Cowen: Great. Thanks, Steve. Let me -- I was wondering if you could talk a little bit about the CELMoDs in your portfolio. Maybe there are several, maybe you give us a lay of the landscape? How are they similar or different from marketed agents? How are they similar or different from each other? And how well-characterized are their targets? How are you positioning them indication?
Sure. And thank you. Because it's a large question and not just specific to multiple myeloma, so I'm glad about that. So, CELMoD certainly from a platform perspective, a very promising way of looking at targeting and building drugs for targets that we're concerned to be non -- are undruggable, right?
So, from a CELMoDs perspective, which leads us into the protein homeostasis and protein degradation aspect of the platform becomes very important and we've begun to see the emergence of the data. When we think about protein degraders, such as the first CELMoDs in multiple myeloma CC-220 and CC-480, that is telling us that our hypothesis is sitting well. We've seen the response rates two years ago for CC-220, with 30% plus response rate. And with 480, we've started to see the 50% plus response rate as this presented recently last year, actually 2020.
From the multiple myeloma perspective, the way we look at the two agents are, there is a higher potency for one, and therefore we do see a profile that has a little bit more neutropenia for 480, as opposed to iberdomide or 220. And we have the larger expansion arms now ongoing for both studies. First of them, the 220 will readout this year, 480 will readout next year. And depending on the magnitude of response -- duration of response, we will be able to then have conversations with regulatory authorities in multiple myeloma.
But beyond that, we have several other agents in development. There is a 282 -- CC282 in lymphoma that is being pursued as well in addition to the other -- the others that I talked about. We have new agents that are being also looked at in the leukemia space. So, I think, we are just at the beginning of the CELMoDs and beginning of discovery of these new molecules that are going to be protein degraders, and really a very promising area where we will be able to go through our library that we've been able to now build and bring new molecules for a multitude of diseases. And just as an extension of that protein degradation platform, we're also looking at LAG of a target. So, such as the first one, which is in the clinic is the androgen receptor degrader, and that is in the prostate cancer setting in the Phase 1 trial. So once that data evolves, we'll learn more.
Great. So you touched on this a moment ago, but could you give us a little more detail around filing timelines for iberdomide you mentioned phase -- early phase data in multiple myeloma at the end of the year. Is that sort of on an accelerated approval pathway in your mind? Or how do you actually think about filing?
So for -- as I said earlier, for both of the studies, so CC-220, or iberdomide, we're looking at the readout of that fourth line plus population data within this year. And so, depending again, as I said, it depends on the magnitude of the results and the durability of those responses that we will hopefully see, will dictate as to how to approach and when to approach regulatory authorities, and what type of approval.
For 480, we are in -- we have just begun the expansion phase. So that readout will be next year. And depending again, on the similar attributes of response and durability and the patient population that will be enrolled in this study, will dictate as to the approach and how we go.
Very importantly, though, if you think about the overall multiple myeloma strategy, we have to not only think about CELMoDs, but the combinations of those CELMoDs with standard-of-care and future therapies. And so, this year we are also launching the Phase 3 program in the earliest setting for iberdomide that you will start to see, and that will pave the way for bringing these CELMoDs to an earlier line of treatment, because the ultimate game is to be able to compete versus IMiDs and at some point replace them.
Okay. You mentioned this as well while you touched upon the androgen receptor degrader, clearly the chemistry associated with CELMoDs and sort of lend itself to some opportunistic avenues that you could go down in terms of looking at other cancers, but also potentially other therapeutic areas. Is that an approach that Bristol is taking? Are you sort of screening your library periodically for targets that might be interesting, in say, immunology or neuroscience or others?
Yes. So, as I said earlier, our understanding of our protein degradation continues to evolve and increase, but we do have several targets that have been identified, but we have not spoken about them publicly. So, I won't go deeper into that. But yes, the areas of our interests, we have several targets that we are continuing to build our molecules already for taking into the clinic. As I said earlier, we already got into lymphoma, we've gotten into multiple myeloma, solid tumors, and we'll continue to evolve. A very exciting field, I truly feel fortunate to be working in that field at this time.