Motoya Koutani: It seems that I am in the Japanese channel. TAK-755, I have a question about TAK-755. If my understanding is correct, this is basically caplacizumab or cTTP, recurrence is suppressed, similar to that drug. And there is no plasma exchange and the bleeding event is fewer with the 755. That’s my understanding. So, is that correct? That’s my first question. And the second question is, I understand that you are going to be filing for this product. It was not part of the press release. But is this only for on-demand, or does it also include a prophylactic use? So, please explain that. That’s my first question.
Christopher O’Reilly: Could you please ask the second question as well?
Motoya Koutani: Yes. My second question is about TAK-341, alpha-synuclein antibody is my understanding. So, in Parkinson’s disease, you are doing Phase 1. And Mr. Plump mentioned that this short target engagement, and this is of course, for MSA, MSA actually involved alpha-synuclein. So, diagnostic criteria for MSA is just symptoms as far as I understand. So, can we really include true MSA patients in the clinical trials? How accurate can you be with that enrollment? And starting from this study, the sponsor started to be Takeda, not AstraZeneca. So, can you please explain why the sponsor has changed to Takeda? That’s my second question.
Christopher O’Reilly: So, I think these are both for Andy. So, the first question on TAK-755. So, understanding similar efficacy is for , but without the need for plasma exchange, is it correct, there is no bleeding events? And then for the filing, would it be on demand or is there also a prophylaxis indication possibly? And then the next question on TAK-341, was in Phase 1 for Parkinson’s now moving into a Phase 2 for MSA. But we €“ certainly, we can enroll the right patients given that a lot of the diagnosis is based on symptoms. So, are we sure we can correctly enroll these MSA patients? And why is Takeda be taking over leading this trial from AstraZeneca? So, I will hand over to Andy, please.
Andy Plump: Terrific. Thank you very much, Koutani -san. This is Andy. So firstly, on TAK-755, the data that we have accumulated in our Phase 3 study is both in prophylactic and in acute settings. cTTP, whether it’s congenital or immune mediated is related to either a complete deficiency or a functional deficiency and ADAMTS13 activity. So, TAK-755 is quite distinct from any existing therapy. It’s a recombinant form of ADAMTS13. And so, we are essentially providing an enzyme replacement therapy. We are placing either the genetic or the acquired deficiency in this enzyme. And the activity that we have seen in the Phase 3 study in cTTP is quite remarkable. TTP is a very complex disease. You have both clotting and bleeding. And so, the endpoints are related to both clotting organ damage that you see when you move blood flow to an organ and also bleeding.
And we saw benefits across all endpoints in our Phase 3 study. And we will be presenting those shortly, and you will have a chance to see them. With respect to TAK-341, you are correct. MSA is a clinical diagnosis and has many overlaps with Parkinson’s disease. There are some distinguishing features. The rapidity of progression is one. And then there are some neuropsychiatric manifestations in MSA, which are different. But it is a diagnosis €“ clinical diagnosis. And so, it’s possible that some of the patients that we would include in our MSA study may not actually have MSA. I don’t think that, that’s necessarily important because our expectation is that not only will TAK-341 be effective in MSA, but we have a strong hypothesis to think that TAK-341 could be effective in Parkinson’s disease.
