 So, let me start with a quote by William Stuart, surgeon general under Nixon administration. The time has come to close the book on infectious diseases. About 50 years later, several thousand people die annually worldwide, now again of antibiotic resistance. So, something must have dramatically changed within this timeframe. It is actually quite a big problem. So, fighting infectious diseases has been officially declared accomplished. No new drugs were discovered, research declined, and at the same time, more and more bacteria gained multi-resistance, with now even strains resistant to all currently known antibiotics. So, how could it happen that bacteria strike back so badly? It's actually tragically that the desired trait of an antibiotic to kill a bacterium also represents its weakest point. Like humans, bacteria do not want to get killed. They rapidly divide and by trial and error, select modifications that renders them insensitive towards the antibiotic, which is termed resistance. Unfortunately, the question is how can we overcome or is there a way to overcome this evolutionary advantage? Bacteria are not bad per se. It's the toxins that they produce which cause the major pathogenic effects in humans. If there's a way that we find a way to dismantle this toxin production, the bacteria would be disarmed and, of course, much less effective and they could not propagate this infection. There would be also, of course, no incentive for further resistance development. So, the question is, could this really work? Isn't an antibiotic that fully eradicates the pathogen better suited for treatment? It's not a toxin that only harms the human body. It also eliminates, as we just heard, the immune response. And if we find a way to get the immune response back in stronger by the reduction of toxins, this would be also a way then to possibly fully eradicate all the pathogens in the cell. Previous studies have shown that individual inhibition of all these toxins led to a positive therapeutic effect. However, it's very difficult to target all of these toxins individually. You have to develop a drug against them. Global regulator of the whole toxin secretion would be much better to address with the therapeutic. So, is there such a switch? Bacteria communicate with each other and they tightly control their population up on a certain threshold concentration. They start with the expression of toxins. This is regulated by a sensual switch which is very fundamental for this bacteria called ClpP. And ClpP is really the gatekeeper of this toxin release. Of course, we know now ClpP is responsible for the majority of all these toxins. It is thus really a prime target for such a just described antivirin strategy. By genetic studies, we could show that when cells are lacking ClpP, they are not infectious anymore. So, they do not produce toxins and thereby they are less infective and much easier to treat also in the mouse model. So, this really confirms that ClpP is a suitable target. However, the question is does this also work in a real infection mode? There are no drugs known against ClpP. But by coincidence, our team has been successful to identify a first generation hibiter that very selectively addressed ClpP and also led to a positive therapeutic effect in a corresponding mouse model with multi-resistant bacteria really showing the proof of concept that is possible. Moreover, the bacteria were incubated over several weeks with the drug and unlike conventional antibiotics, we did not observe any resistance development in this time frame. Moreover, the useful bacteria in our guts, they were preserved under these conditions and not killed like with the conventional antibiotic therapy. So, what are the next steps in development? So, of course, the drug needs to have critical parameter. If you have to have potent activity, stability and low toxicity. Although successful, our first generation unfortunately was very limited in stability. It rapidly hydrolyzed in blood and therefore it was very unsuccessful to use as a drug. We had to go back to the drawing board and systematically optimized by chemical design this first generation hibiter class. And by this we have been now successful in the identification of the second and new generation which exhibits really good efficacy in the mouse model which is stable and also exhibits low toxicity. And we are currently pursuing more preclinical studies meaning mouse studies. This arming bacterial pathogenesis could really be a viable strategy against multi-resistant bacteria. The drug can be applied in a single treatment. You can also use it in combination with established antibiotics to really reestablish maybe their potency. Clipi is a suitable target in this endeavor because it's such an essential regulator of all these violence. So in essence, addressing pathogenesis and virulence in particular could be a viable strategy, could be a good strategy to overcome the problem of multi-resistance. We have been successful in the identification of this compound that showed positive healing in mouse models. So now, as I said, preclinical trials are going on and the aim would be, of course, to move further on into real clinical trials. So antibiotics are around for decades. The use is really safe and if no resistance strain is treated, they fully eradicate the pathogen. So the question is, is it really possible to close the book on infectious diseases maybe in the future by changing a paradigm from antibiotic to anti-violence? Thank you. Thank you.