Sun Pharma Advanced Research Company Limited (SPARC.NS) Earnings Call Transcript & Summary

Ladies and gentlemen, good day, and welcome to SPARC's update on clinical programs and R&D pipeline. [Operator Instructions] Please note that this conference is being recorded. I now hand the conference over to Mr. Jaydeep Issrani. Thank you, and over to you, sir.

Thank you [indiscernible]. Good evening, ladies and gentlemen. I am Jaydeep Issrani. On behalf of SPARC, I welcome you all to SPARC's annual update on clinical programs and R&D pipeline. We have our CEO, Mr. Anil Raghavan; and members of SPARC's senior team on the call today. I hope that you have received the presentation that was sent out some time ago. The slides are also available on our website, that is www.sparc.life. [indiscernible] of the presentation will be similar to what we have been following in the previous versions, that is, our team will present -- or walk you through the presentation and then open the call for questions. Before I hand it over, I want to mention and remind you all that our discussion today includes forward-looking statements that are subject to risks associated with our business, that may cause actual results to differ from those projected in the presentation. I will now hand over the call to our CEO, Mr. Anil Raghavan. Over to you, Anil.

Thank you, Jaydeep. Thank you for the introduction and opening comments. Good evening, everybody. Good morning and good afternoon if you're joining from the U.S. or Europe. A very warm welcome to the 12th edition of our pipeline [indiscernible] engagement makes this [indiscernible] especially when on our calendar. So welcome back to this important call, and thank you for your time. As Jaydeep mentioned, we have our management team on the call today. In the interest of time, though, we don't plan to do detailed intros. Slide 3 has the agenda for the day. We will start with brief comments on our strategy and important program updates, including a brief snapshot of the portfolio performance and the listing of upcoming catalysts. Subsequently, we will dedicate most of our presentation today to provide additional color on 6 opportunities, with the 4 NCE clinical programs, plus 1 important biologics platform with IND visibility, and a new first-in-class [ AMC ] asset in dermatology. Dr. Siu-Long Yao, who heads our Clinical Development, will cover the clinical projects; and Dr. Nitin Damle, our Chief Innovation Officer, will provide an update on the biologics platform and the MUC-1 ADC; and Dr. Vikram Ramanathan, who heads our Translational Development, will speak to us about an interesting collaboration with Hopkins on a potentially first-in-class intervention in alopecia areata, which is the autoimmune [indiscernible] hair loss. We will conclude the presentation with brief comments from our CFO, Chetan Rajpara, on our financial performance and cash situation. So with that, let's start. I'm going to start with Slide 4 here, which is the [indiscernible] summarizing the state of our business. This is meant more as a scorecard, reflecting the current outcomes of a journey, navigating [indiscernible] starting with our [indiscernible] to building an organization, which can now take real bets on new targets and complex modalities. Please allow me to take a few minutes to go over these numbers. On the commercial or close-to-market end of our portfolio, we have 5 assets, Elepsia, which is a high-dose levetiracetam pill is commercialized through a U.S. CNS speciality company called Tripoint Therapeutics; and Xelpros, which is a BAK-free formulation of first-line glaucoma drug latanoprost is the Sun Pharma in the U.S. With now 2 more NDAs under review, and another one is in planning, first one, Phenobarbital, benzyl alcohol and propylene glycol-free formulation is under review with FDA, with the PDUFA date coming up next month. And the second one, brimonidine once-a-day eye drops, [indiscernible] by the project name PDP-716, was submitted recently. PDP-716 and ophthalmic steroid SDN-037 are both licensed to Visiox as we disclosed. These programs, which are either in the market or have a successful clinical outcomes in the late-stage trials, go a long way in validating the SPARC model. In addition to generating cash, these experiences, these offer substantial learnings in terms of building competencies to conceive and convert full development programs. On the second pillar here, we have 6 ongoing clinical trials, leveraging 3 NCEs. These assets offer really significant commercial opportunities, particularly vodobatinib in Parkinson's disease and more broadly across other [indiscernible] conditions, and vibozilimod in dermatology in a spectrum of autoimmune disorders. The primary development space for the NCE leg -- CNS leg of vodobatinib centers around a bunch of diseases driven by the neuronal toxins aggregated alpha-synuclein. Parkinson's disease is the largest slice of the 5 in terms of revenue. Lewy body dementia or LBD or multisystem atrophy or MSA as other 2 components of the spectrum LBD is quite a substantial business in terms of the total disease burden. And while MSA is not a large patient pool, the unmet need is quite high. It doesn't have an appropriate standard of care currently. And unfortunately, these patients deteriorate dramatically in a short window. Vibozilimod can also potentially modifying intervention across alpha-synuclein. Albeit, once we establish ablate a clinical proof of concept, and that's very [ confidential ] for patients across the globe with these debilitating conditions. And on the Vibozilimod, next generation of S1PR1, agonists are becoming class-alternative JAK inhibitors in dermatology after the recent FDA safety warning for the JAK of blood clots. That is quite an the important development and was one of the primary drivers with Pfizer buying our competitor Arena Pharmaceuticals. We are among the 2 players -- few players developing SMPs in dermatology with Arena and BMS being the other 2. On the third column here [indiscernible] our preclinical effort. We intend to bring 2 more projects to clinic in the next 18 months. Alopecia areata program later this year, if everything goes on plan, and MAK-1 ADC next year. But more importantly, we have seen our operating capabilities and external collaborations mature to a point where we feel comfortable taking an early stage risk. I want to leave you with the following thoughts on this slide. SPARC has validated its operating model with a significant number of assets across commercial, late- and mid-stage clinical development and early-stage [indiscernible]. So in that sense, SPARC offers one of the more validated translational features to navigate [indiscernible] to innovate from India for patients across the world. And more importantly, we are approaching some meaningful catalysts in the next 12, 18 months for our stock, and that's what we intend to cover in the rest of the deck. But before we [indiscernible], I want to use the next couple of slides to give some additional color on a few points I just made. Slide 5, please. So on capital efficiency, as a matter of strategy, we went after lower-risk incremental [indiscernible] initially. A positive outcome from that approach versus the nondilutive capital it has generated [indiscernible] to more complex [indiscernible] and build high-value opportunities we've built in the last few years. As you can see in these graphs here, SPARC has spent $500 million up to the end of FY '22, running our operations in the last 15 years and building what we have today. [indiscernible] rights issues in 1012 and 2016 contributed to around $79 million in total, while preferential issues brought in the rest. So in this period, we have invested around $277 million from our internal revenue accruals. Two things of worth noting besides the substantial nondilutive cash flows [ used to trading ] model and the portfolio build-out. These cash flows are primarily coming from our [indiscernible] products, plus some platform licensing transactions and some service revenues in addition to 1 upfront payment on Vibozilimod. [ Timings ] of the majority of the NCE or NVE programs are fully retained [indiscernible] SPARC probably with the exception of Vibozilimod we have significant share retained. So the nondilutive funding mentioned in this slide happened without diluting the more promising programs. Secondly, our journey has been marked by substantial promoter commitment. The lion's share of fresh equity infusion mentioned here in the slide to SPARC has come from our promoter group, and that's huge show of confidence on the SPARC's story and the demonstration of commitment to it's position. Slide 6. We've been Talking about our [indiscernible] from the incremental to the more [indiscernible] opportunities in the past few years. So we have the rationale and nature of that transformation many times. Early on that pivot, we focused on validated targets like [ DCRA ] leukemia and S1PR1 agonist in autoimmunity. But we've now moved to the next phase in that evolution, with increased confidence in taking early stage risk positions with novel biology. These numbers on the chart here, however, [indiscernible] almost 60% of our portfolio is now first-in-class extension and the compensation of the portfolio from a modality mix standpoint continues to evolve. More than almost 1/5 of our programs now are outside of the traditional straightforward new chemistry, and that component is growing faster. The [indiscernible] this transformation wouldn't have been possible without robust external initiative -- I mean external innovation initiative. Most of our ideas involve substantial partnering component, need additional development collaborations or for sourcing important development competencies which is difficult to find a bill in India. In this process, our own identity has shifted quite a bit towards being a translational engine, which look to act as exciting signs and differentiating competencies from wherever we can [indiscernible] from groups across the world. And secondly, the confidence in our portfolio decision-making has evolved quite a bit. Some of that is driven by the disciplined portfolio review process that we have followed to take going over decision. And some of it is driven by the changing emphasis on certain parts of the process itself, like the identification of key experiments, which can give us early signals of proof of mechanism or early signs of potential safety and efficacy or a conscious decision to invest substantially in largest reproducible [indiscernible] in the Phase II state itself. While we are still very much a work in progress, it's important to say that we've taken deliberate steps to mitigate the risk as much as possible while embracing [indiscernible] look at the matter of business reality that we will be dealing with. And last part of that process is our relationship with external advisers and the space that we provide to them to input into a decision-making process. So with that, let's go to the next slide, the Slide 7 for a few examples on these ones. I want to strength upon 3 programs here, Vodobatinib in PD, [indiscernible] junction and SCD-153 targeting a novel immunological target to associate alopecia areata. Starting with Vodobatinib. As is probably the first serious effort to track the oxidative stress response pathway immuno-degenerative diseases. The toxic cascade or event initiated by ABL-mediated oxidative stress response is affected through a complex web of inter-related events involving on one side, the aggregation as an intracellular [indiscernible] and on the other side, compromisation of its multiple protein clearance pathways. Our decision to move to a clinical proof-of-concept study was driven by critical pieces of evidence for the impact of disrupting this cascade is a highly important but super selective c-ABL inhibitor, gathered through [indiscernible] some of the best labs in this area globally. Like Dr. Dawson at Hopkins or [indiscernible] in Canada in addition to what we call our own internal experiment. So the totality of evidence coming from these experiments gave us the confidence to move to clinic. So focus in the clinical study was to establish an appropriate clinical dose, meeting with brain exposure targets indicated by the preclinical programs and confirm the safety of the proposed doses. Once we achieve that, we move to a clinical proof-of-concept study that's large and global enough to provide a comprehensive and reproducible proof of concept for the mechanism. So that's what I was talking about derisking early stage risk-taking through a delivered translation framework. Moving on to the second project here on this slide. Here, again, you can see several parts of the same strategy at [indiscernible]. MUC-1 has been high-interest cancer target for ADC and other tumor targeting programs because of its high tumor-specific [indiscernible]. Our strategy is built on 4 antibodies from the [ Australia ] group called Biomodifying against a cytogenic alpha/beta junctional [indiscernible] looks to avoid the peripheral [indiscernible]. So that gives us a differentiated opportunity to deliver high-potency cytotoxic payloads or other targeted agents using the ADC construct. On a separate note, we are very excited about [indiscernible] of the modality, which has clearly become mainstream on the back of clinical success of products like [indiscernible] recently. These successes and several others have demonstrated the stability and scalability of the linker system and safety windows for the commonly deployed payloads. And in fact, substantial activity using traditional ADC framework as well as with novel constructs involving target agents or immunological intervention and our MUC-1 program and other programs in the preclinical mix give us an opportunity for unique targeting in Oncology. And finally, on the slide on the right column, SCD-153, which we are disclosing for the first time here, SCD-153 is being through an option to license the agreement with a highly accomplished group as Johns Hopkins and [indiscernible] metabolize with significant anti-inflammatory property. As you will see in -- later on in Vikram's slide, we have developed substantial data and are in the process of establishing a topical formulation with appropriate safety margin. We have hopefully headed towards an IND in the early part of 2023. In both these preclinical programs, you can see key elements of our model playing out in terms of an attempt to leverage in our biological insight, willingness to land for an external growth and robust early translational work to set up clinical programs appropriately. We believe that's the right approach and approach offers a responsible path towards growing the portfolio is potentially attractive and clinically rather than [indiscernible]. So let me now give certain near-term considerations before I hand over the call for progress and a cash runway on Slide 8. Let's keep this simple. We had an expected spent of around $60 million in the year. Numbers for the outer years as you can imagine estimates, but we are more or less in the ballpark here. In terms of cash flow, we expect warrant conversions of up to $9 by end of December 2022. In addition, we will have set the milestones in royalties existing and upcoming commercial products and technology licenses. Without taking into account royalties and milestones, we have a cash intake to be added in the next financial year FY '24. Slide 9, please. Now let me spend a few minutes on this slide to give you some [indiscernible]. Starting with a little more context in for covering the projects [indiscernible] on this slide. Market has many marketed products which did not go through the current approval process requiring a clear demonstration of safety and efficacy as they are in medical practice before the current process has established. FDA formulated a plan to [indiscernible] unapproved product, it accompanies an approval through [indiscernible]. The current policy, therefore, aims to remove all unapproved products from the market, then the approvals are given on the basis of [indiscernible]. Policy also offer us certain market exclusivity [indiscernible] new data. Phenobarbital in textbooks is an unapproved product and is primarily used for treating newborns experiencing seizure episode. In addition, current unapproved phenobarbital contains benzyl alcohol or propylene glycol which many regulatory agencies across the globe want to remove because of the potential of toxicity. We filed a new [ drug ] application for phenobarbital in February 2022. FDA has granted us a priority review and pediatric rare disease in designation, which is confirmed in over 7 years of market inclusivity. If approved, SPARC product can become potentially the first approved phenobarbital, which can enjoy the associated market exclusivity, basing certain agency determinations that are set into the approval. SPARC may be eligible for the pediatric rare disease exclusivity and certain other incentives associated with it depending on the outcome of the ongoing [indiscernible]. We are in advanced stages of evaluating [indiscernible] performance of SPARC in the U.S. We started in the U.S. The PDUFA date, as I mentioned, is November 2022. We hope to become exclusively provided as the first approved combination of drug in the U.S. We are looking forward to working with an appropriate commercial partner to grow the franchise responsibly. We can come back to this in more detail, take your questions during the Q&A. Now let's spend a few minutes on Slide 10 to go over the upcoming catalysts for the company. Slide 10. The first column on to discuss is the commercial or late stage clinical program. We had an excellent start for Elepsia as a type 1. These are still very early days. The early performance gives a significant confidence to aggressively scale us for commercial segments for Elepsia. Xelpros is our second product in this category, which is with Sun Pharma in the U.S. We are working very closely with Sun's team to continue to build the franchise. In addition, we expect to see commercialize [indiscernible] later this financial year and reminded him of PDP-716 in the next financial year. We are still discussing the NDA submission for SDN-037 with Visiox. So on the commercial side, we have a few [indiscernible] which we can use to generate additional cash from royalties and regulatory milestone payments in the short to medium term. On the clinical side, Vodobatinib CML program and the [indiscernible] actively recruiting now so slower than we would like given the rare [indiscernible] the indications that we have been doing. We have seen excellent efficacy for protocol eligibility [indiscernible] the study. That we will go on a bit. We are looking to file the NDA in 2024. PROSEEK is a Phase II PD trial for Vodobatinib and we crossed the 70% recruitment mark a few weeks back, and we are pushing forward on all cylinders to complete the accrual by the end of this financial year. And that sets up an important data even in the coming financial year. And Vodobatinib, as you know, is also on a single [ standard ] study in Lewy Body dementia just -- which is expected to read out around the same time. Vibozilimod is on 2 -- Phase II trial in atopic dermatitis and psoriasis. We are ramping up site infrastructure significantly with additional sites in Europe and Latin America. And finally, SC0-120 is the [ oral third ], which is in Phase I patient escalation as inpatient dose escalation studies. And we can hope to get early efficacy signals as early as next year for [ oral third ] program. We are carefully navigating the stage though, given the complex nature of the [indiscernible] right now, and we will set up a go-or-no-go event for this program basis the quality of the efficacy signals that we will see going into next year. And on the preclinical side, I will talk in detail about SB0-154 that's the MUC-1 ADC and SCD-153 in alopecia areata. So I don't go into more details on that. So both projects are on track to go into IND by financial year '24 -- next year. Finally, we will continue to look for additional assets for partnering. We will look for [indiscernible] early signs, this synergizes with our current basket. So we will be considered as it has the potential to grow our clinical spend going into next year and even beyond. So our interest will be primarily driven by strategic portfolio considerations and not opportunism. Now on to Slide 11, this is my last slide in the deck. This chart is the pipeline summary. I guess we've gone through most of this [indiscernible] indication, current development series plus next set of data milestone. And we can come back to this with questions when we meet again for the Q&A. So with that, thanks again for your time today. I will now hand over the call to Dr. Siu-Long Yao, who heads the development for additional detail on 4 clinical programs.

So we understand there is a problem in the line. We are disconnecting and rejoining in a minute. So that may probably improve the connectivity and the line may be clear. Thank you, and sorry for this.

Sure, sir.

Thank you, Anil. And for the audience on the phone [indiscernible] want to show everybody to know [indiscernible] a little. We'll let him recover while I walk you through some of the slides and my colleague will also give you some of those detail. So again, my name is Siu Yao, and I oversee clinical development. The next slide go over Vodobatinib which is SCO-088, which is treatment of chronic myelogenous leukemia. So with SCO-088, we believe that we have a safe, effective option for the treatment of heavily treated last line patients. So this slide, Slide 14, summarizes the clinical development program for this drug. The program started with a healthy volunteer single-ascending dose and food effect study in 40 subjects and then proceeded to a multiple ascending dose study patients. Currently, we're in the midst of a pivotal study involving chronic phase, accelerated phase and last-stage CML. And as noted in the first bullet on the lower right-hand part of the slide, this is last line therapy, so patients are required to have disease that is refractory and/or intolerant to greater than or equal to 3 prior tyrosine kinase inhibitors, 1 of which must have been ponatinib. For this study, we have sites in the U.S., Belgium and there's a host of other sites listed on the slide that you can refer to. This next slide, Slide 15, gives you some of the data we make from the multiple ascending dose study in patients. This slide shows the major cytogenetic response rate that we observed and broke it down into the stages advancing patients at baseline on the top part and what happened to them following treatment on the bottom line. As you can see, 71% of patients came into the study with uncontrolled disease, only 29% had a major cytogenetic reprocess at baseline. Following treatment with Vodobatinib, however, there was a marked increase in the proportion of patients with a major cytogenetic response, as you can see in the lower bar, that said over 2/3 of the patients had disease that was responding to treatment. The next slide, Slide 16, shows results with the -- shows major molecular response rate following treatment. Again, the top bar represents the phase of patients at baseline, just tight enrollment and the bottom bar represents results observed following treatment with Vodobatinib. You can see that the incidence of major molecular response, which represents a 3 log reduction in the number of cancer cells, has increased from 2.8% prior to treatment with 43% following treatment. Finally, Slide 17 here depicts a swimmer's plot that gives you a feel of what we're observing overall with Vodobatinib. On the X-axis is duration of treatment, which is a measure of progression-free survival and on the Y-axis in each row are the results for individual patients. Patients are treated until they no longer respond and the point of which response is sought, is depicted by a dark circle. The duration depicted on the X-axis [indiscernible] to be substantial with time ranging out to 55 months and almost 5.5 years. A swimmer's plot is somewhat of an unequal assessment that doesn't show the maximum benefit because people at the top of the graph only experience treatment for a short period of time, but you don't know if they're going to [indiscernible] like some of those at the bottom of the graph. This was a dose escalation study for that doses at the bottom of the graph, but generally lower than those at the top. Nonetheless, you can see that there has been some dramatic responses with some patients at the lower doses, benefiting from well over 5 years now. So Slide 18 goes over our current plans for the program [indiscernible]. We'll be providing additional updates at the Goldman Conference in October in France, at the Annual Meeting of the American Society of Hematology in New Orleans in December. We're happy to say that our abstract for the ASH meeting has been selected for an oral presentation for the third year in a row now, and results from the pivotal study are anticipated in fiscal year '24. This slide transitions for the use of Vodobatinib for neurodegenerative diseases. The mechanism of action here is relatively unique. I want to point that out in that we are trying to modify the disease force rather than just treat symptoms like the existing therapies do. So Slide 20, it's here to remind you about the underlying signs supporting the role of ABl in neurodegenerative diseases, including Parkinson's disease. As noted in the bullets on the left, ABl from kinase is extracted from all parts of the brain and has a pivotal role in promoting neurodegeneration. Specifically, under conditions of toxic stress, Abl causes cells to die [indiscernible]. Slide 21 goes over results from the preform [indiscernible] slide. So let me walk you through the slide. In this model, [indiscernible] in the disease are injected into the brain to cause Parkinson's disease in mice. The top 2 graphs in the straight title there summarize results from mice turning around at the top of a pole on the left graph and then descending the pole on the right graph. In each graph, time is on the Y-axis and different treatments are on the X-axis. The first 2 groups in each case or in each graph consist of controlled treatments, where disease has not been induced in the mice. The third column in each case is the result you get when you induce disease in the mice. You can see that another time required to turn on top of the pole and then to descend the pole increases in those third columns because [indiscernible] it has disease induced in them. When you treat with a low or high dose of Vodobatinib represented by the fourth and fifth columns, respectively, the time for the mice to increase the [indiscernible] decreases and it's essentially the same as the unaffected mice represented by the first 2 columns in each graph. So our results occur when you look at the strength and breadth of the mice is depicted in the 2 graphs in orange shading at the bottom of the slide. On the Y-axis in these graphs, you have grip strength and going across the X-axis, you have the same treatment as before. Again, the first 2 columns are said unaffected mice, whereas the third column represents second mice not given any treatment. Columns 4 and 5 in the graph represents the results from treatment with Vodobatinib, either in low or high dose. You can see that higher doses of Vodobatinib are able to detect the mice from the insult of the preform [indiscernible] that cause Parkinson's disease in the mice. So this next slide, Slide 22, is from another model of Parkinson's disease, but now in rats. Here, the gene encoding a muted misfolded toxic version of alpha synuclein, originally derived from a person with Parkinson's disease is expressed in the right half of the brain. The left side of the brain is dropped alone as a control to tell you what things would look like in an unaffected brain, not subject to treatment with a toxic disease-inducing alpha synuclein. So following treatment, the whole brain is removed and evaluated for [indiscernible] by using a radioactive probe. Since in each case, the left side of the brain is normal, you want to compare the right side, which has been treated to cause disease with the left normal side each time when you look at the graph. Now the first group of left and right is a control, just to make sure that the virus used to deliver the mutant synuclein is in itself causing some type of unanticipated effect. You can see that the left and right side results, left and right columns there, the first group match so that the delivery system is not causing any real effect. The second group shows you what happens if you induce disease without any treatment. The left side is normal and the right side which has been treated with a toxic synuclein shows much fewer functional cells as represented by the lower bar or column. Groups 3, 4 and 5 represent increasing doses of Vodobatinib. Again, you are comparing the right diseased brain in each case to the normal left brain for each group. You can see that by the time you get the high dose of Vodobatinib shown in the rightmost group, the left and right brain are matching suggesting that Vodobatinib is essentially completely blocking the effects of the disease inducing mutant synuclein. So now we're on Slide 23, and this summarizes the study design of the ongoing PROSEEK clinical study evaluating the effect of Vodobatinib in Parkinson's disease. There are 3 arms here, consisting of placebo in a low and high dose of Vodobatinib. The total sample size is 504, split between the 3 arms. The part 1 is the date study whereas part 2 is an extension where all subjects receive Vodobatinib. As summarized in the bullets on the right there, there are currently 77 active sites and over 70% of the study has been enrolled. Slide 24 here summarizes progress with a Lewy body dementia study that we're collaborating on with an investigator at Georgetown University in The United States. Lewy body dementia is a disease that starts to have or cause similar to Parkinson's disease. So you can see, as noted in the figure in bullet, this is a 45-patient study primarily designed to evaluate safety, tolerability and biomarker results in this population, and we're now about halfway through the study. So this study -- so this slide just summarizes the main milestones for this program. Again, there's the Phase II PROSEEK study and the Lewy-Body dementia study, most of which are maturing in fiscal year 2024. I'm now going to transition to Vibozilimod, a S1PR1 agonist which we believe will be a safer alternative [indiscernible] for the treatment of dermatologic disorders. This is a very busy slide, Slide 27, and I'm going to walk you through some of the bullets here. This provides an overview of Vibozilimod along with some context regarding the therapeutic area and existing molecules. So overall, the goal of our program is to develop an oral standard of care agent for the treatment of dermatologic disorders. And as you may know, the existing oral agents such as methotrexate or [indiscernible] have either limited efficacy and/or significant toxicity concerns, and they're generally unable to reach the efficacy stream with the injectable biologics. Our goal is to have a best-in-class [indiscernible] agonist with efficacy and safety that can approach that of the injectable biologics. So going to the first bullet on the left, as you may know, Fingolimod was the pioneer in this class and served as a proof of principle that targeting this pathway could be effective in autoimmune diseases. Fingolimod, however, has significant cardiovascular limitations and [indiscernible] even overnight inpatient monitoring can be required in some patient populations. All the drugs in the class are approved for nondermatology indications, but they don't always provide selectivity against the S1PR3 receptor, for example, which can lead to hypertension, macular edema, shortness of breath and even cancer. This and other safety concerns have largely limited the ability to explore the use of this class in dermatologic disorders. The last bullet on the left there just reiterate that everyone is looking for an oral agent that treats psoriasis [indiscernible] of the biologic. For a while, it was hoped that the JAK inhibitors, for example, would be able to fulfill that role but the recent addition of Black Box warnings that resulted in roadblocks [indiscernible] agonist actually had a pretty extensive history of thinking now and hence, people are moving to them into this space with some renewed vigor when possible. I've touched on several of the bullets on the right there, they give more details specifically about Vibozilimod. Additional things to know are that we have clear preclinical and early clinical validation and corresponding studies that we're in the midst of clinical trials in atopic dermatitis and psoriasis, and we've seen preclinical synergy with other mechanisms such as the IL-23 pathway in inflammatory bowel disease. So Slide 28 here summarizes the design of the ongoing Phase II study in psoriasis. In this study, 240 patients are randomized amongst 3 doses of Vibozilimod and placebo and treated for 16 weeks to obtain results from PASI75, the primary endpoint for the study. This is basically depicted as the second column on the slide. There are a series of subsequent rerandomization that provide insight and to think about the durability of response on therapy and the durability of response following situation of therapy can be represented by the subsequent columns in the slide. This study has just started and approximately 20% of the subjects have been randomized. This -- Slide 29 now represents the [indiscernible] design of the atopic dermatitis study. This study also consists of 240 patients, randomized to 3 different doses of Vibozilimod or placebo. The primary endpoint also [indiscernible] on the slide reflecting differences in the study. This study is ongoing and involved in U.S., Europe, and Latin America. This slide transitions through our brain penetrate program targeting new estrogen receptor for treatment of [indiscernible]. So Slide 31 here gives you some background and rationale for our estrogen receptor antagonist program. The first bullet points out that Fulvestrant is the main selective estrogen receptor, the greater available for patients failing first-line therapy, but it's limited by the [indiscernible] that is intramuscular and inactivity against mutations at clinically practical dose. Elacestrant, a newer estrogen receptor antagonist with activity against mutant forms of the estrogen receptor, met its primary endpoint in a Phase III study, providing proof of concept for this approach. It's important to note, however, is that other similar drugs in the class have not always correspondingly succeeded. The success seems to be molecule dependent. The last bullet just pointed out that most of these hormonal therapies are now given in combination with other treatments, but that other treatments have not [indiscernible] estrogen receptive degraders and antagonists. Slide 32 goes over our current clinical program for SCO-120 which completed both single ascending and multiple ascending dose escalations in volunteers and we're at or near exposures that we expect to be efficacious at this point. So far, this drug has been generally safe and well tolerated. In the middle of the slide there, we will confirm the tolerability of these doses in patients and see if we can escalate a bit more and part 1 of a patient study that's already in progress with patients who have failed at least 1 prior endocrine therapy and no more than 3 prior chemotherapy. Our main focus will be to confirm the safety of pharmacokinetics [ we saw ] in volunteers except in [indiscernible]. Subsequently, we'll focus on obtaining preliminary efficacy information in several cohorts with the bottom right of the slide. This will include patients with ESR1 mutations and dose resistant aromatase inhibitors as well as dose resistant aromatase inhibitors and Fulvestrant and in a cohort with brain metastasis. Finally, this slide, Slide 33, is just a short summary of our plans for this program. We anticipate a readout from the ongoing study I described in the previous slide in fiscal year '24 followed by initiation of a Phase II study and a potential NDA submission in fiscal year 2027. And with that, I'd like to turn the presentation over to my colleague, Dr. Nitin Damle, who will walk you through some exceptional data with 1 of our upcoming biologics projects. Nitin?

Thank you very much, Siu, and good evening, everyone. My name is Nitin Damle, and I would like to provide an update on our first biologic therapeutic program, SBO-154. During our presentation to this audience a year ago, we had described SPARC's initiative to invest in biologic therapeutics and introduce our strategy to explore antibody-drug conjugates as anticancer therapeutics. SBO-154 is the first product of such exploration and it represents an antibody drug conjugate in which a humanized IgG1 antibody with a high affinity for MUC1 alpha beta heterodimer is linked to a potent cytotoxic drug that preferentially kill dividing cells when delivered to tumors via antibody drug conjugates. The cytotoxic drug used as a payload in SBO-154 is clinically and commercially validated for clinical use in different types of cancers. The tumor target that we have been interested in focusing on is human mucin-1 also known as MUC1, as shown on Slide 36. MUC1 is a glycoprotein overexpressed on the surface of a wide variety of carcinomas and had been the focus of immunotherapies over the last 2 decades. Most of those efforts were clinically unsuccessful in large part due to the presence of a high level of circulating MUC1 carrying the epitope recognized by anti-MUC1 antibodies used in those studies. Mature MUC1 antigen displayed on the cell surface as shown on this slide is a heterodimer of extracellular MUC-1 alpha and a transmembrane subunit MUC-1 beta. In this MUC-1 alpha subunit is the one that gets [ shed ] and can be found in large quantities in the [indiscernible] cancer patients. Such shared MUC-1 in circulation can intercept anti-MUC-1 antibodies used denying them the opportunity to bind to tumor cells resulting in the therapeutic failure. Thus we decided to focus on a unique epitope that is generated by binding of the alpha chain to the beta chain of MUC-1. And this epitope is displayed only on the MUC-1 that is displayed on the cell surface and not represented as shed antigen in the plasma and thereby may be immune from interference from such shed antigens. The MUC-1 alpha beta ethical targeting antibody used by us in creating SBO-154 was originally in licensed as a mouse antibody and was subsequently humanized at SPARC and further covalently linked to a cytotoxic drug to create SBO-154. And we have preclinically evaluated this therapeutic -- curative therapeutic entity. One of the key reasons for the use of anti-MUC-1 antibody for intracellular drug delivery is that any antibody bound to MUC-1 is rapidly internalized and; thus is ideally suited for intracellular delivery of potent cytotoxic agents. The next slide, Slide 37, shows that red fluorescence humanized anti-MUC-1 antibody bound to MUC-1 on the cell surface is rapidly internalized over time and inside the tumor cells. And this is not recognized by green fluorescence secondary antibody outside the cells. Internalized red fluorescence anti-MUC-1 antibody continues to appear as red fluorescence whereas the antibody that is still on the cell surface and hasn't been internalized, is able to be recognized by green fluorescence secondary antibody to create a yellow orange fluorescence, as you see in this slide. In contrast, similar fluorescent -- red fluorescent rituximab targeted at human CD20 and used as a nonbinding control antibody does not show any fluorescence indicating of its lack of tumor bonding and internalization. In the next 2 slides, I would like to share with you antitumor efficacy of SBO-154 against high MUC-1 expressing human pancreatic carcinoma xenografts established in immunodeficient [ mark ]. In this evaluation, pancreatic carcinoma xenografts were first established prior to the initiation of systemic therapy with MUC-1-targeted ADC SBO-154. Similar ADC created using rituximab was used as a nonbinding control in all evaluations. Slide 38 shows that SBO-154 causes dose-dependent inhibition of growth of these xenografts and at the highest dose for the shrinkage of the established tumors. We further evaluated antitumor efficacy of SBO-154, in a model in which xenografts of the same pancreatic carcinoma were allowed to grow to large tumor masses, accounting for up to 5% of the body weight. As shown in Slide 39, SBO-154 was able to cause regression on such preexisting large tumor masses of MUC-1 expressing tumors. In contrast, nonbinder ADC of rituximab allowed for further uninhibited growth of such large tumors. Thus, SBO-154 exhibits the ability to cause strong growth inhibition in a MUC-1 over expressing carcinoma model. We have undertaken detailed antitumor efficacy assessment of SBO-154 in various other carcinomas that express varying levels of MUC-1. These assessments would allow for greater appreciation for the potential of SBO-154 as an anticancer biologic therapeutic. In light of the above preclinical proof of concept and as shown in the next slide, Slide 40, we have advanced SBO-154 program to the preclinical development stage with the intent to file [ IND ] in the U.S. in the financial year '24. With this update, I would like to start and hand further discussion to my colleague, Dr. Vikram Ramanathan. Vikram.

Thank you, Nitin, and good morning, good afternoon or good evening to you all based on where you're located. My name is Vikram Ramanathan, and I'll give you an update on SCD-153. SCD-153 is an NCE that we are working on with potential for use in autoimmune disease, called alopecia areata. SCD-153 is a topical agent for this disease, which has a significant unmet medical need. So Slide 43, gives you some background on the disease. Alopecia areata is an autoimmune disease that causes loss of scalp hair and [ clumps ] and it's a psychologically very debilitating disease. This occurs because the hair follicles which are normally protected from the effects of patrolling immune cells lose their so-called immune privilege. So on the upper left is a diagram of a healthy human hair follicle. At the base is the bulb of the follicle. Immune cells are present, but the bulb of the follicle is normally immune from their effects. To the right of it is the depiction of a disease hair follicle alopecia areata. Some changes are immediately appear. The hair has fallen off and there's a big swarm of immune cells present at the base of the follicle. The text on the right summarizes the changes in the disease. The hair follicle rapidly progresses from the growing anagen phase to the transition of catagen phase and then eventually to the resting of telogen phase. Secondly, there's a collapse of the normal immune privilege at the bulb. The corporate CD4+ and CD8+ T cells infiltrate the area at the base of the follicle. In particular, it's a subset of the CD8+ cells code NKG2D positive CD8+ cells that caused the damage. However, the hair follicle structure and stem cells are preserved suggesting that hair growth is possible in principle if the hair follicle reverts to its original state. Finally, the picture at the bottom left shows how the disease manifests in real life. And this remains an unmet metal need at this time. [ RNCE ] SCD-153 is a topical agent that seeks to reverse these immune changes and allow normal hair growth. So if you move to Slide 44 now, you're looking at in vivo studies in a telogenic hair growth model, the hair on the back of the mouse was clipped at 8.5 weeks of age. The right side is treated with topical SCD-153, and the left side is left untreated. The top row shows that vehicle treatment does not result in hair growth. The images in the second row show that the treated area on the right side of the mouse shows hair growth, but not the untreated left side. In the bottom row, we see the effects of the treatment of the JAK inhibitor tofacitinib. In summary, in this model, SCD-153 simulates robust hair growth after 2 doses given on alternate days. It promotes reentry of the hair follicle into the anagen growth phase possibly by activation of stem cells at the base of the hair follicle. So moving on to Slide 45 now. Here is evidence that the topical SCD-153 also stimulates hair growth in an immune model for alopecia areata. C3H/HeJ mice are a strain that spontaneously developed our alopecia areata in about 20% of the cases. The figure on the left shows pictures before and after topical treatment. The box in green shows good hair growth on the back of the treated area. The head region was not treated and as expected, did not show hair growth. On the right, our images of the alopecic skin of these mice and seen under the microscope. In the untreated skin, there is a strong staining for the corporate CD8+ immune T cells and this staining is greatly reduced in the treated skin. We also have separate evidence for reduction of the inflammatory cytokines in this treated skin. In summary, we are working on a potential topical treatment for alopecia areata. We have data -- separate data which we have not shown here that the compound suppresses inflammatory cytokines in vitro in cell culture. And that here, we have shown you data that show that it promotes high growth in 2 animal models of disease. Finally, Slide 46 indicates that the IND-enabling tox studies are underway and we will be filing an IND soon on the completion of these studies in the early part of 2023. We look forward to sharing an update on this effort in the coming time. This concludes my part of the presentation and I would like to hand over the baton to our CFO, Mr. Chetan Rajpara for his financial update. Chetan?

Thank you, Dr. Vikram. Good evening, everyone. This is Chetan Rajpara, CFO of SPARC. I plan to go over SPARC's financials and cash position at a high level. Slide #48. During FY '22, total income was at INR 144 crores equal to USD 19.3 million, while total expenses were at INR 347 crores, USD 46.6 million, resulting into a net loss of INR 203 crores equal to USD 27.3 million. FY '22 income was lower as compared to FY '21 as previous year income included an upfront nonrecurring receipt of USD 20 million from SCD-044 licensing day. Let me update you on our financial results for first quarter of FY '23. For Q1 FY '23, total income was at INR 29 crores equal to USD 3.7 million, while total expenses were at INR 111 crores equal to USD 14.4 million, resulting into a net loss of INR 82 crores equal to USD 10.7 million. Slide #49. As you may be aware, company raised INR 1,112 crores equal to USD 148 million in July '21 by way of a preferential issue of convertible warrants. The company has already received INR 409 crores, USD 55 million, being 25% payable on application as well as conversion of warrants. The balance sum of INR 703 crores equivalent to USD 93 million is expected to be received by end of December '22, upon the conversion of all warrants by the investors. The company has a line of credit in place for INR 250 crores equivalent to USD 31 million from the parent company. In addition to the bank facilities for INR 245 crores, equivalent to USD 31 million. Bank facilities for INR 183 crores equal to USD 23 million were utilized as of September 30, 2022, which is planned to be repaid in full before March '23. The company has obtained shareholders' approval at the last AGM for raising a sum of up to INR 1,800 crores, that is USD 225 million by way of issuance of securities. The company is in the process of licensing the late-stage clinical asset, which would generate the additional liquidity. For FY '23, approximately 1/3 of our expenses are budgeted for the clinical costs. We are aggressively managing our costs and working to control our nonclinical expenses. That's all from me today on the financial update. A big thanks to all for joining the call. I will now hand over the call to Jaydeep for facilitating the Q&A.

Thank you, Chetan. And we will now open the call for Q&A.

[Operator Instructions] We have a first question from the line of Kunal [indiscernible].

Good evening, and thanks for giving me this opportunity. Sir, my questions are around [indiscernible]. Firstly, you are pitching this as an alternative to JAK inhibitor, right, because of safety signals in JAK inhibitor. But recently, a type 2 inhibitor, Sotyktu, was approved by the FDA. It is the first probably product without the safety warning that has limited the use of JAK inhibitors. So I'm just wondering how do you see your product versus Sotyktu?

Thanks, Kunal, for that question. I think you may be referring to the recent approval of BMS [indiscernible] product, which work through the JAK pathway, but the long-term safety data for the program is it to be awaited, right? So what happened if you look at the JAK as a class in the classical JAK 1, JAK 2 or pan-JAK inhibitor these concerns came through when Pfizer came up with the 5-year data for their first product. And subject to in that sense, it's very early days to conclude that the safety profile is established even if it works through the JAK program. So I think we need to wait for a long-term safety data to surface to have a final verdict on the safety of that class.

I understand. So the reason I asked was because the FDA, I don't think there is any boxed warning that typically comes with other JAK inhibitors. So I thought maybe the physicians might be more amenable to using this.

For sure. I mean, at the moment, they are not treating it as a classical straightforward JAK inhibitor because it works through [ TYK2 ], even though if you look at the downstream of that pathway as a similar message -- I mean, a similar pathway, right? So in that sense, there are apprehensions about how that is going to play out in the long-term safety trials where at the moment, jury led out in terms of long-term safety of that class.

Sir, my second question is also on the same class. So this is an S1P1 receptor. Now the thing is -- I mean, let's say, what kind of advantage would it have, let's say, fingolimod? The reason I asked is maybe fingolimod could be going generic in a couple of years, would be falling let's say 95%. And I mean that's -- even that, that's also a multifunctional [ S1P ] receptor. So I'm just wondering what advantage will this -- your product have over fingolimod?

No, if you look at fingolimod, fingolimod is primarily approved and used in multiple sclerosis, right? And we are seeing the second generation of fingolimod is also coming into the multiple sclerosis space. But our theater for development for the S1P1 program, our internal program, [indiscernible] is in dermatology. And we are not going after the S1P1 pathway in multiple sclerosis. But having said that, I mean if you look at our data on both the agonistic potency and the extended internalization. As we have disclosed in previous presentation, [indiscernible] a best-in-class agent. And we are currently in a clinical trial -- multiple clinical trials, both in psoriasis and atopic dermatitis. And our data from those trials will get at the competitive efficacy of our product against some of the other S1P1 programs, which are actively explored in dermatology.

This is Siu. I just want to add to Anil's comment there that we also believe that we have a very clean compound compared to some of the others. And so because of the great potency, we're hoping to have a better therapeutic index which would give us an advantage over the existing compounds.

Sure. If I can just squeeze in 1 more on this. So there have been a lot of S1P1 products in the market for several years now. So I'm just wondering why they haven't -- why the companies are not pursuing clinical trial in the dermatology space?

No. If you actually look at the dermatology field, which is now [ begin to fund ], there are programs in clinical development, including ours, [ Ionis Pharmaceuticals ], which is now Pfizer, is actively pursuing this. And BMS recently ended not with [indiscernible], but it's a different agent, it's in dermatology, which requires a very keen safety profile as Siu mentioned. So this field is becoming active, especially after the JAK experience both in atopic dermatitis and psoriasis. And we may probably see this even expanding beyond that in the dermatology field.

We have our next question from the line of Narottam Garg from Chanakya.

My question is on what are back here -- so you mentioned that you will complete the recruitment for the program by the end of this financial year. And given that the first study is a 40-week-long study, if I'm not wrong. So would that be fair to say that the first feed out for the Phase 2 will probably be by the end of the next calendar year, which is CY '23. Is that how one should think about it?

So the expectation that we are setting [indiscernible] and also our previous presentation is that we will have top line data readout in the second half of financial year '24. We have made a more precise expectation setting in terms of a specific quarter for data. But our expectation is that we will come with the accrual by this year and then 9 months we'll give you the top line data, which is to us the end 2023 or early part of 2024, calendar year terms.

We have our next question from the line of [indiscernible]. [indiscernible] can you please unmute your line? Since there is no response. We are moving on to the next question from the line of Jayesh Gandhi from Harshad Gandhi Securities.

Sir, can you provide me within a peak sale expectation for PDP-716 and SDN-037?

Sorry, could you repeat your question?

Sir, I was just asking if you can provide me with the peak sales expectation for PDP-716 and SDN-037.

Unfortunately, we don't provide a forecast or an estimate for our products. At the same time, that is dependent on how our partner is commercializing the asset. So we would refrain it from giving any forecast or projections.

Okay. And if you can help me with out-licensing fees that we have got from Visiox Pharma for these 2 programs?

So we've got equity in Visiox, which was created. We had an option to get 10% equity in Visiox but that's subject to the approval from SEBI and we are looking for additional milestones as we proceed with some of the regulatory milestones on the filing and approval of the program.

In addition to the milestone and the 10% equity position, we are also eligible for lower double-digit royalties in this program.

Okay. And 1 last question, if I may ask. We are in process of out-licensing phenobarbital also, any ballpark number which you can -- if you can provide?

Not at this point. I mean, we are in active negotiations on phenobarbital license -- I mean phenobarbital licensing. We hope to conclude the transaction soon as in the PDUFA date for the program is coming up in November of this year. Our hope and expectation is that we will be able to conclude that transaction before the PDUFA outcome so that we can go into a launch as soon as possible. So at the moment, we don't -- we are not in a position to give you details on the transaction that is shaping up.

[Operator Instructions] We have our next question from the line of Manish Jain from GormalOne LLP.

Congratulations on great progress on vodobatinib. So I just wondered on both CML, how are we comparing to asciminib in particular? And later, I'll go to PD on vodobatinib.

Thank you for that question. And on CML, I mean, if you look at the setting that we are pursuing and the data that you have seen in the presentation is different from what Novartis is pursued for their registrational trials and [indiscernible] trial. What we have here is last line setting. These are patients coming off ponatinib, failing 3 lines of tyrosine kinase therapy. And 1 of this needs to be ponatinib. The asciminib trial was in 2 lines of failure against bosutinib. So in that sense, both the severity of resistance and the challenges in the composition of the resistance is significantly more. And there are no last line trials in this setting. So in that sense, it's not -- we cannot directly compare two programs.

Excellent. Excellent. So in terms of additional patients to be recruited on this program. On Slide 14, the numbers highlighted those are enrolled, how many more to get enrolled?

Yes. I think as per the original FDA discussions, the target was in the range of roughly 50 patients, but for registrational submission. But that's something which we hope to discuss with the agency once we go back to them towards the end of this year given the rare disease nature of this indication.

Perfect. Perfect. And on PD, essentially, what kind of risks do you foresee where the peak sales more than looking at the quantum of peak sales, what are the things that can actually determine the sales potential of the product? Where do you -- like risk factors or performance factors, if you can give a little bit of insight on that.

I think we are in a Phase II proof of mechanism study for the Parkinson's disease, where we are exploring the viability of a novel hypothesis. We have seen -- as you've seen in this presentation and also, Manish, earlier presentations, we have presented a fairly large and robust data set. And been fairly transparent in terms of why we think it's a reasonable shorter take. At the same time, the translational risk of failure in this area is quite substantial, right? So the translatability of these preclinical models into clinical outcomes, which we will see once we have top line readout from the program, I think I will rate that as 1 of the more significant risk guidance. And obviously then, if you are successful and if you are unfortunate to get statistically relevant difference between treatment arms and placebo. The extent of that difference is going to be, again, significant in terms of both how much of slowing down of deterioration of the MDS-UPDRS score plus how long you can keep patients from having to need system -- I mean, symptomatic therapy [indiscernible]. They're going to be important factors in this program.

Just 1 last question on this, and I'll join back the queue. Is -- given that vodobatinab is quite significant. So what are our kind of manufacturing plans here to ensure that there is no slippage or delay led to manufacturing concerns?

No. At the moment, we are not looking at diversifying the manufacturing days with the Phase II. What we need to do, and this is an active consideration for us going into Phase III. And once we have success we will definitely expand the manufacturing base for this given both the scale or potential scale of the product plus the potential value impact on our portfolio, and we will not spare any effort in terms of creating multiple manufacturing options for this, but that's more a Phase III question as against the Phase II question.

I have a few more. I'll join back the queue.

For sure. Thanks, Manish.

We have our next question from the line of Girish Bakhru from OrbiMed Advisors LLC.

Just continuing on vodobatinab actually on the PD side. Just wanted your assessment of basically the risk benefit ratio, which I think FDA has been focusing on when they are basically looking at new treatments coming in this class. So I mean from what all approvals have been coming in PD, we have not seen any major breakthrough so far and so many different pathways are being tried like biologics or alpha-synuclein and all these things. So where do you think FDA will focus on the Phase II readout, I mean if it comes to that?

I think as you mentioned, we have seen a [ readout ] of options here, especially after the failure of some of the alpha-synuclein targeted antibody programs. From our standpoint, you're looking forward to FY '24 for readout of the PROSEEK program. What is going to be important is the extent of activity that we will see and the toxicity profile that we see. When we look at our program so far, we have around 350, 355 patients and we are now seeing a significant -- or allowing signals on safety so far. Unlike some of the antibody programs, both in AD and PD it was, I guess, the basis of your [indiscernible] people have seen significant level of neuroinflammation. We haven't seen any alarming signs on toxicity. But when I say this, I'm talking about just blinded visibility of safety data. So a real sense of where we stand in terms of risk benefit can only be commented upon once we have an opportunity to see the data from this. A fairly large as a 55-patient study next year. That would be the broadened proof of concept moment for this hypothesis also is not just for us. So to your earlier point in terms of that of options. If you look at everything that's going on in sporadic PD as a nongenetic PD, BCR -- I mean, ABL inhibitor is probably the most advanced and probably the more viable hypothesis that is being explored at the moment.

And just to clarify, you're not pursuing the PDP, right? PD psychosis?

No, this is -- what we have in PROSEEK trials, these are very early stage Parkinson's patients. They are not -- they haven't experienced symptomatic dopamine [ altering ] therapies like levodopa. So in that sense, what we are trying to catch is early stage neurodegeneration to the extent that's possible and try and slow down the progression of disease. So with the trajectory of our patients as the patients under treatment will be different from the trajectory of patients under placebo. And by slowing down that this is substantially your hope is that you can modify the disease over the course of longer period and keep patients off the need to have symptomatic therapy, which creates subsequent complications like dyskinesia, et cetera.

Yes. And I think we discussed this -- last time you said that there's been, of course, a lot of interest around this asset and several parties are probably looking at it. So you -- I mean, if you could just give some sense on where do you think -- is there a potential of monetizing this soon after positive Phase II readout?

At the moment, we are committed to kind of seeing the Phase II clinical trial through and we are resourced to do that. And it opens up a lot of strategic options to SPARC, both in terms of encashing -- partially encashing or kind of staying on with the asset. And those are all options that we will evaluate as we go into this data even next year. But unfortunately, I don't have a firm guidance on that right now.

Understood. And just last 1 on SCD-153, I couldn't get -- is this asset also [indiscernible] as per alopecia?

Yes. This is an asset. The lead indication for that is a alopecia areata.

I mean there is already like 2, 3 [ tinibs ] like olumiant, I think, got approved recently.

This is not a kinase inhibitor. This is not a tinib. This is a normal mechanism of action. And we haven't disclosed the mechanism of action for IP reasons in this presentation.

Okay. Okay. But any common comment on how -- I don't know if olumiant is expected to do well or what. But I know this is a very high unmet need, but your mechanism of action, you think could be far better than this?

I mean that is probably premature for me to take a position on this, and we are in the late preclinical setting at this point, and we will closely watch the space. And as we accumulate more data going to clinic. I'm sure we will be in a position to kind of articulate the relative performance factors for both these classes.

[Operator Instructions] We have our next question from the line of Ketan Gandhi from Gandhi Securities.

Sir, can you please throw some light on how many programs do we have fast track approval, particularly LBD, PD and CML?

Sorry, I didn't catch the context of the question. I mean LBP, PD and CML these are -- this LBD and PD not in registrational trials, they are in Phase II trials. And in CML, we don't have a fast track, we have an orphan drug designation and a path to an accelerated outcome in a sense -- surrogate endpoint, which needs to be confirmed with confirmatory trials later on. So it's not a priority [ review ] or fast track as you indicated.

Sir, and Xelpros and Elepsia is manufactured where at present?

Xelpros and Elepsia, the manufacturing base is Halol.

Okay. And phenobarbital and brimonidine where we've plan to manufacture?

We have 2 sites for phenobarbital but we haven't disclosed the manufacturing strategy for the product. Once we have a finalization of the commercial partner, we would be in a position to communicate that.

Right. And sir, what would be the timeline for phenobarbital to reach the peak sale potential?

So again, we are expecting an outcome from our current review process by next month. And as you see, this is a conversion of a [ daisy ] product in the sense that there are unapproved product in the market. And the [ daisy ] exclusively works like once you have an approval in using new process, FDA has a commitment to take out the unapproved products in the market. And that decision to enforce the daisy exclusivity is driven by certain determinations the agency need to make during the course of the first year or so in a sense, that August is the manufacturing plan and the unmet need and et cetera, et cetera. So there is a certain set of determinations that the agency need to make in terms of the timing of enforcing that exclusivity. So we don't want to have to set speculative expectations in terms of specific time for seeing the unapproved products going out of the market. But the estimation of the peak sales is going to be linked to that event.

[Operator Instructions] We have a next question from the line of Harith Ahamed from Spark Capital.

My first question is on Xelpros, which is partnered with Sun Pharma. It's been like 3 years since launch. So how has been the plan so far? And have we kind of reached the peak sales of peak [ RX ] for this product?

Thank you for the question, Harith. As I mentioned earlier, this is a program partnered with Sun Pharma, and they would be providing an update on the sales at appropriate time or whenever they disclose about the sales. So we wouldn't be commenting on their -- or how much they are doing. At the same time, peak sales potential is also linked to the performance that has happened. So they will continue to give guidance as they have been doing in the past about the program.

On PDP-716 and SDN-037, just curious as to Sun Pharma is not the partner for these assets given thermology [indiscernible] focused specialty segments. And then we've also partnered with them on Xelpros. And if you could comment a bit on the capabilities at [indiscernible] and your expectations in terms of how they plan to take these assets forward?

For each of these out-licensing commercialization positions, we go through a fairly robust process in terms of identifying the partner who gives us the best shot of maximizing the yield from product. And in this case also, we have gone through a process, and we had multiple players involved in terms of interested parties. And Visiox was probably the most aggressive, both in terms of the investments that they are committing and the quality of the team that they're bringing to the table and past ex -- I mean, their track record in terms of having succeeded in other areas, not in ophthalmology. I mean this is their first ophthalmology effort. So there are several factors which gave us confidence in terms of the trajectory or potential trajectory of the product into this year's proposal. And they also, as Chetan mentioned earlier, gave us an opportunity to have a contingent share of value in addition to a traditional structure. So it's a traditional structure plus access to -- or slice of value that this product may create. So in that sense, both on commercial terms and other dimensions of the proposal both in terms of capability, investments committed, et cetera. That is a very healthy proposal. And that's the reason why [indiscernible].

Okay. And then on phenobarbital. Can you give some color on the other therapies in the [ neonatal ] seizures indication against which phenobarbital will be competing? And given that we are very close to the PDUFA date. Any comment on the interest level in the asset from your licensing discussions with partners, potential partners.

Sure. So phenobarbital is currently -- we're trying to get an indication, which is for treatment of neonatal seizures. For the time being, there are no approved agents for that indication. Phenobarbital, as you would know, is the standard of care currently in the U.S. and other markets. And the second alternative is injectable levetiracetam. So those are the 2 agents, but both of them are unapproved agents being used by the physicians due to lack of other therapies. So that's the answer to your first question and on the interest. Of course, we have been in discussion with potential partners, and we're trying to close this at the earliest possible so that the partner would have enough time and a longer period for commercializing the asset during the exclusivity period that we may get after the approval.

Okay. And last 1 with your permission. On SCD-044, you mentioned that you're expecting completion of Phase 2 in FY '24. So any timelines that we can expect for Phase III trials and maybe filing any target or?

So the practice that we are following on these partner programs, we are basically leaving the disclosure around the execution of those programs to the licensee since we are dealing both parties are dealing with the same set of investors. So we haven't, in this presentation and indicated a timeline. But as you know, we are in do trials in atopic dermatitis, and we are aggressively adding sites. And Sun would be in a position to set expectations in terms of the registration trajectory of the product.

[Operator Instructions] We have a question from the line of Manish Jain from GormalOne LLP.

Yes, hello -- so essentially, I just wanted to know on phenobarbital. My assumption is it will primarily be a hospital setting product. So typically, how many sales reps would be required for such a kind of product?

Manish, the anticipation that this is going to be a hospital product is correct. It will primarily be used in the ICU setting or neonatal centers, which are not many few in U.S., which we are targeting as the primary indication. And the number of reps or the sales team will be dependent on the partner that we engage with and their strategy to commercialize the asset. So I will not be able to give you an exact number, but it will be -- should be in the similar ballpark range as any other asset targeting neonatal centers.

Perfect. Because at some point of time, I had a broader question from this and which I have been raising with you is for such kind of products, at what stage does it make sense for SPARC to actually go out and try and do the marketing on its own rather than being dependent on an external party?

No. Thank you, Manish. I think that's an interesting question. The question is, do you actually try and optimize it for a smaller product, which requires smaller scale of effort or do you go for a bigger product? Because the extent of bandwidth that we need to spend at a management level and also the distraction that it may cause for the rest of the portfolio is going to be considered. So that's an interesting question and an active question in terms of what would be an appropriate time to look at other options for commercialization. But at this point, we have concluded that phenobarbital may not be that opportunity.

Perfect. And given that we've now getting into very interesting biologics like SBO-154 and others. What's going to be our manufacturing strategy there?

At this point SPARC has no plans to invest and build manufacturing capabilities for these normal modalities or for that matter, traditional modalities. So our manufacturing strategy is to broad base the manufacturing of supplier base and deal [indiscernible] as possible. So in this case, also, we will continue to build up multiple options on manufacturing. And as we kind of start preparing for the IND next year for this, and we are already evaluating multiple external vendors for the MUC-1 ADC program.

[Operator Instructions] As there are no further questions, I would now like to hand the conference over to Mr. Jaydeep Issrani for closing comments. Over to you, sir.

Thank you, [indiscernible], and thank you, everyone, for joining today for the call. We try to answer for the questions you had but in case there are any additional questions or follow-on questions, you may reach out to us and we'll respond to you through email. Thank you once again for joining the call today.

On behalf of Sun Pharma Advanced Research Company Limited, that concludes this conference. Thank you for joining us, and you may now disconnect your lines.