A question-and-answer session will follow the formal presentation. This conference is being recorded at the company's request and will be available at the company's website approximately two hours following the end of the call. I would now like to turn the call to your host, Ted Jenkins, Senior Director of Investor Relations and Corporate Communications. Please go ahead, sir. Thank you, operator. Good morning, everyone. At this time, I'd like to remind our listeners that remarks made during this call may state management's intentions, hopes, beliefs, expectations, or projections of the future. These are forward-looking statements that involve risks and uncertainties. Forward-looking statements on this call are made pursuant to the safe harbor provisions of the federal securities laws. These forward-looking statements are based on Corbus' current expectations and actual results could differ materially. As a result, you should not place undue reliance on any forward-looking statements. Some of the factors that could cause actual results to differ materially from those contemplated by such forward-looking statements are discussed in the periodic reports Corbus files with the Securities and Exchange Commission. These documents are available in the investor section of the company's website and on the Securities and Exchange Commission's website, and we encourage you to review these documents carefully. Joining me on the call today are Dr. Yuval Cohen, our Chief Executive Officer, Dr. Barbara White, our Chief Medical Officer and Head of Research, Sean Moran, our Chief Financial Officer, and Craig Millian, our Chief Commercial Officer. With that, it is my pleasure to turn the call over to Yuval. Thank you, Ted. It's my pleasure to welcome everyone to today's call. Thank you for joining us on such short notice. As you know, we have been emphasizing our interest in expanding our pipeline through a series of bolt-on acquisitions. The strategy is straightforward. Leverage our expertise in immunology and our experience in drug development to build a diverse pipeline that mitigates risk by using multiple modalities to focus on inflammation, fibrosis, metabolism, and immuno-oncology. Today, we announce our first transaction, expanding our pipeline by adding two novel anti-integrin monoclonal antibodies that we intend to develop for immuno-oncology and fibrosis, one from University of California, San Francisco, and the other from Panorama Research, Inc. As Barbara will detail shortly, the cytokine TGFβ and its role in promoting inflammation, fibrosis, and cancer has been the focus of extensive academic and industry research, giving rise to testing different approaches to its inhibition. One recent approach is to target specific cell surface integrins that activate TGFβ, and we join others who are pursuing this approach. A number of external clinical studies are underway exploring this mechanism of action in both solid tumors and fibrotic diseases, and there has been significant recent business development activity in integrin-targeting assets. The two antibodies we've acquired have properties we find attractive and we believe position them favorably in the field. CRB-601 is highly specific for the integrin αvβ8 licensed from UCSF and invented in the lab of Dr. Stephen Nishimura. As Barbara will review, CRB-601 has generated preclinical data related to binding and functional activity, showing high potency. We believe CRB-601 could offer advantages over competitor approaches and expect to initiate phase I clinical studies next year. CRB-602 has dual specificity for αvβ6 and αvβ8 integrins and is licensed from PRI. We think targeting both of these integrins may be particularly helpful in targeting fibrotic diseases. Currently, anti-αvβ6 therapeutics are being developed for IPF and PSC. We also plan to start clinical studies with CRB-602 next year. These two new programs fit neatly into our pipeline alongside our existing programs, which focus on the endocannabinoid system. They align with and extend the disease areas we are pursuing and will benefit from our expertise in drug development. Lastly, we reported $125 million in cash as of March 31st, which we expect to fund us through the first quarter of 2024. We are well-capitalized to advance our expanded pipeline to several meaningful clinical milestones. I would now like to turn the call over to our Chief Medical Officer and Head of Research, Dr. Barbara White, to provide us with details of our program expansion plans and the news we announced today. Thank you, Barbara. Thank you, Yuval. We are delighted to have licensed two monoclonal antibodies, or mAbs, that bind to integrins and block integrin-mediated activation of transforming growth factor-beta, or TGFβ. TGFβ needs to be activated from its latent form to exert its biologic activities. Active TGFβ is a multifunctional cytokine involved in many cellular processes, including cell growth and differentiation, immune responses, wound healing, and tissue repair. Our new mAbs will be developed as treatments for solid tumors and fibrotic diseases. CRB-601 was designed in Dr. Stephen Nishimura's lab at UCSF and binds to the integrin αvβ8 with high affinity with IC50 for inhibiting activation of TGFβ in the picomolar range. Integrins are membrane-bound αβ heterodimers that mediate interactions between cells and between cells and extracellular matrix. Integrins are involved in many body processes, including cell growth, differentiation, survival, malignancy, fibrosis, immune responses, wound healing, and angiogenesis. The alpha V integrins, including αvβ6 and αvβ8, activate TGFβ. Some human epithelial malignancies or carcinomas express αvβ8 themselves, which activates latent TGFβ in their microenvironment. Active TGFβ suppresses immune responses that control growth and metastases of established tumors. It converts non-regulatory CD4 + T cells into regulatory T cells, which might be considered checkpoint cells because they suppress activity of other activated immune cells and turn off anti-tumor immune responses. Activation of TGFβ leads to both reduction in CD8 T cell numbers and killing of tumor cells. TGFβ has other effects beyond the immune system that promote tumor growth and metastases. Importantly, overexpression of αvβ8 by tumor cells and expression of TGFβ in tumors have both been linked to poor clinical outcomes. Thus, we and others believe that inhibiting TGFβ activation may provide efficacy in treatment of cancers. CRB-601 is a higher-affinity, humanized version of an anti-αvβ8 monoclonal antibody called C6D4, also developed by Dr. Nishimura's lab, which has been found to be active in animal cancer models. In the MC38 colon carcinoma tumor model, C6D4 reduced tumor volume at day 6 by nearly 50% as a single agent and nearly eliminated tumor growth when combined with anti-PD-1 monoclonal antibody. Complete response rates in the MC38 model were 10% for C6D4, 40% for anti-PD-1, and 60% when the two agents were combined. We look forward to sharing with you data specific to CRB-601 after they are made public by Dr. Nishimura's lab. We believe potential advantages of CRB-601 are the following. It inhibits TGFβ from ever becoming activated. It is very potent, and it has been specifically designed to inhibit activation of TGFβ, not only in a form that is released from its association with the TGFβ latency-associated peptide, but also in a newly described form of active TGFβ that remains associated with the TGFβ latency-associated peptide. This latter form of active TGFβ was recently described by Dr. Nishimura and colleagues and is thought to be the predominant form of TGFβ activated by αvβ8 on tumors. We will develop CRB-601 for the treatment of solid tumors in combination with standard treatments, including checkpoint inhibitors. We expect to be in the clinic in 2022. We've also announced today that we have acquired CRB-602 from Dr. James Larrick and his team at Panorama Research, Inc. CRB-602 is a mAb that binds both αvβ6 and αvβ8 to inhibit their activation of TGFβ. The αvβ6 integrin is expressed by epithelial cells during wound healing and tumors of epithelial cell origin. Overexpression of αvβ6 has been linked to fibrosis in idiopathic pulmonary fibrosis. We expect that CRB-602 may provide potential therapeutic benefit in both fibrotic diseases and cancer. We also expect to complete IND-enabling studies and manufacturing in 2022. With that, I'll turn the call back over to Yuval. Thank you, Barbara. Under the combined terms of the two exclusive licensing agreements, Corbus will pay $2 million upfront and will make potential development and sales milestone payments totaling up to $206 million and pay low single-digit royalties on sales. To close, I want to reiterate how excited we are about our expanding pipeline and also mention that we have posted a new investor presentation on our updated website that details the data and upcoming expected milestones we refer to on today's call. Given our skill set of understanding global, complex clinical programs and our expertise in immunology, along with a strong cash position, we believe we have a significant opportunity to advance novel therapeutics that will have a meaningful impact on patient care. I would like to thank you all for your time and attention. I will now turn the call back over to the operator to open the call for questions from the audience. Thank you. I'll be conducting a question- and- answer session. If you'd like to be placed in the question queue, please press star one on your telephone keypad. A confirmation tone will indicate your line is in the question queue. You may press star two if you'd like to remove your question from the queue. For participants using speaker equipment, it may be necessary to pick up a handset before pressing star one. One moment please while we poll for questions. Our first question today is coming from Brian Abrahams from RBC Capital Markets. Your line is now live. Hey, guys. Good morning. Congrats on the transaction, and thanks very much for taking my questions. I guess maybe starting off for CRB-601, Barbara, I was wondering if you could expand a little bit on how the high potency and differential interactions with LAP and the TGFβ pathway might create ultimately a differentiated mechanism and clinical profile versus other alpha V beta developments. Sure. Thank you, Brian, for the question. The work is a very recent work from Dr. Nishimura's lab and was published in 2020, in which they used some very sophisticated structural analysis and proposed that in the context of tumors, where αvβ8 is expressed on the tumor and TGFβ may be expressed, for example, on a T regulatory cell, that the activation, which means the ability to exert its biologic effect, of TGFβ occurs without TGFβ actually being physically released from the cage that it's in, which keeps it inactive. It remains in close proximity, and that it nonetheless can activate TGFβ on T regulatory cells and cause them on a range of T cells and cause T regulatory cells to exert their activity and induce immunosuppression and tumors. In this actual physically constrained environment, it would be somewhat difficult to target the TGFβ with, for example, an anti-TGFβ monoclonal antibody. The antibody that they've developed is very specifically designed to have high potency to inhibit this type of activation of TGFβ. It's simply that very high potency inhibits the activation of TGFβ that remains associated with its cage, which is thought by their lab at least, to be the predominant form involved in activation of TGFβ in the tumor microenvironment. Got it. That's really helpful. Maybe for CRB-602, can you talk about some of the preclinical work that you might do and some of the preclinical models you'll look at that might best discern the potential differentiation of the dual β6, β8 interaction and where that might be best developed? Sure. We think that the combination of targeting β6 and β8 may be particularly important in fibrotic diseases or in cancers of epithelial cell origin, where both are expressed. We think that what we're looking for in this antibody will again be high potency. We think that's obviously reasonably important, and we will be looking for its ability to have activity in models of both fibrotic disease and tumor. We'll certainly be looking in the tumor models for its ability to augment effects of standard therapy, such as checkpoint inhibitors. We'll be looking to see how it compares to other antibodies or similar antibodies that are being developed in the space. Got it. One more quick one, if I could squeeze it in. Just sort of, I guess, bigger picture. Can you talk about what this means for additional business development plans? You did mention you have a balance sheet that will take you out several more years. I guess, how are you thinking about additional BD potentially for later stage assets and your appetite there? Just your overall, I guess, implications for your overall views and strategy with respect to the landscape that we have coming out there. Thanks. Thanks, Brian. The strategy is as follows. We are looking for assets that are in immunology that we can leverage our expertise. These two assets we think fit uniquely with what we already have, which is the endocannabinoid system. Together, they really focus on these four areas, inflammation, fibrosis, immuno-oncology, and then through the CB1 work on metabolism. Having said that, we're very keen on additional bolt-on acquisitions, and we're particularly interested in one that would be in the clinic or ready for the clinic. Again, this is sort of the filter that we're looking at these opportunities through. It's unlikely, for example, Brian, to use a sort of an extreme example, I can't see Corbus bringing anything around sort of gene therapy. It just doesn't fit who we are and what we do, but expect to look for additional acquisitions. One of the guiding principles there as well to think about is, if you think about our pipeline as it stands now, we have programs that we think have a high probability of success because they're following a validated target, and we have programs where we will be the first to use that mechanism of action. We like to continue having that mix. Expect to see more of that. Great. Thanks so much. Thank you. Next question today is coming from Maury Raycroft from Jefferies. Your line is now live. Hi, good morning, everyone, and congrats on the update today. Question I was going to ask is just whether for both antibodies, do you have rights that go beyond 601 and 602 to next-gen molecules? Do you know for sure that 601 and 602 are going to be the candidates that you eventually move into the clinic? Do you know, Maury, I wonder if you'd repeat that question again. It dropped off, at least I didn't hear it at the end. Sure. Can you hear me now? Yes. Okay. For 601 and 602, I was just wondering if you have rights that go beyond those two candidates to the next-gen molecules from either the lab or from the company, and are these the candidates that you're going to move into the clinic? Thanks. The 601 mAb is actually probably 3rd generation to speak of out of Dr. Nishimura's lab. We do intend to take it into the clinic. We do, as part of the licensing deal, have access to patents that cover a number of other monoclonal antibodies that could be related. It is the one that we plan to take into the clinic. We really are very happy with its properties. Let me say absent a few minor tweaks that may happen. It is basically the antibody we're taking into the clinic. For 602, the arrangement that we have with Panorama Research Inc. is that they have a variety of anti-integrin antibodies and that we will work with them to develop a number of them. This is the first of them. We're most interested in starting with this αvβ6 β8 combo. Again, we are working with them to optimize this particular antibody, but in essence, it's also the one that we will be taking into the clinic. Got it. That's helpful. Also just wondering if you can talk more about how you sourced both of these assets and the deals, and was it a competitive process? Maury, we have been actively looking, as we've been saying, I think pretty much since the end of last year. We're fortunate to have a very, very good BD team, and both of these were assets that we approached. I'd say that it's certainly competitive in terms of the field. We've seen a lot of business development around integrins in general and including αvβ8 integrins. I think that our timing was just especially good, and we picked them at a time where the counterparties were very open to this transaction. Got it. Maybe last quick question just on 601 and the TGFβ tumor signature that you could potentially look for, I guess. First for competitors, are there any updates expected from competitor programs that could help inform Corbus? Do you have a strategy for what an initial clinical study could look like to potentially select patients based on biomarkers? Craig, you want to take the first? Sure. Maury, can you just repeat the question? I temporarily dropped off the call. Sure. Just wondering if there are competitor updates on the horizon that could inform your strategy that you can talk about. Sure. Yeah, that was the first part of the question. Great. Yeah. There's a number of competitive integrins in very early development. I think some have reported some preclinical data. Specifically, Morphic had some early data that they presented at AACR, which was interesting. That's a small molecule program that is slightly ahead of us, but I think some of the learnings there could be leveraged. Most interesting is Pfizer has a phase I integrin program for their αvβ8 in solid tumor. That's an antibody, and they haven't, as far as I know, given specifics in terms of when they'll have data, but that's one we're paying close attention to as well. Beyond that, I'd say those are probably the two that are slightly ahead of us, but that we're anticipating additional data readout on the αvβ8 front. Maury, this is Barbara then. We definitely plan to take advantage of learnings from those in front of us. We think that's a really good thing about what we're doing is that in these particular instances, we will have that advantage, that opportunity to learn from the work that's done by others in front of us, as we think come along with a really great mAb close behind. We think, we believe, we plan to develop biomarkers, tools to identify those patients who are most likely to benefit from the therapy. We think that will be necessary. We have a number of approaches that we are considering, again, we will certainly learn from the work that others are doing. We won't be working in isolation. We plan to do that. In terms of the design of the phase I, we anticipate it'll be a fairly straightforward phase I design in oncology, starting with some tumors in which the αvβ8 is expressed, look for early reads, expand. Sort of the basket philosophy for the early phase I studies. At the same time, we will be evaluating certain potential biomarkers for further development into diagnostics. Got it. That's all very helpful. Thanks for taking my questions. Thank you. As a reminder, that's star one to be placed into question queue. Our next question is coming from Leland Gershell from Oppenheimer. Your line is now live. Good morning. Thanks for taking my question, and thank you for the BD update. Just a couple of broad questions maybe for Barbara, just with respect to the potential for 601. If you have a sense of any particular solid tumor types that may be responsive to the strategy of targeting αvβ8, and furthermore, if you see a role for 601 in being able to address certain tumors that may be refractory to checkpoint inhibitors and have a follow-up. Thank you. Thank you. To start, we don't expect that this therapy will be used as a monotherapy. We certainly expect, as is in the case in most of oncology treatments, that it'll be used in combination, and we think it will be especially helpful and useful in combination with checkpoint inhibitors. That will be an early part of its development. In terms of which particular tumors, there's some work that has been done to look at alpha V beta expression by tumors. We think it should be tumors that have been reported to express αvβ8, and tumors in which we think there's some evidence that activation of TGFβ has played a role, tumors in which perhaps don't have a rich immune inflammatory infiltrate associated with them, those that may have it, those that are more excluded or those that are actually a desert sort of immune responses. There are a couple of things we'll need to look at when we select the tumors, probably not only tumor type, but what is the immune response that's going on in that particular tumor. There are a number that pop to mind upfront, things such as colon cancer or melanoma. Again, there are a number of others, and we will look more broadly initially, have several tumor types that we look at initially in phase I before we focus down in. Thanks. In the press release, you'd mentioned activity in syngeneic tumor models. Just wondering if in the interim between now and perhaps the phase I, we'll be seeing any xenograft-based models? Yes. Data different. Yes. We should expect to see that.