All right, good morning, everyone. Welcome to Oppenheimer's 36th Annual Healthcare Life Sciences conference. My name is Andreas Argyrides. I'm one of the senior biotech analysts at Oppenheimer. Today I have the pleasure to be joined by CEO Jasbir Seehra. Apologies in advance for my, you know, lack of a video. I'm having some technical difficulties, but we'll get through it nonetheless. We'll have a presentation from Jas very shortly. Just a quick background. Keros is a clinical-stage biopharmaceutical company focused on the discovery, development, and commercialization of novel treatments for disorders that are linked to dysfunctional signaling of the TGF-β superfamily of proteins. They aim to target the pathways critical for the growth, repair, and maintenance of blood cells in a number of tissues, including bone, skeletal, muscle, adipose, and heart tissues. Lead candidate, KER-065, is being developed for the treatment of neuromuscular diseases, while elritercept, partnered with Takeda, is being developed to treat ineffective hematopoiesis in both MDS and MF. Great to have you today, Jas. With that, I'll let you take it away with the presentations, and then we'll see if we have time for Q&A. Thank you, Andreas, and for the intro. Thank you also for the opportunity to present Keros today. Usual disclaimer slide, I will be making some forward-looking statements, and the risks associated with those form forward-looking statements are in our 10-Q. That was a quarterly report that was part filed in the webcam. Please take a look. As Andreas talked in his introduction, Keros is entirely focused on the TGF-β superfamily of signaling. We are a clinical-stage pharmaceutical company, and we're developing these differentiated product candidates that target the TGF-β pathway, where the pathway in many diseases is dysfunctional, imbalanced, and that leads to the pathophysiology of the disease. We believe our product candidates have the potential to unlock the full therapeutic benefit of modulating the TGF-β superfamily and provide disease-modifying benefit to patients. As Andreas said, the lead candidate is rinvatercept (KER-065), which is being developed into Duchenne muscular dystrophy and ALS. Our partner drug, it is elritercept, being developed for anemia associated with myelodysplastic syndrome, as well as with myelofibrosis. Behind that, there are numerous preclinical assets ranging from neurodegenerative diseases all the way to other broad diseases such as bone and obesity. Let me talk about rinvatercept (KER-065). KER-065 is a modified activin receptor ligand trap. It's designed to bind to and inhibit TGF-β ligands that are negative regulators of muscle and bone, including activin A and myostatin. Therefore, treatment with KER-065 improves muscle regeneration, which then leads to increased muscle size and strength. KER- 065 also inhibits and reduces fibrosis and inflammation. By increasing skeletal muscle, it reduces fat accumulation because the more muscle burns more energy and thereby reducing fat accumulation, and it is anabolic on bone, increasing bone strength. Previous molecules in this family were not designed to have reduced BMP9 binding, and thereby they had vascular and bleeding events. Rinvatercept is designed to have reduced binding for BMP9, thereby avoiding the vascular and bleeding events associated with the wild type ActRIIB-Fc. When we think about neuromuscular indication, they really fall into two big buckets. One of those is the muscular dystrophies, where mutations in genes coding for the structural proteins that connect the contractile apparatus to the extracellular matrix, those mutations result in inability to connect the extracellular matrix to the contractile machinery. As a consequence, the muscle is weak and breaks down. Similarly, when you fail to transmit the neurological signal to the muscle, that muscle doesn't contract and starts atrophy. Regardless of what the underlying cause of the disease is, the pathology that results is the same. The muscle is either weak and therefore breaks down, or it's not stimulated and starts breaking down, and as a consequence, you get inflammation. Inflammation inhibits muscle regeneration, and that muscle is then replaced with fat and fibrotic tissue. We believe that based upon all of the pharmacology that we have observed in preclinical studies and in the phase I healthy volunteer study, we believe that rinvatercept has the potential in multiple rare neuromuscular diseases where there is a high unmet need. KER-065 in Duchenne's. As you know, DMD is a rare, severe and ultimately fatal genetic disease resulting from lack of dystrophin protein in the muscle. This leads to the muscle being weak and progressively degenerating. About one in 3,500 new births are male births are Duchenne muscular dystrophy, and in these boys, the muscle undergoes continuous rounds of degeneration and regeneration. Every time the muscle is used, it's weak, it breaks down, and there's cycles to try and repair it. Eventually, the ability for that muscle to regenerate declines, due to both a decline in the muscle progenitor cells, known as satellite cells, but also, due to the inflammation, fibrotic tissue, infiltration, and fatty infiltrates. There are currently no cures for DMD. When you look at the landscape, for treatments for DMD, there's the glucocorticoids, which are standard of care. They help maintain muscle function, for short periods of time, Glucocorticoids actually do lose, do result in loss of muscle itself as well as bone, and therefore, the benefit of glucocorticoids is short-lived. Exon skippers, which were roughly less, 40% of the patients have mutations that are amenable to exon skippers, are approved, but have shown minimal benefit to date. Gene therapy, we believe, was going to be the cure, but what we are now seeing is that with the approved therapies, they provide benefit, but that benefit is still limited and eventually starts declining. HDAC inhibitors are approved by the FDA, and they provide benefit by reducing fibrosis, but have associated safety signal. Given the limitations of all of these therapies, we believe that there is opportunity for additional treatments in DMD. When we looked at the preclinical data with rinvatercept, we see that it offers benefits on the muscle, bone, as well as on fat, where we see increases in muscle mass, decreases in fat mass, and improvements in bone mineral density. reduces the negative consequences of glucocorticoids. Even in combination with glucocorticoids, we see both an increase in muscle mass and strength, as well as improvements in bone mineral density. In addition, okay, right, KER-065 is able to ameliorate the inflammation and promote that muscle regeneration, so to contribute to that increased strength. We believe that we can address also the underlying genetic deficiency in combination treatments. When you have the exon skippers, the PMOs, we have observed in combination with KER-065, enhanced expression of the truncated dystrophin. In the absence of exon skippers, there is enhanced expression of utrophin, a homologue of dystrophin. We believe that KER-065 can provide many benefits that are as a consequence of the missing dystrophin in patients with DMD. We've completed a phase I study with KER-065, the drug was generally well tolerated. Our phase I study had both single ascending dose, starting at 1 mg/ kg, going all the way to 5 mg/ kg. In the multiple ascending dose, we explored two doses of 1.25 mg/kg and 2 mg/ kg, with three months of treatment. The drug was well tolerated, and the most of the [AI TAAs] were mild to moderate. There was one patient, okay, that had a very high transient increase in creatine kinase following vigorous exercise just before coming into the phase I center. There were no dose-limiting toxicities or serious adverse events that were observed. Importantly, the earlier molecule that was based upon the native sequences, showed bleeding events, telangiectasias, and that were not observed with KER-065. While we did see injection site reaction, which are common to subcutaneous administration. There was an increase in hemoglobin, but it was asymptomatic and reversible and can be managed through titration in patients. We believe that the healthy volunteer data supports potential for rinvatercept to address multiple aspects of DMD. It can increase lean mass and increase muscle, right? What we observed was increased lean mass, increased thigh muscle volume. We saw that it improved bone mineral density, which boys with DMD become osteoporotic, and therefore, a bone anabolic agent could provide additional benefit. With rinvatercept in the phase I study, we see improvements in biomarker of osteoblasts, the bone-forming cells, bone-specific alkaline phosphatase, reduction in biomarker of bone resorption, and also improvements in bone mineral density. Finally, the decreased mobility and use of glucocorticoids are associated with a high risk of obesity and metabolic syndrome in these patients. Rinvatercept in the phase one study showed increases in adiponectin, a biomarker of fat mobilization, decreases in leptin, a biomarker of fat mass. We saw both decreases in fat mass in whole body as well as in visceral fat in the phase one study. The rationale for rinvatercept in ALS is shown on this slide. ALS is a progressive neurodegenerative disease that destroys motor neurons, leading to muscle weakness, loss of function, and eventually paralysis. There's roughly 30,000 patients that are living with ALS in the U.S. The exact cause of ALS is unknown, 90% of the cases is sporadic with no known familial history. 10% of the ALS patients have familial link to mutations in certain genes. The common feature in all patients is loss of the neuromuscular junction. What you can see in this slide is a healthy motor neuron, single motor neuron that innervates and branches out to excite many muscle fibers. In ALS, some of these muscle fibers are atrophying because the neuromuscular junction has been lost as is shown in the middle figure. We believe that by increasing muscle regeneration, you can increase the size of the adjacent myofibers that still have innervation, and therefore compensate for the loss of some of the myofibers that are no longer innervated. Therefore, rinvatercept has the potential to preserve muscle function and maintain quality of life in these patients. I think the evidence, okay, right, currently from SMA with apitegromab provides a rationale here. apitegromab is being developed for treatment of SMA. The data from the SAPPHIRE phase III trial showed functional gains in these patients, therefore, preservation of muscle function in the face of neural degeneration. Based upon this phase III data, we believe rinvatercept could potentially sustain function in still innervated muscle fibers in patients with ALS. Currently, or mostly, okay, majority of the treatments are focused on preserving or reversing the motor neuron loss. With rinvatercept, we are really targeting the skeletal muscle to potentially preserve the strength of that innervated muscle and provide quality of life benefit. With rinvatercept, skeletal muscle is an active participant in ALS pathology and is not a passive victim of motor neuron degeneration. There is a potential that by promoting muscle growth and function, rinvatercept could counteract not only the muscle atrophy, but there is a potential to change the microenvironment and help preserve some of the motor neuron junctions, reduce the inflammation, and enhance that muscle regeneration. Based upon the clinical and preclinical data we've generated to date, we plan to engage with regulators on the design of a phase II clinical trial, evaluating rinvatercept in patients with ALS in that second half of the year. Just a little bit of preclinical data in the mouse model of ALS. We see the treatment with KER-065, shown in the left-hand panel, preserves a grip strength, and then when you stimulate the nerves, you can actually look at how the muscle functions. You can see that in the vehicle animals shown in red, there is a large decrease in the force being generated, whereas with treatment, you are preserving the force okay, generated by the muscle. I'm going to skip that slide and move next to elritercept. Elritercept is, as I said earlier, an investigational drug, and being developed for treatment of anemia and thrombocytopenia in patients with MDS and in patients with myelofibrosis. In December of 2024, we entered into a global license agreement with Takeda, excluding mainland China, Hong Kong, and Macau. The financial terms for this were that there was an upfront payment of $200 million, and Keros is eligible to receive development and commercial milestones of over $1.1 billion. The tiered royalties start at low double-digit to high teens. Under this agreement, which was entered in January 2025, Takeda became fully responsible for all clinical development, manufacturing, and commercialization of elritercept in their territory. Just in the last minute, we do have a proprietary discovery approach. Keros has a broad approach to target the TGF-β superfamily to develop product candidates with potential to treat broad range of indications, including neuromuscular and neurodegenerative diseases, rare bone and fibrotic diseases, as well as tackle the larger obesity and fertility market. We have a large library of agonists and antagonists, proprietary library of modified activin receptor II ligand traps, mono, bi, and multi-modal antagonists, systemically deliverable ligands. And we have now multiple candidates in preclinical development. Rinvatercept and elritercept were both nominated from our proprietary library of modified ActRIIB-Fc ligand traps for clinical development. Thank you. Quick, I mean, I guess pretty quick summary and a couple of very important updates there. Maybe just to kind of put the presentation, you know, into a nice summary conclusion, what are we looking forward to in terms of catalysts this year? Maybe, also give us a quick snapshot of the financial picture for the company this year? Yeah. On the catalysts this year, we're working hard to start the DMD trial in this quarter. In the second half of the year, we will engage with regulators on the ALS trial. This is a year of execution for us. We have not guided to a timing of data as yet. We need to get these trials running, and then we'll be able to provide guidance. Now, with respect to financials, our third quarter earnings report showed that we had $383 million in the bank at that time, and with a runway into the first half of 2028. That includes the expenses for, both phase II trials, as well as bringing forward, preclinical assets into the clinic. Then lastly, can you remind us, timing on elritercept, phase III and potentially, you know, potential milestones for the progress there? There are development milestones associated with elritercept collaboration. We have not shared the details of those milestones, but there are milestones associated with start of phase III trials. Currently, we're running the elritercept phase III RENEW trial, and Takeda is committed to starting the frontline treatment in the 2025 fiscal year, which ends March 31st of this year. I think you can go back and look at the timeframe for other similar trials and get a guidance that you're looking at roughly two to three years, okay, for enrollment and then with a 12-month endpoint. This will put it towards the end of this decade into early next decade for commercialization. Okay, great. Fantastic. Jas, thank you for the update, the new updates here, all the progress that you guys have made. We're looking forward to progress for the rest of the year. Thank you. we'll stay in touch. Thank you, Andreas, for the opportunity. Yes, let's stay in touch. Yeah, likewise. Thank you for the invite. Appreciate it. Thank you. All right, with that will conclude the call. Thank you, operator.