Good morning, and welcome to the Jefferies Global Healthcare Conference in New York. My name is Nick Pecora with the Jefferies Investment Banking team. It's my great pleasure to introduce Javier Szwarcberg, CEO of Spruce Biosciences. Thank you, Nick, for the intro, and thanks everyone for being here. It's a great pleasure to be speaking with you today and telling you a bit about Spruce Biosciences. I'll be making some statements along the way. I'll refer you to our SEC filings for further reference. Our flagship asset is tralesinidase alfa, which is an enzyme replacement therapy currently being developed. It's an ERT that gets delivered inside the brain through the intracerebroventricular route. It's using a surrogate endpoint approval pathway. Hopefully, that will result in an accelerated approval of a product. We've demonstrated a very profound effect on this endpoint reduction, with normalization of both heparan sulfate and heparan sulfate non-reducing ends, which is a more specific measure in MPS IIIB. This approval pathway was recently validated by the approval of AVLAYAH, a compound that Denali is currently commercializing for MPS II, another neuronopathic disease. The disease is terrible. MPS IIIB affects children and creates incredibly disability that impacts not only the patient, but also the caregivers and family and all that. There's currently no approved therapy for MPS IIIB. We've gotten all sorts of designations from the FDA, including Breakthrough designation, which was granted in October of last year, and have Rare Pediatric Disease designation, which, if approved, will allow us to tap into the PRV opportunity. We also have a monoclonal antibody currently in our pipeline. It's a mAb for congenital adrenal hyperplasia. It binds CRH. It's a CRH ligand, and it's a validated mechanism by virtue of the approval of crinecerfont, a drug by Neurocrine a couple of years ago for CAH. I'll be speaking today about the TA-ERT program and not the CAH program. If there are any questions, happy to address them. The market opportunity is quite large. We've been very conservative, I think, in our estimates on the epidemiology, but we project the incidence to vary by region, but to be between 0.5 per 100,000 to 4 per 100,000 live births. That could give us about 450 patients in the U.S., 500 in Europe, 1,800 in Asia Pacific, and 300 in Latin America, or 350 in Latin America. Non-attenuated Sanfilippo Type B, which is a type of form that we're seeking to address, has a very short lifespan, with most patients living roughly around late teenage years, around 18, 19. Is an autosomal recessive disease, is passed through genes from the parents with each child of an affected family having a 25% chance of getting it. It's highly concentrated in areas where there's consanguinity, and that results in higher rates in Southern Europe, Turkey, Greece, Saudi Arabia, Brazil, and a few other countries. Assuming that we can address half of the prevalent patient pool, we'll probably going to be hitting around five years post-launch around 200, 250 patients treated, with estimates that we might be able to address a total U.S. pool of around 500 patients at peak. There are many other comparators that we can use to benchmark a potential price. This is not yet to provide guidance to the street on what we think the pricing might be. Given that our product isn't weight based and that it is given as a fixed dose through the intracerebroventricular route, we've mapped on this slide compounds that on the far right column tend to be weight based or body surface area based with upper bounds of cost pricing per year that range between $1.3 million and $2.8 million. We think that a price on the lower end of $1.5 million and on the upper end around $2.5 million with an anchor around $2 million might be suitable for this type of disease. I said earlier, MPS IIIB it's a devastating disease. Kids and affected families have to deal with a child that develops semi-normally up to the age of three where they start missing developmental milestones, peak their behavior and cognitive function at around three years of age, and then they decline. They lose brain function, cognitive function. Around 8-1 0 years of age, they've lost the ability to speak, to ambulate, to communicateto feed themselves. They become bedbound, eventually need feeding tubes, tracheostomy tubes for breathing, and they demise from complications of any type of chronic neurodegenerative disease, much like Alzheimer patients. We're trying to revert that route, and the way we revert that route is by removing the glycan that accumulates and builds up in their brains heparan sulfate, which is the glycan that most likely accumulate, given that the enzymatic deficiency builds up in lysosomes. The enzyme, actually, N-acetyl-α-D-glucosaminidase, which is a missing enzyme, sits in lysosomes, and heparan sulfate just builds up and accumulates in that space, which causes inflammation and neurodegeneration. With the advent of therapy that gets administered straight into the CSF, that drug, the enzyme, penetrates into the neural cells through the drug construct, which is NAGLU enzyme, amino acid linker, and a truncated IGF2 molecule. It is primarily through the truncated IGF2 molecule that enables the neuronal penetration. That sets aside, frankly, this compound relative to other ERTs tried in the past and failed for MPS IIIB. We've designed, actually BioMarin on the prior sponsor, have put together a development program that encompasses a feeding study, which is a 902 study, that brought in patients into the 201 trial, which is the treatment trial. We treated around 22 patients for 48 weeks, those 22 went into extension studies. We have about five years' worth of clinical data and biomarker data and safety data on those patients. The efficacy and safety is contrasted relative to the 902 program primarily, which is a natural history study conducted as well by BioMarin prior to our acquisition of a product, which allow us to, in a proper way, have a very valid external control arm to contrast our clinical benefit. We've shown very profound reductions of biomarkers and I think fairly strong clinical evidence of benefit, which I'll show you shortly. Currently planning a confirmatory trial. We're assuming an accelerated approval under our approval framework, or FDA review framework. As such, we would require a confirmatory study that's agreed upon with the FDA at the time of BLA submission, which we have achieved. We currently have a 14-patient trial, seven per treatment arm, randomized controlled in nature. Patients will be treated five years with a BSID, which is called a Bayley Cognitive Raw Score, as our primary endpoint for the confirmatory trial, which will support our full approval. It's a five-year trial. Going back to our clinical data, our biomarker data is very profound. In this slide, on the y-axis, you have the heparan sulfate in the CSF through five years of follow-up, you can see that at most time points, the biomarker was within the limit of normal. This has not been achieved by any other therapeutic, any other ERT, actually, to treat any neuropathic MPS. There's none for MPS IIIB, when you benchmark the effect sizes that we're achieving and seeing are very profound. This is also confirmed by benefit on a more specific biomarker, also part of the HS family, but measuring the non-reducing end, which is the stopping point at which the enzyme stops chopping because it's missing. Very consistent with the data on the overall HS. When one looks at the benefit on cognition, looking at the full approval endpoint, which is what the FDA wants to see in the confirmatory trial, we also see significant benefit. This data was shared with the FDA as part of our October 2025 submission for Breakthrough Designation, and I think had a profound effect on the granting of the BTD. As you see on the purple line at the bottom, patients on the natural history arm decline usually around three, four years of age, all the way down, losing brain function and cognitive function until the end of our follow-up, which was 11. They just plateau and remain flat throughout. We've looked at a number of things derived from another type of a very important questionnaire called the VABS or the Vineland questionnaire. Denali is conducting their confirmatory study using the Vineland questionnaire and not the Bayley's questionnaire. I guess that was an agreement they reached with the agency. We see, again, a very similar degree of benefit on receptive communication, expressive communication, gross motor skills, and fine motor skills in the context of Vineland. We continue to assess endpoints from the Vineland that inform a few areas that are very deemed important by caregivers of patients with this disease, mainly ambulation, feeding, and other type of measures of well-being. Those data are being analyzed and will be presented to the FDA as part of our BLA to demonstrate meaningful functional benefit in addition to biomarker benefit, which I think further reinforces our story. In addition to the clinical data, we have imaging data showing that after six months of treatment in the 201 study, cortical grey matter volume, which is the space or the area of the brain that suffers the most from neurodegeneration in this disease, remains stable. This is in contrast with what you see in natural history patients, where there is an ongoing decline in brain degeneration. We didn't measure cortical grey matter volume or MRIs in our 902 study, but we have an external control trial that actually followed patients over time, and that's very informative, and we're including those data in our BLA as well. Let me give you some context in terms of how the drug gets into the periphery. Through the glymphatic system, the drug escapes the brain and gets cleared. The CSF typically circulates about four times a day, and that allows for the compound to actually reach the systemic circulation, which is a very important component because, over time, if we extend lifespan on these patients, what we would want to achieve also is clearance of heparan sulfate in the periphery and be able to address the potential future cardiovascular, lung, joint, GI complications of this disease, which were not seen because the biggest comorbidity is the brain. We've seen normalization of liver and normalization of spleen sizes, which denote systemic treatment, systemic clearance of heparan sulfate. From a safety point of view, frankly, not much there. Pretty much what one would have expected in the context of a compound that's delivered through the ICV device. Fairly well-tolerated. No meaningful hypersensitivity reactions that we can attribute to compound. Generally well-tolerated. There's usually anti-drug antibodies, some of which are neutralizing antibodies, but to a low degree, and given that antibodies typically don't penetrate the blood-brain barrier too much, there's no reduction in effect size as measured by heparan sulfate and heparan sulfate NRE in patients where neutralizing antibodies were detected. Currently, the company is well-capitalized. We announced closing the quarter with $107 million of cash, which allow us to advance our program and have enough cash beyond our projected approval date. We forecast submitting the product at the end of the year in Q4 and obtaining approval under an assumption of a priority review by the middle part of next year. With that, I'll stop my presentation and open it up for questions if there are any. Yes. How many patients for pilot have you identified? We're currently in the process of identifying patients. The projections that I showed you earlier in the deck are based on publications and on claims database analyses that allow us to get some insights as to the potential projected number of patients. We're currently in the process of hiring and expanding our commercial team, but have already hired a Chief Commercial Officer, a head of commercial operations, and head of market access. Our Chief Commercial Officer, Dale Hooks, was frankly very much responsible for the patient ID efforts that took place for Reata, for Friedreich's ataxia, and be able to get the product approved with about 300 patient forms in the patient hub and about 1,000 patient forms four months after the launch of a product in a fairly uncommon and rare disease. Dale has a very strong track record of rare disease commercial launches, and his top priority is actually doing exactly that, identifying patients that are going to hopefully go on treatment. We're also in the process of initiating an expanded access program, which we hope to have in place in the second half of 2026, which will allow us to segue patients from the trial into commercial product when commercially available. We're partnering with the patient foundations to be able to get that trial enrolled and going. They've been very collaborative and super supportive of the effort. Yeah, we'll be updating the street on our progress made around patient ID in the future. I see no further questions from the audience. Thank you so much for your attention, and looking forward to updating you in the future. Thanks so much