[Translation] A Phase I, open-label, randomized, parallel-group clinical study to evaluate the pharmacokinetic characteristics, safety, tolerability, and immunogenicity of BION-1301 after a single dose in healthy adult Chinese subjects

主要目的：评估中国健康成年受试者单次皮下注射（SC）BION-1301的药代动力学（PK）特征次要目的：评估中国健康成年受试者单次SC BION-1301后对免疫球蛋白的药效学（PD）影响；评估中国健康成年受试者单次SC BION-1301的免疫原性；评估中国健康成年受试者单次SC BION-1301的安全性和耐受性

[Translation]

Primary objective: To evaluate the pharmacokinetic (PK) characteristics of a single subcutaneous (SC) injection of BION-1301 in healthy Chinese adult subjects Secondary objectives: To evaluate the pharmacodynamic (PD) effects of a single SC BION-1301 on immunoglobulins in healthy Chinese adult subjects; To evaluate the immunogenicity of a single SC BION-1301 in healthy Chinese adult subjects; To evaluate the safety and tolerability of a single SC BION-1301 in healthy Chinese adult subjects

Start Date17 Apr 2023

Sponsor / Collaborator

Chinook Therapeutics, Inc.

[+3]

100 Clinical Results associated with Zigakibart

100 Translational Medicine associated with Zigakibart

100 Patents (Medical) associated with Zigakibart

Literatures (Medical) associated with Zigakibart

04 Dec 2023·Clinical kidney journal

The contribution of a proliferation-inducing ligand (APRIL) and other TNF superfamily members in pathogenesis and progression of IgA nephropathy

Review

Author: Barratt, Jonathan ; Yeo, See Cheng

ABSTRACT:

Advances in our understanding of the pathogenesis of immunoglobulin A nephropathy (IgAN) have led to the identification of novel therapeutic targets and potential disease-specific treatments. Specifically, a proliferation-inducing ligand (APRIL) has been implicated in the pathogenesis of IgAN, mediating B-cell dysregulation and overproduction of pathogenic galactose-deficient IgA1 (Gd-IgA1). Animal and clinical studies support the involvement of APRIL in the pathogenesis and progression of IgAN. An elevated level of APRIL is found in IgAN when compared with controls, which correlates with the level of Gd-IgA1 and associates with more severe disease presentation and worse outcomes. Conversely, anti-APRIL therapy reduces pathogenic Gd-IgA1 and IgA immune complex formation and ameliorates the severity of kidney inflammation and injury. Genome-wide association studies in IgAN have identified TNFSF13 and TNFRSF13B, a cytokine ligand-receptor gene pair encoding APRIL and its receptor, respectively, as risk susceptibility loci in IgAN, further supporting the causal role of the APRIL signalling pathway in IgAN. Several novel experimental agents targeting APRIL, including atacicept, telitacicept, zigakibart and sibeprenlimab, are currently under investigation as potential therapies in IgAN. Preliminary results suggest that these agents are well-tolerated, and reduce levels of Gd-IgA1, with corresponding improvement in proteinuria. Further studies are ongoing to confirm the safety and efficacy of anti-APRIL approaches as an effective therapeutic strategy in IgAN.

01 Dec 2023·Clinical rheumatology

A narrative review of potential drug treatments for nephritis in children with IgA vasculitis (HSP)

Review

Author: Lamond, Megan ; Chetwynd, Andrew J ; Marro, Julien ; Oni, Louise ; Williams, Chloe E C

Abstract:

Immunoglobulin A (IgA) vasculitis (IgAV, also known as Henoch-Schoenlein purpura, HSP) is the most common vasculitis of childhood. It usually presents with a simple, self-limiting disease course; however, a small subset of patients may develop kidney involvement (IgAV-N) which occurs 4–12 weeks after disease onset and is the biggest contributor to long-term morbidity. Treatment currently targets patients with established kidney involvement; however; there is a desire to work towards early prevention of inflammation during the window of opportunity between disease presentation and onset of significant nephritis. There are no clinical trials evaluating drugs which may prevent or halt the progression of nephritis in children with IgAV apart from the early use of corticosteroids which have no benefit. This article summarises the latest scientific evidence and clinical trials that support potential therapeutic targets for IgAV-N that are currently being developed based on the evolving understanding of the pathophysiology of IgAV-N. These span the mucosal immunity, B-cell and T-cell modulation, RAAS inhibition, and regulation of complement pathways, amongst others. Novel drugs that may be considered for use in early nephritis include TRF-budesonide; B-cell inhibiting agents including belimumab, telitacicept, blisibimod, VIS649, and BION-1301; B-cell depleting agents such as rituximab, ofatumumab, and bortezomib; sparsentan; angiotensin converting enzyme inhibitors (ACE-Is); and complement pathway inhibitors including avacopan, iptacopan, and narsoplimab. Further clinical trials, as well as pre-clinical scientific studies, are needed to identify mechanistic pathways as there may be an opportunity to prevent nephritis in this condition.Key Points• Kidney involvement is the main cause of long-term morbidity and mortality in IgA vasculitis despite the current treatment recommendations.• The evolving understanding of the pathophysiology of IgA vasculitis is allowing exploration of novel treatment options which target underlying immune pathways.• Novel treatments currently being trialled in IgA nephropathy may have benefit in IgA vasculitis due to the similarities in the underlying pathophysiology, such as TRF-budesonide, B-cell modulators, and complement inhibitors.• Further studies, including clinical trials of novel drugs, are urgently needed to improve the long-term outcomes for children with IgA vasculitis nephritis.

01 Apr 2023·Cell reports

BAFF and APRIL counterregulate susceptibility to inflammation-induced preterm birth

Article

Author: Cappelletti, Monica ; Wayland, Jennifer L ; Doll, Jessica R ; Wilburn, Adrienne ; Salomonis, Nathan ; Chougnet, Claire A ; Stankiewicz, Traci E ; Tilburgs, Tamara ; Divanovic, Senad ; Giordano, Daniela ; Presicce, Pietro ; Moreno-Fernandez, Maria E ; Weinhaus, Benjamin ; Kallapur, Suhas G

Clinical evidence points to a function for B cell-activating factor (BAFF) in pregnancy. However, direct roles for BAFF-axis members in pregnancy have not been examined. Here, via utility of genetically modified mice, we report that BAFF promotes inflammatory responsiveness and increases susceptibility to inflammation-induced preterm birth (PTB). In contrast, we show that the closely related A proliferation-inducing ligand (APRIL) decreases inflammatory responsiveness and susceptibility to PTB. Known BAFF-axis receptors serve a redundant function in signaling BAFF/APRIL presence in pregnancy. Treatment with anti-BAFF/APRIL monoclonal antibodies or BAFF/APRIL recombinant proteins is sufficient to manipulate susceptibility to PTB. Notably, macrophages at the maternal-fetal interface produce BAFF, while BAFF and APRIL presence divergently shape macrophage gene expression and inflammatory function. Overall, our findings demonstrate that BAFF and APRIL play divergent inflammatory roles in pregnancy and provide therapeutic targets for mitigating risk of inflammation-induced PTB.

News (Medical) associated with Zigakibart

28 May 2024

·www.fiercepharma.com

Novartis rides IgAN trioka to 2 trial wins in rare kidney diseases

Novartis is developing three drugs against the kidney disease IgAN. In recent days, the company shared updates on two of them. Novartis is eyeing an FDA filing for a second drug in immunoglobulin A nephropathy (IgAN), as the Swiss pharma goes all-in on the rare autoimmune kidney disease from three different angles. Novartis plans to submit atrasentan to the FDA by the end of June for a potential accelerated approval in IgAN based on positive data from the phase 3 ALIGN trial. In the study, atrasentan led to a significant 36.1% relative reduction in proteinuria compared with placebo after 36 weeks of treatment, according to results presented at the European Renal Association Congress. Atrasentan could be a potential competitor to Travere Therapeutics’ rival drug Filspari (sparsentan). But as analysts from William Blair and Leerink Partners suggested, the Novartis med does not seem to have the upper hand. An IgAN showdown Heading into atrasentan’s 36-week readout, investors were expecting to see at least a 40% placebo-adjusted urine protein reduction because of earlier readouts based on small patient populations and shorter treatment periods, Leerink analysts pointed out in a Monday note. The Novartis drug pulled off a 38.1% reduction in proteinuria, as measured by urine protein to creatinine ratio (UPCR), versus 3.1% for placebo. Both groups also received standard supportive care. By comparison, in the phase 3 PROTECT trial, Travere’s Filspari was associated with an average reduction in proteinuria of 49.8% after 36 weeks, compared with 15.1% for off-label irbesartan. This translates into a 41% relative reduction for Filspari. The two drugs’ trials enrolled roughly similar populations, with some slight differences such as baseline UPCR that are not likely to significantly change the outcome or interpretation of results, William Blair analysts wrote in a Tuesday note. However, a notable difference in the percentage of Asian patients might be a confounding factor for a cross-trial comparison, the team added. Despite the differences between the trials, atrasentan does not appear to be differentiated versus Filspari, Leerink’s analysts said. A recent Leerink survey suggested that doctors would split their use of Filspari and atrasentan equally. Travere’s Filspari may have two advantages. First of all, Filspari already boasts an accelerated approval in IgAN since February 2023, and Travere has already filed for a full approval with a target decision date in September. That gives Filspari a roughly two-year head start against Novartis’ atrasentan, the William Blair team noted. Secondly, Filspari could reduce the number of pills patients have to take, which is an important consideration for many with IgAN, Leerink analysts noted. Filspari is a dual endothelin angiotensin receptor antagonist, while atrasentan inhibits the endothelin A receptor alone. Filspari’s mechanism eliminates the need for an angiotensin receptor blocker such as irbesartan, which is part of the standard of care for IgAN. However, having separate pills allows doctors to adjust the dose of each therapy for a patient, the Leerink team added. In the end, “choosing between the two will likely come down to a case-by-case decision, as well as which therapy is covered by payers/has an easier path to authorization,” the Leerink analysts said. Filspari’s early launch has been progressing nicely, with about 2,000 patient start forms received by the end of March. The drug missed statistical significance on its confirmatory trial endpoint—change in estimated glomerular filtration rate (eGFR) slope, a measure of kidney function—in the PROTECT trial. But Travere believes the results observed in the study could convince the FDA and doctors of its benefits. The confirmatory evidence flop leaves a window open for Novartis’ atrasentan to potentially differentiate itself with an eGFR win. Atrasentan’s ALIGN study remains ongoing and blinded toward its final eGFR analysis, which is expected in 2026. Plus, Filspari is still only penetrating a very small corner of the IgAN at this stage, and there remains significant room for a competitor, Willima Blair analysts aid. IgAN troika Atrasentan, which Novartis believes carries blockbuster potential, is one of the three drugs that the company is advancing in IgAN. Fabhalta, an oral factor B inhibitor, recently showed a 38.3% relative proteinuria reduction versus placebo in the phase 3 APPLAUSE-IgAN trial. The drug got its initial FDA approval in December for paroxysmal nocturnal hemoglobinuria (PNH), and Novartis has filed the IgAN indication with a decision now under priority review. At the ERA Congress, Novartis also shared phase 3 results for Fabhalta in an ultra-rare kidney disease called C3 glomerulopathy. In the APPEAR-C3G study, patients who got Fabhalta achieved a 35.1% reduction in proteinuria compared with placebo after six months of treatment. Novartis plans to file for the indication based on that surrogate endpoint in the second half of this year. At this point, on the eGFR endpoint, Fabhalta showed a numerical improvement of 2.2mL/min/1.73m2. Novartis has estimated Fabhalta could reach over $3 billion in peak sales across PNH, IgAN and C3G. The IgAN candidates target the kidney disease differently, and their ultimate positioning, including sequencing or combinations, will partly be defined by the data they generate, Shreeram Aradhye, M.D., said in a January interview with Fierce Pharma. With Fabhalta, Novartis is targeting the alternative complement pathway. Overactivation of the pathway and deposition of the complement protein could cause kidney damage. So Fabhalta is intervening through that pathogenic mechanism of the injury, Aradhye explained. Atrasentan, by targeting the endothelin receptor, inhibits excess proliferation and inflammatory signaling in mesangial cells, which are involved in IgAN. The third agent, zigakibart, is a subcutaneous anti-APRIL antibody. Aradhye said the drug has the potential to be disease-modifying because it intervenes at an early stage when abnormal IgA is formed. Its phase 3 IgAN readout is expected in 2026, and Novartis also has blockbuster hopes for that drug.

Clinical ResultPhase 3Drug ApprovalAccelerated ApprovalPriority Review

25 May 2024

·www.prnewswire.com

Novartis atrasentan Phase III data show clinically meaningful proteinuria reduction further advancing company's IgA nephropathy (IgAN) portfolio

In the ALIGN study, atrasentan, in addition to supportive care with a renin-angiotensin system (RAS) inhibitor, demonstrated a statistically significant 36.1% proteinuria (protein in urine) reduction vs. placebo + supportive care at 36 weeks1 Endothelin A (ETA) receptor activation contributes to elevated proteinuria in IgAN2-5; atrasentan is a potent, selective ETA receptor antagonist with potential to reduce persistent proteinuria and preserve kidney function for a broad patient population1 IgAN is a heterogeneous, progressive, rare kidney disease with a need for effective, targeted therapies6,7; up to 30% of patients with persistent proteinuria (≥1 g/day) progress to kidney failure within 10 years8 Through its rare kidney disease portfolio, Novartis is committed to exploring a range of treatment options with different modes of action to slow IgAN progression EAST HANOVER, N.J., May 25, 2024 /PRNewswire/ -- Novartis today presented results from a pre-specified interim analysis of the Phase III ALIGN study of atrasentan, an investigational oral selective endothelin A (ETA) receptor antagonist, in patients with IgA nephropathy (IgAN)1. Patients treated with atrasentan, in addition to supportive care (maximally tolerated and stable dose of a renin-angiotensin system [RAS] inhibitor), achieved a 36.1% (p<0.0001) reduction in proteinuria (as measured by 24-hour urine protein to creatinine ratio [UPCR]) at 36 weeks when compared to placebo on top of supportive care1. The results were presented during a late-breaking clinical trials session at the European Renal Association (ERA) Congress1. The study also showed atrasentan has a favorable safety profile consistent with previously reported data1,9. Proteinuria reduction is a recognized surrogate marker correlating with delaying progression to kidney failure and has been used as an endpoint in IgAN clinical trials to support accelerated regulatory approvals10. US FDA submission for atrasentan in IgAN is on track for the first half of 2024. "For those living with IgAN and their families, the disease can have a significant impact not only physically, but also mentally. When my son Eddie was diagnosed with IgAN 20 years ago, there were no FDA-approved medicines developed to treat IgAN. That was as devastating as the diagnosis itself because we felt completely in the dark about how to manage the condition," said Bonnie Schneider, Director and Co-Founder, IgAN Foundation. "It's a disease that affects people differently, and what works for one person may not work for another. We're pleased to see ongoing research into different treatments and are excited for a future where the community will have options to meet their individual needs." The ALIGN study continues in a blinded manner, and therefore only limited interim analysis results can be presented11,12. The final analysis, including the key secondary endpoint of change from baseline in estimated glomerular filtration rate (eGFR) at 136 weeks, and the results in participants receiving a sodium-glucose co-transporter-2 (SGLT2) inhibitor as background care in an exploratory cohort, is expected in 202611,12. "ETA receptor activation causes proteinuria, which is usually one of the first clinical signs of IgAN. Patients with persistent proteinuria have a poorer prognosis and are more likely to progress to kidney failure," said Professor Hiddo Heerspink, Professor of Clinical Trials and Personalized Medicine at the Department of Clinical Pharmacy and Pharmacology at the University Medical Center Groningen and ALIGN blinded Steering Committee Chair. "We need targeted treatment options that can support patients with IgAN across the care pathway. These data from the ALIGN study further demonstrate the ability of atrasentan to significantly reduce proteinuria and, if approved, its potential to become a new foundational treatment for people living with IgAN that can be seamlessly added to current supportive therapy." "Atrasentan has the potential to help transform how IgAN is managed for many people living with this complex illness," said David Soergel, M.D., Global Head, Cardiovascular, Renal and Metabolism Development Unit, Novartis. "Our multi-product IgAN portfolio aims to address the needs of a broad, heterogenous patient population with different modes of action to target distinct drivers of the disease, with the ultimate goal of improving patient care in this therapeutic area." At ERA, Novartis is also presenting new data across its rare disease portfolio, including 6-month data for Fabhalta® (iptacopan) in C3 glomerulopathy (C3G) from the Phase III APPEAR-C3G study, long-term 33-month efficacy and safety data for Fabhalta in C3G from the Phase II extension study, additional data for Fabhalta in IgAN from the 9-month interim analysis of the Phase III APPLAUSE-IgAN study, 1-year Phase I/II data for investigational zigakibart in IgAN, and data from real-world studies in C3G and atypical hemolytic uremic syndrome (aHUS)13-16. About ALIGN The ALIGN study (NCT04573478) is a global, randomized, multicenter, double-blind, placebo-controlled Phase III clinical trial comparing the efficacy and safety of atrasentan versus placebo in patients with IgAN at risk of progressive loss of kidney function11,12. In total, 340 patients with biopsy-proven IgAN with baseline total proteinuria ≥1 g/day despite optimized RAS inhibitor treatment were randomized to receive once-daily oral doses of atrasentan (0.75 mg) or placebo for approximately 2.5 years (132 weeks)11,12. Patients continue receiving a maximally tolerated and stable dose of a RAS inhibitor as supportive care (unless they are unable to tolerate RAS inhibitor therapy)11,12. An additional group of 64 patients receiving a stable dose of SGLT2 inhibitor for at least 12 weeks have also been enrolled11,12. The primary efficacy endpoint of the study is change in proteinuria as measured by 24-hour UPCR from baseline to 36 weeks11,12. Secondary and exploratory objectives include evaluating the change in kidney function from baseline to 136 weeks as measured by eGFR, as well as safety and tolerability11,12. About atrasentan Atrasentan is an investigational potent and selective oral ETA receptor antagonist, currently in Phase III development for IgAN and early-stage development for other rare kidney diseases1,11,12,17. Activation of the ETA receptor contributes to elevated proteinuria, which is associated with kidney damage, fibrosis and loss of kidney function in IgAN2-5. Atrasentan has potential to be added to current supportive therapy to reduce persistent proteinuria and preserve kidney function for a broad patient population1. Preclinical models have also suggested that atrasentan may reduce inflammation and fibrosis in IgAN18-21. About IgA nephropathy (IgAN) IgAN is a heterogeneous, progressive, rare kidney disease6. Each year, approximately 25 people per million worldwide are newly diagnosed with IgAN22. Up to 30% of people who have IgAN with persistent higher levels of proteinuria (≥1 g/day) may progress to kidney failure within 10 years8. There is a need for effective, targeted therapies for IgAN that can help slow or prevent progression to kidney failure6,7,23. Novartis commitment in rare kidney diseases At Novartis, our journey in nephrology began more than 40 years ago when the development and introduction of cyclosporine helped reimagine the field of transplantation and immunosuppression. We continue today with the same bold ambition to transform the lives of people living with kidney diseases. Through our portfolio, we are exploring potential therapeutic options to address the current unmet needs of people living with rare diseases, including IgAN, C3G, aHUS, immune complex membranoproliferative glomerulonephritis (IC-MPGN) and lupus nephritis (LN). Innovative treatment options that target the underlying causes of these diseases may preserve kidney function and help people live longer without the need for dialysis or transplantation. IgAN is a heterogeneous disease presenting with a variety of clinical manifestations, phenotypes, and variable speeds of progression6. In addition to atrasentan, Novartis is advancing the development of two other therapies in IgAN with highly differentiated mechanisms of action: Fabhalta, an investigational oral Factor B inhibitor of the alternative complement pathway, and zigakibart, an investigational subcutaneously administered anti-APRIL monoclonal antibody, which are both in Phase III development24-26. Through our IgAN pipeline, we are committed to creating a portfolio of innovative medicines that improve and extend the lives of people living with kidney disease. Disclaimer This press release contains forward-looking statements within the meaning of the United States Private Securities Litigation Reform Act of 1995. Forward-looking statements can generally be identified by words such as "potential," "can," "will," "plan," "may," "could," "would," "expect," "anticipate," "look forward," "believe," "committed," "investigational," "pipeline," "launch," or similar terms, or by express or implied discussions regarding potential marketing approvals, new indications or labeling for the investigational or approved products described in this press release, or regarding potential future revenues from such products. You should not place undue reliance on these statements. Such forward-looking statements are based on our current beliefs and expectations regarding future events, and are subject to significant known and unknown risks and uncertainties. Should one or more of these risks or uncertainties materialize, or should underlying assumptions prove incorrect, actual results may vary materially from those set forth in the forward-looking statements. There can be no guarantee that the investigational or approved products described in this press release will be submitted or approved for sale or for any additional indications or labeling in any market, or at any particular time. Nor can there be any guarantee that such products will be commercially successful in the future. In particular, our expectations regarding such products could be affected by, among other things, the uncertainties inherent in research and development, including clinical trial results and additional analysis of existing clinical data; regulatory actions or delays or government regulation generally; global trends toward health care cost containment, including government, payor and general public pricing and reimbursement pressures and requirements for increased pricing transparency; our ability to obtain or maintain proprietary intellectual property protection; the particular prescribing preferences of physicians and patients; general political, economic and business conditions, including the effects of and efforts to mitigate pandemic diseases; safety, quality, data integrity or manufacturing issues; potential or actual data security and data privacy breaches, or disruptions of our information technology systems, and other risks and factors referred to in Novartis AG's current Form 20-F on file with the US Securities and Exchange Commission. Novartis is providing the information in this press release as of this date and does not undertake any obligation to update any forward-looking statements contained in this press release as a result of new information, future events or otherwise. A bout Novartis Novartis is an innovative medicines company. Every day, we work to reimagine medicine to improve and extend people's lives so that patients, healthcare professionals and societies are empowered in the face of serious disease. Our medicines reach more than 250 million people worldwide. Reimagine medicine with us: Visit us at and and connect with us on LinkedIn, LinkedIn US, Facebook, X/Twitter, X/Twitter US and Instagram. References Heerspink HJL, Jardine M, Kohan D, et al. ALIGN Phase 3 Primary Endpoint Analysis: Atrasentan Shows Significant Reduction in Proteinuria in Patients with IgA Nephropathy. Presented at European Renal Association (ERA) Congress; May 25, 2024; Stockholm, Sweden. Tycová I, Hrubá P, Maixnerová D, et al. Molecular Profiling in IgA Nephropathy and Focal and Segmental Glomerulosclerosis. Physiol Res. 2018;67(1):93-105. doi:10.33549/physiolres.933670 Lehrke I, Waldherr R, Ritz E, Wagner J. Renal Endothelin-1 and Endothelin Receptor Type B Expression in Glomerular Diseases with Proteinuria. J Am Soc Nephrol. 2001;12(11):2321-2329. doi:10.1681/ASN.V12112321 Zanatta CM, Veronese FV, Loreto Mda S, et al. Endothelin-1 and Endothelin A Receptor Immunoreactivity is Increased in Patients with Diabetic Nephropathy. Ren Fail. 2012;34(3):308-315. doi:10.3109/0886022X.2011.647301 Kohan DE, Barton M. Endothelin and Endothelin Antagonists in Chronic Kidney Disease. Kidney Int. 2014;86(5):896-904. doi:10.1038/ki.2014.143 Kidney Disease: Improving Global Outcomes (KDIGO) 2021 Clinical Practice Guideline for the Management of Glomerular Diseases. Kidney Int. 2021;100(4):S1-S276. doi:10.1016/j.kint.2021.05.021 Boyd JK, Cheung CK, Molyneux K, Feehally J, Barratt J. An Update on the Pathogenesis and Treatment of IgA Nephropathy. Kidney Int. 2012;81(9):833-843. doi:10.1038/ki.2011.501 Reich HN, Troyanov SAA, Scholey JW, Cattran DC. Remission of Proteinuria Improves Prognosis in IgA Nephropathy. J Am Soc Nephrol. 2007;18(12):3177-3183. doi:10.1681/ASN.2007050526 Kim SG, Inker LA, Packham DK, et al. WCN23-1126 Atrasentan for the Treatment of IgA Nephropathy: Interim Results of the AFFINITY Study. Kidney Int Rep. 2023;8(9):1902. doi:10.1016/j.ekir.2023.02.1088 Thompson A, Carroll K, Inker LA, et al. Proteinuria Reduction as a Surrogate End Point in Trials of IgA Nephropathy. Clin J Am Soc Nephrol. 2019;14(3):469-481. doi:10.2215/CJN.08600718 ClinicalTrials.gov. NCT04573478. A Phase 3, Randomized, Double-Blind, Placebo-Controlled Study of Atrasentan in Patients with IgA Nephropathy at Risk of Progressive Loss of Renal Function (ALIGN). Available from: . Accessed May 2024. Lambers Heerspink H, Jardine M, Kohan DE, et al. WCN23-1085 A Phase 3, Randomized, Double-Blind, Placebo-Controlled Study of Atrasentan in Patients with IgA Nephropathy – The ALIGN Study. Kidney Int Rep. 2023;8(3):S279-S280. doi:10.1016/j.ekir.2023.02.630. Kavanagh D, Bomback A, Vivarelli M, et al. Efficacy and Safety of Iptacopan in Patients with C3 Glomerulopathy: Results from the Phase 3 APPEAR-C3G Trial. Presented at European Renal Association (ERA) Congress; May 25, 2024; Stockholm, Sweden. Nester CM, Eisenberger U, Karras A, et al. Update to the Long-Term Safety and Efficacy of Iptacopan in C3G: 33-Month Extension Study Data from Patients Enrolled in a Phase 2 Study. Presented at European Renal Association (ERA) Congress; May 25, 2024; Stockholm, Sweden. Perkovic V, Kollins D, Papachristofi O, et al. Efficacy and Safety of Iptacopan in Patients with Primary IgA Nephropathy: Interim Analysis Results of the Phase 3 APPLAUSE-IgAN Study. Presented at European Renal Association (ERA) Congress; May 25, 2024; Stockholm, Sweden. Barratt J, Kooienga L, Agha I, et al. One Year of Zigakibart Treatment Shows Clinically Meaningful Proteinuria Reduction and Good Tolerability in a Phase 1/2 Study of IgA Nephropathy. Presented at European Renal Association (ERA) Congress; May 25, 2024; Stockholm, Sweden. ClinicalTrials.gov. NCT04573920. A Phase 2, Open-Label, Basket Study of Atrasentan in Patients with Proteinuric Glomerular Diseases (AFFINITY). Available from: . Accessed May 2024. Sasser JM, Sullivan JC, Hobbs JL, et al. Endothelin A Receptor Blockade Reduces Diabetic Renal Injury via an Anti-Inflammatory Mechanism. J Am Soc Nephrol. 2007;18(1):143-154. doi:10.1681/ASN.2006030208 Olson E, McConnell M, Ragan S, et al. MO264: Selective Endothelin A Receptor Antagonist Atrasentan Attenuates Mesangial Cell Injury, Proteinuria and Intra-Renal Proliferative, Inflammatory and Fibrotic Transcriptional Networks in a Rat Model of Mesangioproliferative Glomerulonephritis. Nephrol Dial Transplant. 2022;37:S3. doi:10.1093/ndt/gfac067.063 Cox J, Gunawan M, Wu J, et al. A Central Role of Endothelin A Receptor Activation in Mesangial Cell – Podocyte Crosstalk in IgA Nephropathy and Other Mesangio-Proliferative Glomerulopathies. Glomerular Dis. 2022;2(Suppl 1):1-78. doi:10.1159/000525410 King A, Oballa R, Gunawan M, et al. POS-378 Selective ETA Antagonist Atrasentan, Rapidly Reduces Albuminuria and Downregulates Intra-Renal Pro-Inflammatory and Pro-Fibrotic Transcriptional Networks in the gddY Mouse Model of Spontaneous IgA Nephropathy. Kidney Int Rep. 2021;6(4):S164. doi:10.1016/j.ekir.2021.03.396 McGrogan A, Franssen CF, de Vries CS. The Incidence of Primary Glomerulonephritis Worldwide: A Systematic Review of the Literature. Nephrol Dial Transplant. 2011;26(2):414-430. doi:10.1093/ndt/gfq665 Xie J, Kiryluk K, Wang W, et al. Predicting Progression of IgA Nephropathy: New Clinical Progression Risk Score. PLoS ONE. 2012;7(6):e38904. doi:10.1371/journal.pone.0038904 Novartis. Novartis completes acquisition of Chinook Therapeutics. Available from: . Accessed May 2024. Novartis. New Novartis Fabhalta® (iptacopan) data show clinically meaningful and statistically significant proteinuria reduction of 38.3% versus placebo for patients with IgA nephropathy (IgAN). Available from: . Accessed May 2024. Perkovic V, Kollins D, Renfurm R, et al. WCN24-1506 Efficacy and Safety of Iptacopan in Patients with IgA Nephropathy: Interim Results from the Phase 3 APPLAUSE-IgAN Study. Kidney Int Rep. 2024;9(4):S506. doi:10.1016/j.ekir.2024.02.1414 SOURCE Novartis Pharmaceuticals Corporation

Clinical ResultPhase 3Phase 2

25 May 2024

·www.prnewswire.com

Novartis presents latest Phase III Fabhalta® (iptacopan) data in C3 glomerulopathy (C3G) showing clinically meaningful and statistically significant 35.1% proteinuria reduction vs. placebo

Secondary endpoint data for estimated glomerular filtration rate (eGFR) showed numerical improvement over 6 months vs. placebo1; additional 6-month open-label data to be presented at a future medical meeting2,3 Fabhalta showed a favorable safety profile with no new safety signals1 C3G, an ultra-rare kidney disease caused by alternative complement pathway overactivation, progresses to kidney failure in ∼50% of patients within 10 years4-7; currently there are no treatments approved for C3G7-9 Fabhalta, an oral Factor B inhibitor of the alternative complement pathway, selectively targets the underlying cause of C3G1; late-stage development program ongoing across several other rare diseases10-13 EAST HANOVER, N.J., May 25, 2024 /PRNewswire/ -- Novartis today presented results from the 6-month, double-blind period of the Phase III APPEAR-C3G study of Fabhalta® (iptacopan) at the late-breaking clinical trials session of the European Renal Association (ERA) Congress1. Patients treated with Fabhalta in addition to supportive care achieved a 35.1% (p=0.0014) reduction in proteinuria (as measured by 24-hour urine protein to creatinine ratio [UPCR]) at 6 months when compared to placebo on top of supportive care1. In many kidney diseases, proteinuria reduction is an increasingly recognized surrogate marker correlating with delaying progression to kidney failure14,15. Fabhalta is an oral Factor B inhibitor of the alternative complement pathway being investigated in adult patients with C3 glomerulopathy (C3G)1-3. Regulatory submissions, including to the FDA and EMA, for the adult C3G indication are planned for the second half of 2024. "C3G is an overlooked and devastating illness that often strikes when people are young. The prognosis for patients with C3G is poor, and around half of the affected patients progress to kidney failure requiring dialysis or transplant within 10 years of being diagnosed," said Marianne Silkjær Nielsen, Founder of CompCure, a Danish non-profit association committed to improving outcomes for individuals with C3G and immune complex membranoproliferative glomerulonephritis (IC-MPGN). "Currently there are no therapies approved for C3G, but research into potential new treatments developed specifically for this disease gives us hope that we can improve outcomes for patients and blunt its emotional, physical and social effects." Additional data on the secondary endpoint of estimated glomerular filtration rate (eGFR), a measure of kidney function, showed a numerical improvement of +2.2 mL/min/1.73 m2 (p=0.1945) over 6 months with Fabhalta compared to placebo1. The study also showed Fabhalta has a favorable safety profile with no new safety signals1. "This is an exciting milestone for patients and the potential future management of C3G. The hallmark of C3G is overactivation of part of the immune system called the alternative complement pathway, which damages the kidneys and leads to severe loss of kidney function in many patients. Currently used treatments don't address the underlying biology of C3G and often come with significant side effects that add to the burden of the illness," said Professor David Kavanagh, Professor of Complement Therapeutics & Honorary Consultant Nephrologist at the Faculty of Medical Sciences at Newcastle University and APPEAR-C3G Steering Committee Member. "Fabhalta is the first potential treatment that targets the alternative complement pathway in C3G, and its impact on measures of kidney damage and kidney function in this study, in addition to its safety profile, is encouraging for patients and the clinical community." The APPEAR-C3G study continues with an additional 6-month, open-label period following the 6-month double-blind period, in which all patients receive Fabhalta, including those previously receiving placebo2,3. These data will be presented at an upcoming medical meeting when available.  At ERA, Novartis is also presenting new data across its rare disease portfolio, including results for investigational atrasentan in IgA nephropathy (IgAN) from the 36-week interim analysis of the Phase III ALIGN study, additional data for Fabhalta in IgAN from the 9-month interim analysis of the Phase III APPLAUSE-IgAN study, long-term 33-month efficacy and safety data for Fabhalta in C3G from the Phase II extension study, 1-year Phase I/II data for investigational zigakibart in IgAN, and data from real-world studies in C3G and atypical hemolytic uremic syndrome (aHUS)16-19. "Our ambition is to transform the care of patients living with rare kidney diseases by discovering, developing and delivering innovative treatment options," said David Soergel, M.D., Global Head, Cardiovascular, Renal and Metabolism Development Unit, Novartis. "The APPEAR-C3G results add to the growing body of evidence demonstrating Fabhalta's potential to target the underlying pathophysiological drivers and to provide clinically meaningful outcomes in a range of rare conditions." About APPEAR-C3G  APPEAR-C3G (NCT04817618) is a Phase III multicenter, randomized, double-blind, parallel group, placebo-controlled study to evaluate the efficacy and safety of twice-daily oral Fabhalta (200 mg) in C3G patients2,3. In addition to the results from adult patients with C3G, enrollment is ongoing in a separate cohort of adolescent patients with C3G2,3. The study comprises a 6-month double-blind period where adult patients were randomized 1:1 to receive Fabhalta or placebo on top of supportive care, followed by a 6-month open-label period where all patients receive Fabhalta (including those who were previously on placebo) 2,3. The primary endpoint for the double-blind period was proteinuria reduction from baseline at 6 months for Fabhalta compared to placebo as measured by 24-hour UPCR2,3. The primary endpoint for the open-label period is proteinuria reduction from baseline at 12 months for both treatment arms and proteinuria reduction from 6 to 12 months for the placebo arm2,3. Secondary endpoints for the double-blind period include change in eGFR, proportion of participants meeting composite renal endpoint criteria (≤15% reduction in eGFR and ≥50% reduction in UPCR), change in glomerular inflammation (as measured by disease total activity score in renal biopsy), change in patient reported fatigue (as measured by FACIT-Fatigue score), and safety and tolerability2,3. About Fabhalta ® (iptacopan) Fabhalta (iptacopan) is an oral, Factor B inhibitor of the alternative complement pathway1.  Discovered at Novartis, Fabhalta is currently in development for a range of rare diseases including IgAN, C3G, aHUS, IC-MPGN and lupus nephritis (LN), and, as such, the safety and efficacy profile have not been established in these indications2,11-13,20. There is no guarantee that Fabhalta will become commercially available for these indications. Fabhalta was approved by the FDA in December 2023 and the EMA in May 2024 for the treatment of adults with the rare blood disorder paroxysmal nocturnal hemoglobinuria (PNH)21,22. About C3 glomerulopathy (C3G)  C3G is an ultra-rare, progressive kidney disease that initially presents in mostly children and young adults4-6,23. Each year, approximately 1-2 people per million worldwide are newly diagnosed with C3G, a form of membranoproliferative glomerulonephritis (MPGN)4. In C3G, overactivation of the alternative complement pathway – part of the immune system – causes deposits of C3 protein to build up in kidney glomeruli (a network of blood vessels that filter waste and remove extra fluids from the blood)4,7,23-25. This triggers inflammation and glomerular damage that results in proteinuria (protein in urine), hematuria (blood in urine) and reduced kidney function4,7,23-25. Approximately 50% of C3G patients progress to kidney failure within 10 years of diagnosis, at which point they will require dialysis and/or kidney transplantation6,7, with over 55% of patients with C3G experiencing disease recurrence post-transplant26-29. Novartis commitment in rare kidney diseases At Novartis, our journey in nephrology began more than 40 years ago when the development and introduction of cyclosporine helped reimagine the field of transplantation and immunosuppression. We continue today with the same bold ambition to transform the lives of people living with kidney diseases. Through our portfolio, we are exploring potential therapeutic options to address the current unmet needs of people living with rare diseases, including IgAN, C3G, aHUS, IC-MPGN and LN. Innovative treatment options that target the underlying causes of these diseases may preserve kidney function and help people live longer without the need for dialysis or transplantation. Disclaimer This press release contains forward-looking statements within the meaning of the United States Private Securities Litigation Reform Act of 1995. Forward-looking statements can generally be identified by words such as "potential," "can," "will," "plan," "may," "could," "would," "expect," "anticipate," "look forward," "believe," "committed," "investigational," "pipeline," "launch," or similar terms, or by express or implied discussions regarding potential marketing approvals, new indications or labeling for the investigational or approved products described in this press release, or regarding potential future revenues from such products. You should not place undue reliance on these statements. Such forward-looking statements are based on our current beliefs and expectations regarding future events, and are subject to significant known and unknown risks and uncertainties. Should one or more of these risks or uncertainties materialize, or should underlying assumptions prove incorrect, actual results may vary materially from those set forth in the forward-looking statements. There can be no guarantee that the investigational or approved products described in this press release will be submitted or approved for sale or for any additional indications or labeling in any market, or at any particular time. Nor can there be any guarantee that such products will be commercially successful in the future. In particular, our expectations regarding such products could be affected by, among other things, the uncertainties inherent in research and development, including clinical trial results and additional analysis of existing clinical data; regulatory actions or delays or government regulation generally; global trends toward health care cost containment, including government, payor and general public pricing and reimbursement pressures and requirements for increased pricing transparency; our ability to obtain or maintain proprietary intellectual property protection; the particular prescribing preferences of physicians and patients; general political, economic and business conditions, including the effects of and efforts to mitigate pandemic diseases; safety, quality, data integrity or manufacturing issues; potential or actual data security and data privacy breaches, or disruptions of our information technology systems, and other risks and factors referred to in Novartis AG's current Form 20-F on file with the US Securities and Exchange Commission. Novartis is providing the information in this press release as of this date and does not undertake any obligation to update any forward-looking statements contained in this press release as a result of new information, future events or otherwise. About Novartis Novartis is an innovative medicines company. Every day, we work to reimagine medicine to improve and extend people's lives so that patients, healthcare professionals and societies are empowered in the face of serious disease. Our medicines reach more than 250 million people worldwide. Reimagine medicine with us: Visit us at and and connect with us on LinkedIn, LinkedIn US, Facebook, X/Twitter, X/Twitter US and Instagram. References Kavanagh D, Bomback A, Vivarelli M, et al. Efficacy and Safety of Iptacopan in Patients with C3 Glomerulopathy: Results from the Phase 3 APPEAR-C3G Trial. Presented at European Renal Association (ERA) Congress; May 25, 2024; Stockholm, Sweden. ClinicalTrials.gov. NCT04817618. A Multicenter, Randomized, Double-Blind, Parallel Group, Placebo-Controlled Study to Evaluate the Efficacy and Safety of Iptacopan (LNP023) in Complement 3 Glomerulopathy (APPEAR-C3G). Available from: . Accessed May 2024. Bomback AS, Kavanagh D, Vivarelli M, et al. Alternative Complement Pathway Inhibition with Iptacopan for the Treatment of C3 Glomerulopathy – Study Design of the APPEAR-C3G Trial. Kidney Int Rep. 2022;7(10):2150-2159. doi:10.1016/j.ekir.2022.07.004 Schena FP, Esposito P, Rossini M. A Narrative Review on C3 Glomerulopathy: A Rare Renal Disease. Int J Mol Sci. 2020;21(2):525. doi:10.3390/ijms21020525 Smith RJ, Alexander J, Barlow PN, et al. New Approaches to the Treatment of Dense Deposit Disease. J Am Soc Nephrol. 2007;18(9):2447-2456. doi:10.1681/ASN.2007030356 Martin B, Smith RJH. In: Adam MP, Feldman J, Mirzaa GM, et al., editors. C3 Glomerulopathy. GeneReviews® [Internet]. Updated 2018. University of Washington, Seattle; 1993-2024. Available from: . Accessed May 2024. Smith RJH, Appel GB, Blom AM, et al. C3 Glomerulopathy – Understanding a Rare Complement-Driven Renal Disease. Nat Rev Nephrol. 2019;15(3):129-143. doi:10.1038/s41581-018-0107-2 Goodship TH, Cook HT, Fakhouri F, et al. Atypical Hemolytic Uremic Syndrome and C3 Glomerulopathy: Conclusions from a "Kidney Disease: Improving Global Outcomes" (KDIGO) Controversies Conference. Kidney Int. 2017;91(3):539-551. doi:10.1016/j.kint.2016.10.005 Kidney Disease: Improving Global Outcomes (KDIGO) Glomerular Diseases Work Group. KDIGO 2021 Clinical Practice Guideline for the Management of Glomerular Diseases. Kidney Int. 2021;100(4S):S1-S276. doi:10.1016/j.kint.2021.05.021 Perkovic V, Kollins D, Renfurm R, et al. WCN24-1506 Efficacy and Safety of Iptacopan in Patients with IgA Nephropathy: Interim Results from the Phase 3 APPLAUSE-IgAN Study. Kidney Int Rep. 2024;9(4):S506. doi:10.1016/j.ekir.2024.02.1414 ClinicalTrials.gov. NCT04578834. A Multi-Center, Randomized, Double-Blind, Placebo-Controlled, Parallel Group, Phase III Study to Evaluate the Efficacy and Safety of LNP023 in Primary IgA Nephropathy Patients (APPLAUSE-IgAN). Available from: . Accessed May 2024. ClinicalTrials.gov. NCT04889430. A Multicenter, Single-Arm, Open Label Trial to Evaluate Efficacy and Safety of Oral, Twice Daily LNP023 in Adult aHUS Patients Who Are Naive to Complement Inhibitor Therapy (APPELHUS). Available from: . Accessed May 2024. ClinicalTrials.gov. NCT05755386. A Multicenter, Randomized, Double-Blind, Parallel Group, Placebo-Controlled Study to Evaluate the Efficacy and Safety of Iptacopan (LNP023) in Idiopathic Immune Complex Mediated Membranoproliferative Glomerulonephritis (IC-MPGN) (APPARENT). Available from: . Accessed May 2024. Thompson A, Carroll K, Inker LA, et al. Proteinuria Reduction as a Surrogate End Point in Trials of IgA Nephropathy. Clin J Am Soc Nephrol. 2019;14(3):469-481. doi:10.2215/CJN.08600718 Caravaca-Fontán F, Díaz-Encarnación M, Cabello V, et al. Longitudinal Change in Proteinuria and Kidney Outcomes in C3 Glomerulopathy. Nephrol Dial Transplant. 2022;37(7):1270-1280. doi:10.1093/ndt/gfab075 Heerspink HJL, Jardine M, Kohan D, et al. ALIGN Phase 3 Primary Endpoint Analysis: Atrasentan Shows Significant Reduction in Proteinuria in Patients with IgA Nephropathy. Presented at European Renal Association (ERA) Congress; May 25, 2024; Stockholm, Sweden. Perkovic V, Kollins D, Papachristofi O, et al. Efficacy and Safety of Iptacopan in Patients with Primary IgA Nephropathy: Interim Analysis Results of the Phase 3 APPLAUSE-IgAN Study. Presented at European Renal Association (ERA) Congress; May 25, 2024; Stockholm, Sweden. Nester CM, Eisenberger U, Karras A, et al. Update to the Long-Term Safety and Efficacy of Iptacopan in C3G: 33-Month Extension Study Data from Patients Enrolled in a Phase 2 Study. Presented at European Renal Association (ERA) Congress; May 25, 2024; Stockholm, Sweden. Barratt J, Kooienga L, Agha I, et al. One Year of Zigakibart Treatment Shows Clinically Meaningful Proteinuria Reduction and Good Tolerability in a Phase 1/2 Study of IgA Nephropathy. Presented at European Renal Association (ERA) Congress; May 25, 2024; Stockholm, Sweden. ClinicalTrials.gov. NCT05268289. An Adaptive, Randomized, Double-Blind, Dose Exploration, Parallel Group, Placebo Controlled, Multicenter Phase 2 Trial to Evaluate the Efficacy, Safety and Tolerability of LNP023 in Combination with Standard-of-Care with and without Oral Corticosteroids in Patients with Active Lupus Nephritis Class III-IV, +/- V. Available from: . Accessed May 2024. Novartis. Novartis receives FDA approval for Fabhalta® (iptacopan), offering superior hemoglobin improvement in the absence of transfusions as the first oral monotherapy for adults with PNH. Available from: . Accessed May 2024. Novartis. Data on File. Medjeral-Thomas NR, O'Shaughnessy MM, O'Regan JA, et al. C3 Glomerulopathy: Clinicopathologic Features and Predictors of Outcome. Clin J Am Soc Nephrol. 2014;9(1):46-53. doi:10.2215/CJN.04700513 Ravindran A, Fervenza FC, Smith RJH, Sethi S. C3 Glomerulopathy Associated with Monoclonal Ig is a Distinct Subtype. Kidney Int. 2018;94(1):178-186. doi:10.1016/j.kint.2018.01.037 Caravaca-Fontán F, Lucientes L, Cavero T, Praga M. Update on C3 Glomerulopathy: A Complement-Mediated Disease. Nephron. 2020;144(6):272-280. doi:10.1159/000507254 Servais A, Noël LH, Roumenina LT, et al. Acquired and Genetic Complement Abnormalities Play a Critical Role in Dense Deposit Disease and Other C3 Glomerulopathies. Kidney Int. 2012;82(4):454-464. doi:10.1038/ki.2012.63 Zand L, Lorenz EC, Cosio FG, et al. Clinical Findings, Pathology, and Outcomes of C3GN after Kidney Transplantation. J Am Soc Nephrol. 2014;25(5):1110-1117. doi:10.1681/ASN.2013070715 Regunathan-Shenk R, Avasare RS, Ahn W, et al. Kidney Transplantation in C3 Glomerulopathy: A Case Series. Am J Kidney Dis. 2019;73(3):316-323. doi:10.1053/j.ajkd.2018.09.002 Caravaca-Fontán F, Polanco N, Villacorta B, et al. Recurrence of Immune Complex and Complement-Mediated Membranoproliferative Glomerulonephritis in Kidney Transplantation. Nephrol Dial Transplant. 2023;38(1):222-235. doi:10.1093/ndt/gfac148 Novartis Media Relations E-mail: [email protected] Novartis Investor Relations E-mail: [email protected] SOURCE Novartis Pharmaceuticals Corporation

Clinical ResultPhase 3Phase 2Drug Approval

100 Deals associated with Zigakibart

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Indication	Highest Phase	Country/Location	Organization	Date
Glomerulonephritis, IGA	Phase 3	US	Chinook Therapeutics, Inc.	27 Jul 2023
Glomerulonephritis, IGA	Phase 3	AR	Chinook Therapeutics, Inc.	27 Jul 2023
Glomerulonephritis, IGA	Phase 3	AU	Chinook Therapeutics, Inc.	27 Jul 2023
Glomerulonephritis, IGA	Phase 3	CA	Chinook Therapeutics, Inc.	27 Jul 2023
Glomerulonephritis, IGA	Phase 3	KR	Chinook Therapeutics, Inc.	27 Jul 2023
Plasma cell myeloma refractory	Phase 2	US	Chinook Therapeutics, Inc.	15 Nov 2017
Relapse multiple myeloma	Phase 2	US	Chinook Therapeutics, Inc.	15 Nov 2017

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT03945318 (ERA2023)	Phase 1/2	Glomerulonephritis, IGA	103	Cohort 1	haorjodibo(newvzmvhqs) = ieqxxcvkue wglilegnjb (wsyovtkmwy )	-	15 Jun 2023
				Cohort 2	haorjodibo(newvzmvhqs) = dscelwktzr wglilegnjb (wsyovtkmwy )
NCT03945318 (Phase 1/2 Study of BION-1301, ASN2022)	Phase 1/2	Glomerulonephritis, IGA APRIL \| IgA \| Gd-IgA1 ... View more	20	BION-1301 450 mg IV	yxxmxxevjm(xfftbewvyt) = ynzcokclct yaicxfecoq (gmbbkayfud )	Positive	04 Nov 2022
				BION-1301 600 mg SC	yxxmxxevjm(xfftbewvyt) = xchihijccf yaicxfecoq (gmbbkayfud )
NCT03945318 (Corporate Publications) Manual	Phase 1/2	Glomerulonephritis, IGA	40	BION-1301 (450 mg Q2W IV → 600 mg Q2W SC, up to 104 weeks ‖)	ekqhzdvubt(bbzcpnevdi) = fkvbgkrfhr abfcokdmii (hqwavyemla ) View more	Positive	01 Nov 2022
				BION-1301 (600 mg Q2W de novo SC, up to 104 weeks)	ekqhzdvubt(demeyfjchm) = frtwvizcae mtyyrbmbdk (graagdilws )
NCT03945318 (Corporate Publications) Manual	Phase 1/2	Glomerulonephritis, IGA	10	BION-1301	fymxygitil(pvckxkyqcr) = hqydimirnu umvyniukwb (uhcpvpelvv ) View more	Positive	04 Nov 2021
NCT03340883 (CTgov)	Phase 1/2	Relapse multiple myeloma \| Plasma cell myeloma refractory	21	BION-1301 (BION-1301 50 mg Q2W)	hidiceuxry(zfhakqmakc) = jnagcizulc diirieqgez (pohjtrizst, ymmlsephpz - zjrmswnurp) View more	-	07 Sep 2020
				BION-1301 (BION-1301 150 mg Q2W)	hidiceuxry(zfhakqmakc) = ekcjkircgj diirieqgez (pohjtrizst, beeyueiakp - sivdysmeyn) View more
NCT03340883 (ASCO2019) Manual	Phase 1	Plasma cell myeloma refractory	15	Zigakibart	bgwztsqfob(sktcdbudfh) = none tgvnbcapkd (tharpfuppi ) View more	Negative	03 Jun 2019
BION-1301 (ASN2018)	Not Applicable	Glomerulonephritis, IGA APRIL \| BCMA \| TACI	-	BION-1301	ojpmlldvzn(vrsjxsxnnp) = ixuuithpse wtqfabzwst (dqyawiscne, 0.89) View more	Positive	23 Oct 2018

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