Welcome, everyone, and thank you for joining us today for another Virtual Investor: What This Means segment. My name is Janine Thomas. I am CEO of JTC IR, and I will be the moderator for today's segment. I am very pleased to be joined by Dr. Reid Bissonnette. He heads the Translational Research and Development at Xenetic Biosciences. Before we get started, I just want to remind our audience that Xenetic Biosciences is publicly listed on NASDAQ and trades under the ticker XBIO, and during today's discussion, the company will be making forward-looking statements, and I encourage everyone to view the company's latest SEC filings on their website at xeneticbio.com for the latest information. So, Reid, we are so happy to have you. We're going to dive right in, so to get started, can you please provide an overview of Xenetic and your innovative DNase I platform? Xenetic Bio is a small biopharma company based in Boston, which is developing an oncology drug pipeline around the nuclease DNase I. Now, DNase I is an enzyme which breaks down DNA in a variety of ways. And physiologically, DNase I is responsible for cleaning up cell-free DNA and preventing that DNA from becoming a health issue. For example, cell-free DNA is implicated in certain types of autoimmunity. Xenetic Bio is developing DNase I as a drug targeting a physiological structure called neutrophil extracellular traps, or NETs. And these are expelled by activated neutrophils, which is a type of white blood cells. For context, neutrophils are the body's equivalent to the Marine Expeditionary Force. They're the tip of the spear for dealing with infections and other insults. Now, these neutrophil extracellular traps, or NETs, are actually web-like structures composed of extracellular chromatin, or DNA. And these are coated with histones and other proteins that are derived from the neutrophils. NETs are beneficial in the case of microbial infections, where they actually trap microbes, net them, so to speak, and hold them for destruction by the immune system. In cancer, however, NETs, neutrophil extracellular traps that are associated with tumors can create a host of problems. NETs are actually pro-tumor, meaning they can contribute and promote tumor progression. They can promote and facilitate metastasis and can contribute to an immunosuppressive tumor microenvironment, which then hinders and inhibits the anti-tumor immune responses and the ability of the immune system to control and kill tumor cells. They can actually physically interfere with the ability of immune cells, such as killer T cells, to detect and engage tumor cells. NETs are also known to contribute to resistance to chemotherapy, immunotherapy like immune checkpoint inhibitors and other immunotherapies, and radiotherapy. And of course, that's what Xenetic Biosciences is pursuing: DNase I as a means of targeting NETs in order to improve patient responses to cancer therapies. To that end, we are accumulating preclinical proof of concept and mechanistic data that demonstrates DNase I, by targeting and destroying NETs, can improve significantly the efficacy of several cancer therapy modalities. And in particular, our interest is in immunotherapies and chemotherapy. Appreciate that, Reid. So can you now summarize for our audience the recent data that was presented at SITC? Yes. We presented some of our preclinical data at SITC 2024. This is the Society for the Immunotherapy of Cancer and is arguably the place to be if you're an immuno-oncologist. We showed data demonstrating that DNase I significantly improved the efficacy of an antibody directed against CTLA-4, which is an important immune checkpoint. Immune checkpoints are essentially natural brakes on the immune response and can prevent an overstimulated immune response. However, in cancer, immune checkpoints result in suppression of the immune response and block anti-tumor immunity. Some examples of clinically used CTLA-4 antibodies include ipilimumab, or Yervoy, and others. What's important here is that we showed this DNase I-mediated efficacy bump in a model of colorectal cancer that represents about 85% of all CRC patients, or colorectal cancer patients. And where immunotherapies like immune checkpoint inhibitors, like CTLA-4 or PD-1 antibodies, have really failed so far to show any clinical benefit. This subset of colorectal cancer patients that fails to respond to immune checkpoint inhibitors is commonly known as microsatellite stable mismatch repair proficient, or MSS-MMRP-CRC. There are a number of possible mechanisms for how this DNase I anti-CTLA-4 combination therapy works in this setting, but I believe that there are at least three or four mechanisms at play. I believe that DNase I relieves the NETs-mediated immunosuppression and inhibition overall of the anti-tumor immune response. And there are multiple aspects to that that I won't go into now. DNase I likely promotes the release of things like tumor antigens and facilitates their presentation to the immune system, which is a problem in this particular subset of colorectal cancer, and that this can then lead to increased anti-tumor immunity. Finally, DNase I improves access of tumor cells to immune cells, leading to the tumor cells' demise. So, Reid, we are here for a What This Means segment. So I have to ask, what does your data mean for your DNase platform and your overall development strategy? These are an important proof of concept data. Together with some other very positive data we have collected from evaluating combinations of DNase I with other immune checkpoint inhibitors, such as antibodies to immune checkpoint PD-1, for example, which you typically hear of as nivolumab, or Opdivo, or pembrolizumab, or Keytruda, our data indicate that the administration of systemic DNase I has the potential to significantly improve the anti-tumor efficacy of and patient response to what are now commonly used immune checkpoint inhibitors. Essentially, what this will do is flip the switch. It'll convert a nonresponse to immune checkpoint inhibitors to a positive response in CRC and other cancers where NETs are likely a factor in therapy resistance. Obviously, these POC data and proof of concept data will guide us as we march towards the clinic. Okay. So with that, this concludes Xenetic Biosciences' What This Means segment. I would like to thank Dr. Bissonnette of Xenetic Biosciences for joining us today. And I'd also like to thank our audience for your time and attention. As a reminder, Xenetic trades on NASDAQ under the ticker XBIO. And if you like what you saw today, I encourage you to visit xeneticbio.com for more information on the company, to sign up to follow the company to receive their alerts, as well as follow their social channels to stay current on the latest information. And you can also visit virtualinvestorco.com for our latest segments and event calendar. I'd like to thank everyone and wish you a great rest of your day.