The Phase IIb miracle trial aims to confirm the additive benefits of both balcinerone combined with dapagliflozin, and we will have beta later this year. We have shown significant benefits of zibotentan, our selective endothelin receptor antagonist in combination with dapagliflozin and improving fluid dynamics and reducing the risk of adverse kidney events. We presented data from our Phase IIb venous CKD trial at the American Society of Nephrology, which I will cover in the next slide. And finally, we are in advanced stages of planning Phase III trials for baxdrostat monotherapy in patients with treatment resistant, uncontrolled hypertension, and in combination with dapagliflozin for patients with CKD and hypertension. Baxdrostat has been shown to be effective at reducing systolic blood pressure without off target inhibition of cortisol synthesis.
This treatment paradigm would offer a much-needed option for patients with CKD and hypertension. We have already initiated a Phase III trial for zibotentan and dapagliflozin, with plans to initiate baxdrostat monotherapy by the end of the year. We are also in advanced stages of planning Phase III trials for the other two combinations. Our ambition is to develop these four potential new medicines to extend Cardiorenal protection while addressing specific symptoms of disease. Next slide, please. Data from the Phase II ZENITH CKD trial investigating zibotentan and dapagliflozin in patients with CKD and residual high proteinuria showed clear benefit in reducing the urine albumin creatinine ratio, a key indicator for kidney function. Zibotentan improves fluid dynamics and reduces the risk of adverse kidney events.
When combined with dapagliflozin’s ability to reduce extra vascular volume, these two medicines have been shown to provide significant benefit over endothelin receptor antagonists alone, where fluid retention has been a barrier to uptake. The complementary mechanisms deliver superior efficacy and acceptable tolerability both doses were well-tolerated and offer benefits across glomerular filtration rates supporting our path to Phase III. On the right-hand side, our IL-33 inhibitor tozorakimab has proven ability to inhibit dual pathways ST2 and RAGE/EGFR. This is important as these independent pathways are involved in different inflammatory cascades. Dysregulation of ST2 pathway drive airway inflammation, while dysregulation of RAGE/EGFR pathway is linked to epithelial remodeling and mucus overproduction, hallmarks of chronic lung diseases.
This September data was presented from the Core 2 trial for patients hospitalized with COVID-19. Patients receiving tozorakimab had a substantially lower risk of respiratory failure or death at day 29 versus standard of care alone. These data build confidence in tozorakimab and its mechanism of action and inflammatory lung diseases. The recently dosed MIRANDA trial updates the range of doses being investigated across our COPD program, which includes the ongoing Oberon and Titania Phase III trials. We will have data from our Phase II FRONTIER-3 trial in asthma, as well as FRONTIER-4 in COPD, which we hope to present in due course. Please advance to the next slide. As announced this morning, we have licensed and oral glucagon like peptide one receptor agonist for the treatment of obesity, Type 2 diabetes and other cardiovascular, renal and metabolic diseases.
ECC5004 is a once daily, oral small molecule, and preliminary results have shown a potentially differentiated clinical profile. Obesity is a significant and growing market. With over 1 billion patients living with obesity today. The majority of these patients are suffering with comorbidities such as Type 2 diabetes, heart failure, hypertension, and renal disease. We are well placed to address the spectrum of disease associated with obesity with potential oral combinations in our existing and pipeline medicines. For example, we have recently seen data on our oral PCSK9 where the product profile is in line with our expectations and is differentiated with limited food interactions. We are excited about the opportunity for a monotherapy and dyslipidemia as well as in combination with ECC5004.
We are building a robust portfolio of novel medicines to address a broad range of cardiovascular, renal and metabolic diseases. Please move to the next slide and I will now hand over to Mark who will cover our Rare Disease portfolio.
Marc Dunoyer: Thank you, Sharon. Can we go to next slide please. Rare Disease delivered total revenue of $5.8 billion in the first nine months of 2023 at 12% year-over-year, driven by increased patient demand and new launches globally. Ultomiris grew 49% in the third quarter driven by patient demand, particularly patient naive to go on the treatment in generalized myasthenia gravis as well as successful conversion on Soliris across all indications. As a consequence of this conversion dynamic, Soliris declined 12%. [Indiscernible], both Strensiq and Koselugo grew 21% and 81% respectively, reflecting strong underlying patient demand. Looking at the regional breakdown in the middle, I want to highlight the performance of emerging markets, which grew 70% in the quarter.
Global expansion is an important part of our strategy and we continue to benefit significantly from the AstraZeneca footprint. We have now launched in 64 countries globally, are on track to delivering on our ambition to reach 100 countries by 2030. Lastly, I wanted to provide some context regarding our C5 franchise across neurological diseases, myasthenia gravis as well as NMOSD, as well as [indiscernible] disease atypical HUS, and PNH. We continue to see neurology indication grow as launch is continued globally. And in the case of mg, the patient population is significantly larger [indiscernible] rare diseases. The pie chart on the right panel, they represent revenues in the U.S., whereas the two other panels show global sales. Please advance to the next slide.
Last week, we presented Phase II data at the American Society of Nephrology demonstrating the clinically meaningful efficacy of Ultomiris in IgA Nephropathy. Ultomiris demonstrated rapid, complete and sustained complement inhibition characterized by significant and potentially disease modifying reduction in proteinuria from week four, as well as a stable mean glomerular filtration rate over 26 weeks. IgA Nephropathy is characterized by the deposition of immune complexes in the kidney that activates the complement system, which then triggers inflammation, and causes glomerular damage. At the most prevalent, primary glomerular disease relative to other rare disease in the renal area, IgA Nephropathy is associated with substantial morbidity and mortality with approximately half of patients experiencing end stage kidney disease or death.
We see the opportunity for Ultomiris as an add on therapy to patient optimize on standard of care renin-angiotensin-aldosterone system inhibitors, and SDLT2. This data not only affirms the whole of complement intergenic property, it provides confidence for Phase III, but also accelerates our ambition to expand Ultomiris into additional indication and border patient population. With that, please advance to the next slide. And I will hand over the call back to Pascal for his closing remarks.
