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Lineage (LCTX) Q3 2026 Earnings Call Transcript

The Motley Fool·11/13/2026 16:13:56
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DATE

Thursday, Nov. 12, 2026

CALL PARTICIPANTS

  • Head of Investor Relations - Ioana Hone
  • Chief Executive Officer - Brian Culley
  • Chief Financial Officer - Jill Howe
  • Senior Vice President and Head of Clinical - Dr. Priyantha Herath

TAKEAWAYS

  • Cash and Marketable Securities -- $45.2 million as of Sept. 30, 2026, which the company expects will fund planned operations into the second quarter of 2028.
  • Total Revenue -- $1.5 million, representing a decrease of $2.2 million from the same period in 2025 due to lower collaboration revenue recognized from the Roche agreement.
  • NeuroAirmid Acquisition Cash Consideration -- $2.4 million paid upfront to shareholders and $1.9 million paid to third parties, totaling $4.3 million in day one cash payments.
  • NeuroAirmid Acquisition Equity Consideration -- 2.2 million common shares issued at closing, valued at approximately $2.1 million.
  • Deferred Acquisition Payments -- $2.6 million in cash and $2.4 million in common shares due on the first anniversary of closing to fulfill upfront obligations.
  • HUNT1 Operating Costs -- Less than $2 million per year, which includes a co-funding obligation for the $12 million CIRM grant.
  • HUNT1 Patient Enrollment -- Six patients dosed as of the call date in the Phase Ib/IIa REGEN4HD study, with no serious adverse events reported.
  • REGEN4HD Study Scope -- 21 patients in total, evaluating dose escalation from 2 million to 16 million cells for the treatment of Huntington's disease.
  • OpRegen Material Shipment -- Hundreds of vials of GMP drug product were recently released and shipped to Genentech for clinical trial use.
  • Research and Development Expenses -- $3.8 million, an increase of $0.5 million from the prior year driven by higher spending on preclinical and ReSonance programs.
  • General and Administrative Expenses -- $4.9 million, an increase of $0.7 million year over year primarily due to personnel and stock-based compensation costs.
  • Net Income -- $4.2 million, or $0.02 per share basic, reflecting a quarterly fair value noncash remeasurement of warrant liabilities.
  • AlloSCOPE 5D Patent -- U.S. Patent No. 12,692,476 issued with an expiration date of June 9, 2043, covering methods to capture adherent cell features in 3D culture.
  • AlloSCOPE Scaling Progress -- 5D technology successfully scaled from 100 milliliters to 3 liters.
  • COR1 Development Timeline -- Preclinical animal data is expected to be shared publicly in the first quarter of 2027.
  • ReSonance Collaboration -- $12 million partnership with William Demant Invest extended into its second year following successful first-year milestones.
  • OPC1 DOSED Study -- Third patient scheduled for surgery on Dec. 8, 2026, with a fourth patient expected to be dosed in the first quarter of 2027.
  • Islet Cell Differentiation -- First reported successful differentiation of pluripotent stem cells into islet cell precursors using the 5D system.
  • Milestone Eligibility -- Up to $615 million in remaining development and commercial payments eligible under the Roche and Genentech agreement.

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RISKS

  • Culley stated, "Approvals for novel modalities can take longer than we'd all like," regarding the clinical development timeline for the OpRegen program.
  • Culley noted that while Lineage is the only company with a neural progenitor cell transplant in the clinic, competitors are focused on reducing mutant huntingtin, and one competitor's Phase Ib trial has been delayed to Dec. 31, 2027.
  • Howe reported that the cash runway guidance of the second quarter of 2028 is one quarter earlier than prior guidance, reflecting the financial impact of the NeuroAirmid acquisition.

SUMMARY

Lineage Cell Therapeutics, Inc. (NYSEMKT:LCTX) announced the acquisition of NeuroAirmid Therapeutics, adding the clinical-stage HUNT1 program for Huntington's disease to its pipeline. Management reported that this acquisition completes an initiative titled Lineage 3.0, designed to diversify the company's portfolio into three clinical-stage assets alongside OpRegen and OPC1. The company stated that the HUNT1 program utilizes the same proprietary cell line as existing internal programs, which allows for immediate integration into the AlloSCOPE manufacturing platform. Financial results reflected a shift in cash runway guidance to the second quarter of 2028 and a decrease in quarterly revenue due to the timing of deferred revenue recognition from the Roche collaboration. Management stated that the company remains focused on capital efficiency and the industrialization of cell therapy manufacturing through its AlloSCOPE 5D technology.

  • Culley stated that the successful differentiation of islet cell precursors in the 5D system "opens multiple options to continue development, either independently or in an alliance with specialized parties."
  • Dr. Herath noted that the HUNT1 program addresses neurodegeneration through both cell replacement and the release of brain-derived neurotrophic factor to support surviving host neurons.
  • Management confirmed that the company has already filled a GMP master cell bank of the cell line underlying the HUNT1 program to accelerate tech transfer and industrialization.
  • The company highlighted its competitive position in the RPE transplant field, noting that OpRegen remains the furthest along in clinical development despite a competitor's reported delay.
  • Culley indicated that the COR1 program for corneal dystrophies moved from concept to animal testing in less than a year, reflecting the speed of the AlloSCOPE platform.
  • The company scheduled a scientific advice meeting with the Danish Medicines Agency for Dec. 2026 to discuss regulatory development plans for the ReSonance auditory neuron therapy.

INDUSTRY GLOSSARY

  • AlloSCOPE: Lineage's proprietary allogeneic cell manufacturing platform designed for scalable, off-the-shelf cell production.
  • 5D Technology: A specific application of AlloSCOPE that attempts to combine the features of 2D adherent cell manufacturing with 3D bioreactor scale.
  • HUNT1: An allogeneic neural progenitor cell therapy program for the treatment of Huntington's disease.
  • OpRegen: A retinal pigment epithelium cell replacement therapy for the treatment of geographic atrophy secondary to age-related macular degeneration.
  • OPC1: An oligodendrocyte progenitor cell therapy for the treatment of cervical spinal cord injuries.
  • CIRM: California Institute for Regenerative Medicine, a state agency that provides grant funding for stem cell research.
  • Striatum: A deep brain structure that is the primary site of neuronal loss in Huntington's disease.
  • Islet Cells: Cells found in the pancreas that produce insulin, targeted for the treatment of Type 1 diabetes.
  • RPE: Retinal pigment epithelium, a layer of cells in the eye essential for vision.
  • BCVA: Best corrected visual acuity, a standard measure of vision used in clinical trials.

Full Conference Call Transcript

Operator: Welcome to the Lineage Cell Therapeutics' Third Quarter 2026 Conference Call. [Operator Instructions] An audio webcast of this call is available on the Investors section of Lineage's website at www.lineagecell.com. This call is subject to copyright and is the property of Lineage and recordings, reproductions or transmissions of this call without the expressed written consent of Lineage are strictly prohibited. As a reminder, today's call is being recorded. I would now introduce your host for today's call, Ioana Hone, Head of Investor Relations at Lineage. Ms. Hone, please go ahead.

Ioana Hone: Thank you, Audra. Good afternoon, and thank you for joining us. A press release reporting our third quarter 2026 financial results was issued earlier today, November 12, 2026, and can be found on the Investors section of our website. Please note that today's remarks and responses to your questions reflect management's views as of today only and will contain forward-looking statements within the meaning of federal securities laws. Statements made during this discussion that are not statements of historical fact should be considered forward-looking statements, which are subject to significant risks and uncertainties. The company's actual results or performance may differ materially from the expectations indicated by such forward-looking statements.

For a discussion of certain factors that could cause the company's results or performance to differ, we refer you to the forward-looking statements sections in today's press release and in the company's SEC filings, including its most recent annual report on Form 10-K and in the Form 10-Q filed today. We caution you not to place undue reliance on any forward-looking statements, which speak only as of today and are qualified by the cautionary statements and risk factors described in our SEC filings. With us today are Brian Culley, our Chief Executive Officer; Jill Howe, our Chief Financial Officer; and Dr. Priyantha Herath, our Senior Vice President and Head of Clinical. I'll now hand the call over to Brian.

Brian Culley: Thank you, Ioana. Good afternoon, everyone, to what I expect will be an important and memorable earnings call. Just a few minutes ago, we announced that we had acquired NeuroAirmid Therapeutics, a private biotech company founded on technology licensed from the lab of world-leading Huntington's disease researcher, Dr. Leslie Thompson. NeuroAirmid holds certain rights to HUNT1, formerly known as hNSC-01, which is a clinical stage neuro stem cell program currently enrolling patients in a Phase Ib/IIa clinical trial for the treatment of Huntington's disease, a fatal neurodegenerative disorder. With this transformational deal, we have secured an entirely new clinical-stage cell therapy program, which immediately becomes a key part of Lineage's clinical portfolio.

I plan to spend most of today's call outlining in detail why we are so excited about this acquisition and how we believe the addition of a third clinical stage asset to our pipeline alongside OpRegen and OPC1 will enhance our business and drive future value. But before I dive into this breaking news, I want to provide some short updates on our other programs. I will start with OpRegen, which, of course, remains tremendously important as our lead program. OpRegen continues to be evaluated by Genentech in a Phase IIa study named GAlette in patients with geographic atrophy secondary to age-related macular degeneration.

GAlette is intended to optimize surgical delivery to the subretinal space and evaluate the safety and efficacy in OpRegen in patients with GA. As you're all aware, we are not able to provide guidance on our partners' timing for further clinical development, but we remain confident that the OpRegen program is being well supported within the Roche and Genentech organizations. Some of you have asked me recently about public records found on an FDA website and that disclose information about several hundred vials of OpRegen drug product labeled for clinical trial use that has recently been shipped to Genentech from our GMP manufacturing facility.

Under the terms of our agreement with Roche and Genentech, I cannot comment on anything outside of publicly available facts. So today, I can only affirm that the information regarding the production, release and shipment of clinical material for multiple batches of OpRegen is accurate. The other note I will share today about OpRegen is to call out some activity in the RPE transplant competitive landscape, which we observed on Bloomberg. Apparently, a clinical trial sponsored by an OpRegen competitor has been significantly delayed with a new anticipated primary completion date of their ongoing Phase Ib trial pushed out to December 31, 2027.

While it's clearly not good for patients in need of treatment to experience extended time lines, this might also serve as a reminder that Lineage and our partners at Roche and Genentech remain furthest along in clinical development in this important and innovative field of RPE cell transplantation. Approvals for novel modalities can take longer than we'd all like, but we remain hopeful that OpRegen, which has previously demonstrated retinal restoration and improved visual acuity scores will ultimately reach the market for the benefit of patients around the world. Moving next to AlloSCOPE, our proprietary manufacturing platform.

I want to highlight that we recently announced the issuance of a patent underlying an application of the AlloSCOPE platform that we call 5D. 5D is a term we use to describe certain methods we employ to try and capture the positive features of 2D adherent cell manufacturing when performed in a 3D culture environment. We are doing this to try and capture the high-volume advantages and lower production costs for cell therapies that are expected to have high cell dose requirements, such as an islet cell therapy for the treatment of Type 1 diabetes, which is expected to require hundreds of millions of cells or even a billion cells per patient. But 5D offers more than just greater scale.

So we are using 5D methods for other programs in our pipeline. This patent, therefore, is fundamental to our business, and we are extremely happy to have a new proprietary position for our platform with an expected patent expiration date into 2043. Speaking of islet cells, we believe the highest and best opportunity for our 5D technology may be for the production of islet cells because islet cells don't easily expand in culture. Yet as I said, the dose requirement for an islet cell therapy is likely to be extremely high.

We believe a cost-effective cell therapy for T1D will need to start with a huge number of undifferentiated cells that importantly, retain their capacity to scale and specifically their pluripotency and response to differentiation factors before you even start turning them into islet cells.

Our engineering efforts with ILT1 to date have focused on producing cells with these critical features and on a modality that can support both expansion and differentiation entirely in a closed culturing system with no inefficient 2D plating steps or vessel transfers, because if this approach to generating large numbers of undifferentiated pluripotent stem cells is successful and applied to an islet cell differentiation protocol, it could potentially solve a major hurdle to production and commercialization of an islet cell therapy product for the treatment of Type 1 diabetes. We have been successful this year in showing the scalability of our new 5D technology from 100 mls to 500 mls and more recently to 3 liters.

With those achievements behind us, we more recently shifted our effort to showing that our 5D cells could actually differentiate into endodermal precursors, which is the first and necessary step for all islet differentiation protocols. I'm pleased to share today for the first time that our R&D team was able to differentiate pluripotent stem cells into islet cell precursors in a 5D system and that those precursors exhibited the desired attributes when compared head-to-head against islet cell precursors made on a 2D system. Importantly, because these precursors are a common cell type to all islet differentiation protocols, this work opens multiple options to continue development, either independently or in an alliance with specialized parties.

I will just note that regarding potential alliances, we are not interested in becoming a contract manufacturer. So I would anticipate that any such alliance would reflect the value of our enabling technology. I'm both pleased and impressed with how quickly this work has proceeded and because we believe our 5D approach provides a differentiated solution to a major challenge facing the cell therapy industry, which is enabling commercially scalable, consistent and cost-effective manufacturing of pluripotent cell-derived therapies, I will continue to keep you informed of our progress. In parallel to ILT1, we also have a deploying 5D platform to produce corneal endothelial cells. So I'll discuss that program next.

I am sometimes asked when we will have data from the COR1 program for the treatment of corneal dystrophies. So I just want to start by reminding everyone that the COR1 program is barely a year old. We disclosed it less than 8 months ago, and it's already moved into preclinical animal testing. So we are moving very quickly, and we hope to continue to go quickly. As I just mentioned, we used our AlloSCOPE platform with the 5D technology and successfully achieved seamless precursor expansion and differentiation in a 3D bioreactor to produce corneal epithelial cells, which together with our proprietary thaw-and-inject formulation, meet our internal criteria for continued development.

Knowing that our audience is eager to know how our cells perform in the established translational models, we then advance those cells promptly into preclinical testing. We expect to have initial preclinical data internally by year-end and to share that data publicly in the first quarter of 2027. So that is something we can all look forward to from the COR1 program. The other internally developed program that we successfully moved from product concept into preclinical testing in less than a year is ReSonance, our auditory neuronal cell therapy for the treatment of hearing loss.

After producing these cells and generating some initial in vitro data with our academic collaborators at the University of Michigan, we entered in August 2025 into a $12 million research collaboration funded by William Demant Invest, or WDI. WDI continues to fund preclinical development of this program. And at our recent joint steering committee meeting, we jointly decided to advance the collaboration into a second year. We also already scheduled our first regulatory interaction for ReSonance, a scientific advice meeting with the Danish Medicines Agency, which is scheduled for December.

I want to pause here to highlight that we have shown not only for ourselves, but also for external partners that we have moved 2 completely new and internally developed product candidates quickly and successfully through the early stages of manufacturing and development, and we've done this with capital investments that we invite to be compared with our cell therapy peers. We know innovation in cell therapy can be a long journey, so we strive to extract a return from each of our invested R&D dollars. We believe we have developed a track record to support our commitment to fiscal discipline, something we believe is prudent in good markets and essential in bad ones.

Our plan is to continue to build a diversified portfolio of allogeneic cell transplant programs that rely on our proprietary manufacturing platform, which leads me to the headline of today's call, our acquisition of NeuroAirmid and the HUNT1 neuronal cell therapy. On this call, we will refer to NeuroAirmid as NAM and the lead asset as HUNT1, reflecting Lineage's pipeline nomenclature. We have reduced the highlights of the deal down to 10 key points, which the team will review next. Dr. Herath will first review the technology and scientific rationale for HUNT1. Jill will then provide the economic implications, and I will close with the strategic fit. We will begin with Dr.

Herath, who actually embodies the first of our 10 key points, which is internal expertise because he is a bona fide expert in Huntington's disease. And I will invite you to examine Dr. Herath's full bio on our newly updated website. I will also just point out that he has cared directly for many HD patients as a specialized attending neurologist. In his industry career, he led the work on 2 separate first-in-human Huntington's trials and even has formal training in stereotactic procedures in Parkinson's disease, which is the delivery method being utilized in the ongoing HUNT1 trial. We are delighted to be able to hit the ground running with these internal capabilities, and I know Dr.

Herath is particularly excited that we were able to complete this transformative acquisition.

Priyantha Herath: Thank you, Brian, and thank you all for joining us today. For those of you who may be less familiar with Huntington's disease, it is a rare inherited neurodegenerative disease caused by a mutation in the Huntington or HTT gene. Over time, that mutation leads to the dysfunction and loss of neurons that are important for decision-making, thinking, emotions, behaviors as well as movement. HD is a particularly devastating disease because it affects people across multiple aspects of their lives and in its later course can resemble a cruel combination of dementia, Parkinsonism and psychosis. The early clinical course of HD is characterized in part by the loss of neurons in a structure deep within the brain called the striatum.

The striatum is a major node in the neural circuitry that supports cognitive, behavioral psychiatric and motor functions. It is in the striatum that neurons, especially a type of neurons called medium spiny neurons are lost earliest and most severely in HD. When these medium spiny neurons are destroyed, performance of the neural networks that do all of this work degrades and beyond a certain threshold, the functions that those networks support become abnormal, thereby causing symptoms and signs of the disease. Then it continues to progress until you can somehow stabilize or replace the lost cells. Existing HD treatments are largely aimed at managing individual symptoms rather than stopping or reversing the underlying neurodegeneration.

That is because for a long time, the field held that the mutant protein itself was the immediate cause of neuronal cell death. Various approaches to reduce mutant protein have been the mainstay of HD therapeutics for many years, and some of these huntingtin reduction strategies remain under investigation in clinical trials, while a number of them have already failed. More recently, though, new research has redefined our understanding of processes that likely initiate the neuronal cell death. You hear about this in various programs that attempt to reduce what is called somatic instability in HD.

With this, the focus in Huntington's disease research has been shifting because the mutant huntingtin may not be the most proximate cause that leads to neuronal cell death. I should note that neither addressing the DNA mismatch repair in the case of somatic instability nor reducing the mutant huntingtin protein itself is designed to support the surviving cells or to restore the neurons that have already been lost. And so based on the more recent understanding of the disease, we and others believe cell replacement could be an effective approach to treating symptoms of HD.

Knowing that one of the earliest and most critical places where the cell loss occurs is in the striatum, we believe that administration of replacement neurons directly into the striatum could help restore and stabilize this critical node of the brain. The HUNT1 clinical program embodies this approach and is designed to address cell loss in 2 ways. First, the cells differentiate into different kinds of neurons that may form connections with the host brain circuitry. Second, the implanted cells produce permissive growth factors, especially brain-derived neurotrophic factor, BDNF, a protein that supports neuronal survival. It is deficient in Huntington's disease.

We believe that the former will restore some of the lost cells and the latter will support the remaining cells in the circuitry, thereby stabilizing the network and therefore, symptoms. And as you've heard today, this novel mechanism has reached clinical testing. And if restoration is robust, symptoms might not only stabilize, but could also improve. The HUNT1 program is being studied clinically at hNSC-01. It is an allogeneic neural progenitor cell therapy and was created from the same cell line that we have used with our AlloSCOPE 5D technology as well as for our COR1 program, giving us experience and confidence in this line.

HUNT1 is currently being administered to symptomatic HD patients as a single direct injection into the striatum in an ongoing Phase Ib/IIa clinical study called REGEN4HD. Before the REGEN4HD trial was initiated, a robust preclinical package was developed. HUNT1 cells were studied in vivo in several well-characterized mouse models of Huntington's disease. In vivo differentiation into different neuronal subtypes was observed with neuronal markers expressed for at least 8 months after administration. Synaptic contacts with host neurons were also observed and BDNF release was measured. Most importantly, improvement in HD-associated pathology and behaviors were observed in these studies in these animals.

Regarding preclinical safety in pivotal 9-month GLP toxicology and tumorigenicity study, no treatment-related adverse findings and no tumors were observed. Survival, neuronal differentiation and short-term safety were also shown in nonhuman primates. This robust preclinical data set supported the advancement of this program into clinical testing in the REGEN4HD study, where we hope that these effects will be translated into patients. REGEN4HD is an open-label Phase Ib/IIa study sponsored by University of California, Irvine. It enrolls adults aged 18 to 65 with genetically confirmed early manifest Huntington's disease. The Phase Ib portion reflects dose escalation from 2 million to 16 million cells through 4 cohorts of 3 patients each. Each increase is gated by independent Data Safety Monitoring Board.

The planned Phase IIa portion then adds 9 patients at the maximum tolerated dose for 21 patients in total. Cells are delivered under real-time MRI guidance and patients received 12 months of a modest but well-established immunosuppression regimen with monitoring for immune responses against the graft. The primary endpoint of this trial is safety at 6 weeks after surgery. This period covers surgical complications, signs of graft rejection, seizures, infection and complications of immunosuppression. Long-term safety is being assessed at 12 months. Exploratory measures include Unified Huntington Disease Rating Scale, UHDRS, motor and functional scores, cognitive and behavioral scales, volumetric MRI, FDG-PET, which together would provide insights into potential treatment activity.

Fluid biomarkers include neurofilament light chain in CSF and plasma and proenkephalin in CSF that will be measured. Notably, proenkephalin is produced by medium spiny neurons, the very population of neurons that this therapy is intended to support. Active follow-up of these patients will continue for 2 years with long-term safety follow-up to 15 years, which is standard for cell and gene therapy clinical studies. With respect to data to date, Cohort A and B enrollment are now complete with a total of 6 patients dosed as of this call. To date, no serious adverse events have been reported. And with that, I'll turn the call to Jill to discuss the economics of this acquisition.

Jill Howe: Thanks, Priyantha. This was a transaction that involved 4 significant parties. So I think it makes sense to go beyond the headline numbers and explain why we saw this as a great business opportunity for Lineage. Starting with the upfront consideration, we have made a cash payment of $2.4 million to NAM shareholders as well as issuing approximately 2.2 million common shares, or $2.1 million worth of Lineage equity. In addition, we made cash payments of $1.9 million to third parties in connection with the transaction.

In the aggregate, our external cash payments on day 1 were approximately $4.3 million, a number we feel not only reflects exceptional value for clinical stage assets, but also fits well within our capability for investment. Following these upfront payments, we have updated our run rate guidance into Q2 2028, which is 1 quarter earlier than our prior guidance. On the first anniversary of the transaction closing, we expect to make a final installment of the upfront payment and plan to pay NAM shareholders up to approximately $2.6 million in cash and $2.4 million worth of Lineage common shares as well as a $356,000 cash payment to CIRM.

And at that time, we will have fulfilled all of our upfront payment obligations. All of the remaining payments to NAM shareholders arising from this transaction are contingent and based upon substantial clinical progress. Clearly, these are payments we would be happy to make because they reflect success of this program. And as with the upfront, all of the contingent payments can be paid half of Lineage stock at our election, reducing the burden on our cash runway. In terms of the ongoing and expected operational costs, the REGEN4HD trial is being funded by a $12 million CIRM grant awarded to UC Irvine.

We estimate that our clinical costs for the program will run less than $2 million per year, which includes our obligation to co-fund a portion of the CIRM grant up to $3.1 million. We believe these investments will fit well within our historic budget run rate of approximately $30 million per year. As you can see, this is a transaction that we felt was extremely attractive for us from both a scientific and financial perspective. And in addition to the novel approach and the acceptable price tag, there are some important strategic reasons for us to have entered into this acquisition, which Brian will cover next. Brian?

Brian Culley: Thanks, Jill. So we heard about the strong scientific rationale from our in-house HD expert, Priyantha, and heard about the compelling economics and relatively modest impact to our cash runway from Jill. So next, I'm going to provide additional context on 4 final points from a strategic perspective, which will complete our 10-point list. First, it's vital to understand that Lineage already held commercial development rights to the underlying cell line upon which HUNT1 was developed. Many years ago, the Thompson Lab obtained a research use license to that line, but that license did not include clinical or commercial rights.

Those pre-existing rights were held by Lineage and provided us with both strategic insight into the program and leverage in negotiating mutually favorable deal terms. Perhaps not coincidentally, the line they chose as the best option for HUNT1 development was also one that we independently selected to utilize with our AlloSCOPE 5D technology and for our COR1 program. I want to emphasize the convergence of 2 independent R&D groups honing in on this key cell line. It is probably not a coincidence that among hundreds of possible choices we each independently chose the same line for further investment. This line's characteristics give us additional confidence in its potential clinical performance.

In addition to the line, Lineage also offered something even more important and useful to the future of this product candidate. We have already demonstrated the capability to produce a large-scale GMP production system, which is not yet available for HUNT1, but would be highly desirable to have. And so the second key contribution that Lineage brings to this deal is the ability to industrialize the HUNT1 manufacturing process. Because the team at NAM has a sophisticated understanding of the importance and difficulty of securing a credible manufacturing partner, we believe they appreciated the value and enablement that a proven team like ours could bring to the program.

So in addition to assuming responsibility for clinical development of the HUNT1 program following completion of the REGEN4HD clinical study, we'll also assume responsibility for all future cell manufacturing, process development, scale-up and optimization activities. Regarding the competition, in addition to what Dr. Herath mentioned, I would just add that while there is clinical data suggesting that lowering mutant Huntington does not lead to clinically meaningful outcomes, it remained plausible that one or more of these approaches will reach the market while HUNT1 advances through clinical testing. If that occurs and some attenuation of the disease is achieved through mHTT reduction, it still will not address the restoration side of the disease.

Just as complement inhibition can slow the progression of geographic atrophy, but it cannot restore vision. Restoration of lost neural tissue might only be possible with a cell transplant. And then regarding the clinical program, the ongoing HUNT1 study is primarily about collecting safety data, but it also will be collecting functional assessments, including TFC, which I'll note is the same assessment that FDA intends to rely on for the proposed confirmatory trial of uniQure's AMT-130 program.

And as I have explained on prior calls, one of the drivers of Lineage's choices of which cell therapies to develop is the potential to collect efficacy signals in a Phase I setting rather than having to wait for larger and more expensive Phase II comparative studies. This approach has allowed some cell therapy product candidates to advance directly to Phase III, a strategy we've seen employed by companies like Bayer and Aspen, which are working on similar cell transplant approaches, but for Parkinson's disease. And then finally, regarding delivery, we're pleased that the study is using a proprietary stereotactic delivery system from ClearPoint Neuro. Stereotactic delivery has become widespread with thousands of treated patients.

And conveniently, ClearPoint is located just down the road at Fletcher Cove, one of my favorite locations here in San Diego. So I said at the outset that we would review 10 key points of support for this deal, and I just want to ensure nothing was missed. So in more or less, their order of appearance on this call, I will begin with number one, which is that we have both internal disease expertise with Dr. Herath and external disease expertise with the Thompson Lab at UC Irvine. Second, HUNT1 offers the field a novel therapeutic approach, one that is aligned with the emerging views of Huntington's disease pathology. Three, HUNT1 has a robust and directionally positive preclinical package.

Four, this program has a strong strategic fit with our maturing clinical pipeline in neurology. Five, the competition is mostly focused on reducing mutant huntingtin, which has already failed in some iterations. Meanwhile, we are currently the only neural progenitor cell transplant currently in the clinic. Six, if corporate partnering makes sense for us, we believe HUNT1 could be highly attractive to big pharma, and we have retained significant economic ownership of the asset if that path makes sense for us. Seven, we envision a reasonable time to clinical data and value creation with a 21-patient Phase Ib/IIa trial currently enrolling. Eight, we have taken on manageable upfront and near-term payments with no anticipated impact to our preacquisition plans.

Nine, we benefit from external funding provided by CIRM, which is supporting a majority of the current trial. And finally, point 10, aside from the upfront payments in the first year, the remaining milestones are contingent and payable half in stock and more than 90% of the remaining biobucks do not occur until high-value events like Phase III trial initiation and product approvals. So to conclude, what we have achieved is the addition of a clinical stage asset aimed at treating a leading unmet medical need in a neurodegenerative disease with no disease-modifying approvals that is based on an increasingly promising and highly differentiated mechanism of action and built on a cell line for which we have experience and confidence.

The HUNT1 program brings external grant funding to defray approximately 2/3 of the expected Phase Ib/IIa trial costs, and it has already been administered to 6 patients, giving us an early read on product and delivery safety. And finally, we believe the deal satisfies our commitment to capital efficiency. Ultimately, we see this acquisition as transformative to the overall value of Lineage, and it reflects our confidence in our long-term business opportunities.

And then just before I ask Jill to provide our financial review, I want to mention that we are continuing to enroll patients in the dose study of OPC1, which is evaluating the safety and utility of a novel delivery device to deliver OPC1 directly to the area of injury. We also continue to be satisfied with the performance of this new device because to date, the patients who have been administered OPC1 with this device have not experienced any unexpected procedural product or device-related adverse events and no significant design changes have been required for continuation of the DOSED study.

The third patient in the DOSED study is scheduled for surgery before year-end, and we believe a fourth patient will be dosed in Q1. Jill?

Jill Howe: Thanks, Brian. I'll begin with an update on our cash runway. As of September 30, 2026, we had $45.2 million in cash, cash equivalents and marketable securities, which we expect will fund planned operations into the second quarter of 2028. Beyond our current cash on hand, we also remain eligible for several other sources of capital. We remain eligible to receive approximately $32 million from the cash exercise of warrants issued in November 2024, which have a strike price of $0.91. Importantly, those warrants have a 3-year term, and that term will accelerate to 90 days if Roche and Genentech publicly disclosed their intent to advance OpRegen into a multicenter trial that includes the control or compared arm.

And we also remain eligible for up to $615 million in development and commercial milestone payments under the Roche and Genentech collaboration agreement. And last, we continue to evaluate potential partnerships similar to our Roche and Demant collaborations, which we could enter into in the future. Now I will review our third quarter results. Our revenue is generated primarily from collaboration revenues, royalties and other revenues. Total revenues for the 3 months were approximately $1.5 million, a net decrease of $2.2 million as compared to $3.7 million for the same period in 2025.

The decrease is primarily due to lower collaboration revenue recognized from deferred revenues under the Roche agreement, reflective of measured progress towards completion of the first performance obligations. Additionally, revenue from our research collaboration agreement with WDI was lower, both decreases were driven by fewer services provided in the current year. Operating expenses are comprised of research and development and general and administrative expenses. Total operating expenses were approximately $8.8 million, an increase of $1.3 million as compared to $7.5 million for the same period in 2025. R&D expenses were $3.8 million, an increase of $0.5 million as compared to $3.3 million for the same period in 2025.

The net increase is primarily driven by $0.8 million for our preclinical programs and other undisclosed programs and $0.5 million for our ReSonance program, partially offset by $0.2 million for our OPC1 program and $0.6 million for our OpRegen program. G&A expenses were $4.9 million, an increase of $0.7 million as compared to approximately $4.2 million for the same period in 2025. The net increase was primarily driven by personnel costs and stock-based compensation expense. Our loss from operations was $7.3 million, an increase of $3.5 million as compared to $3.8 million for the same period in 2025.

Other income and expenses reflected other income of -- excuse me, $12 million compared to other expenses of $26 million for the same period in 2025. The net change was primarily attributable to the quarterly fair value noncash reimbursement of the warrant liability driven by a decrease in our share price as compared to an increase in the prior year's quarter. The net income was $4.2 million or $0.02 per share basic and $0.03 loss per share diluted compared to a net loss of $28 million or $0.13 per share of both basic and diluted for the same period in 2025. The change was primarily driven by the quarterly fair value noncash remeasurement of the warrant liability.

And with that, I'll hand the call back over to Brian.

Brian Culley: Thanks, Jill. So to sum up, with this acquisition, we have completed an initiative we call Lineage 3.0, which is intended to make us a leader in developing next-generation cell therapies. In addition to our lead program, OpRegen, and reflecting the confidence we have in that program's continued development, we have added 3 new allogeneic cell transplant campaigns over the past 12 months or so. Two of these programs were invented completely in-house and one was acquired, but even the acquired one was built on a cell line that we originally owned and have extensive experience with.

And throughout this campaign of expansion and diversification, we have not only maintained a stable and reasonable level of investment of approximately $30 million per year, but also demonstrated proprietary and valuable technical capabilities on the manufacturing side. These initiatives and decisions are meant to signify another step forward in our goal of being the dominant leader in allogeneic cell therapy, not only on the technical side, but also in the clinic. We appreciate your support and belief in our vision. And with that, operator, we are ready for any analyst questions that we may have.

Operator: [Operator Instructions] We'll take our first question from Mayank Mamtani at B. Riley Securities.

Mayank Mamtani: Congrats on this deal announcement. A lot of good detail here. So Brian, as you know, the bar in Huntington's has been, as you mentioned, set by the Huntington lowering programs where FDA accepts this composite UHDRS as the intermediate endpoint with CSF, NfL as supporting evidence and these things take as long as 3 years of follow-up with need to show differentiation versus external control. HUNT1 works downstream of that, as we know, with cell replacement. So I was wondering how as you collect data, I understand you're still early in the study, what would good look like with this 12-month follow-up on some of the clinical and the biomarker endpoints you're looking at?

And is the goal here stabilization as we see with the these gene targeted approaches versus actual improvement, which you're trying to do with OpRegen? And then I have a couple of follow-ups.

Brian Culley: I appreciate the question, Mayank. It's correct that it's early. We've owned it for 8 hours. So I'm going to direct that question to Dr. Herath about the mechanism.

Priyantha Herath: Mayank, thanks for the question. So first of all, this particular study is about safety, as you know. As far as the efficacy from this approach, we are obviously looking at early signals even in the Phase Ib/IIa, which include some of the clinical/functional measures, which are part of the UHDRS scoring system. That includes, as Brian mentioned, TFC, for example, SDMT, which is a cognitive test and a few other things. Beyond that, NfL, as you mentioned, and there's obviously going to be other imaging findings such as MRI and FDG-PET. There are other ways of getting faster clinical signals, but those are yet to be discussed and maybe we will share those things in a future call.

Mayank Mamtani: Understood. And then on the immunosuppression regimen you're using, if you could maybe just clarify, at what point that would -- what are you using? And how do you monitor graft rejection and at what point that would be withdrawn?

Priyantha Herath: So patients received tacrolimus, mycophenolate -- so tacrolimus for 12 weeks, mycophenolate for 12 weeks, and we dosed them with basiliximab on day 0 and day 4 of surgery. And then, of course, they'll have an initial administration of methylprednisolone, which will be tapered off after a few days, followed by low dose maintenance of prednisone for the entirety of the remaining 52 weeks. And they, of course, have Bactrim coverage for potential infections that could occur in immunosuppressed patients.

But the point that I want to make is, besides what I just mentioned, we consider this particular regimen and we will be closely monitored, including its drops of the tacrolimus levels is far less potent than some of the other regimens that were used in other clinical trials where there had been some problems.

Mayank Mamtani: Okay. And maybe just a manufacturing scale question. And here, obviously, the dose levels that you're using are -- from what I understand, 16 million cells, it's smaller relative to your islet cell work. So maybe just talk a little bit about how much of the AlloSCOPE specific work has already happened to scale these cells up? What tech transfer may need to happen? And just kind of walk us through how between the many initiatives you have across different cell types, how does this -- what should we be tracking to understand the commercial kind of viable doses you'll be producing for this program?

Brian Culley: Thanks, Mayank. So I think what we've been able to demonstrate with AlloSCOPE and the multitiered banking approach that we use is that we have a capability of producing numbers of cells that are going to exceed the needs even in very aggressive adoption models. We have not initiated work on this process per se, but we did actually make a decision to go at risk with the underlying cell line and to begin work on the master cell bank that will support it.

And I'm happy, although I haven't cleared this with R&D, but I'm happy to tell you that they just filled earlier this morning, California Time, a GMP master cell bank of the cell line that underlines this program. So we are careful not to make statements that we can absolutely make millions of vials of every cell type that could be posed at us, but we can point to significant success with neural cell types, especially those that have common features and common early differentiation steps. And we did at risk, make the decision to work on a master cell bank, which it hasn't undergone the lease testing and all the analytical testing, but those vials were filled today.

So we're really hitting the ground running and benefiting from our prior expertise. And as manufacturing continues to be of elevated importance and we achieve additional milestones, we will be delighted, I'm sure, to share those with you and others.

Mayank Mamtani: So just to clarify, you have enough material to dose all 21 patients already manufactured and you will hold the master cell bank and IND essentially as part of this acquisition going forward?

Brian Culley: Currently, there is material to support 21 patients with the original NeuroAirmid process. NeuroAirmid or UC Irvine holds the IND. We will be the holder after the current study is complete. And in parallel, we are working on developing -- we're doing the process development in order to establish a new efficient and industrial capable method of manufacturing the same cell type. So at some point in the future, there will need to be some kind of bridging or comparability testing, but we're quite confident that we will achieve this. We would not have entered into this agreement if we thought we had to start that process from square one.

Operator: We'll move next to Joe Pantginis at H.C. Wainwright.

Joseph Pantginis: Very exciting news. Thanks for sharing all the details today. So Brian, you just spent some time on the manufacturing process. Maybe I can dig in a little bit more, especially with the transition from academic manufacturing to the industrialized process that you're talking about. Can you talk a little bit more to the work plan and what you think the rate-limiting steps are? How much of that lab tech currently and their know-how can be brought over? And then ultimately, do you think you can cut the time and the cost of the manufacturing cells for ultimate COGS?

Brian Culley: Thanks, Joe. Good, good questions. I think you and others who have listened to our calls in the past are aware that we proudly talk about something that we call better from the beginning, which is that when we are initiating a new program that is internally developed, we try to put all the right features and attributes for production in place at a level that is not likely to be changed because we know that very small changes can have an effect on your therapy.

The partner to that concept is working with a group that has a process that has reached the clinic, which is very exciting, but perhaps does not have in place the kind of process and industrialization and scale and control and purity that you would prefer for the consistent performance of a new therapy. So the rate-limiting work is very difficult to project because even a highly experienced company like ours doesn't necessarily have an ability to anticipate what the major hurdles will be. However, there are still another 15 patients to enroll in the current study, data collection and analysis that provides a large window for us to be able to begin this work.

And if that bank I referred to in the prior question is, if it's performance, it's analytical testing passes, we will be able to do work directly with GMP material. So it's notable that a little bit below the surface, there are things like we have patents that have issued and we think we can use aspects of our existing proprietary methods to apply or deploy onto the current process to make it more in line with what we think of as a commercially viable therapy. So it really speaks to the value of what the AlloSCOPE platform can bring. We have demonstrated ability to do this.

We can go into these programs with a probably different view of the risk of failure than others because of our familiarity with not only the line, but also the steps and having prior success of putting material from multiple discrete batches into clinical testing. And I want to just confirm and ask whether or not that actually got to the question you were asking or if there was something more nuanced that I might have missed.

Joseph Pantginis: No, it does. And then I guess just the second part of the question, and I guess this is nuanced, too, because it's a long-term goal here. Do you think the manufacturing process would look to cut time and also reduce cost for ultimate COGS, if approved?

Brian Culley: Yes. Everything that we are doing is not just allogeneic, but it's meant to be off the shelf and have cryopreservation formulation. So when you think about production scale, when you have contributing advantages like a tiered banking system and you're able to freeze this material, it's normal that you expect that frozen cells could last for many years, you get the dual benefit of high production along with the ability to have very long-term storage.

The other thing that maybe I haven't been highlighting strongly enough is that the cost -- the production cost per vial of an off-the-shelf therapy like the ones that we do are vanishingly lower than what you are familiar with in oncology sub-cell therapy for autologous treatments, which are custom and specific to one individual where you go through all of the manipulation for weeks or months in order to manufacture material just for one patient. And that's why you see over in cancer, people have to charge $400,000, $500,000 for some of those therapies.

In our case, it is a completely different situation because we have already shown an ability to do steps that generate thousands of vials and by repeating those steps, we could, therefore, do millions of vials. And so we're really changing the mathematics around what it costs to produce material that is off the shelf and allogeneic. So absolutely, and actually, your question is a good reminder that I might not emphasize that our cost of productions are probably a very small fraction of what you find for autologous therapies.

Joseph Pantginis: Very helpful. And if I could just ask 2, I guess, logistical questions for the company as a whole. So for COR1, with the preclinical data coming out in the first quarter, if that was correct, as you said, what kind of data could we expect or metrics? And then the second logistical question is, I just want to make sure I'm up to date on this. What is the current CIRM cycle with regard to any of your internal applications or goals?

Brian Culley: Thanks again, Joe. So COR1, the preclinical animal models are pretty well established in the literature. I'm always reluctant to mention species by name because people have pets. But we have 2 models that we are going to perform. One of the advantages, I believe, is that because a lot of work has been done on these models, we don't have to reinvent them. We already know how cells should perform so we can be really efficient rather than, for example, in our hearing loss work. We have to do more exploratory. We're still trying to figure out the best models, what gives us quality information.

But with corneal epithelial cells, reliable, predictive translational models have already been established, which allows us to use fewer samples to get the same robust and actionable information. Regarding CIRM applications, we don't have any CIRM applications at this time. We are certainly eligible to apply for them in the future. The one that we are essentially inheriting is the one that was granted to UC Irvine with Dr. Thompson as the primary investigator. And just to the extent that it might look a little odd that we are providing a certain amount of cash to CIRM, that is because that CIRM grant to the University of California at Irvine was fully funding that work.

When we acquire NeuroAirmid, we are stepping into the customary normal sponsor role, which means we become the co-funder of that grant. So that's normal and expected for a CIRM grant is that they expect corporate entities like us to be participating and contributing to the grant. So we are stepping in for the academic place and providing some of that co-funding back to CIRM. But again, it's a approximately 30% co-funding, it's a very tolerable number over the life of that grant, which I believe is 3 or 4 years in duration.

Operator: We'll take our next question from Jack Allen at Baird.

Jack Allen: Congrats on the progress and the acquisition here. Maybe I'll start with one on the Huntington's program. I was hoping you could provide a little bit more color as it relates to the extent that these cells are differentiated, how naive are these cells or to what extent are they differentiated internally? And then additionally, how pure is the cell product that you're bringing forward here? I know you're using a similar cell line that you have a lot of experience and confidence in. And I'm just curious how pure the product is that they brought in the clinic. And those are the questions on Huntington's. And I just have one brief follow-up on OPC1 as well.

Brian Culley: Yes. Thank you, Jack. We -- with the exception of OpRegen, which was our pioneering program, we tend not to or prefer not to share our proprietary information or our confidential information regarding things like purity or identity markers or other aspects of our material that people might use as a base case to try to develop superior products. What I think I'm comfortable saying is that it would be normal and expected that academic material may not be as robust and pure as material that a company like Lineage might be able to manufacture simply in part of the experience that we bring into this work.

So we are very comfortable with all of the features that, of course, the FDA is looking for regarding safety and the characterization of the material that's being used in the clinic right now. We even now have 6 patients of relatively short-term, but still important safety data regarding this material. But we think there are opportunities for improvement beyond just scale. So we will be bringing those into this product candidate.

And if in the future, we see a little bit of crowding in Huntington's the way that there's starting to be a little bit of crowding in Parkinson's, if people do start to make comparisons around other attributes, we would be loud and proud about sharing what we have. But I don't think it's necessary at this time. It just gives people a target to aim at.

Jack Allen: Got it. And then maybe just a little bit more color on the degree of terminal differentiation of these cells, like where do they sit in the differentiation cascade?

Brian Culley: Thank you. I neglected to answer that. Yes, it's between -- they're not fully differentiated. So...

Priyantha Herath: Yes. So we expect that these cells will divide at least a few more generations and differentiate. They're not fully differentiated.

Jack Allen: Got it. And then on the OPC1 program, it sounds like you've dosed an additional patient here. I just wanted to see if there's any color around whether that was an acute patient or a chronic patient and how you're thinking about the future enrollment of different types of patients in this study as well?

Brian Culley: Yes. Right now, it's chronic, and we've got a -- do we have a surgery date for our...

Priyantha Herath: It's on December 8.

Brian Culley: Okay. We've got a chronic patient coming up in early December. It is slow because there is a stagger. And so we have a narrower criteria. After 4 patients are treated, it allows us to go into open enrollment, so we might be able to go a little bit faster. But we have a third patient coming up in a few weeks. And then we think that there will be a fourth one in Q1. All of these patients that we're talking about are chronic. I won't go into it on this call because I have gone into it in depth in prior calls. But we have biological and strategic reasons to be emphasizing chronic patients now with this program.

And maybe, again, just for sake of time, maybe we will dig deeper into that, maybe especially as we get into the open phase of that program, which is still very important to us.

Operator: We'll take our next question from John Newman at Canaccord Genuity.

John Newman: Really exciting acquisition today. A lot of questions have been asked on Huntington's. So I will ask something a little bit different. I wonder if you could give us an update on the ILT1 program in Type 1 diabetes. Obviously, lots of exciting things going on in the eye, spinal cord injury and now Huntington's. But curious as to how things are coming along in Type 1 Diabetes.

Brian Culley: Yes. Thank you, John. I spend a lot of time, and Jill also spends a lot of time talking with investors about the need for a solution to a seed scale problem. So it's very easy to imagine manufacturing large numbers of islet cells in large vessels. But you can't put 1 million cells into a 10-liter vessel and think that you're going to produce 10 billion or 20 billion islet cells. You have to have a seeding density of material that itself is quite large. And you can only get that from dividing the cells and from those dividing those cells.

So what we try to focus on as the solution is generating a very large number of cells that retain their pluripotency, that retain the response to differentiation factors. So these are undifferentiated cells that are queued up and are going to perform in the right way because if you think about how sensitive cell division is to things like changing media or changing surfaces or time, you can accumulate mutations in cells that will outcompete and lead to the wrong target cell type. It's almost like an evolution in a production system. So the only way that we believe that you can solve this is you need to have very synchronous identical behavior from an enormous number of cells.

That is profoundly difficult to do. And if you consider that, well, maybe the opportunity to solve this problem is to just let your islet cells continue to divide, as I said earlier on the call, they don't like to do that. These are not rapidly dividing cells like auditor neurons or RPE cells. So we have been focused on creating a solution where you can get the proper performance and synchrony of undifferentiated cells as they grow as adherent cells because they tend to behave a little bit better if they're adherent. So we put them on to microcarriers so that they are adherent, but then those microcarriers are loaded into 3D vessels.

There's more to it than just that. I don't want people to think that we invented putting cells on microcarriers as a solution to volume. But it does serve our purposes as a solution to try to get cells that will respond to differentiation queues in a synchronized and unified way and not wander off and become fibroblasts when you want islet cells. So we started this process at very low scale, and we showed that we could have some success at 100 mls and then we did it at 500 mls and then we did it at multiple leaders.

And we said, well, we should really ask the question, are the cells that we're making, are they able to differentiate into the islet precursor? And we were successful, as I announced today for the first time that we've done that, too. So the next logical step, of course, will be to continue that work, will be to take those precursors further down the road to make actual islets, let those islet cells get compared against other cells that are being made.

And if they look and feel and behave like other islet cells that are made by leaders in this space, leaders that probably roll off the tongue from every person who's on this call today, but they were manufactured on a modality that has already shown itself to be able to support high synchrony, high response de factors. I think it changes the risk of scale-up analysis dramatically in our favor. So I appreciate that, that's highly technical, but that is the nature of this particular project. It's not about being the first in the clinic. It's not about debating whether our hypoimmunity strategy is better than worse than anybody else's.

It's that none of this matters in our minds unless you can actually make hundreds of millions of cells per patient in an affordable way.

Operator: And next, we'll move to Sean McCutcheon at Raymond James.

Sean McCutcheon: Very interesting acquisition here. For the REGEN4HD study, how much control do you have over the timing of a data disclosure from that study? Is there a lever to share interim results ahead of the study and perhaps ahead of expanding at that MTD? And then can you maybe speak a bit more to what you've seen from NeuroAirmid database from the ongoing study that gives you confidence in the viability of this asset in Huntington's? Understanding it's very early, only 6 patients started in April, so limited follow-up. But it would be good to get a sense of what you know so far on the clinical profile in addition to the preclinical profile.

Maybe speak to the cadence of scans and biomarker assessments in the study.

Brian Culley: Thanks, Sean. I mean I'll pick up on your comment that it started in April, and it's already got 6 patients. So I think that enrollment going so quickly probably reflects the opportunity and the enthusiasm and the need in this patient setting. The study is being run by UC Irvine. It's a collaboration very much. So we don't have control necessarily over the information, but I think that they have been already very good about sharing updates. So we will continue to work with them in that way. And then Priyantha, is there anything you would add about the study? Confidence in the team's ability to execute because we are not the operators of the study.

We are more of advisers at this time.

Priyantha Herath: Correct. So Dr. Thompson, as he mentioned, is a very highly regarded researcher in the Huntington field, in fact, in all of the neurodegenerative disorders. But beyond that, the clinician who is enrolling these patients is an extremely well-trained MD, PhD neurologist with movement disorders, subspecialty training. And he has a very large clinic. So he has access to a large number of patients. In fact, the only reason why we are at patient #6 right now is because of the DSMB gating, which we go through for the next 3 months just to assess the safety. So in terms of finding patients for this trial, that's a very straightforward thing.

And I believe that there are other plans to work with other academic centers. In terms of the patients themselves, these are early manifest patients and there are plenty to go around also. And so yes, if there are any other questions, I can try to answer specific questions.

Sean McCutcheon: I just -- I was curious as to how much information you've received from the study, how much you've been able to see behind the curtain in the database for the study? And I guess, any high-level commentary on -- you mentioned safety, but any high-level commentary on early clinical indications?

Brian Culley: Thanks. I can add because I can maybe divine from the question that it's frustrating for a lot of people that we don't have the same level of information with respect to the OpRegen program. This is completely different. Obviously, we had abundant access through diligence and confidentiality. We have incorporated certain requirements regarding reporting, but I don't think we're ever going to need them. This is a collaboration, and we are involved with the strategic planning committee. Dr. Herath sits on that committee.

So we have -- I don't want to necessarily say full access because I don't think that phrase is a defined term in our agreement, but this does not resemble the arm's length relationship that we have with OpRegen, and Roche and Genentech, which was in place due to the materiality. This is a different situation here where we have a lot more information and insight as to the progress on this program. And operator, if there's a burning question that's short, I think we could take it, but we are already over an hour. We did want to accomplish a lot and provide a lot of information.

So let's just check and see if we are complete here in the queue.

Operator: And yes, we are. That was our final question. I'll turn it back over to you, Brian, for closing remarks.

Brian Culley: Great. Thank you, everyone. Look, we're focused on replacing cells that have become dysfunctional or destroyed because we believe that this might someday reshape many treatment paradigms for a lot of diseases. So we thank you for joining us on this mission, and thank you for your participation on the call today. Have a great one.

Operator: And this concludes today's conference call. Thank you for your participation. You may now disconnect.

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