Please note that this conference is being recorded. I now hand the conference over to Mr. Jaydeep Israni from SPARC. Thank you, and over to you. Thank you, Yashree. Good evening, ladies and gentlemen. My name is Jaydeep Israni. I head the Business Development and Investor Relations at SPARC. On behalf of SPARC, I welcome you to SPARC's yearly update on strategy and program updates. I'm joined by our CEO, Mr. Anil Raghavan, and members of SPARC's senior management team for the call today. The format for today's discussion will be similar to our previous presentations. That is, SPARC presenters will walk you through these slides, after which the call will be open for questions and discussions. The presentation for today's discussion was shared earlier. We hope you have received it. Before we start today's discussion, I would like to remind you that our discussion today includes forward-looking statements that are subject to risks and uncertainties associated with our business. Hence, actual results may be different from those projected in today's presentation. I'll now hand it over to Mr. Anil Raghavan for his presentation. Over to you, Anil. Thank you, Jaydeep, for the introduction, and good evening, everyone. It gives me great pleasure to welcome you to SPARC's 14th annual portfolio update. Thanks so much for your continued engagement and continued trust. We couldn't have reached where we have reached without your steadfast support every step of the way. Thanks again, and thank you for taking the time to be with us today. As Jaydeep said, we will follow our regular discussion flow, starting with a commentary on our strategy and operational priorities, followed by a report on the progress of key programs. My intent is to capture the most important elements of our post-PROSEEK plan and set expectations for the short to medium term. I will also touch upon several programs which we do not plan to cover in the program update. On that part of the presentation, we will focus on reviewing the progress made on two specific programs, which is super important for SPARC going forward. I'm delighted to introduce Dr. Mudgal Kothekar and Dr. Sandeep Inamdar, who recently moved to therapeutic leadership roles for immunology and oncology. Mudgal and Sandeep have been with SPARC for many years and will play important leadership roles in shaping our portfolio in their respective therapeutic domains. Mudgal will discuss our SCD-153 program for alopecia areata and potentially other dermatology autoimmune conditions. Sandeep will go over the MACH-1 ADC program, that's SBO-154. So with that, let's start where we have left off in our last call, slide four, please. This is an overview of the PROSEEK pooled result. As we mentioned during the interim analysis call, we have closed the study at 491 patients almost immediately after the interim analysis results were out. We have also discontinued the long-term extension study with roughly maybe under 100 patients completing that leg of the program. We have now completed the full analysis, including the planned biomarkers, and we've also completed several post-hoc questions we had. Unfortunately, the results from the full analysis closely match the interim analysis trends that we shared with you. The MDS-UPDRS part three trends are shown here in the graphs below. Mean of the change from baseline was the primary endpoint, which also showed a similar trajectory without adjusting for dropouts. That's not on the chart here. But in a model-based analysis, adjusted for dropouts during a drug arm marginally deteriorated and underperformed the placebo. The placebo performance in the study has been a clear outlier, with a modest improvement in MDS-UPDRS part three versus both natural history and trends that we have seen from other trials in early Parkinson's disease, and on biomarkers, while most markers mirrored the clinical trend, a key mechanistic marker, that's alpha-synuclein and CSF, bucked that trend and demonstrated a reduction in the high-dose arm, a result that actually supported the c-Abl hypothesis. Pharmacokinetics, peaking from both plasma and CSF, were consistent with prior studies and expectations. In fact, in the CSF, even at the lower dose, we had multi-fold coverage for the c-Abl IC50. We also analyzed the LTE trends, which was not a controlled part of the study, so we didn't have a placebo. All placebo patients transitioned to high dose post week 40, in line with the LTE study design. Patients who remained on the drug continued to deteriorate slightly when we adjusted for dropouts using a statistical model. We used something called MMRM, a widely used statistical technique for making corrections for randomly missing data. While it is difficult to draw a firm conclusion without a placebo arm, it appears that these patients deteriorated slower than expectations based on natural history studies, even in the long-term extension arm. We plan to review the full results with our scientific advisory board later this month, and looking forward to publishing the study formally as soon as possible. That's all what I wanted to say about PROSEEK at this point. We will revisit PROSEEK during the Q&A if you have questions, and I'm sure some of you may have. Let's move to slide five, please. Understandably, PROSEEK was a significant turn for us. Now, as we pivot from that chapter, we have to address the important top-of-the-mind question that ourselves and our investors have regarding the value of the residual portfolio and how do we resolve them. We spent a lot of time after PROSEEK data readout analyzing our other active programs and potential options and settled on three important priorities for SPARC going forward. First pillar is having an optimized portfolio with a narrow therapeutic area focus and SCD-153 and SBO-154 as anchor assets. That's Itaconate and MACH-1 ADC. Secondly, we have to adopt a more flexible business model for resourcing and cashing our assets and capabilities. This means, for example, a willingness to partner key assets much earlier than we have been traditionally exploring or we were comfortable exploring. Finally, we need to have a sharper focus on execution of short-term cash-generating opportunities. We have several milestones varying degrees of likely impact, varying probabilities of success, and time to event horizon. Now, let me take. We are going to talk to all of these pillars in a bit more detail in the rest of the presentation. So let's start with slide seven on portfolio optimization. Let's first look at what is not here. Neurodegenerative disease is missing. While our challenges with Vodobatinib were truly multifactorial, a couple of key ones stood out on reflection: reliability of animal models and variability of appropriate clinical trial design in terms of duration of the study, number of patients needed, availability of reliable biomarkers, etc. These were two of the most important ones. We had several programs in the neurodegenerative diseases area going into the PROSEEK data event, pursuing similar or complementary hypotheses. Since the outcome of PROSEEK, which was a real downer for these programs, we have parked all but a couple of early platform-building efforts in the neurodegeneration space, pending our review with our staff and determination of ways to mitigate the key risks. In the interim, oncology and immunology will remain mainstay of our portfolio, and they are somewhat natural choices for us, both from an opportunity attractiveness standpoint and capability maturity perspective. Oncology represents significant unaddressed disease burden and pricing support in spite of intense competition. We will focus on two key themes which enjoyed a lot of success of late: smart delivery of cancer drugs mediated either through an antibody or small molecule ligand. We will look to deliver a variety of payloads, including chemotherapeutics, immunoactivators, and other targeted therapies. Another theme we are excited about is new synthetic lethality targets, which can work in either PARP resistance or in new synthetic lethality pairs. We have a couple of interesting ideas there that we are currently pursuing. So one key element of this approach, especially the smart therapeutic part, is its modular nature. Many of its components, be it targeting moieties, linkers, or payloads, can work in multiple combinations and permutations, which gives us significant efficiencies in terms of discovery and early preclinical development. Immunology is a bit more nuanced picture. The autoimmune field has seen a significant level of success, moving the standard of care substantially in recent years, mostly on the back of resounding success of antibodies blocking key cytokines such as IL-23 and IL-17 in psoriasis and IL-4 and IL-13 in atopic dermatitis. The field really has a suboptimally addressed need for a safe oral or subtopical alternative for biologics depending on disease severity. JAK inhibitors, which provide an effective alternative, have their own liabilities on safety. That's where SPARC is trying to position in immunology: novel mechanisms which can lead to safe topical alternatives to biologics and JAKs. We believe it will also meet another key unaddressed need in this space. That's for combinations which can improve efficacy and therapeutic window. And we will have more to say on that later on. Now, let's move to slide eight, please. Here we have a bit more on 154 and 153 programs. We've introduced these programs in our earlier calls last year. Let me give you a quick recap of these programs as a refresher. SBO-154 is an antibody-drug conjugate which targets a novel combinatorial epitope of the tumor-associated antigen called mucin-1. As you know, we have in-licensed these unique antibodies from the University of Tel Aviv startup called Biomodifying. 154 is the first product on that platform, and it leverages a robustly validated linker and payload, that's MMAE using a PABC linker. We've already achieved preclinical validation for several key aspects of the hypothesis, which we will go over in the next slide. SCD-153, on the right side here, is a prototype of an analog of an endogenous immunosuppressive metabolite called Itaconate, which was originally developed by a team at Johns Hopkins. We have built the 153 program on multiple topical formulations of this Itaconate analog, which we believe can be effective intervention in autoimmune disorders like alopecia areata and vitiligo. The program has completed its first-in-human single-ascending dose recently, and multiple-ascending dose study in alopecia areata patients is expected to start in early part of 2025. Mudgal will walk us through the program in a bit more detail. As I mentioned earlier, we are really excited about the platform nature of both these assets. Upon clinical validation, both assets can deliver multiple indications and products in the monotherapy setting as well as in combination, and I want to talk a bit more about the promise of these two opportunities in the next couple of slides before I move on from the portfolio optimization priority, starting with slide nine. The ADC field has been on fire recently on the back of the success of products like Enhertu and Trodelvy, and in fact, a lot more is in the works, making ADC one of the hottest, busiest areas for innovation in oncology, and hopefully even beyond, particularly in immunology in the future. What is making this search possible is the evolving maturity of linker payload technologies. That's a big factor. And also the opening up of several key technology elements, such as linker systems again, giving broad freedom to operate from an IP perspective. The field is also learning from the growing clinical experience about optimal DARs, drug-antibody ratios, that's effective ways of management of critical adverse events and viable dosing regimens, and so on and so forth. SBO-154 looks to leverage some of these key learnings from the field's recent success with a potentially novel targeting moiety, that's the SEA domain of MUC1. Why is that important? Let's go to slide 10, please. As you can see, a lot of intense activity that we are currently witnessing in the ADC space is driven by classic herd mentality. Take a look at the antigens targeted. A lion's share of these programs target less than 10 cancer-specific antigens. Even within that distribution, two antigens, HER2 and TROP2, account for a vast majority of current active programs. In our view, HER2 and TROP2 both have already failed for classic ADCs with chemotherapeutic payloads, which is what almost all of these programs are trying to do. So there's a real dearth of potentially high-impact targeting agents, and that's what we believe will give MACH-1 ADC a distinctive edge. MUC1 alpha has been and continues to be a target of active interest for ADCs and even other approaches like cancer vaccines. All these programs need to swim against substantial blood levels of cleaved alpha, which makes tumor targeting difficult. 154 overcomes that issue by focusing on the SEA combinatorial epitope, which improves the tumor specificity significantly. We now have, as I said, validation for two key elements of this idea. That's the relatively low levels of floating SEA compared to the floating alpha in patient plasma and appreciable surface expression of the epitopes of high interest in highly prevalent tumor types. Sandeep will later in the presentation talk to both these elements of data validating our hypothesis. As I said earlier, if we successfully reproduce these outcomes in the clinical setting, that gives us a new viable targeting entity which can be used extensively with other types of modalities such as other cytotoxins, immunoactivators, and T cell engagers. And that's certainly exciting. Now, for a brief update on 153, slide seven, please. This slide, particularly, builds on a couple of points I mentioned earlier. In spite of its enormous commercial success, the clinical impact of biologics is limited to more advanced patients fighting severe manifestations of certain diseases like atopic dermatitis, psoriasis, or IBD, rheumatoid arthritis, etc. The number of lives impacted is far fewer than patients who are managed with small molecule orals or topicals. The real issue here is the stagnation in non-biologic standards of care, both in terms of safety and efficacy. So moving the therapeutic needle will require new approaches which expand choice of decisions and patients fighting these difficult diseases, either as standalone agents or potential combination partners. That's the real promise of SCD-153. We have learned so much about the pathway and the new chemical entity itself in our productive collaboration with JHU. And we're really looking forward to subsequent phases of clinical development. We will review our science and other early clinical outcomes that we had from the phase 1 so far later in the presentation when Mudgal comes in. So let me leave this segment with two or three key messages. SPARC will pursue select teams in oncology and immunology for its portfolio build going forward. That's leveraging tumor-specific delivery options and synthetic lethality in oncology and novel pathways which can become topical options in certain dermatology autoimmune conditions. SCD-153 and SBO-154 offer potentially high-value options and ideal vehicles to test this approach with great upside if they're successful. We will direct our resources preferentially to developing these programs to its clinical inflection points. These will remain the primary focus of our process with SPARC. Let me go over the next two tenets of our strategy going forward, starting with a key shift on our partnering approach. I will use the SBO-155 program to illustrate the change we are trying to highlight. Slide number 13, please. Certainly, one of the challenges we have coming out of a costly clinical data setback is the resource constraints that we have to navigate. Committing to continue developing the prioritized assets will consume a significant share of resources that we have access to. That leaves several important programs in our portfolio with very difficult choices. Historically, our intent has been to stay on to the program at least till we obtain a clinical proof of concept and enter late-stage clinical development. We need to re-examine that construct, and that's what we are intending to do. We will look for partnerships at an earlier stage of development. In addition, we will also look for alternative structures like asset-specific new co-creation. We have a specific example for this shift in approach coming out of our work with UCSF. I want to go over the program and the construct in a bit more detail in the coming slide. Before I do that, let me also make a brief comment on another business model opportunity which we have shied away from in the past. That's leveraging our discovery and translational capabilities in a services model to de-risk SPARC. Even though there are really strong tailwinds in terms of market forces supporting India-based service delivery and India-based services businesses and a real need to de-risk SPARC for downside protection, we continue to stay on the sidelines for several reasons that we have spoken about in many of our past calls. While that remains the case, we will continue to review our options and risk carefully and take a final position on this opportunity in the coming year. Now, to get back to our collaboration with UCSF, slide 14, please. This slide captures the broad timelines of our relationship with UCSF. UCSF was one of our earlier strategic collaborations with the Master Collaboration Agreement taking shape in 2017. The program that led to SBO-155 was conceived in 2020, and we could identify a lead candidate with preclinical validation two years flat. We are proud of the quality of collaboration we are having with UCSF and the accelerated nature of the early development. We've explored setting up a new core for advancing this asset, and that thought led to the formation of Thila Therapeutics, a company founded by a team of UCSF investigators, SPARC and UCSF itself. Earlier this week, we announced the successful closure of the letter of intent between SPARC and UCSF to go ahead with this construct. SPARC and UCSF will license rights to its joint IP to Thila Therapeutics, and Thila will raise external dollars to fast-track SBO-155 to clinic. We believe this is an exciting business model option which we can explore with many other programs in our early-stage pipeline, which in the broader scheme of things allows more shots in the goal and a certain level of risk mitigation at the portfolio level. Slide 15 has more color on the program per se. PSMA has been targeted for tumor-specific delivery of chemotherapeutics for a long time. The field had its first major breakthrough with a radioligand therapy called Pluvicto, which uses a small molecule ligand of PSMA to deliver radiotherapy. In spite of its impressive data early on, the RLT field faces many challenges, leaving alternatives to come in and improve the outcomes. There is a significant opportunity to reduce the variability of therapeutic benefits, plus improve overall safety profiles, particularly reducing the bone marrow toxicity. Alternatives can also help overcome limitations in terms of lifetime heart caths, in addition to all the logistical challenges in putting together and distributing radiotherapy. SBO-155 provides a differentiated approach using a synthetic PSMA ligand for targeting, but delivering alternative payloads. We believe this approach helps to overcome some of the limitations of the radioligand therapy, as well as PSMA-targeted ADCs which have been tested so far. In an indication where, unfortunately, there is progression with tragic quality of life and survival implications, SBO-155 we believe can offer a very useful treatment option. Now, let's please move to slide 16, which discusses some illustrative data from this program. The graph on the left highlights efficacy in an in vitro system with ta floors, PC3 prostate cancer cells for both PSMA over-expressing PC3-PIP cells and PSMA null PC3-flu cells. SBO-155 efficiently inhibits the PIP cells at less than a picomolar IC50 and has a thousandfold advantage over the null flu cells. Over on the right side of the chart, we have an in vivo proof of concept on PC3 xenograft model. Our small molecule drug conjugate at 60 micrograms per kilogram dose is tested in both PIP and flu xenografts against the vehicle, while SBO-155 in the flu xenografts and vehicles in both xenografts did not make any impact. Look at the growth curve on the over-expressing PIP model. It leads to a complete regression of the tumor. These and other critical pieces of data validating this asset have paved its way to a set of IND-enabling studies which are currently going on, setting up its clinical entry in the short to medium term. Slide 17, please. As I said earlier, Thila Therapeutics was formed between SPARC, UCSF, and its scientific founders. SPARC will receive 55% of Thila's initial shares in two tranches. The equity will be issued in full within six months of signing the definitive agreement. Thila plans to build its pipeline focusing on the small molecule drug conjugate modality with additional targeting ligands and payloads in a wide variety of solid tumor media. We are super excited about many things here. Firstly, SBO-155 as an asset and its potential to emerge as a true alternative to other PSMA-targeted approaches, and that is foremost. We are working with a very high-profile and potentially high-impact team of scientific founders at Thila. We believe in their ability to follow through and develop a pipeline using this approach. And finally, this experiment offers a viable alternative, as I said earlier, to advancing interesting programs, particularly in the face of resource constraints. That's very promising as we continue to build differentiated preclinical programs all fighting to find a way to clinic sooner than later. That takes me to the final set of slides on my part of the presentation, which aims to cover certain short-term cash catalysts which we are tracking very closely. Let's move to slide 19, please. In the next few slides, I want to focus on two things. On the left bucket here, we have a bunch of short-term milestones with potential cash events. They come with a mix of probabilities which will be difficult to estimate accurately at this moment. But they all offer a definitive path to adding additional resources to support the prioritized programs and beyond. And therefore, very important. Equally important is optimizing our cost structure to the demands of our current portfolio and intent. Not just structural adjustments, though, but finding ways to do more with less constantly. And we've done quite a bit of this since proceeding interim analysis itself and may have potential additional adjustments to make in the coming year depending on where the chips fall on the first bucket. Let's take a look. Slide 20, please. We have four programs which can potentially lead to cash-generating milestones in the short term. Let's go one by one, starting with Sezaby, which is our benzyl alcohol-free phenobarbital formulation which got approved in November 2022. There are two potential opportunities which we are aggressively pursuing. That's finding a way to convince the agency to reconsider the denial of a pediatric rare diseases voucher which we believe we were eligible for, and secondly, convincing the agency to enforce the orphan drug exclusivity that Sezaby was granted. I'll cover both these opportunities in a bit more detail in the next slide. Vodobatinib's CML part is the next one in the set. It has always meant as a head for the PD program, and I will update you on where we stand at the moment on our efforts to find a development and commercialization partner. PDP-716 is another asset on the chart with potential access to cash. As you remember, we received a Complete Response Letter which primarily cited the unacceptable regulatory status of our API partner. Since then, we've replaced the API source and made several changes to the process, primarily moving to a higher volume capacity for the finished product manufacturing. On the partner end, we just went through a couple of ownership transitions involving a SPAC deal which did not conclude and a merger with another pharmaceutical company. We are working very closely with the current management of ORQX, that's their new name, to complete the CRL response by the second quarter of the next financial year and ensuring a successful launch once we get the approval, which we hope to get sometime in financial year 2026, and PDP-716 launch as a significant milestone attached to it. We also made substantial progress with revolutimodl, which is a couple of phase two studies targeting AD and PSA, which I'll talk to you in a bit. We'll start with Sesadine over to slide 21. Let me start with a caveat on the potential pediatric rare diseases voucher. This matter is the subject of an active litigation, and there are significant restrictions in terms of how much we can discuss. So I'll limit my comments to providing necessary background and the potential impact in case of a positive outcome. The PRV voucher program was established with an intent to incentivize the development of better and safer medications for pediatric rare diseases. The PRV statute lays down very specific qualifications for a product to meet in order to be eligible for a pediatric rare diseases voucher. During the approval of Sezaby in 2022, FDA denied us the voucher and shared with us the agency justification supporting the denial, which is built on certain interpretation of the FDA PRV statute. SPARC believes that the agency interpretation led to an unfair denial of the voucher, and we are committed to exploring all available options to correct it. We've been on this path since the approval, including directly presenting our case for reconsideration to the agency. After exhausting all available reasonable options, we approached the court for direction in February 2024, and we expect the court's initial opinion on this matter in the last quarter of this financial year. We hope for a positive turn of events, and if we get a favorable outcome, as you can see from the rest of this slide, PRV is a highly valued tradable device which has recently been sold for valued in excess of $150 million. Unfortunately, we cannot go into any more detail on this here, given the active status of this matter. But as things evolve, we will keep you posted. And now, on the exclusivity piece, let's see slide 22. When the agency approved Sesadine, they granted SPARC a seven-year orphan drug exclusivity, which we've enforced will force marketers of unapproved formulations of phenobarbital IV out of the market. FDA follows a longstanding policy of risk-based enforcement of exclusivity. We've been working with the agency through this period to remove unapproved products from the market. We've been in touch with the agency through direct representation and using formal devices such as citizens' petitions. Given the complexity of the case, FDA has indicated to us that they need more time to formally respond to our citizens' petitions. In the meantime, we've been communicating with the marketers of unapproved formulations, making them aware that they cannot continue to be in the market as Sesadine is now formally approved in the U.S. market, and this was done through a formal cease and desist letter. We've also been working to make our supply chain more robust by adding additional external capacity, which is under agency review as we speak. We remain hopeful that the exclusivity will be enforced, as it is just not a matter of getting unapproved products out. In addition to being the only approved IV phenobarbital in the U.S., ours is the only product which does not have potentially harmful excipients such as benzyl alcohol. FDA has a stated intent to remove products containing benzyl alcohol, especially when it poses significant potential risk to vulnerable populations such as neonates. So going into 2025, all hands on the deck and staying hopeful. Now, Vodobatinib CML on slide 33, please. Post-closing interim analysis results. We engage with the U.S. FDA for CML to have clarity on registration expectations, and they agree on key elements of the phase three design. The schematic here on the top half of this slide captures the expected phase three program. There are a couple of major elements to note in terms of FDA expectations. First is the population, patients who have failed at least one second-generation TKI. And we also need to include a smaller dose-finding leg. So in this design, we have 20 patients at 200 milligram and 130 milligram each. And we've kept this an integrated protocol which can move to the phase three part of the program post-analysis of the randomized dose-finding part. We have to get an agreement on the phase 3 dose with the agency at this stage before we initiate a formal comparative study against 500 milligram drug called bosutinib. Our intent is to keep the program at a state of readiness to launch a registration program while we finalize the potential development and commercialization partner. We've initiated that process in the second half of this year and have completed our initial outreach. As you can expect, given the niche orphan indication, we are working with a limited field here. We are working towards identifying a partner by the end of this financial year, and the final program on this list is uncertain That's SCD-044, which is licensed to Sun Pharma on slide 24. I have a brief update. As you know, we have two active phase 2 trials for ongoing in atopic dermatitis and psoriasis. The most important update here is we've achieved enrollment completion for both these programs earlier this year. Atopic dermatitis is expected to read out top line for its 16-week part one in Q4 of this year, but psoriasis is expected to reach top line readout in the first quarter of next financial year. At this point, we are really looking forward to seeing the data and looking forward to working with our commercial partner to advance the program to phase three. Slide 25, please. Coming into this year on the back of preceding outcomes, one of the key objectives was to find ways to preserve capital without sacrificing the most important portfolio priority. As you can see, we've prioritized MACH-1 ADC and Itaconate AA program as our top execution priorities, plus wanted to continue to shape these programs and its extensions preclinically without losing momentum in addition to exploring some of our more promising discovery programs. What are the implications of this? We minimized all additional spend on the ongoing CML program and decided to focus on transitioning the asset to a potential partner with the fully conceived development program for phase three. We found an alternative model for developing the SBO-155, as we explained. We are really excited about that. And even on our high-priority program, we've significantly increased the India clinical component to keep the overall cost of the clinical POC under check. On the organizational side, coming into this year, we were gearing up for a significant Vodobatinib phase three program or even multiple late-stage programs. Even the early-stage nature of the assets, we are assigning higher priority to now. There was a significant mismatch between the scale of our clinical development team and our current scope, or even the scope we are expecting in the short term. As you can see here on these charts, we're currently at 324 against the planned FY 25 headcount of 400 plus. This reduction is driven by significant downsizing in the clinical development capability here in India and also substantially in the U.S. Our U.S. headcount dropped from 37 at the beginning of the year to 7 currently. Our resourcing is certainly an evolving situation. We started the year with INR 15.2 million in operating cash. But with proceed turning out the way it turned out, we had to rely on our smaller operating cash flows and approved debt limits, which are primarily coming from our promoter group companies or from commercial banks with promoter group guarantees. This may take us to middle of Q1 next year. But as I mentioned, we have several potentially cash-generating catalysts in the short term. We will review these, and we will review where we stand at the end of the year before finalizing a medium-term resourcing plan for the company, and we will keep you posted. Slide 26, please. Here is a snapshot of our short to medium-term execution priorities. I've touched on the objectives for Sesadine, Waterbattner, PDP-716, and Revolt Elimon in detail in the previous slides, which I don't plan to go over again. We have additional objectives set for SCD-153 and SBO-154 on this slide. But in the subsequent sections, Mudgal and Sandeep will give you additional color on the status and plans for these programs. So let me not steal their thunder. So in closing, let me say this. We've tried to turn the page and focus on two very promising assets to have additional shots to SPARC. We have several other interesting ideas preclinically, which are important data milestones coming up in the short order. What we did with SBO-155 may give us a good template to progress these programs without committing additional resources on our end. In the short term, we will stay super focused on achieving potentially cash-generating milestones, which we have listed at this presentation. Once we are through with that, we will take a hard look at where we are at the end of the year and our options going forward and go from there. So thank you for your time today. I will transition the call now to Dr. Mudgal Kotekar for an update on SCD-153, and looking forward to seeing you back during the Q&A. Thank you. Thank you, Anil. Good afternoon. So I will provide an update on the SCD-153 program for the treatment of alopecia areata. As shown here on slide 28, alopecia areata is an autoimmune disorder that results in patchy hair loss, as shown in the diagram on the left side. So this disease affects 2% of the global population, and the prevalence is increasing. Some patients, mainly those with a mild disease, they do recover spontaneously, but most of the patients need medical intervention for hair growth. The corticosteroids are often used off-label with limited efficacy, and they carry a risk of side effects on the long-term use. Even the recently approved JAK inhibitors carry black box warnings for some serious side effects, such as cardiovascular events, infections, and malignancies. Now, in terms of pathogenesis, the hair loss in alopecia areata is the cause of infiltration of immune cells, such as the CD8 positive T cells around the base of the hair follicles that attack these hair follicles and result in hair loss. Next slide, please. So this SPARC has developed a topical agent called SCD-153 for the treatment of alopecia areata. This is a first-in-class compound that targets the basic pathogenesis of the disease. SCD-153 was evaluated in an animal model of alopecia areata in mice. The pictures on the left side show the animals that were treated in this model. As shown in this diagram, SCD-153 at various doses and dosing regimens resulted in growth of hair in this model, while the animals that were treated with vehicles showed no hair growth. Now, the figure on the right-hand side shows the hair growth in terms of hair growth index in these animals. So you can see that SCD-153, at most of the dosing regimens, resulted in hair growth over time, but there was no hair growth in the animals that received the vehicles. The dose three regimen one showed the most remarkable hair growth. So this animal model experiment showed that SCD-153 resulted in a dose-dependent increase in hair growth in the animal model of alopecia areata. Next slide. Now, in the same study, we evaluated the effect of SCD-153 on the CD8 T cell infiltration around the hair follicles. The figure on the left side shows a reduction in the CD8 T cells at the base of the hair follicles in the animals that received SCD-153 compared to the animals that received the vehicles. As shown on the right side, there was a significant and dose-dependent reduction in CD8 positive and NKG2D positive CD8 T cells in the skin of the animals that were treated with SCD-153. Now, these NKG2D positive CD8 T cells are a type of CD8 T cell that are specifically implicated in the pathogenesis of alopecia areata. On slide 31 is an update on the phase one program. So we have recently completed a phase one study in healthy volunteers. In this study, single ascending doses of SCD-153 were evaluated in five sequential cohorts of healthy volunteers with eight healthy volunteers in each cohort. Now, in this study, measurable concentrations of SCD-153 were detected in dermis and epidermis of the skin with increase in concentration with increase in dose, indicating that the drug is reaching its site of action. In terms of safety, SCD-153 was well tolerated up to the highest dose that was evaluated in this study. The maximum safe dose was not reached because the highest dose itself was found to be safe. No subject in this study experienced any dose-limiting toxicity. Next slide. This slide shows the drug-related adverse events that were reported from this study. One subject at the dose level four experienced mild eczema and burning sensation. Now, at the dose level five, two subjects experienced mild eczema and one subject experienced burning sensation. Now, all of these events were mild in severity and resolved without treatment. Next. On the next slide, slide 33, is an update on the planned study. So we have planned a phase one B study in patients with alopecia areata in India. So the protocol of this study has been submitted to the DCGI. So this is a randomized double-blind study to evaluate the safety, efficacy, and pharmacokinetics of SDD-153 compared to vehicles in alopecia areata patients. The flow chart shown here describes the overall design of the study that I will describe in short. In this study, patients will be randomly assigned in a four-to-one ratio to receive SDD-153 or vehicle in sequential cohorts of four dose strengths of SDD-153. Initially, patients will be enrolled in the first cohort of the dose level one. These patients will initially receive a single application of the assigned treatment, that is SCD-153 or the vehicle on day one, which will be followed by safety assessments up to day eight. After the safety assessment following a single dose, these patients will continue to receive once-daily treatment throughout the treatment period. Now, the patients that are initially randomized to SCD-153 will continue to receive SCD-153 for a total duration of 24 weeks. While the patients that were initially randomized to vehicle, they will be switched to SCD-153 at week 13 and then receive the active treatment for the next 12 weeks. Now, patients will be enrolled in the subsequent higher dose levels after the evaluation of safety data up to day 22 from a previous dose level cohort. Next slide, please. Now, to summarize, SCD-153 employs a new mechanism of action to address the complex immune pathogenesis that could be implicated in a diverse range of clinical disorders. In addition to providing an alternative option for treatment as a single agent, SCD-153 has a potential to be used in combination with established treatments to improve their efficacy in terms of durability of the response or in terms of increasing their response rates. SCD-153 has a potential to be explored in multiple dermato-immunological disorders, and multiple topical formulations of SCD-153 could be explored. So, in short, SCD-153 is a topical first-in-class alternative that has a potential to address the limitations of existing therapeutic options. On the next slide, that is slide 35, are the projected milestones for this program. Now, the phase 1b study in alopecia areata patients will be initiated in quarter one of the next financial year. We will get the interim readout from this study in quarter one of FY 27, and we target to initiate a global phase 2b study of SDD-153 in Q4 of FY 27. So here, I conclude the update on SDD-153, and I hand over to Dr. Sandeep Inamdar for an update on SBO-154. Thanks, Mudgal. So we will now shift our focus to SBO-154 and anti-MUC1 antibody drug conjugate with a monomethyl auristatin, or MMAE, payload being developed for the treatment of multiple advanced solid tumors. The next slide. So MUC1 is a highly glycosylated transmembrane protein consisting of an extracellular alpha subunit, a membrane proximal beta subunit, and a short cytoplasmic tail. It is widely expressed in normal glandular epithelial cells, such as the lining of the gastrointestinal and respiratory tracts. It is normally expressed exclusively on the apical or glandular surface of the epithelial cells. However, during malignant transformation, there is an increase in the cell surface expression of MUC1, along with a change in the normal pattern of the expression, resulting in MUC1 expression across the entire cell surface in cancer cells, as opposed to the apical expression that is seen in normal cells. This change in expression pattern may allow anti-MUC1 ADCs to selectively target the tumor because the apical surface in normal tissues is not usually accessible to administer drugs. The next slide. SBO-154 is a first-in-class humanized IgG1 antibody targeting what is known as the SEA domain of MUC1. The SEA domain is located in close proximity to the cell surface at the junction of the extracellular alpha subunit and the partially embedded beta subunit. Historically, it has been easier to develop antibodies against the alpha subunit, particularly the VNTR region, and therefore most of the previous clinical efforts that have been directed against this region of the protein. However, the VNTR region is subject to significant proteolytic cleavage, resulting in a large amount of circulating MUC1 in the peripheral circulation that may have originated from the tumor cells. In fact, the well-known cancer antigens CA15-3 and CA 27.29 that are overexpressed in breast and some ovarian cancers are circulating MUC1 entities that have been cleaved off from the tumor cells. Large amounts of circulating alpha subunit MUC1 in the periphery may sequester or bind to exogenously administered therapeutic ADCs, resulting in a sink effect, thereby limiting the access of the antibody to the actual site of tumor. Since the SEA domain is not subject to the same level of proteolytic cleavage as the VNTR region, it is unlikely to be subject to the sink effect in the plasma. Next slide. SPARC has evaluated the cell surface levels of SEA domain MUC1 in various patient-derived tumor tissues using a proprietary immunohistochemistry assay. We have seen high levels of SEA domain-specific MUC1 expression across a variety of common tumors, such as the adenocarcinoma of the lung, ER-positive breast cancer, and ovarian cancer. The median H-score, which is a measure of cell surface expression of the protein, exceeded 200 out of a maximum possible score of 300 in most of these tumors that were predominantly stage IV tumors. For context, an H-score greater than 100 would be considered moderate, and scores exceeding 150 are generally considered high. It also appears that the level of MUC1 expression increases with increasing stage of the disease. Among these, breast and lung cancer samples had broad circumferential expression. The expression pattern in ovarian and pancreatic cancers was predominantly apical. However, given that tumors generally lose the typical glandular architecture that is present in normal tissue, the extent to which this apical expression will restrict access to SBO-154 is unclear. However, given the very high expression levels in ovarian cancer, we plan to enroll a cohort of these patients in our phase one study, which I shall discuss in the next couple of slides. So, in order to further test the sink effect hypothesis, we have also evaluated the levels of circulating sea domain MUC1 and compared that to the VNTR domain in plasma samples of patients with advanced cancers. Across all tumor types tested, we find that the levels of circulating SEA domain are significantly lower than the VNTR domain from the alpha subunit, indicating that SBO-154 may not suffer from the same sink effect that impacted the earlier generations of MUC1-targeted therapies. Next slide. We have evaluated the activity of SBO-154 in in vitro cell lines and in vivo animal models with different levels of MUC1C expression. The in vitro cytotoxicity data are depicted in the tables at the top of this slide, where it's evident that SBO-154 shows higher potency as seen by lower IC50 values in the higher-expressing COLO357 and MCF7 cell line compared to the lower-expressing HT-29 cell line. Similarly, when the COLO357 cells were xenografted in nude mice, the tumor volume reduction was significantly greater upon treatment with SBO-154 compared to vehicle control. In contrast, SBO-154 resulted in relatively modest reduction in tumor volume in the H-T29 xenograft study, indicating that the pre-clinical efficacy of SBO-154 correlates well with target antigen expression. Next slide, please. Preliminary non-GLP toxicology studies have been completed in Cynomolgus monkeys, which is the pharmacologically relevant species for this antibody. In an exploratory seven-week dose range finding study in two animals each, SBO-154 was administered at doses of one, three, and six milligrams per kilogram for three doses at an every three-week dosing schedule. SBO-154 was generally well tolerated up to the highest dose of six milligrams per kilogram. There was no mortality or adverse clinical signs, with no effect on body weight and food consumption. There were lab abnormalities of bone marrow suppression, such as reduction in blood cell counts, which is consistent with the known adverse event profile of MMAE. Histopathology was also consistent with the observed lab value changes. There was a dose-proportional increase in exposure of SBO-154, and the highest non-severely toxic dose, or the HNSTD, was established at six milligrams per kilogram. A repeat dose GLP tox study is currently ongoing as part of the pre-IND requirement. This will help confirm the preliminary tox results and estimate the starting dose in our phase one study. Onto the next slide. Now, I would like to provide a program update in terms of next steps for this molecule. We had submitted a pre-IND meeting request to the U.S. FDA, for which we received a detailed written response in late November. Their response indicates broad agreement with SPARC's proposed IND data package, and we do not anticipate any barriers to the IND filing early next year. We proposed a multi-country phase one dose escalation and expansion study in patients with advanced epithelial solid tumors and standard eligibility criteria for a study like this. The dose escalation portion is expected to enroll approximately 30 unselected solid tumor patients who have failed available therapy. Once a maximum tolerated dose has been established, we plan to open three tumor-specific expansion cohorts of approximately 30 patients each in tumors that are known to highly express MUC1 SEA. This includes ER-positive breast cancer, adenocarcinoma of the lung, and ovarian cancer. This will be an adaptive design with the goal of establishing early clinical proof of concept for the program. Next slide, please. Finally, a quick update on the upcoming milestones for this program. We anticipate an IND filing by the end of Q4 FY 2025, followed by initiation of the phase one study in the subsequent quarter. Next slide. So, while that concludes my specific discussion of SBO-154, I'd like to highlight that the MMAE payload-based approach is only one of the multiple ways we can leverage MUC1 targeting. This uniquely targeted antibody has the potential to serve as a platform for other payloads, including other chemotherapeutic agents, such as cytoskeletal disruptors or DNA-damaging agents, immunotherapy-based approaches using both immune agonists as well as checkpoint inhibitors, and agents targeting angiogenesis. We have very early programs in development for some of these approaches. I've now handed back over to Jaydeep to direct the rest of this session. Thank you, Sandeep. This is the last slide for discussion today, and it summarizes SPARC's pipeline of disclosed assets and their stage of development. We have multiple other programs under development that are not disclosed, and we will share details of those programs at appropriate time in future. With that, we would now open the call for question and answer session. Thank you very much. We will now begin the question and answer session. Anyone who wishes to ask a question may press star and one on their touch-tone telephone. If you wish to remove yourself from the question queue, you may press star and two. Participants are requested to use handsets while asking a question. Ladies and gentlemen, we will wait for a moment while the question queue assembles. Ladies and gentlemen, to ask a question, please press star and one on your phone. We have a first question from the line of Vishal M. from Systematix. Please go ahead. Thanks for the opportunity. I'm audible. Yes, please go ahead. We are. Yeah. Yeah. So, my question is, assuming we have some milestones coming up wherein we can potentially generate cash. So, one is a licensing deal for your CML candidate, and there is a priority review voucher that you might get issued. But in a worst-case scenario, assuming there is a delay in monetization of these opportunities, what is the cash level we have currently, and how long we can continue to fund our operations? So, no, Vishal, thank you for the question, and that's really. I'm sure it's top of the mind for a lot of investors. And as I said, we have a significant number of opportunities here, not just the two that you noted, that is the priority voucher and potential licensing. We have other options like the PDP-716 launch, the exclusivity enforcement on Sezaby. So, there are four or five potential areas where we can have access to short-term cash. But if you come back to where we are in terms of operating cash flows and access to debt that we have, it will probably take us to the early part of next year. And then, depending on where we reach with the short-term cash generating opportunities, which we will have visibility by the end of this year, we will have to take a position in terms of how we plan to resource the continuing development of these programs, which we are committed to do. But we haven't had a final decision on how we will go forward from there, even though we have some options, which we will disclose once we reach that point in the first quarter of next year. Right. So, you also expect phase two data on revolutimod and psoriasis and atopic dermatitis. Assuming the data is positive, so do you expect milestone income on a positive data there? It is, yeah. So, once it reaches the next level of development, it should move to a phase three program. It is a milestone event for us. It's listed as one of the short-term opportunities in our presentation. That's the reason. Right. And so, just any sense that you would have gathered on the efficacy of Revolt Elimon in psoriasis from your early data that you would have, both in psoriasis and atopic dermatitis versus the other oral options in the same therapy? While you are targeting these, while you are kind of, while safety is one of the topmost priority, but just getting a sense on the efficacy that you would expect from these drugs compared to the other oral options in the market. Vishal, we are in a blinded study at the moment. So, we have no visibility in terms of early signals of efficacy. And the studies that we have done earlier were phase one trials, right? So, the only human trials that we had were multiple phase one trials. I don't know whether you've been part of the previous discussion. The translational case for S1P modulator was built on two things. One, we have seen significant ALC reduction, that is, lymphocyte reduction in circulation. That is the mechanistic marker at the dose that we are studying in phase 2 setting. If you look at literature, there are other products in this class which were tested in atopic dermatitis and alopecia, I mean, atopic dermatitis and psoriasis. There is a certain threshold of ALC reduction that was required for competitive activity. We reached that level of ALC reduction in the phase 1 setting. That was the translational case for initiating these phase 2 programs. We do not have any inkling of what is in store, given the blinded nature of the study. Right. Right. Just one final one on Sezaby. Any technical hurdles there in terms of getting exclusivity? I just wanted to understand whether it is a process or there is also uncertainty around the process. It is a process in the sense the process that FDA follows is a risk-based assessment of how and when to enforce the exclusivity, right? FDA usually gives this time when a new product comes to establish a robust supply chain to be in the market before they start enforcing the exclusivity. It is a process, and we are in the process of engaging with the agency. We are hopeful, as we have indicated, by the third quarter of this coming financial year, we hope to have exclusivity. Right. Sorry, just one more. On the in-licensed asset, SCD-153, would you kind of, would you need to pay some milestone income there whenever you get positive data? Or these are completely your own assets now? No, we have these are licensed very early. That was a multi-year option agreement that we had on an early-stage preclinical asset. And we have milestones and royalties, which are typical to those kinds of deals, which is usually in small, I mean, it's in low single-digit%. So, we have a structure which has both milestones and royalties. But given the early-stage nature, it is not like commercial licensing. Right. Got it. Thank you very much. Thank you, Vishal. Thank you, Vishal. We'll take our next question from the line of Bino Pathiparampil from Elara Capital. Please go ahead. Hi. Good evening. A couple of questions from my side. Do you have any estimate of the unapproved phenobarbital market size in the pediatric market? We haven't specifically disclosed a market size. But if you look at the current usage in the unapproved market, it's in several scores of billions of dollars. But I don't want to give you a top-of-the-mind number, but it is publicly available. The second is that the number of units being sold in the U.S. is in excess of two million injectable units, which we believe is primarily used for neonatal population. Two million units. Okay. Got it. Second, on the Sezaby PRV, when you say in 1Q, sorry, 4Q FY25, that would be an opinion of the court, is there a trial that has already taken place, and it will be a final verdict by the court, or what exactly would we expect? So, the process is that we have to have written submissions from us and FDA and HHS and back and forth on those written submissions. And now, later this month, early January, they will decide whether an oral argument is required. And that would be the first indication. And then if that's required, we expect that to complete in the first quarter, I mean, the last quarter of this year. Expected to complete in the last quarter of this financial year? Yep. Okay. Which means this coming next three months. Right. That's our expectation and hope. Okay. Understood. And last on these two ophthalmic products, PDP-716 and SDN-037, I think I'm a little bit less updated. I was going through an earlier presentation from early this year. These two assets were not there. So, could you give a bit of background on how these came in, what is the market potential, etc.? Yep. PDP-716 is a reformulation of brimonidine, which is a widely used second-line drug in glaucoma. And we give a significant dosing benefit for this product. And we have disclosed the clinical results in previous presentations. We met the regulatory standard from a clinical data expectation standpoint. And when we filed, we filed this with an external API source. And that external manufacturer of the API had regulatory issues, and that led to a complete response letter. And before we got there, we had licensed this product to a commercialization partner, a company called VisiOx, which is a specialty ophthalmology company in the U.S. And VisiOx has gone through a transition. It's now sold to a different company, and we are working with their management to respond to the complete response letter. We replaced the API source with a new source, and we also made changes to the manufacturing process because we expect higher volumes for this. So, we are moving to a higher volume facility for this. So, our expectation is that by second quarter of next financial year, we will be in a position to file from the new facility, and then it has a six-month review time. So, we're working very closely with ORQX. And the second product in this group was the steroidal reformulation. And there also we have very good clinical results. But with the commercialization partner, what we agreed was we will schedule these submissions sequentially in the sense we will first complete PDP-716, and then we'll go with the steroidal product. So, we will wait for the closure of PDP-716 to take a position on the regulatory process for that product. Understood. Thank you very much. Thank you. Thank you. Ladies and gentlemen, to ask a question, please press star and one on your phone now. As there are no further questions, I would now like to hand the conference over to Mr. Jaydeep Israni for closing comments. Over to you. Thank you. Thank you, everyone, for being on call today. In case you have any additional questions, feel free to reach out to us on the number that we have provided on the website, and we'll be happy to answer your questions. Thank you once again for being on call today. Thank you. Thank you. On behalf of Sun Pharma Advanced Research Company, that concludes this conference. Thank you for joining us, and you may now disconnect your lines.