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Momenta Pharmaceuticals Inc (MNTA)
Q1Â 2019 Earnings Call
May. 02, 2019, 8:30 a.m. ET
Contents:
- Prepared Remarks
- Questions and Answers
- Call Participants
Prepared Remarks:
Operator
Good day, ladies and gentlemen. And welcome to the Momenta Pharmaceuticals First Quarter 2019 Earnings Conference Call. At this time, all participants are in a listen-only mode. Later we will conduct a question-and-answer session, and instructions will follow at that time. (Operator Instructions) As a reminder, this conference call is being recorded.
I would now like to introduce your host for today's conference, Ms. Patty Eisenhaur, Vice President of Investor Relations and Corporate Communications. Ma'am, you may begin.
Patty Eisenhaur -- Vice President, Investor Relations and Communications
Thank you, operator, and good morning, everyone. And thank you for joining us today for Momenta's conference call to discuss financial results and operational highlights for the first quarter of 2019. Today's call is being webcast and you can view the slides we will be presenting in the Investor section of our website at momentapharma.com. Joining me on the call with prepared remarks are Craig Wheeler, President and Chief Executive Officer; and Michelle Robertson, Chief Financial Officer. Young Kwon, our Chief Business Officer; and Tony Manning, our Chief Scientific Officer, will be available for the Q&A portion of the call. Following our remarks, we will open up the call to questions.
Before we begin, I'd like to mention that our call will contain forward-looking statements about our financial outlook, business plans and objectives, and other future events and developments, including statements about our strategic plan and our restructuring, the use, efficacy, safety, potency, tolerability, dosing, convenience and market potential in reception of our products and product candidates, including their potential as best-in-class agent, development timelines and strategies, development of our product candidates, including the design, timing and goals of clinical trials and availability of data, hypotheses regarding certain effects of our product candidates and clinical studies, the timing of regulatory filings, regulatory approvals and market formation and launches of our product candidates and products, potential competition and revenues for our products, accounting treatment for payments from our collaborators, our current and potential future collaboration, and non-GAAP operating expense guidance, including our anticipated collaborative revenues and restructuring charges.
These statements are subject to risks and uncertainties that may cause actual results to differ materially from those projected. These risks and uncertainties include those described in the slide entitled Cautionary Note regarding forward-looking statements included in the presentation accompanying this call and under the heading Risk Factors in our most recent annual report on 10-K filed with the Securities and Exchange Commission, as well as other documents we may file from time to time with the SEC. Any forward-looking statements speak only as of today's date and we assume no obligation to update any forward-looking statements made on today's call.
On the call, we will also discuss first quarter 2019 non-GAAP operating expense. Please see the presentation accompanying the call for further information and reconciliation of this measure.
With that, I will now turn the call over to Craig.
Craig A. Wheeler -- President and Chief Executive Officer
Thank you, Patty, and good morning, everyone. On today's call, I'll focus on updating you on progress for our three lead novel drug programs, M281, M254 and M230, all of which will have meaningful clinical data readouts in the next 12 months to 18 months. As you know, Momenta is now focused on developing drugs to treat rare immune-mediated diseases. All three of our initial clinical programs are focused on various elements of Fc biology to develop treatments for these diseases.
I'll also spend some time highlighting our promising research platform utilizing Fc multimerization, which was developed by leveraging insights from our clinical portfolio. Finally, I'll discuss our legacy development programs, which we retained following our restructuring to help fund our promising novel portfolio. I'll then turn the call over to our CFO, Michelle Robertson, who will discuss our first quarter 2019 financial results and reiterate our guidance for 2019. Following closing remarks, we will open up the line to your questions.
This year we are focused on clinical execution as we work toward generating Phase 2 readouts from our ongoing trials. These programs are all derived from the rich protein engineering heritage that has been the core capability of Momenta for many years and the deep immunology expertise that we have built more recently. We believe the combination of these capabilities provides us with a distinct advantage over others in the field.
I'll begin with our FcRn program, M281. As a reminder on the biology, FcRn is essentially a rescue or transport receptor for IgG antibodies, inhibiting this receptor allows dramatic reduction in the circulating level and cross tissue transfer of pathogenic IgG antibodies, which are at the root of a broad range of auto and alloimmune diseases with high unmet need. We believe targeting FcRn has the potential to improve overall care in terms of safety, efficacy and patient convenience versus existing therapies, including steroids, immunosuppressants and IVIg.
I know it is not lost on our investors that the FcRn space is a competitive field. Our strategy from the start has been to develop a best-in-class product. We believe this is a category that similar to the TNF antagonist space, we'll have multiple approved competitors. Our goal is to be the HUMIRA of the FcRn space. To do this we are focused on five key elements.
First, potency efficacy. Our antibody, a purpose built high affinity aglycosylated fully human IgG1 has already demonstrated the highest potency in the class with full receptor occupancy from a single dose. Our Phase 1 data demonstrated that we can safely lower circulating IgG by up to 85%. We believe this potency will translate to superior efficacy in many diseases.
Safety, so far our molecule, thanks to a careful design, has shown no evidence of effector function-related toxicity or infusion-related reactions. There were no SAEs in our Phase 1 studies and the product has been very well tolerated. If this continues to bear out in our future clinical trials, we will have a best-in-class safety profile.
Dosing, we believe our superior potency provides an opportunity for best-in-class dosing. In autoimmune disease, we believe we can achieve once monthly dosing with a 30 mg per kg IV. We have an ongoing infusion study, which we are encouraged by and believe we will be able to get to short infusion times. We also have developed a subcutaneous formulation, which we will advance further into development as we define our optimal efficacious dose.
Breadth of use, our preclinical and clinical strategies are focused on demonstrating the broad and in some areas potentially unique capabilities in autoimmune disease, fetal maternal disease and in combating product immunogenicity. Specifically in combination with AAV gene therapy.
And finally, the label, all of the activities I have described are focused on building a comprehensive clinician-friendly label for our product. In addition, I'll point you to the comprehensive dosing data, which will come from our Phase 2 MG trial and evidence of safety for use in women of child-bearing age from our HDFN trial. All of which will support use of our agent in a broad population.
I'll now update you on our clinical programs for M281. Our first autoimmune trial called Vivacity-MG is a Phase 2 study in Myasthenia Gravis. This is a 60-patient, five-arm trial with one placebo and four dose arms. Our goal is to demonstrate strong efficacy and establish optimal dosing. We believe that we should be able to achieve best-in-class efficacy in MG with once monthly dosing in this trial. The comprehensive dosing dataset will also allow us to fully understand the dose response in chronic treatment for MG and other autoimmune diseases. We believe the data when included in our label will also be valued by physicians as they learn how to utilize the product. Further, if our agent does demonstrate higher efficacy, we should be able to run a smaller Phase 3 study in MG based upon the better effect size. Side initiation is going well and patient enrollment is under way. We continue to anticipate top-line data in the second quarter or third quarter of 2020, assuming a successful pace of enrollment. We plan to initiate another clinical trial of M281 in a second autoimmune indication in the second half of this year and we'll announce the indication at that time.
In the fetal maternal disease area, we have also initiated our first trial. First, a quick summary of the biology. The fetal maternal diseases we are focused on are caused by the transfer of allo or autoantibodies from the mother's circulatory system to the fetus. This transfer enables those maternal antibodies to attack various targets in the fetus, resulting in significant morbidity and mortality. This transfer is accomplished by FcRn binding and subsequent transfer of IgG antibodies across the placental circulation from mother to fetus. M281's ability to maintain full receptor occupancy enables total blockage of all antibody transfer from the mother to the fetus through the placenta.
This was demonstrated by our preclinical data featured in a February presentation at the Society of Maternal-Fetal Medicine Annual Meeting and published in the American Journal of Obstetrics & Gynecology in March. These publications outlined an ex vivo placental perfusion model. The gold standard model of the human term placenta, which demonstrated M281's potential to safely inhibit IgG transfer from maternal to fetal circulation. The study also showed insignificant transfer of M281 to fetal circulation, which importantly limits the exposure of the drug itself to the fetus.
Our first Phase 2 study in this area, known as the unity study is in hemolytic disease of the fetus and newborn or HDFN. HDFN is a rare condition that we estimate affects 4,000 to 8,000 pregnancies each year in the U.S. It is caused by red cell alloimmunization, where antibodies from the mother target proteins on the fetal red blood cells. This leads to fetal red blood cell destruction and anemia and in severe cases, can result in long-term neuro-developmental delays, including cerebral palsy and bilateral deafness, fetal heart failure and fetal death. Currently, there are no FDA approved therapies to treat women at risk for HDFN. The standard-of-care is intrauterine blood transfusions. And even with these interventions there's a 20% rate of fetal mortality and significant morbidity in newborns.
We have initiated the trial and have opened sites in the U.S., Canada and Europe. We are continuing to open additional sites and patient screening is under way. This study will take some time to enroll, because women must be pregnant to be eligible. The protocol itself is also rather long, M281 administration starts around the beginning of the second trimester and is weekly after that. After birth, both the mom and the neonat must be followed. We expect this 15 patients study to readout in 2021.
I will note that due to the profound unmet need in this population, this study could potentially lay the foundation for accelerated approval. I will also note that success in HDFN may open the door to all other allo and autoantibody based fetal maternal diseases, which though they are caused by antibodies to different fetal targets are all driven by the exact same mechanism of FcRn transport across the placenta.
And finally, we are exploring M281 as a supportive therapy in combination with AAV gene therapy. As maximal lowering of IgG could open the therapeutic window, allowing these products to overcome anti-AAV antibodies and retain their efficacy. This could potentially enable more people to receive gene therapy or even allow for multiple doses, which hasn't yet been achieved in the field.
At this time, we have a research collaboration under way with a gene therapy Company to explore M281 as a supportive regiment to an AAV-mediated gene therapy candidate. We are working to establish proof-of-concept in the lab. We do not anticipate clinical work until we have established proof-of-concept efficacy for M281 and the gene therapy on a stand-alone basis.
I hope you can all see the tremendous opportunity for this molecule that we are building toward. There have been very few agents in recent years that have had this type of broad potential. We remain confident for the purposeful design of our molecule, the strong data generated to-date in the clinic and in our preclinical models, and the strong patient and physician-friendly strategies we are pursuing, give us a chance to truly create a best-in-class product that will benefit many thousands of patients.
I'll now turn to M254, our hypersialylated IgG program. This program often takes a backseat to the FcRn discussion but it is equally promising. Our research team once again showed their mettle with this program. Their research into the effects of lengthening the Fc bound glycans on IgG antibodies and terminating those glycan with sialic acid groups showed that these modifications drive enhanced anti-inflammatory behavior in many animal models of autoimmune disease. They then tapped into our protein design team to create an enzymatic process to raise a very low level of sialylation present in IVIg to about 90%. In animal models of ITP and other autoimmune diseases, the effect has been dramatic. We have been able to consistently show that our hypersialylated IgGs are 7 times to 10 times more potent than IVIG.
Why is this important? Today the IVIg market is estimated to be a $4 billion plus market in autoimmune disease and it is supply constrained as suppliers can't collect enough plasma to meet demand. IVIg also has a very high treatment burden for patients because of the large volumes that must be used to show efficacy. Often patients must endure multiple days of infusion and most suffer from infusion-related side effects that require additional treatment. This often results in the use of IVIg being pushed to second or third-line despite its efficacy advantages.
If we can demonstrate the same advantages in humans that we have shown in animals, this agent should be able to demonstrate enhanced safety, tolerability, patient convenience, lower overall use of resources and possibly higher efficacy than IVIg. This could transform and grow the already $4 billion IVIg market in autoimmune disease. We have started our first trial with this agent in immune thrombocytopenic purpura or ITP. Enrollment is under way in this four part Phase 1/2 study, which includes both healthy volunteers and patients. This study has one objective to show how much M254 is needed to show dose equivalents to IVIg in humans.
We are currently advancing through the various cohorts of Part A, the single ascending dose arm of our study. In Part B, patients will receive both M254 and a standard dose of IVIg, which will allow us to understand the relative dosing ratios for going into our Part C crossover study. M254 could be the first of our novel programs to achieve proof-of-concept for efficacy, which we are currently expecting in the first half of 2020. If we can show in humans the same potency advantages we have shown in animals, these results could be a potent catalyst for our Company and offer a dramatic step forward for many autoimmune patients currently being treated with IVIg.
Lastly, M230, our novel program being developed in collaboration with CSL. It's a recombinant Fc multimer that works by antagonizing the -- and the activating Fc gamma receptor system and blocking immune complex mediated tissue damage. It is currently being evaluated in an ongoing Phase 1 study, which CSL anticipates will be completed in 2019. As I've said in the past, we are a bit arms length on this program as CSL is running the program for the terms of the contract. However, we co-fund 50% of the program and per our agreement we share in the U.S. profits of the product 50/50 with CSL. We are also eligible for attractive ex-U.S. royalties, as well as significant milestone payments if the product succeeds. We believe M230 to be another program with blockbuster potential in our portfolio. We will update you as we learn more.
I now would like to briefly update you on some of our research work relating to our SIFbody platform. We were excited to present two posters at the American Association for Cancer Research Annual Meeting in late March, showing the potential for the application of our Fc multimerization technology when applied to cell depleting therapies. Our SIFbody platform combines fabs with an Fc multimer to achieve targeted cell depletion. These agents work by binding the cellular target with the fab and then taking advantage of the ability of the SIFbody portion of the molecule to bind with high affinity to Fc gamma receptors activating effector cells, as well as the fixed complement initiating the complement cascade. This leads to very efficient cell killing.
Well-known therapeutics like Rituxan and Darzalex, engage the Fc gamma receptor and complement systems to mediate cell depletion. They are important standards of care for patients with cancer and autoimmune diseases. However, they do not have strong enough effector function to effectively mobilize the immune system in all cases. This characteristic can limit their efficacy and can often contribute to drug resistance.
At AACR, we described the discovery of a novel anti-CD38 Fc multimer with superior efficacy and potency to existing anti-CD38 therapeutic antibodies in both cell systems and in non-human primates. And also with the ability to efficiently deplete Darzalex resistant multiple myeloma patient tumor cells.
We also described the discovery of a novel anti-CTLA-4 Fc multimer that maintains checkpoint blockade activity, while simultaneously enhancing the ability to deplete CTLA-4-expressing Treg cells with immune-suppressive activity. Such an agent has the potential to enhance anti-tumor activity through the dual mechanisms of checkpoint blockade and Treg depletion. This shows the power of the technology to enable the discovery of potentially best-in-class agents targeting CD38, CTLA-4 and other targets of therapeutic interest. We view these two SIFbodies as test cases for our platform and believe that we can apply this technology to enhance antibodies across a range of immuno-modulating targets. This platform has already generated a fair amount of BD interest. We look forward to sharing results of our continued investment in this area in the future.
I'll finish with a brief update on our legacy development programs. First on M923, our wholly owned biosimilar to HUMIRA. As a reminder, we have secured a U.S. launch date in November of 2023 and have the ability to launch in the EU on approval, contingent on securing a partner. Our discussions with potential commercialization partners are continuing.
And finally, I'll touch on M710, our proposed biosimilar to EYLEA. Our partner Mylan is conducting a Phase 3 study and we expect U.S. market formation in 2023 subject to positive Phase 3 results, marketing approval and patent considerations. We believe we are currently in the lead for developing this asset and believe M710 could provide a more affordable treatment option and bring in significant revenue to support our expanding novel pipeline. We will continue to keep you updated as this trial progresses.
With that, I'll turn the call over to Michelle to review the first quarter 2019 financial results and then I'll close with some final comments.
Michelle Robertson -- Chief Financial Officer
Thanks, Craig. Good morning, everyone. We reported a net loss for the first quarter of $45 million, compared to a net loss of $48 million in the same quarter last year. Revenue for the first quarter totaled $4 million, compared to $5 million for the same period in 2018. Product revenue which includes profit-share earned from Sandoz' sales of our Glatopa products was $2 million in the first quarter of 2019 and reflects a $1.5 million legal settlement and royalty payments to Teva. Product revenue in the first quarter of 2018 was $4 million and included a deduction of approximately $10 million for our share, a 50% of Glatopa 40 mg inventory reserves. The decrease in product revenue quarter-over-quarter was primarily due to lower net sales of Glatopa, driven by continued market competition.
Research and development revenue was $2 million, an increase from $1 million in the first quarter of 2018. The increase was primarily due to higher revenue recognized on the collaborative upfront payment as part of our biosimilars collaboration with Mylan, offset in part by lower reimbursable expenses. First quarter total GAAP operating expenses were $52 million, compared to the $54 million for the same period in 2018. The first quarter GAAP operating expenses included $3 million of stock compensation expense.
First quarter R&D expense decreased to $28 million when compared to $33 million in the same period in 2018. The decrease was primarily due to cost savings following our workforce reduction in the fourth quarter and lower lease costs, offset by increased costs related to our affinity M281 clinical trial.
First quarter G&A expense increased to $24 million , compared to $21 million in the same period in 2018. The increase was primarily due to increased depreciation and legal costs, offset by cost savings following our workforce reduction in the fourth quarter of 2018.
For the first quarter of 2019, our non-operating expense -- non-GAAP operating expense was $48 million, within the range of previously provided guidance of $45 million to $55 million. Our non-GAAP operating expense is defined as total operating expenses less stock-based compensation, restructuring costs and collaborative reimbursement revenue.
Turning briefly to our balance sheet. We ended the first quarter with $416 million in cash, cash equivalents and marketable securities, compared to $449 million at the start of the quarter. Also during the quarter, we adopted ASC 842, a new lease accounting standard. This includes the addition of a lease liability of $94 million in recognition of rate of use assets of $77 million. The adoption of this new standard had no impact on our P&L in the quarter. There will be more detail in our 10-Q footnote disclosures. Going forward, these numbers will be adjusted as we look to reduce our real estate footprint post our 2018 restructuring.
Turning now to our guidance for 2019. We are reaffirming the guidance we provided in November for non-GAAP operating expense between $45 million and $65 million on a quarterly basis. We expect fluctuations in cost quarter-to-quarter as our studies get under way and patients are enrolled. As a reminder, our non-GAAP operating expense is defined as total operating expenses less stock-based compensation, less restructuring cost and less collaborative reimbursement revenues.
I'll now turn the call back over to Craig for closing remarks.
Craig A. Wheeler -- President and Chief Executive Officer
Thanks, Michelle. As you heard from Michelle, we are well-capitalized to drive our programs toward meaningful data readouts next year and look forward to continuing to update you on our programs as the trials advance.
Thank you again for joining us. And I'll now turn the call over to the operator to get Q&A under way.
Operator
Thank you. (Operator Instructions) Our first question comes from Derek Archila with Stifel. Your line is open.
Unidentified Participant -- -- Analyst
Hi. Bill (ph) on for Derek. Thanks for taking our question. Can you provide color -- more color on the M281 studies and how enrollment has been progressing, given that there's so many competitive studies in MG and HDFN is such a unique indication? Thanks.
Craig A. Wheeler -- President and Chief Executive Officer
Sure, Bill. Yeah. I can't really give you any specific guidance on that now. We have the site signed up and enrollment is under way, but it's still early in the trial. I'll have a better read on it as a year goes on, but it's really a little bit early right now to be able to give you any guidance on that.
Unidentified Participant -- -- Analyst
Thanks.
Operator
Our next question comes from Eric Joseph with J.P. Morgan. Your line is open.
Unidentified Participant -- -- Analyst
Hey, all. This is Turner (ph) on for Eric. Thanks for taking the question. The first one is just on the subcu formulation of 281. It really sounds like you're honing in on the go ahead dose, so I'm just curious if you can expound a little bit on the formulation and any specifics like volume per injection, number of injections required and delivery injection like is there an auto-injector in neophyte decided yet?
Craig A. Wheeler -- President and Chief Executive Officer
Yeah. I think it's a little early for us to be speculating in terms of the -- what's going to be required. We are very satisfied with what we've been able to do in terms of the concentration and we are confident we'll have a very available subcu for folks. But we're really focusing on the conclusion of the MG study to truly understand dosing. So, for example, in that study you remember we're doing -- looking at once monthly 30 mg per kg or 60 mg per kg once. And so until we really nail down exactly how much we need and what that dosing interval is, it's like it's a little early to be to be predicting exactly what we'll be doing with the subcu, we're ready with it to go, but we're really trying to make sure we understand the dosing and the dosing intervals first.
Unidentified Participant -- -- Analyst
Okay. Got it. And just a quick follow up to that, are there any types indications for subcu over IUV formulation that you're prioritizing or would potentially be most beneficial for patients?
Craig A. Wheeler -- President and Chief Executive Officer
We're not at this time, I think, what we're looking at is the comparison between a -- potentially a smaller volume subcu more frequently or a rapid infusion because we think we will be able to infuse our IV rapidly in a longer intervals at -- in home infusions or doctor's offices and so we're really trying to understand all that and we'll get a better read on that when we have the Phase 2 data.
Unidentified Participant -- -- Analyst
Okay. Thanks.
Craig A. Wheeler -- President and Chief Executive Officer
Sure. Thank you.
Operator
Our next question comes from Brandon Folkeswith with Cantor Fitzgerald. Your line is open.
Brandon Richard Folkes -- Cantor Fitzgerald & Co. -- Analyst
Hi. Thanks for taking my question. I was just wondering, could you share any feedback you have received following the publication of the M281 data, as well as the presentation of the data at the Maternal-Fetal Medicine Meeting? Thank you.
Craig A. Wheeler -- President and Chief Executive Officer
I think, the feedback has generally been extremely positive. I think, the people are looking at this as an opportunity to transform the space. Obviously, the data that we got from the placental perfusion model gave people a lot of confidence that we can both block the transfer of maternal antibodies, as well as prevent the transfer of our drug to the fetus. And so that's -- that -- I think that has been very positively received by the community. Tony, anything you would add on that?
Anthony Manning -- Chief Scientific Officer
Yeah. No. I wouldn't -- I -- (ph) the overall data was very positively received and we've had good interactions with investigators around their enthusiasm for the study.
Craig A. Wheeler -- President and Chief Executive Officer
Yeah.
Brandon Richard Folkes -- Cantor Fitzgerald & Co. -- Analyst
Okay. Thank you very much.
Craig A. Wheeler -- President and Chief Executive Officer
Sure.
Operator
Thank you. (Operator Instructions) Our next question comes from Danielle Brill with Piper Jaffray. Your line is open.
Unidentified Participant -- -- Analyst
Hi. Good morning, everyone. This is a Neeraj Lad (ph) on for Danielle Brill. I just had a quick question related to Derek's question. Would you be able to give us any insights into how many targets site numbers you have for the HDFN trial?
Craig A. Wheeler -- President and Chief Executive Officer
It's a pretty low number. I can't give you the specific numbers, but it's low because most of these -- these patients are treated in specialty centers. And so where we're going is in the country by country basis to those specialty centers, because if you think about what the standard-of-care is with that intrauterine transfusions, particularly in the -- beginning in the second trimester. Those are very, very difficult procedures. And so we really have the start of this kind of worked collaboratively with those thought leaders in each of the countries. And so it will be a relatively low number of sites, but those sites are kind of regional draws for the patients with these conditions.
Unidentified Participant -- -- Analyst
I see. Okay. Thank you. And my second question was, would you be able to give us some color on the types of indications of interest you're looking for at -- looking at for M281, specifically if there's any specific technologies you're looking at or commercial opportunity thresholds?
Craig A. Wheeler -- President and Chief Executive Officer
So I'll just say generally that our belief is in autoimmune disease. We want to begin to cover the different disciplines that might be prescribing this. So neurology is obviously one space we can go and we can think about where we go in places like dermatology or other places that we can potentially use this agent. So we're thinking about as we get from the -- to the label back we want to make sure we get as much broad exposure, because these clinicians are each treating multiple diseases where these agents could be used. But beyond that we're kind of keeping it pretty close to the vest until we have aligned with the FDA in terms of where we're going next and we'll announce it as we go into the clinic, which should be midyear, I would say in the early second half.
Unidentified Participant -- -- Analyst
Got it. Thank you so much.
Craig A. Wheeler -- President and Chief Executive Officer
Certainly. Thank you.
Operator
Thank you. And I'm not showing any further questions at this time. I would now like to turn the call back to Mr. Craig Wheeler, Chief Executive Officer for any closing remarks.
Craig A. Wheeler -- President and Chief Executive Officer
Sure. Thanks everybody for joining us. And we look forward to keeping you updated on our exciting portfolio. So talk to everybody soon. See you.
Operator
Ladies and gentlemen, thank you for participating in today's conference. This does conclude today's program and you may all disconnect. Everyone have a wonder day.
Michelle Robertson -- Chief Financial Officer
Good-bye.
Duration: 35 minutes
Call participants:
Patty Eisenhaur -- Vice President, Investor Relations and Communications
Craig A. Wheeler -- President and Chief Executive Officer
Michelle Robertson -- Chief Financial Officer
Unidentified Participant -- -- Analyst
Brandon Richard Folkes -- Cantor Fitzgerald & Co. -- Analyst
Anthony Manning -- Chief Scientific Officer
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