预约演示
更新于：2026-10-21
Plonmarlimab
普那利单抗
更新于：2026-10-21
概要
基本信息
原研机构 |
在研机构 |
权益机构- |
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 528352742H
来源: *****
Sequence Code 528352747L
来源: *****
关联
7
项与 普那利单抗 相关的临床试验NCT07453004
A Multicenter, Randomized, Double-Blind, Double-Dummy, Active-Controlled Phase II Clinical Study to Evaluate the Efficacy, Safety, Tolerability, Pharmacokinetics, and Immunogenicity of Punarlimab in Subjects With Acute Gouty Arthritis
NCT07208058
An Open-label, Single-arm, Multicenter, Phase III Clinical Study to Evaluate the Efficacy, Safety, and Tolerability of Plonmarlimab in Subjects With Relapsed/Refractory Rheumatic and Immunologic Disease-associated Haemophagocytic Lymphohistiocytosis (Also Known as Macrophage Activation Syndrome [MAS])
NCT07034209
An Open-label, Single-arm, Multicenter Clinical Study to Evaluate the Efficacy, Safety, Tolerability, Pharmacokinetic Characteristics, and Immunogenicity of Plonmarlimab in Subjects With Rheumatic and Immunological Disease-associated Haemophagocytic Lymphohistiocytosis (HLH) (Also Known as Macrophage Activation Syndrome (MAS))
100 项与 普那利单抗 相关的临床结果
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100 项与 普那利单抗 相关的转化医学
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100 项与 普那利单抗 相关的专利（医药）
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75
项与 普那利单抗 相关的文献（医药）2026-03-17ONCOGENE
BRD4 orchestrates the metabolic-epigenetic regulation of GM-CSF expression and secretion to drive PD-L1⁺ macrophage-mediated immune evasion in triple-negative breast cancer
Article
作者: Diao, Haizhou ; Dong, Menghao ; Chen, Jian ; Jin, Wei ; Pan, Yueyin ; Zhang, Jinguo ; Yang, Xiuwei ; Cao, Yueyue ; Chen, Jingxiong ; Han, Xinghua ; Zhang, Yan ; Shan, Benjie ; Hua, Hui
Immune checkpoint blockade targeting the PD-1/PD-L1 axis shows promise in triple-negative breast cancer (TNBC), yet durable responses are limited by immune escape. Here, we identified tumor-derived bromodomain-containing protein 4 (BRD4) as a critical mediator of tumor-associated macrophage (TAMs)-driven immune evasion in TNBC. Using syngeneic TNBC mouse models, we found that BRD4 promotes PD-L1 expression on TAMs by increasing GM-CSF production from tumor cells. Mechanistically, BRD4 binds to the GM-CSF promoter enriched with H4K8 lactylation (H4K8La) and H3K27 acetylation (H3K27Ac). BRD4 further sustains pyruvate and lactate pools via upregulation of PKM2, thereby amplifying H4K8La and H3K27Ac on the basis of modifications at the GM-CSF locus. Functionally, exogenous GM-CSF supplementation rescued impaired tumor growth and defective activation of TAMs caused by BRD4 inhibition, establishing a direct BRD4-GM-CSF-TAMs regulatory axis. Therapeutically, combined treatment with the BRD4 inhibitor JQ1 or the first bromodomain (BD1) selective inhibitor MS402 and an anti-GM-CSF antibody markedly suppressed TNBC progression and converted the tumor immune microenvironment from "cold" to "hot". In conclusion, our study reveals a previously unrecognized metabolic-epigenetic mechanism through which BRD4 drives GM-CSF-dependent TAMs activation and immune evasion in TNBC. Targeting BRD4 in combination with GM-CSF blockade represents a promising therapeutic strategy to overcome immune resistance in this aggressive breast cancer subtype.
2025-12-01Life Science Alliance
Lnk/Sh2b3 regulates initiation and severity of autoimmune insulitis and contributes to diabetes risk
Article
作者: Tenno, Mari ; Takaki, Satoshi
The Lnk/Sh2b3 adaptor protein functions as a regulatory molecule for cytokine signaling in lymphohematopoiesis. A missense variant of the LNK/SH2B3 gene is reportedly a risk variant common to several autoimmune diseases, including type 1 diabetes (T1D). However, roles of Lnk in T1D development remain elusive. We found that Lnk−/− mice showed increased susceptibility to diabetes following treatment with fairly low doses of streptozotocin, manifested by hyperglycemia and insulitis accompanied by accumulation of CD8+ T-cells and loss of pancreatic β cells. The high susceptibility of Lnk−/− mice to islet damage was abolished in crosses with Rag2−/− mice lacking lymphocytes or MyD88−/− mice carrying various defects in activation of innate immune cells. In Lnk−/− mice pancreata, dendritic cell (DC) fractions were altered and showed augmented expression of CD40 and IL-27. Treatment with anti-CD40L or anti-GM-CSF antibodies suppressed β cell damage and prevented diabetes. Thus, Lnk regulates T-cell priming and expansion via GM-CSF- and possibly IL-27-dependent activation of pancreatic DCs after islet damage.
2025-12-01Current Hematologic Malignancy Reports
The Role of Inflammation in CMML Pathobiology and Progression
Review
作者: Padron, Eric ; Neupane, Niraj
PURPOSE OF REVIEW:
Chronic myelomonocytic leukemia (CMML) is a clonal hematopoietic malignancy characterized by monocytosis and dysplasia. While mutations in genes like TET2 and SRSF2 have helped us understand its molecular foundations, the role of inflammation in driving disease behavior is becoming increasingly evident. This review explores the role of inflammation in the biology and clinical progression of CMML, with a focus on its impact on disease initiation, progression, and potential therapeutic strategies.
RECENT FINDINGS:
Recent studies have shown that inflammatory cytokines, especially IL-6, TNF-α, and IL-8, are not just bystanders but active participants in promoting clonal hematopoiesis, immune dysregulation, and bone marrow dysfunction in CMML. Patients with systemic inflammation or autoimmune conditions are at a higher risk of developing CMML, suggesting a potential causal relationship. On the therapeutic front, drugs targeting cytokine pathways, such as ruxolitinib (a JAK inhibitor) and lenzilumab (an anti-GM-CSF antibody), have shown early promise in modifying disease activity and improving symptoms. Inflammation plays a central role in CMML, from disease onset to transformation into acute leukemia. Understanding and targeting these inflammatory circuits may not only help slow disease progression but also improve quality of life for patients. As our knowledge grows, incorporating inflammation into both our diagnostic frameworks and treatment approaches will likely become standard in the care of CMML.
100 项与 普那利单抗 相关的药物交易
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研发状态
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| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 噬血细胞性淋巴组织细胞增多症 | 临床3期 | 中国 | 2025-11-21 | |
| 巨噬细胞活化综合征 | 临床3期 | 中国 | 2025-11-21 | |
| 新型冠状病毒感染 | 临床3期 | 美国 | 2020-04-11 | |
| 原发性痛风 | 临床2期 | 中国 | 2026-03-26 | |
| 类风湿关节炎 | 临床1期 | 中国 | 2020-08-06 | |
| 类风湿关节炎 | 临床1期 | 中国 | 2020-08-06 | |
| 脓毒症 | 临床申请批准 | 中国 | 2026-07-01 |
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临床结果
临床结果
适应症
分期
评价
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临床2/3期 | 149 | (TJ003234 6mg/kg (Part 1)) | 膚鏇獵鬱齋繭簾顧廠鑰(製積獵鹽襯簾淵繭願鹹) = 憲鏇淵齋構簾窪獵醖壓 願顧積構觸選構選簾淵 (艱網獵網夢鹹範獵鹽鏇, 艱製艱繭鑰遞構鹹鑰願 ~ 鑰顧襯醖蓋齋襯簾製廠) 更多 | - | 2023-05-06 | ||
Placebo (Placebo (Part 1)) | 膚鏇獵鬱齋繭簾顧廠鑰(製積獵鹽襯簾淵繭願鹹) = 簾築鹽憲淵鏇夢範齋範 願顧積構觸選構選簾淵 (艱網獵網夢鹹範獵鹽鏇, 範構鏇蓋築襯襯齋構壓 ~ 壓壓鏇觸夢製壓窪鏇醖) 更多 | ||||||
临床2/3期 | 91 | 憲鹹襯齋獵構壓衊遞鏇(顧網淵鑰獵選觸壓獵製) = 鹽網選鹹膚憲製簾壓齋 範觸製顧選選觸糧夢壓 (衊獵鹹築觸鬱簾製鏇範 ) 更多 | 积极 | 2021-08-11 | |||
Placebo | 憲鹹襯齋獵構壓衊遞鏇(顧網淵鑰獵選觸壓獵製) = 鹽構艱選築鑰窪艱糧廠 範觸製顧選選觸糧夢壓 (衊獵鹹築觸鬱簾製鏇範 ) 更多 |
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