Arrowhead Pharmaceuticals Q4 2023 Earnings Call Transcript

Quartr
Provided by Quartr
November 29, 2023

There are 15 speakers on the call.

Operator

Ladies and gentlemen, welcome to the Arrowhead Pharmaceuticals Conference Call. I will now hand the conference call over to Vince Anzalone, Vice President of Investor Relations for Arrowhead. Please go ahead, Vince.

Speaker 1

Thank you, Justin. Good afternoon and thank you for joining us today to discuss Arrowhead's results for its fiscal Q4 year ended September 30, 2023. With us today from management are President and CEO, Doctor. Chris Anzalone, who will provide an overview of the quarter Doctor. Javier San Martin, our Chief Medical Officer, who will provide an update on our mid and later stage clinical pipeline Doctor.

Speaker 1

James Hamilton, our Chief of Discovery and Translational Medicine, who will provide an update on our earlier stage programs and Ken Myszkowski, our Chief Financial Officer, who will give a review of the financials. In addition, Tracey Oliver, our Chief Commercial Officer and Patrick O'Brien, our Chief Operating Officer and General Counsel will be available during the Q and A portion of the 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 are forward looking statements and are subject to numerous risks and uncertainties that could cause actual results to differ materially from those expressed in any forward looking statements. For further details concerning these risks and uncertainties, please refer to our SEC filings, including our 10 ks filed today and our quarterly reports on Form 10 Q.

Speaker 1

I'd now like to turn the call over to Chris Anzalone, President and CEO of the company. Chris?

Speaker 2

Thanks, Vince. Good afternoon, everyone, and thank you for joining us today. Arrowhead made significant progress toward reaching our 2020 and 2025 goal to grow our pipeline of RNAi therapeutics to a total of 20 clinical stage or marketed products by the year 2025. With yesterday's announcement of a CTI filing for ARO DM1, our newest skeletal muscle targeted program being evaluated as a treatment for Type 1 myotonic dystrophy. We now have 15 clinical stage programs, 10 are wholly owned and 5 are being developed with partners.

Speaker 2

We expect these 15 clinical programs to grow to 16 over the next month with the addition of 1 more CTA this year. This will complete an extraordinarily productive year on the development front. In 2023, we will have nominated 9 new potential clinical candidates using our TRiM platform across 4 different tissues: liver, pulmonary, CNS and skeletal muscle. In addition, we will have filed 4 CTAs for new clinical candidates during the calendar year. We believe this type of productivity is simply unmatched in our field and is particularly impressive given the size and market capitalization of our company.

Speaker 2

Even so, we expect more in 2024. To understand these 15 clinical programs now, the 20 we will shortly have, the new targets we are planning to address and the new cell types we will target over the years is to understand the magnitude of patients we expect to treat and the value we can create over the long term. Of course, there is too much there to discuss in this setting. So today, we will focus on some of the accomplishments, events and considerations that may drive and unlock value in the near term. I see 3 primary areas.

Speaker 2

First, we are derisking our pulmonary platform with knockdown and safety data in our clinical trials and toxicity data from our chronic tox studies. These enable us to move toward mid stage studies addressing 3 main categories of chronic lung disease: inflammation, mucal obstruction and interstitial lung disease, each of which have unmet treatment needs. 2nd, we are making good progress toward becoming a commercial company. We expect our initial commercial product to be plazasarin, formally ARO APOC3, in the treatment of familial chylomicronemia syndrome, for which we will complete a Phase 3 study in Q2 2024, followed by our anticipated second indication for treating patients with severe hypertriglyceridemia or SHTG and a later potential and lastly, we have directional guidance towards strengthening our balance sheet in a shareholder friendly way. Let's start with the pulmonary platform.

Speaker 2

We believe that Arrowhead is the 1st and only company to show clinically that RNAi can be harnessed to silence the gene expression in the human lung. This is important and marks the accomplishment of a key long term goal we set for ourselves several years ago. We've always thought that once we have we will conduct value in the entire platform and provide confidence that other programs could work similarly, much like our current expectations for new liver programs. So let's talk about important de risking steps. First, we think we have confirmation we have adequately addressed the chronic GLP toxicology issues of our 1st generation ARO ENAC candidates.

Speaker 2

In that program, we saw findings of local lung inflammation in chronic rat and monkey toxicology studies. We determined that this result was consistent with macrophage overload syndrome and thus we needed to make next generation candidates with improved potency and enhanced duration of effect, so we could stretch out the dosing interval and reduce exposure. I think we are now over that initial hurdle. We've received chronic oncology results in both rodent and primate species for ARO LRAGE and ARO MMP 7. James will talk about the specifics, but the takeaway is that the no AELs or no observed adverse effect levels suggest sufficient safety margins to move confidently into Phase 2 studies.

Speaker 2

These were welcome results, I believe represents substantial derisking for the entire pulmonary platform. Once we select the dose and dose interval for each candidate, we plan to interact with the regulatory authorities in 2024 to discuss all results to date, including toxicology and our plans for further clinical development. Next, we want to ensure that clinical safety and tolerability are acceptable. We now have 3 pulmonary programs in first in human studies and safety results have been consistent with no concerning safety signals across all three programs in 145 patients or healthy volunteers on active drug. We need to ensure that our pulmonary drug candidates are doing what they are intended to do.

Speaker 2

We still need patient data in ARO NMP7 and ARO MUC5AC to understand this, but ARO RAGE data have been very encouraging. Normal Healthy volunteers showed 89% mean max knockdown 95% max knockdown of circulating SRH after 2 doses of 184 milligrams ARO range. At 92 milligrams healthy volunteers showed a mean max knockdown of 80% and max knockdown of 90% after 2 doses. We are still collecting data from asthma patients, but so far they are mapping on top of those from normal healthy volunteers as we expected. Together, I believe these data are important for the ARO RAGE program and more broadly serve to derisk the entire pulmonary franchise.

Speaker 2

These data give us confidence that one, we have chronic tox coverage to move confidently into Phase 2 studies for ARO RAGE and ARO MP7. 2, the drug candidates have been generally well tolerated in humans and 3, we are seeing deep and durable knockdown in the ARO RAGE clinical program that tracks with what we saw in animal studies. The next step is to interrogate whether RAGE knockdown leads to a favorable clinical effect in patients. Upstream of hard clinical outcomes or FEV1, there are biomarkers that can inform on whether ARO RAGE is engaging inflammatory pathways. We are approaching a time during the coming months where we may have data on ARO RAGE and asthma patients to make that assessment.

Speaker 2

We are currently dosing mild to moderate asthma patients and enrolling patients with high baseline FeNO to potentially enrich for an anti inflammatory signal. I believe that signal would represent a significant further derisking event. So we are working quickly to get high FeNO patients enrolled. The next area where I think we are creating substantial value is our progress toward becoming a commercial company. Our Phase 3 study of plazasiran in patients with familial calendocrineemia syndrome is approaching completion and we expect the last patient visit to be in the Q2 2024.

Speaker 2

That is a big step for development stage biotech company. We are carefully considering launch strategies for plazasiran and look forward to speaking more about those soon. We will go after FCS. Data from Phase 2 studies of both podaciran and zodaciran, formerly ARO ANG3, have been very compelling, and our presentations and webcast around the American Heart Meeting earlier this month were well received by physicians, industry and the investment community. For plazasiran, we see a clear opportunity to treat patients with severe hypertriglyceridemia or SHCG.

Speaker 2

We believe there are 3000000 to 4000000 people in the U. S. With triglycerides over 500 milligrams per deciliter with approximately 1,000,000 of them with TGs greater than 880. There are very limited treatment options for these patients. Further, we anticipate an SHTG approval based upon studies demonstrating a lower rate of triglycerides during one year of treatment with an adequate safety profile.

Speaker 2

In Phase 2 studies, plazasiran reduced TGs to lower than 500 in virtually all and many had TGs fall to normal levels. We are presented with a compelling set of facts, a large pool of patients without adequate treatment options, a clear and relatively short regulatory pathway and a drug candidate that has been consistent and very effective in Phase 1 and Phase 2 studies with good tolerability. We've had productive interactions with FDA, including end of Phase 2 meeting to discuss the design of a Phase 3 clinical program in SHTG patients. We are finalizing planning and I expect we will launch the studies early in 2024. Beyond FCS and SHTG, we continue to see attractive opportunities to help a broader population of patients with plazasiran or with zodasiran.

Speaker 2

Both candidates have shown a substantially have shown to substantially reduced remnant cholesterol, increasingly appreciated risk factor of cardiovascular disease. I expect that we will conduct a cardiovascular outcome trial or CVOT that we will launch and that we will launch it in the middle of 2024. We have been planning to run cbot with plazasiran, but given the exciting data we presented at in mixed dyslipidemia patients, we are now considering whether plazasiran or zodasiran would be a better candidate. We expect to decide which is better suited for this patient population over the coming months.

Speaker 3

This is

Speaker 2

a good problem to have as both appear to be potentially powerful agents in this large market and we simply want to try to ensure we are moving the best candidate forward in this space. Also on the late stage side of our business, Takeda is enrolling patients in the Phase 3 study of fisiriran. It is my understanding that they intend to open approximately 90 sites worldwide to help ensure the program moves quickly to an approvable endpoint that could be met after 2 years of treatment. Our wholly owned programs, Discovery Engine and burgeoning commercial presence are all exciting components of our business that we believe will create substantial value going forward. They will also require significant capital over the coming years we are focused on building out our balance sheet to ensure that we can make these important investments.

Speaker 2

To that end, are actively working on opportunities to bring in capital in shareholder friendly ways, and we believe there are several good options in front of us. For instance, we are exploring specific product financing for the plazasiran SHTG Phase 3 study and separately a possible CBOS, whether done with plazasiran or zodasiran, we believe we can source sufficient capital for those studies and return for limited royalties on those products. In addition, we have discussed business development in the past. We now have 5 different platforms that incorporate the design of high quality RNAi molecules that target 5 different cell types: hepatocytes, skeletal muscle, pulmonary, adipose and CNS. We believe this broad ability to deliver highly potent RNAi we believe there is ample work there's ample room to work with partners and also continue to build an extensive wholly owned pipeline.

Speaker 2

That is intended to continue to let our discovery engine move quickly while ensuring that, one, we focus on a more limited set of wholly owned assets that provide our commercial team with a level of synergy and efficiency 2, we continue to have access to necessary capital outside the capital markets 3, we can continue to build more passive value as our partners invest in development and commercialization and 4, we can continue to serve patients. As we are able to provide better clarity related the sources and magnitude of new capital, I believe a clear overhang in our stock may be removed. There's a lot of high quality work going on in Arrowhead and substantial potential value to be unlocked as we solidify our balance sheet. Stay tuned for details when we're able to talk more about it. I want to highlight one last event from the quarter that is important.

Speaker 2

We announced that GSK reached an agreement with Janssen to transfer exclusive worldwide rights to further develop and commercialize JNJ-three thousand nine hundred and eighty nine to GSK. If you recall, Janssen announced that they were discontinuing hepatitis B research later announced that they were winding down most of their infectious disease and vaccine programs. JNJ-three thousand nine hundred and eighty nine was one of the discontinued programs of the strategic decision that created uncertainty about the future. Janssen was a good partner and we are confident that GSK will continue the diligent work the Janssen started. This transaction also builds on Arrowhead's relationship with GSK, which includes the 2021 exclusive license of GSK-four fifty three-two thousand nine hundred and ninety, formerly ARO HSD, an investigational RNAi therapeutic currently in a Phase 2 study as a potential treatment for patients with alcohol related and non alcohol related liver diseases.

Speaker 2

We look forward to continuing our productive relationship with GSK. I'd now like to turn the call over to Doctor. Javier Sanmartis. Javier?

Speaker 3

Thank you, Chris, and good afternoon, everyone. I want to focus on the significant progress we've made on plusasiran, formerly ARO APOC3 and zobasiran, formerly ARO ANG3. This includes presentations at the American Heart Association meeting with Phase 2 data on the NIEER and SHASTA-two studies of trozaciran and the ARCHES II study of sodasiran, a KOL webinar on the significance of this data and recent interactions we have had with the FDA on our plans for Phase 3 studies. Let's start with review of what plosasiran is and then that's the data presented at the AHA. Triluziran is designed to reduce production of apolipoprotein C3 or apoc3, a component of triglyceride rich lipoproteins or TRL and a key regulator of triglyceride metabolism.

Speaker 3

APOC3 increases plasma DG level by inhibiting breakdown of TRLs by lipoprotein lipase and uptake of TRL REMA by hepatoreceptors in the liver. Clozartiran is being developed as a for patients with familial calendrotronemia syndrome, severe hypertriglyceridemia and mixed dyslipidemia. These are 3 distinct patient with very different phenotypes. Familial chalomochromia syndrome or FCS is severe and ultra rare genetic disease characterized by extremely high TG levels, typically over 1,000 milligrams per deciliter, leading to high risk of acute pancreatitis that usually requires hospitalizations and can be fatal. We're currently conducting the PALISADE Phase 3 study in 75 patients with FCS, the primary endpoint of the study is percent change from baseline and fasting TG.

Speaker 3

PALISADE is scheduled to complete in Q2 of 2024. Sever hyperpressiveemia or SSTG it's characterized by marked elevation in TG levels, typically over 500 milligrams per deciliter, which can also lead to increased risk we conducted the Phase 2 SHASTA-two study and reported data at We're also working on initiating Phase 3 studies, SHASTA-three and SHASTA-four in early 2024. I will discuss the data and Phase 3 study design in a moment. Lastly, myxdeaflipidemia is the presence of high TGS and REMMAN cholesterol often with low HDL cholesterol. REMMAN cholesterol is believed to be a major contribution to the residual risk of atherosclerosis cardiovascular disease after LDL is well controlled.

Speaker 3

We conducted the Phase 2 NEAR study in patients with mixed is lipidemia unreported dose data at We're currently working on key features of the study design, including patient population selection for a potential Phase 3 study in patients with ACVD and mixed dyslipidemia. We presented data at for these last two patient population, FFTG and MEGTISLE PDIMA. The Phase 2 SHASTA-two study of processiran in 226 subshells with SFTG who had baseline TGS greater than 500,000,000 2 doses of 10, 25 or 50 milligram of posaciran once every 12 weeks reduce CGs to near normal level and more than 90% of patients achieve CG levels below 500 milligrams per deciliter, which is the risk threshold for acute pancreatitis. Losacitam achieved mean maximum reduction of 90% in APOC3 and 87% in TGS. At 24 weeks, 12 weeks after the second dose, 7 APOC3 we remain 79% below baseline, antigens were 74% below baseline with reduction in Renmann cholesterol of 63%, while HDL cholesterol increased 58% above baseline.

Speaker 3

In the Phase 2 NEAR study of in 353 subjects with mixed dyslipidemia who had fasting digits between 150 and 499 milligrams per deciliter and either LDL cholesterol greater than 70,000,000 ounce per deciliter or non HDL cholesterol greater than 100,000,000 ounce per deciliter. Fabius in this study received 2 doses of 10, 25 or 50 milligrams of processiran at baseline and at week 12 for 2 doses of 50 milligrams at baseline and week 24. Trosufcedent treated subjects demonstrate a mean maximum reduction in APOC3 of up to 89% and robust reductions in atherogenic lipoproteins. At 24 weeks, prostacinan reduced stitches by 64%, Renmin cholesterol by 54%, APOB by 19% and non HDL cholesterol by 27%, while increasing HDL cholesterol by 51%. These were very encouraging results and they received a lot of attention at After the presentations, we hosted a webcast featuring 3 experts in the treatment and management of lipid and lipoprotein disorders.

Speaker 3

Daniel Gaudet, Professor of Medicine at Universite Montreal, who discussed processiran in the context of the current treatment last case for severe hypertriglyceridemia, Borje Nordiskar, Professor and Chief Physicians, Copenhagen University Hospital, University of Copenhagen, Denmark, who discussed the emergent goal of renmincholestar in cardiovascular disease and Stephen Nissen, Chief Academic Officer for the Heart and Vascular Institute at the Cleveland Clinic, who discuss why the decrease in atherogenic lip proteins observed with prosacitam has the potential to prevent cardiovascular outcomes. A replay of that webcast is available on our website if you missed it. My takeaway was that all three experts agree that prostasinab has a unique profile and great potential in SCS, SSTG and in patient with ASCVD and mixed dyslipidemia. The support of these notable experts gives us additional confidence as we embark on Phase 3 studies to further evaluate PROCESSIA. So what will the FSDG Phase 3 studies look like?

Speaker 3

We had an end of Phase 2 meeting with the FDA and our plan is to do 2 similar studies, Shasta 3 and Shasta 4, that together will be composed of approximately 700 patients, all with TGS greater than 500 milligrams per deciliter. The primary endpoint is lowering TGS after 1 year. We will include a subset of patients at higher risk of acute pancreatitis. We will provide more detail on that as we get the studies initiated in early 2024. We will also have a 3rd study that involve patients with moderately elevated tissues to add to our safety database.

Speaker 3

We expect these studies to all be completed around the same time. All in all, our interactions with FDA have been productive and helpful. We believe that we have incorporated their feedback and look forward to continue the dialogue with the agency as we get closer to an NDA filing following completion of the PALASADE study in patient with FCS and as we move forward with additional Phase 3 studies in we also presented data at on zobasiran, which received a lot of attention. Sebastiran is designed to reduce production of angiopoietin like protein 3 or ANGPTL3, which is hepatocyte expressed regulator of lipid and lipoprotein metabolism with multiple potential modes of action, including inhibition of lipoprotein lipase and endothelial lipase. In the Phase 2 ARCHES II study of rosuvastiran in 204 subjects with mixed dyslipidemia who had baseline TGS between 150 and 4.99 milligrams per deciliter and either LDL cholesterol greater than 70 milligrams per deciliter or non HDL cholesterol greater than 100 milligrams 2 doses of 50 milligrams, 100 milligrams or 200 milligrams of solvacitam once every 12 weeks reduce expression of HPT L3 and decrease atherogenic lipoproteins.

Speaker 3

Treatment with zobasiran resulted in substantial reductions of HPT L3 up to 74%, stitches up to 63%, LDL cholesterol up to 20%, Renmin cholesterol up to 82% and ApoV up to 22%, all at week 24. Sovaciran was also associated with a relative reduction in liver fracture at week 24 with no adverse events related to liver function test changes reported to date. Plasasiran and zobasiran continue to show favorable safety profiles. Treatment emergence adverse events reported today reflect the comorbidities and underlying conditions of this study population. As I mentioned before, we're currently considering multiple Phase 3 study I'm making decisions on patient population selection for myxislipidemia in patients with atherosclerotic cardiovascular disease.

Speaker 3

We'll talk more about that in 2024 after we have further interactions with FDA about our proposed plan. I will now turn the call over to Doctor. James Hamilton. James?

Speaker 4

Thank you, Javier.

Speaker 5

I believe the productivity of our discovery organization is unrivaled. This is partly due to the efficiency and scalability of siRNA therapeutics and specifically of our proprietary TRiM platform, but more importantly, we continue to find ways to outperform others in the RNA therapeutic space, we are in a highly productive and lean organization. In 2023 alone, we completed discovery and optimization across 5 different delivery platforms and nominated 9 clinical candidates. Each then may go on to the IND enabling phase, including GLP toxicology studies, clinical supply manufacturing, as well as preparation and submission of regulatory filings. We are also working on a discovery pipeline of similar size for 2024.

Speaker 5

This high level of productivity is how we intend to reach our 2020 and 25 development goal. Our discovery stage pipeline is for the most part kept confidential until we are approaching a CTA 4 times until we file a CTA. So you will likely start hearing more about the newly nominated clinical candidates over the coming quarters. For example, yesterday we announced that we filed the CTA for ARO DM1, our clinical candidate for the treatment of patients with Type 1 myotonic dystrophy or DM1 and our second clinical program using the TRiM platform for delivery to skeletal muscle. The Phase 1, 2a dose escalating study will evaluate the safety, tolerability and PKPD profile of single and multiple ARO DM1 is designed to reduce expression of the dystrophia of myotonic protein kinase or DMPK gene.

Speaker 5

TM1 is the most common adult onset muscular dystrophy and there is currently no approved disease modifying therapy. Treatments have focused on symptomatic management, including physical therapy, exercise, ankle foot orthoses, wheelchairs and other assistive devices. ARO DM1 represents a novel approach to treat DM1 by silencing aberrantly transcribed GMPK mRNA, which could lead to improvements in multiple symptoms, including muscle strength

Speaker 6

and function.

Speaker 5

We have several exciting early stage clinical programs that target genes expressed in the liver, lung, muscle and CNS, each of which is moving towards proof of concept data. However, I will focus on the 3 pulmonary programs. Specifically, I'd like to review safety and tolerability data to date, recent chronic toxicology results that I think helped derisk the pulmonary platform broadly as well as some new PD data that further for our plans to rapidly move all programs forward. To review, our 3 clinical stage pulmonary programs are the following: ARO RAGE is designed to reduce expression of the receptor for advanced glycation end products or RAGE as a potential treatment for inflammatory pulmonary diseases. ARO MUC5AC is designed to reduce production of mucin5AC or MUC5AC as a potential treatment for mucobstructive pulmonary diseases, an ARO MMP7 is designed to reduce expression of matrix metalloproteinase 7 or MMP7 as a potential treatment for idiopathic pulmonary fibrosis or IPF.

Speaker 5

All three of these programs are in Phase 1, 2a clinical trials evaluating single and multiple doses in normal healthy volunteers and in patients. Across the 3 programs, 145 total subjects, both normal healthy volunteers and patients have received active drug via inhalation with another 31 receiving aero rage via the subcutaneous route. There have been no serious adverse events deemed to be related to drug. There have been no patterns of drug related adverse events, pulmonary adverse events such as cough or shortness of breath or adverse changes in lab or spirometry values. There has also been no evidence of local lung inflammation based on bowel cell count evaluation and all chest x rays have been read as normal.

Speaker 5

These safety and tolerability results have largely been consistent across the 3 programs and are highly encouraging for the Next, I'd like to cover the chronic toxicology results for ARO RAGE and ARO MMP7, which we recently received. These results are also highly encouraging and suggest that we have sufficient safety margins to proceed confidently to Phase 2. Specifically for ARROWAGE, the No Observed Adverse Effect Level or NOAEL in the 6 month RAT study was the mid dose and in the 9 month monkey study, it was the highest dose study. For ARO MMP7, the rat NOL was highest dose and the monkey NOAL was the mid dose. Keep in mind that dose levels selected per GLP toxicology studies our high multiples of the desired clinical dose, so some findings in the toxicology study are expected.

Speaker 5

The results for both ARO RAGE and ARO MMP7 suggest that the learnings and improvements we have made since our 1st generation pulmonary candidate, ARO ENAC have improved the therapeutic index for our inhaled siRNA programs. Any feedback from regulatory authorities, we are confident that we will have the required safety margins to begin Phase 2 studies. This is an important step for the pulmonary platform at an important time as we look to design and initiate Phase 2 studies in 2024. We will be conducting a new pharmacodynamic data. ARO RAGE continues to yield promising dose defendant target engagement results.

Speaker 5

We previously reported impressive reductions in soluble RAGE protein or SRAGE in serum and in bronchoabiola lavage fluid or BALF and healthy volunteers. Previously reported at our June Analyst R and D Day, after 2 doses of 92 milligrams given on days 1 and 29, serum SRAGE mean maximum reduction was 80% with a maximum reduction of 90%. After a single dose of 184 milligrams, we observed a mean reduction of 90% and maximum reduction of 95 we will be in a listen only mode. After the presentation, we will be in a listen only mode. With mean maximum serum SRH reduction of 76% and maximum reduction of 91%.

Speaker 5

We have since received additional SRAGE data after 2 doses of 184 milligrams in healthy volunteers. After a second dose of 184 milligrams, serum SRAGE mean maximum reduction was 89% with a maximum knockdown of 96%. Additionally, reduction of serum SRH was similar in healthy volunteers and in patients with asthma at the 44 milligram dose level. So what are the next data points that we are watching? We are currently enrolling the top dose cohort in the mild to moderate asthma patients and have initiated a cohort of asthma patients with high baseline levels of fractional exhaled nitric oxide or FeNO, which is a biomarker for the degree of IL-thirteen driven type 2 inflammation in the lung.

Speaker 5

These are both important to watch. If we continue to see consistency of PD effect in asthma patients, that would be encouraging. Also it would be highly encouraging if RAGE Lung knockdown leads to an anti inflammatory effect via the FeNO biomarker and either the mild to moderate asthma patient cohorts or more likely in the high FeNO cohort. The former should have data available during the coming months and the latter, we'll have the data around Q3 of 2024. I will now turn the call over to Ken Myszkowski.

Speaker 5

Ken?

Speaker 7

Thank you, James, and good afternoon, everyone. As we reported today, our net loss for fiscal 2023 was 205,300,000 we will be

Speaker 8

in a listen only mode.

Speaker 7

After the presentation, we will be in a $1.92 per share based on 106,800,000 fully diluted weighted average shares outstanding. This compares with a net loss of $176,100,000 or $1.67 per share based on 105,400,000 fully diluted weighted average shares outstanding for 2022. Revenue for fiscal 2023 it was $240,700,000 compared to $243,200,000 for 2022. Revenue in the current period primarily relates to our collaboration agreements with Takeda, GSK and Amgen. Revenue is recognized as we complete our performance obligations or key development milestones are reached.

Speaker 7

For Takeda, revenues recognized commensurate with our performance obligation, which includes managing the ongoing AAT Phase 2 clinical trials, remains $866,000 of revenue to be recognized associated with the Takeda collaboration, which will be recognized in the next fiscal quarter. Revenue in the prior period primarily related to the recognition of payments received from our license and collaboration agreements with GSK and a portion of the payments received from our license and collaboration agreements with Takeda and Horizon. Total operating expenses for fiscal 2023 were $445,700,000 compared to 421,700,000

Operator

again, please remain on the line. Your conference will resume shortly. We are currently experiencing technical difficulties and we are trying to get back online. Please bear with us. We are currently having technical difficulties and we're trying to get back online.

Operator

Please stand by and thank you for your patience.

Speaker 3

Hello?

Operator

Hello? Yes. You are now back online.

Speaker 7

Sorry folks, we lost our Internet connection. We're calling in as a cell phone. And I'll continue where I think we left off. Total operating expenses for fiscal 2023 were $445,700,000 compared to $421,700,000 for 2022. This increase is driven primarily by increased candidate specific and discovery R and D costs as the company's pipeline of clinical candidates we have both increased and advanced into later stages of development.

Speaker 7

Net cash used by operating activities during fiscal 2023 was $153,900,000 compared with net cash used by operating activities of $136,100,000 during 2022. The increase in cash used by operating activities is primarily driven by higher research and development expenses. We expect our operating cash burn to be $110,000,000 to $130,000,000 per quarter in fiscal 2024, we expect full year capital expenditures of approximately $150,000,000 as we near completion of our GMP manufacturing facility. Turning to our balance sheet, our cash and investments totaled $403,600,000 at September 30, 2023, compared to $482,300,000 at September 30, 2022. The decrease in our cash and investments was primarily due to cash used for operating activities and capital expenditures, partially offset by cash inflows from financing activities.

Speaker 7

Our common shares outstanding at September 30, 2023 were $107,300,000 With that brief overview, I will now turn

Speaker 4

the call back to Rick.

Speaker 7

Thanks, Ken. Arrowhead

Speaker 2

had another productive quarter and we see wide open space to accelerate our growth over the coming year. We expect 2024 to be a data and event rich year with many expected opportunities to create value, including readout of the plazasiran FCS Phase 3, filing our first NDA, launching a Phase 3 for SHTG with plazasiran, launching a Phase 3 cVAT with either plazasiran or zodasiran, readout in various patient populations with ARO C3, initial CNS data in patients with ARO SOD1, ARO RAGE, FeNO and Knockdown data in asthma patients ARO MMP7 Knockdown data in IPF patients ARO MUC5AC knockdown data in asthma and COPD patients and initiation of 1st in human studies with our 1st adipose targeting candidate. Thank you for joining us today. And I'd now like to open the call to your questions. Operator?

Operator

Please press star 1 and And our first question comes from Edward Tenthoff from Piper Sandler. Your line is now open.

Speaker 8

Great. Thank you very much and thanks for taking the question. I'm excited about all the progress on the cardiovascular side. I wanted to ask about the DM-one filing today, because now with this, I think you guys also recently maybe filed on DUX4, if I'm remembering correctly. So this is really a franchise is starting to build in muscle.

Speaker 8

Is this going to be a core area or could this be one of the areas for potential partnership that you were highlighting, thanks.

Speaker 2

Hey, Ted. Thanks very much. And again, we're really sorry for the technical problems.

Speaker 8

No worries.

Speaker 2

I think you're right. We view skeletal muscle as potentially another vertical, another franchise. We think both DM1 and DUX4 are good targets. We think these are 2 large numbers of patients who Desperately need treatment options and so we're excited about these. We are looking at some additional targets as well and so we'll see if this can grow to be something as large as we foresee pulmonary being for instance.

Speaker 2

At this point, it's a little bit too early to tell, but I would agree that right now it appears to be a pretty interesting burgeoning franchise for us.

Speaker 8

Awesome. Great. Thank you. Looking forward to hearing more about it.

Speaker 5

Thank you, Ted.

Operator

And thank you. And our next question comes from Ellie Merle from UBS. Your line is now

Speaker 9

open. Hey guys, thanks so much for taking my question and all the color on the timeline for the pulmonary program. Maybe just in terms of understanding the biology of RAGE, particularly in the high FeNO cohorts, I guess, what are you looking to see there? And what would you view as clinically meaningful? Thanks.

Speaker 5

We would expect to see the reductions in FeNO primarily based on our animal data and the work we did in the alternate area model Showed steep reductions in IL-thirteen. We can't measure FeNO in the rats, but a large reduction in IL-thirteen should translate into a reduction in FeNO and in terms of what would be clinically meaningful based on what was seen with tislepilumab or Dupixent, I think something in the 30% or so range would put us In the range of what those other molecules have been able to show.

Speaker 2

Javier, do you think that?

Speaker 3

No, I think that's

Speaker 9

Great. Thanks.

Speaker 7

Thank you.

Operator

And our next question comes from Maury Raycroft from Jefferies. Your line is now open.

Speaker 10

Hi, thanks for taking my question. I was going to ask one on ARO RAGE 2. You mentioned that in patients, the data is mapping with what you observed in healthy volunteer data. Can you elaborate on whether you're seeing this for your 90 2 in 184 mg asthma patients. And could you have the FEV1 data from these non FeNO patients, potentially even by year end or Q1 of next year, I guess maybe if you could provide more granularity on the time line there.

Speaker 10

And also, you talked a little bit about the subcu aero rage data. Can you remind or can you talk about what you're seeing there and remind what the purpose is of assessing that route of administration?

Speaker 5

Sure. So I'll take those in reverse order. Subcu, we're still about halfway through that study, the study is fully enrolled, but with healthy volunteers we're just collecting the data from some of the earlier cohorts. So we're not ready to share the SRAGE data from those studies yet. The idea there is that based on the animal work we've done, we were able to see significant levels of knockdown in both rodents and in monkeys with subcu administration.

Speaker 5

So we wanted to we view that as a potential additional option, an optional route of administration. It could be different from an inhaled route of administration. Then the next question I think was on FEV1. We've seen those data as they come in and it's primarily in there as safety endpoint and the cohort sizes are very small, we've not analyzed those data in the patient cohort that we have filled at this time, so I think it's too early for us to say anything about FED-one changes. Suffice it to say that The cohort sizes are single digits and PD-one can be a noisy metric.

Speaker 5

And then the first question was? It was mapping of Yes, that's right. We only have the S antigen data or the S RAGE reduction data from the 44 milligram dose level in the patients. So we've not seen the SRH reduction data from 92 milligrams or 184 milligrams.

Speaker 10

Got it. Okay. And for FEV1 at baseline, is that something you can comment on for the asthma cohorts, The higher dose cohorts?

Speaker 5

Yes. Again, I think we don't have all of the aggregated data as of yet, but

Speaker 3

for the senior cohorts and in the MAG 5AC program, but in the RAGE, asthma, they are mild patient by

Speaker 7

definition. Got

Speaker 10

it. So more mild patients in and the asthma patients for those 2 higher dose cohorts. Okay. Thanks for

Speaker 7

taking my question. Thanks, Marty.

Operator

And our next question comes from Mani Faroohar from Leerink Partners. Your line is now open.

Speaker 11

Thanks for taking the question.

Speaker 4

I guess I'm going to zoom out on an ultimately more macro and philosophical question. You talked about monetize some type of synthetic royalty or royalty sale monetization. You talked about a couple of different approaches to finance the ongoing CBOT, that in my mind raises 2 questions. One that is by definition anything that's royalties it's a fairly high duration financing instrument and that it's essentially a form of synthetic debt. How do you think about timing a royalty or I guess convert any type of debt any type of rate dependent transaction given how volatile the funding rates of anyone who would be buying that royalty from you would be, do you want to wait until rates come down, see if you could potentially get a tighter spread, etcetera?

Speaker 4

Just how do you think of that from a purely financial CFO macro perspective? And then secondarily, You know what, I'm going to stop. I'll ask my follow-up afterwards.

Speaker 2

Sure. So the short answer is no. We are we would not wait for macro environments to change. Who knows where those are going to there are several funders, multiple funders that do this kind of work. And we have been chatting with some of them for a bit now and we believe that there are there could be attractive opportunities there that are not dependent upon fundamental changes in the macro environment.

Speaker 2

So we feel comfortable that there are that there is capital there at a reasonable rate for us to finance these in this kind of manner, will we ultimately pull that lever? We have made that decision, but we just wanted to make clear that that is a lever and potentially an attractive lever that we could pull as part of an overall financing strategy.

Speaker 4

Great. And I guess my follow-up is, if you're going to be selling part of the economics of an asset that you're going into a CDOT, How do you think about that versus partnering the asset entirely rather than the Cbot yourself? Presumably, a large pharma partner would ascribe a lower operational discount to their own carrying out of a CVOT versus you guys doing your first CVOT implying a more attractive NPV if they were to acquire the asset from you in a partnership, Whether 100% purchase, royalty, fifty-fifty, under any terms, by definition, the economics of A partnership would be better than doing raising capital during itself. So like how do you so is there a reason why you see retaining it and then raising at an implied higher cost of capital as a better strategy rather than Selling it at an implied lower or partnering at an implied lower cost of capital and eliminating the operating risk of having to do a CVOT yourselves.

Speaker 2

Yes. Look, those are all things that we consider as we look at the array of funding opportunities ahead of us. Paying some amount of royalties on these is relatively cheap for us because we're not stacking royalties. We don't owe royalties on any of these assets. And so and presumably also those royalties will be capped.

Speaker 2

Presumably, they would not go indefinitely, but you're right, as we look at all these opportunities, we need to take all those things into consideration. Look, we see ourselves as a commercial company and we think we can create a lot of value as a commercial company. And so assuming that our the relative cost of capital, while holding on to these assets is reasonable, then that's something that we would do.

Speaker 4

All right. Thanks guys. That's really helpful. Yes, you're welcome.

Operator

And thank you. And our next question comes from David Lebowitz from Citi. Your line is now open.

Speaker 6

Thank you very much for taking my question. Just piggybacking on the last question, as far as any licensing agreements you're looking at, are you planning to wait until after the pivotal data? And also what activity level are you intending to really take within the partnership, is this something where you're going to be very active licensing to kind of one of these royalty companies or would this be something more specific where you're basically giving control of the asset to a larger pharmaceutical player?

Speaker 2

Yes. The answer to that just depends upon the asset, of course. We have done and we'll continue to do asset licenses like we do with HSD or HBV or AAT, I guess AAT is a little bit different, because we do have 50 giga profit share there, but or Lp we will do those going forward, depending upon the asset. Look, our here's our goal. We have a very large pipeline and it's only going to get larger.

Speaker 2

And so we've got plenty of room to license out some individual assets, what we want to end up with is a series of verticals where we can concentrate commercial build out and we can give our commercial team several drugs the hold in the bag to sell into various channels. I think we can do that given our franchises were pulmonary, muscle, cardiometabolic, CNS, etcetera, adipose, etcetera. So, I think we can do that. And as we look at how to cluster those, we will find that there are some outliers, if you will, some that may not fit well into a commercial strategy, and those would be the easy ones. Those would be the easy ones to license out.

Speaker 2

We also have the opportunity to do platform deals. We've talked about this in the past. I like that a lot. We now have 5 platforms, 5 different cell types that we can address. I like the idea of working with partners who can bring in targets to us and we can help to create drugs for those partners.

Speaker 2

That for me is found value as long as those targets are not what we're working on right now. And so maybe it's an unsatisfying answer because we'll be doing a number of different things, but that's the way we see the Waterfront. And again, if we are 1 or 2 asset company, then the answer would be much simpler. But we are a 20 plus asset company. And so we have the ability to structure a number of different partnerships and go to market strategies for ourselves.

Speaker 6

Thanks for taking my question.

Speaker 2

You're welcome.

Operator

And our next question comes from Luca Issey from RBC Capital. Your line is now open.

Speaker 11

Great. Thanks so much for taking my question. Congrats on the progress. I have a quick one maybe Javier, if I may. I was under the impression that you were planning a cardiovascular Come trial with APOC3, while it sounds to me that you're not planning cardiovascular come trial either with APOC3 or ANG3, Assuming that that is correct, what drove the change in strategy?

Speaker 11

Was this informed by conversations with the FDA? And is this related in any sort of form or shape with the numerical worsening in glycemic control that we've seen for APOC3? Any color there much appreciated. Thanks so much.

Speaker 3

Thank you for that question. It's really important. And I think this highlights how dynamic is So development today, how fast science change in our plans. If we go back, I would say 6 to 9 months when we already were thinking and working on a simple trial design for trosacitabonopec3, the focus was triglycerides and the field was focused on triglycerides as a key component of the receivable base. In the last 6 months, I think that focus changed.

Speaker 3

And I'm saying in the last 6 months, because I don't know if you Calling to the KOL webinar at the American Heart Association, Doctor. Nodarbar showed a slide while you see the number of publications in Renmin Cholesterol as a company of residual risk in the last 10 years, which was 10 or 20 papers a year versus 1,000 in the last 1 year. That means the change in this field is happening as we speak and the understanding that it's not just PG, but it's Renmin Cholesterol and it's the totality of the atherogenic lipoprotein is a new development. And frankly, 6 months ago or 9 months ago, it wasn't a key component of our decision making and it is now and it's been in the last 3 months. So now when you look at the 2 molecules and you focus on the concept of totality of atherogenic lipoproteins, not TG or not TG only, you can remember for TG AOC has better efficacy than HETO ANG3.

Speaker 3

But when you look at the totality of heterogeneic lipoproteins, HEDO ANG3 reduced LDL cholesterol by 20 plus percent, reduced REMA cholesterol by 80%. So it is substantially different. The population that we should address may not be exactly the same and that's something that we're thinking and talking to experts right now. So I think we're while changing following the science, we did have conversation with some experts. We did not have any conversation about this with the FDA yet and within the next month or so, we're going to get close to make a decision and start to define our next step from the regulatory perspective and from the clinical trial design perspective.

Speaker 2

And I don't think this was I don't think you were getting towards this, but let me just say our increase in interest in ANS-three doesn't reflect a lack of confidence in APOC3. We were moving forward to that forward on that as you point out for CBOT. But as the science has been moving, as Javier said, over the last 6 months, we've had this growing wait a minute moment where we should be looking also at ANS III just to ensure that we are pushing the best candidate that we can into a specific type of CVOT, we are still moving as quickly as we can. Obviously, with FCS, we'll be finished with that Phase 3, I think, in Q2, we'll be starting the SHCG Phase 3 early 2024. Now we've got a little bit of time to figure out where we're going to place our bet with the C bond.

Speaker 3

Got it. Thanks so much, guys. You're welcome.

Operator

And thank you. And our next question comes from Brendan Smith from TD Cowen. Your line is now open.

Speaker 11

Great. Hi, guys. Thanks for taking the questions. Congrats on the progress. Just a couple of quick ones, if I could.

Speaker 11

I also want to have a follow-up just on the timing to pulmonary data. Is it fair to say we'll see the high dose RAGE data in asthma patients by Q2 of next year, with the high CINO data in Q3. And then really just any color you can give us on MUC5aC and MMP7, maybe when we might see some of that data next year would be great. And then quickly, I just wanted to see if there's any updates on the ARO C3 program and if there's any plans to put out any data from that next year either? Thanks.

Speaker 5

Sure. James? Sure. Yes. The intention would be to release the SRAGE data from the asthma cohorts when it becomes available to us, so probably middle of the first half of next year, I think for the asthma, the high dose asthma, esterase data.

Speaker 5

And then in terms of FeNO in the high FeNO cohorts, we're able to meet Q3 for, for pheno data in those patients. And then MUC-five AC has been a little more challenging to enroll Some protocol requirements in there and the requirement of those patients being severe asthmatics, But likely towards the middle of the year for MUC5AC data, we still need to enroll the highest dose cohort of those patients. In terms of C3, we are in the process of enrolling the patient cohorts, the IgA nephropathy patients as well as the C3G patients. So probably the second half of twenty twenty four for proteinuria data.

Speaker 11

All right, great. Thanks very much. Appreciate it.

Operator

Thank you. And our next question comes from Mayank Mamtani from B. Riley Securities, your line is now open.

Speaker 12

Good afternoon. Thanks for taking our questions. So maybe James, if you could dive a a bit deeper on the safety margin difference that you've seen between MUC5 versus RAISE in the recent preclinical data that we And if you're able to comment on how the Noelle doses for VUMPD5 correlate with the top dose that's being tested in the clinic? And maybe a high level question on like what for MUC5 would be human proof of concept like we like investors think about For atorage, in terms of the high asthma patients, like you just commented, it's severe asthmatic But what sort of biological signal would be relevant here given obviously this is more downstream physiology to IL-four after 13.

Speaker 5

Yes. I think on the last question, it's a bit tough to pin down what's clinically relevant in terms of MUC5AC knockdowns, since there's not a great correlate out there from other drugs. So I can't give you an exact number on that. In terms of the safety margins comparing MMP-seven or RAGE with ENAC, I guess it depends on the dose level. We used a low, mid and high dose level for all of those chronic tox studies in the rats.

Speaker 5

If you compare the cumulative dose given over a 6 month RAD study at the high dose level for wage, we had there's a sevenfold difference between the high dose level used in ENAC and in RAGE and the 4 to 5 full difference for MMP-seven in the RAD, so it's significant difference between the total cumulative doses that were administered In those 2 with those 2 different molecules.

Speaker 12

Got it. Thank you. And then just on the muscle targeting programs that's for DM1, could you just remind us the targeting receptor ligand approach here? And as obviously you guys know, it's an active field. There are alternative antibody ASO approaches.

Speaker 12

Maybe how does sort of your preclinical data inform what you've seen? And maybe related to that, is the plan to secure non dilutive capital for that no longer a near term event, Chris? Or you're just going to be opportunistic recognizing that there might be some more clinical data coming from these targets from any of your peers.

Speaker 2

I'm sorry, I misunderstood the what kind of capital? Say that again.

Speaker 12

Yes. I think you had plans for non dilutive capital at some point, which delayed the DUX4 program. So I'm just curious if you're no longer going to do anything strategically there for the mass of in the near term.

Speaker 2

Right. Yes, yes, yes. That ran its course for now. We are happy to run the DUCs IV as well as DM1 clinical programs and then which does not mean that we will never partner them, but we were exploring as you know, we were exploring potentially partnering DUCs IV. It just made sense to us to stop those discussions and we're moving ourselves for right now.

Speaker 5

James, do you want Sure. And then on the comparison with the other muscle targeting platforms that are out there, for DM1, we've worked and knockdown in the syno and have achieved, I think compared to similar knockdown or similar duration of effect with what's been published for example, the transfer targeted platforms, we use the peptide targeting the AlphaB Beta 6 integrin. So it's a different way of getting the sRNA into the cell. I think we in terms of total drug dosage, our dosages should be much lower compared to the transferring conjugates, which of course conjugating sRNA to a monoclonal antibody. And then I would also anticipate that we would not expect to see some of the transferring related safety issues that have been out there, of course, time will tell and the data will tell us, but it's something we would not anticipate.

Speaker 12

Okay. Thanks for taking my questions, please.

Speaker 2

You're welcome.

Operator

Thank you. And our next question comes from Patrick Trucchio from H. C. Wainwright and Company. Your line is now open.

Speaker 8

Thanks. Good evening. Just regarding the 2025 targeting goals, can you give us a sense of from which platforms the 20 drug candidates are expected to emerge from understanding several have been announced this year and if along with CNS pulmonary liver adipose and muscle, if additional tissues may be targeted with TRiM?

Speaker 2

I don't have any guidance to tell you on additional cell types other than the fact that we will be in new cell types. We've said publicly that we think we can get into a new cell type every 18 to 24 months. I think that continues. Look, I expect by the year 2025, we will have new or additional candidates in every one of those verticals.

Speaker 8

Got it. And then just a few follow ups on the pulmonary compounds. Just first regarding initial chronic tox results So the ARO RAGE and ARO MP7, I'm wondering if you can tell us if or when further chronic tox data is expected and the level of that data should continue to support advancement of those programs and when you might have similar data for ARO MUC5AC in 2024. And just to follow-up on ARO REACH, if you can discuss the targeting mechanism of the subcu administration and advantages that would be expected for this route relative to the inhaled route?

Speaker 5

Yes, sure. So in terms of the chronic rat or the chronic tox data for the pulmonary programs, that's it. I mean, that's the final that's from the final report. So there's no more expectations. We won't be getting any more data around chronic tox for MMP-seven or RAGE.

Speaker 5

From up 5AC, We're still planning the chronic tox study. We wanted to get some biomarker data from the clinical study to better inform on the dose frequency for the chronic tox studies since frequency of administration seems to be really important to avoid entering into dose levels where we see toxicity, we really wanted to nail down dose frequency. So we need to get a duration of effect from the clinical studies before we finalize the chronic tox study for MUC-five

Speaker 2

And regarding the subcu, our thinking there was twofold. 1, there could be other targets and other indications where subcu administration is just preferred to inhaled. And second, that could potentially also broaden or widen out our therapeutic index.

Speaker 8

Great. Thank you very much.

Speaker 2

You're welcome.

Operator

And thank you. And our next question comes from fracar agrawal from Cantor Fitzgerald. Your line is now open.

Speaker 13

Hi, thanks for taking my questions and congrats on the progress. So on your ARO X DH program that was partnered with Horizon, it seems that Amgen has decided to terminate this agreement. Was there any data generated by XTH program or was it just part of the recent And what are your plans for this asset now develop internally or will you be looking for a partner again? Thank you.

Speaker 2

So it's early to say on that. We haven't seen data. I don't know that we will, but at least so far we haven't seen any of the clinical data. And so and we've not been told you know, why that was being discontinued, whether it's strategic or something else. We have some theories.

Speaker 2

James, do you want to talk about the Amylin program for instance?

Speaker 5

Sure. Yes. I think another company had a mesyronate targeting the same gene target XDH. It was also discontinued due to lack of decline in uric acid in the blood, plus immunogenicity knockdown All of

Speaker 2

the MycetiGH

Speaker 5

in the liver, there are still hepatic sources. So liver knockdown might not have been enough.

Speaker 7

Thank you.

Speaker 3

Thank you.

Operator

And one moment for our next question. And our next question comes from Mike Alts from Morgan Stanley. Your line is now open.

Speaker 14

Hey guys, thanks for taking the question. Maybe just a quick one on ARROWAGE. Just in terms of timing of a potential Phase 2 study there. Now that the clinical chronic tox studies are done for ARROWAGE, do you have enough data to now start to engage with the FDA or is the plan more to wait for some of the other cohort data like the asthma patients or hyfino before you

Speaker 3

We're thinking about starting Phase 2 2024 for sure, and there's already work going into that, that we design, patient populations, selection of we are also we are already planning as the data is coming in, it will help us to decide the dose of the dose frequency, But we are already planning on the next stage development for the 8 0 range.

Speaker 4

Okay. Thank you.

Speaker 5

Welcome.

Operator

And thank you. And one moment for our next question. And our next question comes from William Pickering from Bernstein. Your line is now open.

Speaker 11

Hi, thanks so much for squeezing me in. I had a few follow ups on the DM1 announcement. So how is the drug designed to get your siRNA inside the nucleus for example, splicing assessment or any functional endpoints? Thank you.

Speaker 5

Sure. Yes. So we will look at some of the same endpoints that other companies have looked at and we'll look at total DMPK knockdown, changes in spliceopathy and we'll also look at the video end opening time as well as some of the other functional endpoints. And so your other question on knocking down siRNA in the nucleus, we've done some work in animals. We haven't published this yet or started publicly via poster or presentation.

Speaker 5

We've shown at doses similar to what we had planned on administering in the clinic that we are able to get a level of knockdown of nuclear RNA and that translates into improvements in spliceopathy. So that was the impetus for us moving this program into the clinic that we could get even with some modest levels of nuclear RNA knockdown, we could get improvements in spliceopathy.

Speaker 11

Great. Thanks so much and congrats on the progress.

Speaker 5

Thanks.

Operator

Thank you. And I would now like to turn the call back over to Chris Andy Lonsie for closing remarks.

Speaker 2

Thanks very much everyone for joining us today and I wish you all a happy holiday season.

Operator

This concludes today's conference call. Thank you for participating. You may now disconnect.

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Earnings Conference Call
Arrowhead Pharmaceuticals Q4 2023
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