Thanks so much, Paula, and hello to everyone on the call. Let me begin with a quick refresher on chronic neutropenia. The hallmark of chronic neutropenia is abnormally low levels of circulating neutrophils that are the defense mechanism our body uses to fight pathogens. As we've presented previously, there is a well-established correlation between circulating levels of neutrophils or absolute neutrophil count, ANC, and the risk of frequent and/or serious infection. Note that the lower limit of normal for neutropenia diagnosis is 1,500 cells per microliter. Below that, grades are divided based on the infection risk in increments of 500 cells per microliter from mild to moderate to severe. As you can see, severely neutropenic patients have ANC of less than 500, and this corresponds to the highest risk of infection. To reduce the risk of infection in these patients, it is critical to move them from the most severe grade towards less severe grade to achieve as normal a level of neutrophil as possible. Therefore, an increase of 500 cells per microliter is an important clinical practice objective. Through its mechanism of action, mavorixafor has been shown to do precisely that, increase the number of circulating neutrophils. This ability is clearly stated in the mavorixafor label from the FDA approval in WHIM syndrome based on results from a pivotal Phase III trial. These results demonstrated that mavorixafor sustainably raised ANC over the 52 weeks of the trial and consequently reduced the annualized rate of infection along with the duration and severity of infections in trial participants. This infection benefit was achieved through an increase in mean ANC of more than 500 cells per microliter. These results and the WHIM approval in the U.S. provide confidence in our plan to potentially bring mavorixafor to those with other chronic neutropenic conditions where significant unmet needs remain. The gap in addressing these unmet needs results from the significant lack of innovation in the field. The only currently available therapy is G-CSF, which was approved almost 30 years ago. It's an injectable drug that is associated with dose-dependent and often treatment-limiting side effects as well as long-term risk of certain malignancy. As you've heard in our previous investor presentations, CN patients and the physicians that treat them are dissatisfied with G-CSF and its side effects, especially fatigue and bone and muscle pain. Unfortunately, these side effects are often dose-dependent and can limit the use of G-CSF or prevent its use at a fully effective dose. We believe there is an urgent need for a new innovation like mavorixafor, which data now suggests could be used, if approved, as a monotherapy or in combination with G-CSF while also allowing for reduced doses of G-CSF to limit side effects and long-term cancer risk. Our market research indicates there are approximately 50,000 people diagnosed with CN in the U.S. Of this population, it's estimated that about 15,000 have high unmet need, including recurrent infection despite the available standard of care. Our Phase III 4WARD trial focuses on this population with the highest unmet need, enrolling adolescents and adults with ANC below 1,500 cells per microliter and a history of recurrent and/or serious infection. To meet the multiple needs of this population, we envision two potential opportunities for oral once-daily mavorixafor within this market. One, it could be used as a monotherapy in newly diagnosed CN patients or to replace G-CSF treatment; and two, in combination with G-CSF, enabling a meaningful reduction in G-CSF dosing, lessening pain, discomfort and long-term risk of malignancy. Our Phase II CN study set out to evaluate those opportunities. And as you will see in just a minute, we believe the data from this study supports the potential for mavorixafor to transform the chronic care of this neutropenic population. As shown here, the main goal of the Phase II study were to confirm the durability of the Phase Ib results that showed 100% response to a single dose of oral mavorixafor plus or minus G-CSF across multiple CN types. We also aim to assess the long-term safety and tolerability of mavorixafor use with and without G-CSF in people with CN. In addition, we wanted to explore the feasibility and the willingness of physicians to safely reduce G-CSF with mavorixafor; and a key goal was also to inform the design of our Phase III pivotal trial and, in doing so, derisk the trial. The Phase II study was a six-month study with monthly visits and comprehensive assessment at baseline in months one, three and six. Two quick notes on the design of this study. First, since the neutrophil life cycle is about 10 to 14 days, we believe that a study of this length provides a good indication of the bone marrow's long-term ability for stable neutrophil production; and second, modifications to G-CSF dosing were permitted in the combination group following participants' month two visit. So the first assessment of those on an adjusted dose would have been at the month three visit. These adjustments were decided between physicians and their patients and were not protocol mandated. Let's start by looking at the final participant disposition in the study, a population typical of those with chronic neutropenia and high unmet need. We enrolled a total of 23 participants in the 6-month, single-arm, open-label study with the mix of idiopathic and congenital CN and even a few with cyclic presentation. There was a typical gender distribution in the study and a mean age of 34 years. We also note here that there was a good mix of genetic backgrounds with the congenital group, also representative of what you might see across the full CN population. We analyzed the data in two groups: mavorixafor monotherapy comprising 10 participants; and the mavorixafor plus G-CSF group with 13 participants, nine of whom ended up having their G-CSF dose reduced in the study. In addition, we evaluated neutrophil functionality pre- and post-treatment in a sub-study population of nine evaluable participants and compared those results to a group of healthy individuals. To address the unmet needs existing with current chronic CN therapy, our objective is to sustainably increase circulating functional neutrophils using oral mavorixafor. Thus, the results presented today are focused on answering the following four questions. One, in the monotherapy group, did mavorixafor increase and durably sustained absolute neutrophil count at clinically meaningful levels; two, in the combination group, were physicians willing and able to adjust their patients' G-CSF dose when adding mavorixafor; three, could G-CSF be reduced while maintaining clinically meaningful ANC levels; and four, are the neutrophils that are mobilized into the peripheral blood by mavorixafor functional throughout the six month study? First, let's look at the monotherapy results. Consistent with our data presentation in June, mavorixafor durably and meaningfully increased mean ANC, bringing levels into normal range at month three and month six. As an oral once-daily treatment delivering this level of ANC increase, you can begin to appreciate the potential for mavorixafor as monotherapy. In addition, mavorixafor also durably and meaningfully increased mean ANC level in the severe CN study participants. Those starting with levels below 500 cells per microliter had more than two-fold increase in mean ANC versus baseline throughout six months of mavorixafor treatment. As a reminder, such an increase in ANC in our Phase III WHIM trial led to a decrease of 60% in infection rate. So this similar increase in ANC here is not only clinically meaningful, but also helps increase our confidence in achieving a positive infection rate readout for this monotherapy population in the ongoing pivotal Phase III trial in CN. Let's move now to the combination results. In this group, we started with 13 participants entering the study on G-CSF at baseline. One dropped out almost immediately, so we had 12 eligible to have their G-CSF dose reduced following their month two visit. Notably, clinicians chose to reduce the G-CSF in nine of these 12, with three being fully taken off G-CSF prior to their six month visit, finishing the study on mavorixafor monotherapy. Thinking back to the market opportunity and unmet need slide, you can now see why we're so excited about the data. This is the first look at how physicians could potentially use mavorixafor in their CN patients who are already on G-CSF, should it gain approval. Today, we're not presenting the data from the three participants who remain on stable dose G-CSF. But we know that the final data set from this group was consistent with the results we shared this past June, showing robust and sustained increases in mean ANC from baseline levels. Let's look now only at participants who were dose-adjusted. As shown here, the G-CSF reductions were quite substantial, and mean ANC were able to be maintained at normal levels throughout the study. At month three, where eight of the nine have been adjusted, physicians were comfortable lowering G-CSF by 52% on average. This average increased to 70% reductions by month six, with three of the nine adjusted dose participants taken completely off G-CSF. Anecdotally, physicians and academic experts have told us that they believe a 25% reduction in G-CSF would be clinically meaningful to their patients. So seeing this level of G-CSF reduction reinforces the potential benefit of mavorixafor and role in the treatment of CN. We now turn our attention to assessing the functionality of the increased levels of circulating neutrophil in the Phase II sub-study. As mentioned, the purpose of this sub-study was to assess the percentage of functional neutrophils in people with CN, including those with congenital genetic variations associated with neutrophil maturation arrest. We used two well-accepted functionality assays: the phagocytosis assay, which assesses the neutrophil's ability to engulf pathogens; and an assay for ROS production, ROS is reactive oxygen species, or the ability to damage or kill pathogens that have been engulfed. These neutrophil function studies were conducted on the sample from nine eligible participants with a mix of CN types and monotherapy and combination use. We also recruited five healthy individuals to provide a benchmark for comparison. For simplicity today, we are only showing the phagocytosis data, but we note that the ROS assay results closely mirrored the phagocytosis results. While participants with chronic neutropenia have fewer neutrophils than healthy donors, you can see here that those neutrophils that do make it into the circulation are, in fact, functional with a similar percent of functionality between the neutropenic and healthy donor population. Note that the bars here represent the percentage of neutrophils that demonstrated phagocytosis after challenge with opsonized bacteria. We've also broken out the congenital CN subset to see if genetic variant affects functionality differently than in the other groups. Looking now at the full results, we see that the percentage of functional neutrophil in the healthy donors, the full group of participants and the congenital CN subset are essentially the same following six months of mavorixafor therapy. And note, while we are showing you here the data for fibrocystic function, we generated very similar data on the percentage of neutrophils generating ROS after bacterial challenge. Recall in our 52-week WHIM Phase III clinical trial, we saw that an increase in circulating mature neutrophils corresponded with a 60% reduction in the annualized infection rate as well as reduction in the severity and duration of infection. By increasing the number of functional circulating neutrophils, we believe that mavorixafor treatment could correspondingly reduce the infection rate in the larger chronic neutropenia population. And we are hopeful to see similar results in our ongoing registrational Phase III chronic neutropenia trial. Mavorixafor with or without concurrent G-CSF therapy was generally well tolerated throughout the study. The overall safety profile was consistent with previous studies. And the most frequent treatment-related, treatment-emergent AEs were GI-related, nausea and diarrhea, which were mild to moderate and typically resolved over time. As we noted in our June presentation, we did see three discontinuations in the study. These occurred early in the execution of the study. And after implementing an education program on possible GI side effects, there were no further discontinuation. Rest assured, we have incorporated this education into the Phase III CN trial. In summary, we could not be more pleased with the results of this Phase II study having met all of the goals we set forth. We have shown that mavorixafor can durably and meaningfully increase mean ANC as a monotherapy even in the most severe CN population and can do likewise when dosed in combination with G-CSF. We show that mavorixafor enabled clinicians and their patients to meaningfully lower the use of G-CSF while maintaining mean ANC at normal levels. Critically, we showed that mavorixafor increased total count of functional circulating neutrophils even in the most difficult-to-treat individuals with CN. And importantly, we demonstrated that mavorixafor was generally well tolerated on its own and in combination with G-CSF. These results give us great confidence in the chance of success of our ongoing Phase III trial and mavorixafor's potential to reduce infection rate. They also provide hope that mavorixafor could be the innovation that the CN community is looking for. As you've heard previously, through our interviews with physicians and CN patients, what they need and want is a well-tolerated oral option, one that can enable them to safely reduce the use of injectable G-CSF. And so far, our results have shown that mavorixafor fits that profile well as either a monotherapy or in combination use. I'll now turn it back to Paula to conclude. Paula?