预约演示
更新于：2025-01-29
Tozorakimab
更新于：2025-01-29
概要
基本信息
原研机构 |
最高研发阶段临床3期 |
首次获批日期- |
最高研发阶段(中国)临床3期 |
特殊审评突破性疗法 (中国) |
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结构/序列
Sequence Code 20819666L
来源: *****
Sequence Code 616717178H
来源: *****
关联
20
项与 Tozorakimab 相关的临床试验NCT06304961
A Randomised, Single-dose, Parallel Group Study in Healthy Volunteers to Assess the Relative Bioavailability of Two Different Dosage Forms for Tozorakimab Via Subcutaneous Administration
CTIS2023-508041-40-00
- D9180C00011
CTRI/2023/09/058035
A Phase III, Multicentre, Randomised, Double blind, Parallel group, Placebo controlled Study to Evaluate the Efficacy and Safety of Tozorakimab (MEDI3506) in Patients Hospitalised for Viral Lung Infection Requiring Supplemental Oxygen (TILIA).
100 项与 Tozorakimab 相关的临床结果
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100 项与 Tozorakimab 相关的转化医学
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100 项与 Tozorakimab 相关的专利（医药）
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9
项与 Tozorakimab 相关的文献（医药）2024-07-01European Journal of Internal Medicine
Towards precision medicine in COPD: Targeting type 2 cytokines and alarmins
Review
作者: Varricchi, Gilda ; Poto, Remo
Chronic obstructive pulmonary disease (COPD) is a main global epidemic increasing as population age and affecting approximately 10% of subjects over 45 years. COPD is a heterogeneous inflammatory disease with several endo-phenotypes and clinical presentations. Although neutrophilic inflammation is canonically considered a hallmark of COPD, eosinophilic inflammation can also be present in a subgroup of patients. Several other immune cells and cytokines play a key role in orchestrating and perpetuating the inflammatory pathways in COPD, making them attractive targets for treating this disorder. Recent studies have started to evaluate the possible role of type 2 (T2) inflammation and epithelial-derived alarmins (TSLP and IL-33) in COPD. Two phase III randomized clinical trials (RCTs) showed a modest reduction in exacerbations in COPD patients with eosinophilic phenotype treated with mepolizumab (anti-IL-5) or benralizumab (anti-IL-5Rα). A phase III RCT showed a 30% reduction in exacerbations in COPD patients with ≥ 300 eosinophils/μL treated with dupilumab (anti-IL-4Rα). These results suggest that blocking a single cytokine (e.g., IL-5) or its main target (i.e., IL-5Rα) is less promising than blocking a wider spectrum of cytokines (i.e., IL-4 and IL-13) in COPD. TSLP and IL-33 are upstream regulators of T2-high and T2-low immune responses in airway inflammation. Several ongoing RCTs are evaluating the efficacy and safety of anti-TSLP (tezepelumab), anti-IL-33 (itepekimab, tozorakimab), and anti-ST2 (astegolimab) in patients with COPD, who experience exacerbations. In conclusion, targeting T2 inflammation or epithelial-derived alarmins might represent a step forward in precision medicine for the treatment of a subset of COPD.
2024-06-01Kidney International Reports
Inhibition of Interleukin-33 to Reduce Glomerular Endothelial Inflammation in Diabetic Kidney Disease
Article
作者: Selvarajah, Viknesh ; Bhat, Maria ; Baker, David ; Conway, James ; Woollard, Kevin ; Slidel, Tim ; Musial, Barbara ; Tu, Xiao ; Hofherr, Alexis ; Hansen, Pernille B L ; Heerspink, Hiddo J L ; Bartesaghi, Stefano ; Pecoits-Filho, Roberto ; Liarte Marin, Elena ; Challis, Benjamin ; Seth, Asha
Introduction:
Inflammation is a significant contributor to cardiorenal morbidity and mortality in diabetic kidney disease (DKD). The pathophysiological mechanisms linking systemic, subacute inflammation and local, kidney injury-initiated immune maladaptation is partially understood.
Methods:
Here, we explored the expression of proinflammatory cytokines in patients with DKD; investigated mouse models of type 1 and type 2 diabetes (T2D); evaluated glomerular signaling in vitro; performed post hoc analyses of systemic and urinary markers of inflammation; and initiated a phase 2b clinical study (FRONTIER-1; NCT04170543).
Results:
Transcriptomic profiling of kidney biopsies from patients with DKD revealed significant glomerular upregulation of interleukin-33 (IL-33). Inhibition of IL-33 signaling reduced glomerular damage and albuminuria in the uninephrectomized db/db mouse model (T2D/DKD). On a cellular level, inhibiting IL-33 improved glomerular endothelial health by decreasing cellular inflammation and reducing release of proinflammatory cytokines. Therefore, FRONTIER-1 was designed to test the safety and efficacy of the IL-33-targeted monoclonal antibody tozorakimab in patients with DKD. So far, 578 patients are enrolled in FRONTIER-1. The baseline inflammation status of participants (N > 146) was assessed in blood and urine. Comparison to independent reference cohorts (N > 200) validated the distribution of urinary tumor necrosis factor receptor 1 (TNFR1) and C-C motif chemokine ligand 2 (CCL2). Treatment with dapagliflozin for 6 weeks did not alter these biomarkers significantly.
Conclusion:
We show that blocking the IL-33 pathway may mitigate glomerular endothelial inflammation in DKD. The findings from the FRONTIER-1 study will provide valuable insights into the therapeutic potential of IL-33 inhibition in DKD.
2024-06-01American journal of physiology. Endocrinology and metabolism
Advancements in diabetic kidney disease management: integrating innovative therapies and targeted drug development
Review
作者: Raina, Rupesh ; Ghose, Shaarav ; Satariano, Matthew ; Shah, Raghav ; Cahill, Thomas ; Korada, Saichidroopi
Diabetic kidney disease (DKD) is a leading cause of chronic kidney disease and affects approximately 40% of individuals with diabetes . Cases of DKD continue to rise globally as the prevalence of diabetes mellitus increases, with an estimated 415 million people living with diabetes in 2015 and a projected 642 million by 2040. DKD is associated with significant morbidity and mortality, representing 34% and 36% of all chronic kidney disease deaths in men and women, respectively. Common comorbidities including hypertension and ageing-related nephron loss further complicate disease diagnosis and progression. The progression of DKD involves several mechanisms including glomerular endothelial cell dysfunction, inflammation, and fibrosis. Targeting these mechanisms has formed the basis of several therapeutic agents. Renin-angiotensin-aldosterone system (RAAS) blockers, specifically angiotensin receptor blockers (ARBs), demonstrate significant reductions in macroalbuminuria. Sodium-glucose transporter type 2 (SGLT-2) inhibitors demonstrate kidney protection independent of diabetes control while also decreasing the incidence of cardiovascular events. Emerging agents including glucagon-like peptide 1 (GLP-1) agonists, anti-inflammatory agents like bardoxolone, and mineralocorticoid receptor antagonists show promise in mitigating DKD progression. Many novel therapies including monoclonal antibodies CSL346, lixudebart, and tozorakimab; mesenchymal stem/stromal cell infusion; and cannabinoid-1 receptor inverse agonism via INV-202 are currently in clinical trials and present opportunities for further drug development.
100 项与 Tozorakimab 相关的药物交易
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研发状态
10 条进展最快的记录, 后查看更多信息
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| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 急性呼吸道感染 | 临床3期 | 美国 | 2022-12-13 | |
| 急性呼吸道感染 | 临床3期 | 中国 | 2022-12-13 | |
| 急性呼吸道感染 | 临床3期 | 日本 | 2022-12-13 | |
| 急性呼吸道感染 | 临床3期 | 阿根廷 | 2022-12-13 | |
| 急性呼吸道感染 | 临床3期 | 澳大利亚 | 2022-12-13 | |
| 急性呼吸道感染 | 临床3期 | 比利时 | 2022-12-13 | |
| 急性呼吸道感染 | 临床3期 | 巴西 | 2022-12-13 | |
| 急性呼吸道感染 | 临床3期 | 保加利亚 | 2022-12-13 | |
| 急性呼吸道感染 | 临床3期 | 加拿大 | 2022-12-13 | |
| 急性呼吸道感染 | 临床3期 | 哥伦比亚 | 2022-12-13 |
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临床结果
临床结果
适应症
分期
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RONTIER-4 (NEWS) 人工标引  | 临床2期 | - | 鏇糧遞廠鏇鏇壓繭構蓋(壓餘憲網積顧鑰網淵範) = 窪蓋願選齋範憲窪選糧 蓋鑰醖構廠範鏇簾鬱繭 (夢鏇願構鬱衊鹹膚觸餘 ) 更多 | 不佳 | 2024-09-11 | ||
临床2期 | 609 | Placebo (Placebo) | 遞淵簾鹹艱襯糧糧壓積(齋願積壓鬱鏇選製鑰廠) = 鏇衊膚窪選壓鏇鹽鬱襯 簾鹽蓋艱憲遞顧夢網窪 (鹽範衊廠鏇膚獵觸蓋獵, 糧壓網糧鹹鑰網膚製醖 ~ 獵鹹鏇壓餘觸獵襯構簾) 更多 | - | 2024-07-10 | ||
(MEDI3506 30 mg) | 遞淵簾鹹艱襯糧糧壓積(齋願積壓鬱鏇選製鑰廠) = 憲膚醖範壓醖鬱夢網醖 簾鹽蓋艱憲遞顧夢網窪 (鹽範衊廠鏇膚獵觸蓋獵, 觸壓範獵艱鑰餘鏇醖範 ~ 鹽積醖壓築蓋鏇膚鬱艱) 更多 | ||||||
临床2期 | 250 | Placebo | 衊壓艱蓋願積遞襯餘衊(鏇構獵糧網築網醖積鹽) = 顧繭遞願壓衊範蓋鬱積 選願觸鑰壓簾膚鹽積願 (衊膚鏇齋廠範壓築築齋, 窪獵襯衊繭範憲鹹醖願 ~ 鏇壓選衊獵範製簾鏇顧) 更多 | - | 2024-01-30 | ||
临床2期 | 148 | Placebo | 膚鏇餘艱膚廠構製築選(糧淵蓋願窪觸廠獵醖觸) = 夢鹹廠遞壓夢簾衊夢鹹 淵鬱獵齋鏇糧廠製憲簾 (醖遞艱餘糧獵齋顧積積, 蓋壓簾鹹淵壓鹽鹹獵觸 ~ 顧範蓋膚簾網構鬱遞廠) 更多 | - | 2023-09-28 | ||
临床2期 | 574 | 積糧餘夢願夢遞餘憲齋(製築夢築積廠鹽觸醖膚) = 鑰衊壓鹽顧範壓鏇鹹壓 簾廠繭鹽鏇糧網構範壓 (築遞鹽顧觸簾顧鹹衊醖, 775) 更多 | 积极 | 2023-06-14 | |||
N/A | - | 願壓製築顧艱壓製壓遞(鏇憲壓顧鑰夢夢夢鹹鏇) = 選艱壓鹹積範鏇鬱醖鏇 構廠積鹽積範膚築構獵 (糧窪簾鬱簾膚網糧選築, 0.008 ~ 0.062) | - | 2022-09-04 |
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