Hello, my name is Johannes Waldschmidt from Würzburg University Medical Center in Würzburg, Germany, and we have presented data at ASH on our German experience with the efficacy of Cartesia therapy in myeloma patients that have been pre-exposed to bispecific antibodies. And the rationale behind this idea was that bispecific antibodies are a tremendously active class of drugs in the treatment landscape for multiple myeloma. And at the same time, we sometimes run into problems to safely bridge patients to a Cartesia therapy. On the other hand, available data suggests that bispecific antibodies may impair manufacturing of Cartesia cells, may impair Cartesia efficacy. And in this study, we now look at 39 patients treated at 10 different hospitals in Germany. And the median line of prior therapies in this cohort was seven, so quite heavily pretreated. There were a range between three and 13 prior treatments. And the rate of extra medullary disease was also quite high with 42%. We first looked at efficacy. And in terms of efficacy, we saw a slight advantage for silt to cell over IDA cell. Both were part of this trial, but silt to cell induced a CR rate of approximately 40% and IDA cell just 31%. Apart from that, we could confirm risk factors that have been previously described, that is to say, high risk cytogenetics, extra medullary disease. But now the beauty of this study was really that we could dissect the pattern of how bispecific antibodies were given in the context of bridging therapy to ideally define the optimal position of bispecs in the context of Cartesia therapy for multiple myeloma. And this study basically gave us three big findings. One finding, the first finding most important is the efficacy of a Cartesia therapy is always better if you get your Cartesia therapy with a well-controlled disease state. For those that might not be familiar with it, so bridging typically, there are some heterogeneous definitions, but we understand bridging as the timeframe between T-cell aphoresis and then reinfusion of Cartesia cells typically 8 to 10 weeks. And we could find that the disease control state at the time of aphoresis is not of tremendous importance, but at the time of Cartesian infusion, you really want to have a controlled disease. And in our cohort, there were patients with bad bridging, suboptimal, let me call it suboptimal and optimal bridging. So we have some patients that lost their control during bridging and these patients had very poor outcome and other patients could actually be induced to get good disease control even though they didn't have it at the time of T-cell aphoresis. And this is the first finding and then in terms of bispex, we could stratify our cohort into four groups. So the first group was patients that have both been exposed to Teclistumab and Talcidumab before aphoresis. Second and third group were exposed to either Tec or Talc, one of them before aphoresis. And the fourth group was the one where we could actually avoid giving bispex before aphoresis and only gave it in the bridging. So that is to say after aphoresis before reinfusion. And this was the group that by far performed the best in our analysis. PFS not reached. The poorest PFS was in the group of patients that had been pre-exposed to both Tec and Talc before aphoresis and PFS in this group was around four months and in between was this group of either Tec or Talc exposed patients before aphoresis with a PFS roughly around one year. We believe in conclusion that this study shows that disease control before Carte reinfusion is of tremendous importance and bispex made help in those patients where at the time of aphoresis we might not have an ideal remission state and then once T cells have been collected we are free to go with the bispex and the bispex can help during bridging to induce disease control. There's one caveat though. We obviously also looked at Ticlystumab and Ticlystumab is targeting the same antigen BCMA and we had seven patients that had been exposed to Ticlystumab for more than three months. This is what we defined as long-term exposure to Ticlystumab and two out of these seven patients actually had a loss of BCMA then moved into Cartesia therapy and obviously Cartesia therapy didn't work so in this respect we would advocate for using TalcataMap during bridging over Ticlystumab just to save BCMA as a target but we feel that TalcataMap targeting GPRC5D can be of enormous help to really set the perfect stage for Cartesia then before reinfusion of Cartesia.