but we’ve kind of got caught here in the middle and the abstract that we wrote, the late-breaker we wrote for AAC — ACC, we knew it was going to be pretty borderline because we just had sold little patient data at that time.

Esther Rajavelu — Oppenheimer — Analyst

Got you. Okay. And then maybe one for Ken. Can you talk about how we should be thinking about opex specifically, R&D spend over the course of the year with some of these CTAs and Phase 1s getting started?

Ken Myszkowski — Chief Financial Officer

Sure. So our R&D spend for this quarter was $23.4 million, about $21 million of that was kind of cash expenses excluding our R&D depreciation and stock comp. You will see that increased throughout the year and if you look at our, our cash burn, we’re looking at, I would say $25 million to $30 million per quarter.

Esther Rajavelu — Oppenheimer — Analyst

And that’s sort of a steady state as you’re thinking about the course of the year, for the rest of the year.

Ken Myszkowski — Chief Financial Officer

Yeah, we’ll see that increase a little bit, but we think it’s going to stay in that range for the next, for the rest of this fiscal year.

Esther Rajavelu — Oppenheimer — Analyst

All right, thank you.

Bruce Given — Chief Operating Officer

Thank you.

Operator

Thank you. And our following question comes from the line of Keay Nakae with Chardan. Your line is open.

Keay Nakae — Chardan Capital Markets, LLC. — Analyst

Yeah. Just with respect to HSD, can you now tell us a little bit more about the protocol for the NASH patients or maybe specifically, the timing of the biopsies?

Christopher Anzalone — President and Chief Executive Officer

Bruce?

Bruce Given — Chief Operating Officer

I’m sorry, so the timing of the biopsies. We have early biopsy that’s around, I’m looking at Javier here that’s around six weeks?

Javier San Martin — Chief Medical Officer

Six weeks.

Bruce Given — Chief Operating Officer

And then we have the second — and then a different cohort that has a later biopsy that I want to say is what around 12 weeks or so, do you remember exactly, Javier?

Javier San Martin — Chief Medical Officer

Yeah —

Bruce Given — Chief Operating Officer

Yeah, I’m sorry. It should be on our clintrials.gov I think it’s not, but anyway we are, we’re trying to look at depth around when we think would be peak effect, which is usually around six weeks and the duration where we’re stretching out closer to three months to four months to get a sense of duration, but it’s a challenge of course because we can’t do multiple biopsies. The way we could do multiple blood tests for other things.

Keay Nakae — Chardan Capital Markets, LLC. — Analyst

Okay. And I think you’ve clarified this now with the comments, Bruce. But the reason for the early glimpse of the data from the ANG3 and APOC3 in the press release was because you weren’t going to have anything to — you’re going to be able to present at ACC and you’re not certain of when — when the next scientific meeting where you’ll have some data to present it?

Bruce Given — Chief Operating Officer

Yeah. I suspect that that we will have an opportunity around mid-year would be my guess. It would be when it’s we’re likely to to do it. If there is an opportunity earlier, I’m sure we would just because there is already I think pretty interesting data to show, but the next set of of cardiology/lipid meetings that at least are on our radar screen right now show up around the middle of the year.

Christopher Anzalone — President and Chief Executive Officer

Yeah. And your interpretation is right. As Bruce mentioned, we just didn’t have as much data, but the deadline of the abstract submission for late breakers for ACC, and so now we’re sort of in this no man’s land for the next several months and we’re sitting on some very exciting data. So it made sense to give you a flavor for it. So you can see that these drug candidates are working at least as well as we expected and frankly a bit better than we expected, and then you’ll have — you will have a fuller dataset later in the year.

Keay Nakae — Chardan Capital Markets, LLC. — Analyst

Okay, very good. Thank you.

Bruce Given — Chief Operating Officer

Yeah. Frankly that APOC3 data kind of blew us away.

Operator

Thank you. And I’m not showing any further questions at this time, I would now like to turn the call back to Chris Anzalone.

Christopher Anzalone — President and Chief Executive Officer

Well, thank you very much everyone for joining us today. And we look forward to seeing you next quarter. [Operator Closing Remarks]