Good morning, and welcome to today's joint conference call regarding the Tectonic and AVROBIO merger. At this time, all participants are in a listen-only mode. Please be advised that the call is being recorded. Now I'd like to turn the call over to Erik Ostrowski, Interim Chief Executive Officer and Chief Financial Officer of AVROBIO. Please go ahead. Thank you, operator, and good morning, everyone. Joining me on today's call is Alise Reicin, Tectonic's President and CEO. Before I begin, I want to remind everyone that this discussion and the accompanying presentation will contain forward-looking statements based upon the current expectations of AVROBIO and Tectonic, which include, but are not limited to, statements regarding the expected timing, completion, effects, and intended outcomes for the proposed transactions and our future expectations, plans, and prospects for the combined company. Such statements represent management's judgment and intention as of today and involve assumptions, risks, and uncertainties. Further, as indicated on these slides, AVROBIO intends to file a registration statement and accompanying proxy statement and prospectus with the Securities and Exchange Commission relating to the proposed transactions. Please be advised to read, when available, these and other relevant documents filed with the SEC. Please refer to the accompanying slides for more details on these forward-looking statements. Turning to the transactions. Earlier today, we issued a press release that outlines a merger agreement between AVROBIO and Tectonic Therapeutic, a privately held clinical-stage biotechnology company focused on developing GPCR-targeted therapeutic proteins and the related private placement financing. This release is available at avrobio.com under the Investors & Media tab. As we communicated in July of last year, AVROBIO halted further development of its programs and conducted a comprehensive review of strategic alternatives for its business, with a focus on maximizing shareholder value. Following this thorough review, our board of directors believes the proposed merger announced this morning is in the best interests of our shareholders. Tectonic is advancing a pipeline of novel therapies made possible by unlocking the potential of biologics in the GPCR space. The company is at an exciting stage in its development, having generated exciting initial clinical data with its Fc-relaxin fusion protein, TX45, a potential best-in-class agent focused on addressing areas of high unmet need in cardiopulmonary indications. Tectonic's programs are enabled by its proprietary GEODe platform, which aims to overcome major limitations of antibody discovery addressing GPCRs and has the potential to develop novel compounds across a broad range of indications. I will now provide an overview of the transactions, including the private placement financing. In support of the combined company's future operations, Tectonic has entered into subscription agreements for a $130.7 million private placement with a syndicate of new and existing leading institutional life sciences investors. These proceeds, together with the existing cash expected from both companies at closing, are expected to provide the combined company with approximately $165 million of cash and cash equivalents at closing. These cash resources are currently expected to fund operations into mid-2027 and intended to be used to advance Tectonic's pipeline through multiple clinical data catalysts. After giving effect to the private placement financing, pre-merger AVROBIO shareholders are expected to own approximately 22% of the combined company. Pre-merger Tectonic stockholders are expected to own approximately 40% of the combined company, and purchasers in the private placement are expected to own approximately 38% of the combined company, subject to certain assumptions. The percentage of the combined company that AVROBIO shareholders will own as of the close of the transaction is subject to adjustment based on the amount of AVROBIO net cash at the closing date. The merger and related financing are expected to close in the second quarter of 2024, subject to satisfaction of closing conditions for each transaction. Upon closing of the merger, the combined company is expected to operate under the name Tectonic Therapeutic, Inc. and to trade on NASDAQ under the ticker symbol TECX. Philip Donenberg from the AVROBIO Board of Directors will join the Tectonic board at the time the transaction closes. We believe this transaction will result in a combined entity with a strong cash position, backed by an impressive investor syndicate, and are confident in the Tectonic leadership team's ability to deliver on their vision. I'd now like to turn the call over to Alise, who will present an overview of Tectonic's business and plans. Alise? Thank you, Erik. The Tectonic team and I are also delighted with this transaction, and I want to start by thanking the AVROBIO team for their really outstanding collaboration throughout this process. The total funds generated from this process will be critical to advancing Tectonic's vision of creating novel biologic therapies for patients and creating value for our shareholders, and we're excited to share that vision with you today. At Tectonic, we're leading the way in the development of GPCR-targeted biologics, the development of which has been a real challenge in the field. To be successful, we need the right technology, the right assets and development plans, and the right people, and I believe we have all of these. Tectonic now has a validated platform that we call GEODe, that enables us to reproducibly discover GPCR-targeted biologics. GPCRs have been a really rich area of drug discovery and development, but the overwhelming majority of approved drugs against this class of targets are small molecules. We're not aiming to replace small molecules where these have worked well. Instead, our focus is on those targets where we think a biologic is the optimal modality to unlock the potential of that target. We have a rich emerging pipeline with our first three compelling targets against high unmet need indications, including two where there is no approved therapy. Our lead asset, an Fc-relaxin fusion protein, is in phase I, and the early data is quite promising, suggesting it has the potential to be a best-in-class therapy for a mechanism that has blockbuster potential in cardiopulmonary diseases. We will have more complete PK/PD data later this year to reinforce the profile of the drug. This will be followed by phase I-B hemodynamic data in 2025 and randomized phase II data in 2026. Tectonic's leadership team and founders have an extensive history of drug discovery and development success, resulting in the first approval of 20 drugs and many life cycle management indications. We have a great group of investors, and post-closing, we'll have cash that is expected to provide runway into mid-2027, with multiple value-creating inflection points along the way. I want to spend a few minutes telling you about my leadership team with a focus on the scientific leaders. I'm a physician, scientist, and a 25+-year pharma veteran. My first 19 years were at Merck Research Labs, where I worked across more than 10 therapeutic areas in both early and late drug development. I led the KEYTRUDA program from its first-in-man study through its initial approval. Prior to coming to Tectonic, I was President and Head of Global Clinical Development at Celgene. Peter McNamara, our CSO, joined us after 15 years at Novartis, where he worked across therapeutic areas and modalities. He's had 16 INDs and 2 approved drugs. Tony Muslin, our CBO, was a professor of cardiology at WashU, and then spent 10 years at Novartis and Sanofi in leadership roles in cardiovascular and metabolism. Marcie Ruddy, our Chief Medical Officer, spent 10 years at Merck, working across therapeutic areas in early development, and most recently was VP of Clinical Immunology at Regeneron, where she led the DUPIXENT team through multiple phase II, III, and life cycle management approvals. Tim Springer and Andrew Kruse are founders who both remain active in the company or professors at Harvard Medical School. Tim is not only a highly respected scientist and recent winner of the Lasker Award, but also a very successful serial entrepreneur. Andrew is a world-renowned expert in the biochemistry of GPCRs. Now, let me give you a sense of the breadth of the opportunity available to us. GPCRs are cell surface proteins that play a major role in transmitting signals from the outside of the cell to the inside of the cell. They've been an incredibly rich area for drug discovery, with over 30% of all currently marketed drugs modulating GPCRs. But these approved therapies only address 12% of known GPCRs, so many potentially compelling targets remain untapped. Because of the challenges of making GPCR-targeted biologics, of the approved drugs, there are only three GPCR-targeted antibodies, so there's a significant opportunity for biologics to play a much bigger role in this space. The right hand of the slide outlines those places where we think a biologic might be the better modality over a small molecule. First, there are GPCRs that have been very difficult to target with small molecules, where we believe a biologic is more likely to be successful. Also, there are families of GPCRs where the target site is very similar across members of the family, and small molecules often cannot provide the needed specificity, resulting in off-target toxicity. Biologics are likely to provide that specificity. We also have a use case where small molecules have been on the market for decades, but there's a black box warning for a high unmet need indication because of very specific tissue toxicity in that indication. We have the ability to make a biologic that can avoid that specific tissue, potentially enabling the development of a novel drug in an indication without approved therapy. Lastly, you can develop bi or trispecifics to achieve multi-target impact, which you can't do with small molecules. Now, turning to the first three programs in our pipeline. Our lead program, as I mentioned, is an Fc-relaxin fusion protein, optimized using the protein engineering part of our GEODe platform. We are initially developing it for a subset of Group 2 pulmonary hypertension, which is pulmonary hypertension in patients with left-sided heart failure. I'll describe this program in detail in the coming slides, but we believe we have an ideal match between the mechanism of our drug and the pathophysiology of the disease. Next, we have a GPCR antagonist, which was discovered using all three pillars of our GEODe platform. It acts as an anti-angiogenesis agent, targeting hereditary hemorrhagic telangiectasia, otherwise known as HHT, which is a disease arising from abnormal vascular formation. It is the second most common hereditary bleeding disorder, and there are no approved therapies for patients affected. There are mouse models of HHT, which have been shown to translate into efficacy in the clinic, and we have early data demonstrating efficacy in one of these mouse models of the disease. We anticipate choosing a development candidate later this year. In our third program, we are taking a bispecific approach to fibrosis, targeting two targets expressed on the same cell, but with complementary pathways. One of the targets already has proof of concept in the clinic, and we believe that this has the potential to be a best-in-class approach to treating fibrotic diseases. In every one of our programs, we know how to efficiently get to proof of concept in a capital-efficient way. In terms of timelines, we expect this raise will give us a greater than three-year runway, which enables us to achieve multiple value-creating milestones across our program. This should include getting us through proof of concept for relaxin and getting our second program in HHT into the clinic in Q4 2025 or Q1 2026, with the potential to start phase II in 2026. Other assets can then be used for partnership opportunities, and discovery deals using our platform can be considered. We believe there's no systematic platform risk because the risk of the assets are uncorrelated. Now, let's turn to the challenges in the discovery of biologics targeting GPCRs and how our GEODe platform addresses them. First, GPCRs are embedded in the cell membrane, and if you extract them from the lipid membrane to produce material for screening, the receptors often cannot retain their native conformation. Second, GPCRs are often expressed at very low levels, which creates an additional obstacle to purifying enough material for a screen. Third, they're often conserved across species, so trying to induce antibody formation against them through immunization in animals is often unsuccessful because it requires breaking tolerance. Last, because GPCRs spend most of their time in an inactive state, developing agonists is especially challenging, as you need to stabilize the receptor in an active form for agonist discovery. The GEODe platform we assembled over the last three years consists of three main pillars to address these challenges. First, it includes a wide range of biochemistry techniques and GPCR structural insights that help us boost receptor expression and stabilize them outside the cell membrane. Second, we have proprietary yeast display libraries and sorting protocols to productively generate hits without the need for animal immunization. And finally, the platform has protein engineering techniques to produce chaperones that can stabilize GPCRs in active form and also to optimize these molecules as they arise. So switching to our lead program, TX45, which is an RXFP1 agonist based on a relaxin fusion protein. So what do we know about the human hormone, relaxin? Well, it's often referred to as the hormone of pregnancy because it's upregulated during pregnancy. And what it does in pregnancy helps inform what we hope it will do in patients. First, it's a pulmonary and systemic vasodilator, which enables the pregnant person to increase cardiac output to accommodate the increased demand from the developing fetus. It also demonstrates antifibrotic effects, as it remodels the pelvic ligaments to enable a vaginal birth. What else we know about relaxin came from the Novartis serelaxin program, the first major attempt at developing a recombinant form of the hormone as a cardiovascular therapy. But the major issue with serelaxin was its short half-life, which required that it be given by continuous IV infusion. This limited development to acute heart failure, where a two-day infusion was given on top of standard of care. A meta-analysis of six studies with more than 11,000 patients demonstrated both its safety and activity, with a 23% reduction in five-day worsening heart failure. However, one of two pivotal studies, which included six-month cardiovascular mortality as a co-primary endpoint, failed. Expecting a two-day infusion to impact a five-day endpoint, let alone expecting an impact on an endpoint six months later, was a high bar to set for the study. We've used our engineering capabilities from our platform to address the half-life issue and enable development in the optimal disease settings. Specifically, we increased the half-life by making an Fc-relaxin fusion protein. On the right, you can see rat PK for one of our early compounds in black and for a competitor relaxin Fc fusion in orange. For both, you can see the half-life is prolonged from minutes to days, but you can also see you're losing 90% of the exposure in the first few hours, which is not typical for Fc fusions. It turns out it is typical for Fc fusions or antibodies with a high isoelectric point, and both of these molecules have a high pI, as does native relaxin. The high pI means these are highly charged proteins, which have been shown to bind to heparan sulfate in the glycocalyx, which traps them so they get pulled out of the blood, reducing the free drug that then can get into the tissues. We hypothesized that we could increase overall exposure and improve free drug that could penetrate the tissue if we engineered our compound to lower its isoelectric point. Our clinical compound, TX45, can be seen in green, and as you can see, with a reduced pI, we have a tenfold increase in exposure. How does this translate into potency in animals? Renal blood flow in rats is an excellent pharmacodynamic marker for relaxin because it captures its rapid systemic vasodilatory effects. That makes it an ideal setting to benchmark our compounds against a high pI comparator. Start on the left of this slide. As I mentioned, when you give equal amounts of these drugs, you get a 10-fold increase in exposure with TX45. However, engineering to reduce the pI did also result in a decreased potency in vitro by a factor of 10. If this was just about optimizing blood PK, one would expect then that equal amounts of the two drugs would show equal in vivo potency because you would need 10 times more TX45 to activate RXFP1. However, despite the decreased in vitro potency, in vivo, as you can see, our drug is 10x more potent than the comparator compound. Zero point three mg/kg of the high pI comparator compound had similar effects on renal blood flow as 0.03 mg/kg of TX45. In contrast, 0.3 mg/kg of TX45 shows much greater effect than the comparator, and we attribute this to less drug trapping in the glycocalyx, resulting in more free drug becoming available to activate the receptor in tissue. We have data suggesting we have a potential best-in-class relaxin fusion protein, and we've chosen Group 2 pulmonary hypertension in patients with preserved ejection fraction heart failure, HFpEF, as our first indication for several reasons. First, Group Two 2 with HFpEF is a substantial unmet need population with no approved therapies. It's a large population in the U.S., and the five-year mortality in this disease is high. Second, the mechanism of action of relaxin matches the pathophysiology of the disease. We also believe there's a clear, reasonably quick path to approval because an outcome study is not needed to get approval or reimbursement in Group 2 PH, which should enable an earlier entry to market compared with CHF. Also, there may be a pricing and reimbursement advantage if the first indication is in a subset of CHF with highest unmet need. Beyond Group 2 PH, there is the potential to expand to other types of pulmonary hypertension, to larger heart failure indications, and also renal diseases. When people talk about pulmonary hypertension, they're usually referring to Group 1 PH, also known as PAH, because that is where most drug discovery and development efforts have focused to date. Group 2 PH is pulmonary hypertension associated with left heart failure, and over the last few years, two subtypes have been identified, which I'll describe on the next slide. HFpEF affects several million patients in the U.S., and more than 600,000 of those have elevations in their pulmonary artery pressure, and therefore, they have Group 2 pulmonary hypertension. More than 500,000 of these have IPCPH, isolated post-capillary pulmonary hypertension. With these patients, elevated pressures in the left side of the heart backflow into the pulmonary circulation, leading to elevated pulmonary pressures. Their pulmonary vasculature is normal, and if you can treat their heart failure adequately, which has been difficult with current therapy, their pulmonary artery pressure should come down. In contrast, combined pre- and post-capillary pulmonary hypertension, CPCPH, represents more than 100,000 patients in the U.S. These patients have both increased pulmonary pressure due to backflow, but in addition, their pulmonary vasculature starts to look like Group 1 PH. They get muscularization of the arteries and a narrowing of the lumen. As blood is pushed through a smaller lumen, you get an increase in pulmonary vascular resistance, which is how you differentiate them from patients with IPCPH. In our phase II study, we're going to enrich for CPCPH patients because if we ran an all-comer study, it would mainly enroll IPCPH. With a more balanced population, we'll be able to determine whether TX45 works in either or both subsets, which gives us two shots on goal. How does TX45 work, and why do we believe it's going to be ideal in this study? First, as I mentioned, it's both a pulmonary and systemic arterial vasodilator, and it does this by inhibiting endothelin-1 on the left and by activating the production of nitric oxide, NO, in the middle. It's also an antifibrotic and remodeler of both the pulmonary arteries and the heart, and it does this by activating matrix metalloproteinases 2 and 9 and by inhibiting the TGF-beta pathway via inhibition of SMAD 2 and 3. So putting it together, you can see the pathophysiology of Group 2 PH on the left in this table and how relaxin's mechanism of action addresses this on the right. We've already spoken about pulmonary artery narrowing in CPCPH and the fact that relaxin both dilates and remodels the pulmonary arteries. Furthermore, long-standing Group 2 PH can lead to dysfunction of the right side of the heart, and preclinically, relaxin has been shown to improve this. In preserved ejection fraction heart failure, you get a stiff and thick left ventricle that doesn't relax to allow adequate filling of the heart in diastole. Right, relaxin could increase cardiac output via three different mechanisms. One, by dilating the peripheral circulation, making it easier to pump blood out of the heart. That's called decreasing afterload. Two, by relaxing the heart muscle, diastolic filling should improve. Lastly, with long-term treatment, remodeling of the left ventricle should further enhance function. Lastly, many of these patients have compromised renal function, and relaxin, via dilation of the renal vascular system, has been shown in the clinic to improve kidney function. In sum, relaxin's actions really match the pathophysiology of the disease. Just a brief comparison of Group 2 PH versus Group 1 PAH. Group 2 PH has many more patients than PAH, and like PAH, is likely to be a multi-billion dollar opportunity. In the middle, you can see that survival is similar to or worse than PAH, so the unmet need is high. And lastly, unlike PAH, where there are many approved drugs, there are no approved therapies for Group 2 PH, aside from drugs used to treat heart failure. A logical question is whether the drugs approved for PAH also work in Group 2 PH. To date, studies evaluating these have failed, and we think one reason is that some of these drugs mainly work by dilating the pulmonary vasculature. And if you're doing nothing to enhance cardiac function, you're going to push more blood into the left side of the heart, but the heart can't push that blood out, and heart failure can worsen. The PDE5 inhibitors also failed in an all-comer Group 2 PH population, but in three separate studies in patients with CPCPH, they demonstrated improvement in hemodynamics, exercise tolerance, and a reduction in heart failure hospitalizations. We think this increases the probability that TX45 will work in CPCPH. The reason for that is reflected on this side. PDE5 inhibitors work by activating the nitric oxide pathway, by inhibiting the breakdown of nitric oxide. I think of relaxin as being a PDE5 inhibitor plus, because it not only activates that same nitric oxide pathway, it does all of the other things that we just talked about. Based on this, we believe TX45 has the potential to be effective both in CPCPH and in IPCPH. The other data that we believe increases our probability of success in Group 2 pulmonary hypertension comes from the serelaxin program. A right heart cath study was done in patients with acute heart failure, where pulmonary and cardiac hemodynamics were measured pre and post starting a serelaxin infusion. In orange are the data from patients treated with 20-hour infusion of relaxin, and in blue are data from placebo. Focus on the first eight hours, as diuretics were allowed after that. You can see a drop in pulmonary artery pressure on the left, a drop in pulmonary vascular resistance in the middle, and a drop in systemic vascular resistance on the right. Not shown here was the drop in pulmonary capillary wedge pressure, which is a measure of heart failure, and also an increase in cardiac index. In a similar study in chronic heart failure, an increase in cardiac output and a decrease in wedge pressure was demonstrated. We're going to do a very similar study to this in phase I-B in patients with Group 2 PH and HFpEF. We're in the middle of our phase I study. In addition to getting pharmacokinetics, we're getting renal blood flow data several time points after dosing. We found that the exposures that give you near maximal effects on renal blood flow are the same exposures where you get the chronic effects in pulmonary hypertension and congestive heart failure preclinical models. So at the end of the phase I study, we should have a very good idea of the target dose and dosing interval. In just a few months, we plan to start our phase I-B right heart cath study in patients with Group 2 PH, looking at hemodynamic effects. In the second half of the year, we plan to start a placebo-controlled, six-month study in Group 2 PH patients with HFpEF. We've completed dosing of the first three cohorts of our phase I study, as outlined on the right-hand part of this slide, and we've started dosing the next two cohorts. To date, TX45 has been well-tolerated, with minimal adverse effects and no drug-related SAEs. Based on 42-day data from the 0.3 mg/ kg cohort and 14-day data from the 1 mg/kg and 150 mg cohort, the drug appears to be well-behaved, with low variability and dose- proportional PK. We've also seen a 38% increase in renal blood flow at the lowest dose, which is in line with what has been reported with serelaxin and which meets our go criteria. Shown here on the left is the preliminary PK from the 0.3 mg/kg IV cohort. Six patients were dosed with drug, but you can only see four patients because the variability is so low that two of the patient data lines are not visible. You'll also note the curve starts to become linear after day 14. On the right is day two and day eight renal blood flow data from the same cohort, demonstrating that the increase in renal blood flow is maintained through day eight of dosing. Longer-term renal blood flow measurements are pending. Based on available data, a PK model was constructed, which suggests that with monthly dosing of 150 mg subcu, the trough levels exceed the levels predicted to provide maximum effects on renal blood flow. Given that we can go up to 300 mg monthly with a single shot, we anticipate monthly dosing. There are two major biopharma companies who are also attempting to develop longer half-life forms of relaxin. This is validation of the substantial market opportunity for drugs that effectively tackle this mechanism and speaks to the potential strategic value of our program if we can confirm that we have a best-in-class molecule. So in summary, I want to close by reiterating how strongly I believe that the combination of our assets, our expertise, and our capital will enable us to develop transformative biologic therapies for patients and create substantial value for our shareholders over the coming years. Our lead asset is ideally matched mechanistically to address the treatment of Group 2 PH and HFpEF, a disease without approved therapy. Our platform has the potential to consistently generate compelling pipeline candidates across therapeutic areas, and our team is unmatched. Thank you very much. This concludes the AVROBIO and Tectonic call today. A recording of today's call will be available for playback, and more details can be found on the AVROBIO's website, avrobio.com, later today. Thank you for joining. You may now disconnect.