Stephen Scala, Cowen
Great. Let's spend a moment on deucravacitinib. So, when we get the full Phase 3, as you mentioned later this year, what would you suggest that investors focus on -- in Phase 2 deucravacitinib was about twice as effective in achieving PASI 75 as was OTEZLA, should that be the bar in Phase 2 or sometimes Phase 2 trials aren't quite as good. What -- how would you ask us to approach this data?
Sure. And thanks for reminding everyone that there are two Phase 3 studies that have recently laid out. And we recently got confirmation. So, this is sort of breaking news in a way. We will have the ability to present both of these Phase 3 studies at AAD in April. So, you will be able to see the full dataset, and certainly that will pave the way for our discussions with the authorities as we continue to get engaged in that side. We will not get into the specificity of the data. Now we are only six to eight weeks away, so you will get to see that yourself.
We do believe from our perspective, deucravacitinib will probably be the oral agent of choice because of the profile that we continue to see and as it is evolving with the data that we have. And the reason I say that is if you look at it from an efficacy perspective, not only is there the statistical significance that is required for the filings, et cetera.
But it is clinically meaningful improvement versus the currently used oral medication, which is OTEZLA and because of its mechanism of action through TYK2 specificity in terms of inhibition of IL-12/23, I think the safety profile will also define itself. So something to look at to pay attention to both from an efficacy perspective and safety perspective. And because of that specificity and where it is hitting in terms of the pathways, it opens up the space for looking at future indications as a broader medicine for autoimmune diseases of multiple indications, such as IBD SLE, et cetera, that will start to show data later in the year.
Why don't we spend a moment on some of those potential new indications? I think there were five or six that were mentioned at the R&D event you hosted in June. Can you kind of just maybe rank them the top two or three in terms of their potential and ability to really influence the trajectory on the molecule -- of the molecule? What are the ones that you think could really be a meaningful commercially?
Absolutely. Being an R&D person, let me say that, first of all, from a mechanistic perspective, it is a differentiator in medicine that will have applicability probably to a larger extent in multiple autoimmune diseases. So, first of all, psoriasis we just talked about, but then we also have shared the data in psoriatic arthritis in the Phase 2 study. We are imminently starting the Phase 3 program in the psoriatic arthritis space, as you will see coming through.
You know that we have studies that are already ongoing in ulcerative colitis. And the Phase 2 study will have a readout at the end of this year, and that will pave the way for future development options for that disease.
We will have the Phase 2 readout for systemic lupus erythematosus as well at the end of the year or very early next year. So, looking forward to that, which will also then lead us into that indication. Study also ongoing in Crohn's disease and that data evolves in 2022. And so that will lead us to that indication in the future of data supportive.
And then there are multiple other indications that will continue to emerge and we'll pay attention to them as we build towards a larger program for deucravacitinib in the future.
I should have mentioned at the outset any investor on the line has a question. You can either email me or Mike, or you can submit it online and we will read your question to Samit.
Maybe we can move on and let me preface this by saying Sanofi was at our conference yesterday. And as you can imagine, they were citing some of the potential risks with agents, which were worked through the pathway that deucravacitinib works through. And they were basically arguing that there's a common pathway and all agents, whether they're regardless of their configuration within the JAK family are funneled through the same pathway. And therefore, there's this potential risk. Why is that not correct, Samit?
So, I think scientifically speaking, and we've done multiple experiments, and we should certainly start to understand that not all pathways work in the same way and not all the molecules are JAK inhibitors. Certainly, we know what the concerns are around the JAK inhibitors.
When we think about deucravacitinib and the reason we continue to say that it's a TYK2 inhibitor is because we've done the medicine chemistry. Our scientists have really designed the molecule for that specificity to work through that pseudo kinase domain of TYK2 to have a very specific downstream effect on IL-12 inhibition, IL-23 inhibition and interferon health inhibition.
And what that leads us is into that profile from both efficacy perspective, which as you will see the data will continue to show how it lines up with those inhibitors of IL-12/23. And from a safety perspective that we are not seeing those signals of lab abnormalities. We are not seeing signals of those cardiovascular events or VTEs, that would be of concern.
So, we do believe from a preclinical perspective, from a clinical data perspective, it just informing our hypothesis. We feel very comfortable as we look forward to presenting these data and taking them to the authorities. Now, of course, what the authorities will decide based on the data will conform to that. But we do believe that the differentiation that we have brought together in the design of the molecule and the conduct of the trials and the data that we've been able to generate differentiates itself.