BE-MOBILYZED: BElimumab to MOBIlise memory B-cells from secondary LYmhoid organs to improve memory B-cell HLA-specificity profiling to support delisting for transplant access in highly-sensitiZED.

开始日期2025-09-01

申办/合作机构-

NCT07138898

/ Not yet recruiting临床2期IIT

Immunosuppressant Management in Rheumatology Patients Undergoing Elective Total Shoulder Arthroplasty

The purpose of this study is to assess the incidence of rheumatologic flares, changes in pain scores (VAS), changes in functional outcomes (PROMIS), wound complications, surgical site infections, and return trips to the operating room for rheumatology patients following shoulder replacements, comparing those who stop their immunosuppressants preoperatively for the same amount of time as suggested in the literature for hip and knee arthroplasty versus those who hold the medications for a shorter period of time preoperatively.

开始日期2025-09-01

申办/合作机构

NYU Langone Health

NCT06716606

/ Recruiting临床3期

An Open Label Study to Investigate the Long-term Safety and Efficacy of Belimumab in Adults With Interstitial Lung Disease (ILD) Associated With Systemic Sclerosis (SSc) and Other Connective Tissue Diseases (CTD)

This is an open label extension (OLE) study of an ongoing randomized controlled parent clinical studies 218224 (NCT05878717) and 221672 (NCT06572384) which aim to assess the efficacy and safety of belimumab on reducing the decline in lung function in participants with interstitial lung disease associated with diffuse cutaneous systemic sclerosis (dcSSc-ILD) and interstitial lung disease associated with other connective tissue diseases (CTD-ILD), respectively. The OLE study will describe how well tolerated belimumab will be long term, and whether it might continue to slow progression of lung function decline, slow overall disease progression and improve quality of life.

开始日期2024-12-12

申办/合作机构

GSK Plc

[+1]

100 项与贝利尤单抗相关的临床结果

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100 项与贝利尤单抗相关的转化医学

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100 项与贝利尤单抗相关的专利（医药）

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1,285

项与贝利尤单抗相关的文献（医药）

2026-01-01·CURRENT OPINION IN RHEUMATOLOGY

Advances in the diagnosis and treatment of Sjögren disease

Review

作者: Karampela, Asimina I. ; Tsironis, Christos ; Mavragani, Clio P.

Purpose of review:

Sjögren disease (SjD) constitutes a diagnostic and therapeutic challenge due to its clinical heterogeneity and complex pathophysiology. This review synthesizes recent advances in diagnostics, disease stratification, and targeted therapies, highlighting their potential to optimize patient care.

Recent findings:

Emerging diagnostic approaches include advanced salivary, lacrimal, and serum biomarkers, refinements of established diagnostic tools, role of specific autoantibodies, and AI-assisted histopathology, improving early detection and risk stratification, particularly for lymphoma-prone phenotypes. Novel immunological insights have enabled phenotype-based classification, guiding the development of targeted therapies against B-cell pathways, cytokines, and co-stimulatory molecules with several agents (e.g., belimumab, ianalumab, telitacicept) showing promise in reducing disease activity scores.

Summary:

Recent advances provide a framework for precision medicine in SjD, integrating molecular and imaging biomarkers into patient selection and treatment monitoring. Clinically, this could enable earlier diagnosis, individualized risk assessment, and tailored therapy. Research priorities now include validating diagnostic innovations in diverse populations, elucidating phenotype-specific mechanisms, and conducting adequately powered, biomarker-driven trials to optimize therapeutic efficacy.

2025-12-31·RENAL FAILURE

Biological targeted therapy for lupus nephritis–the role of BLYS and APRIL

Review

作者: Yang, Xin ; Li, Longzhu ; Zeng, Ying ; Deng, Qing ; Wang, Yu ; Liu, Xiu-Juan ; Liu, Siyi ; Wen, Dan ; Zhou, Yan ; Chen, Qinkai ; Lv, Jinlei

Lupus nephritis (LN) is a frequent and serious complication of systemic lupus erythemosus (SLE). Both innate and adaptive immunity play essential roles in the initiation and progression of LN. B-lymphocyte stimulator (BLYS) and a proliferation-inducing ligand (APRIL), members of the tumor necrosis factor superfamily, bind to receptors such as B-cell activating factor receptor 3 (BR3), transmembrane activator and CAML interactor protein (TACI), and B-cell maturation antigen (BCMA). BLYS and APRIL are often overexpressed in LN, showing a positive correlation with disease activity. Therapeutic targeting of BLYS/APRIL has demonstrated efficacy in reducing LN activity. Traditional immunosuppressants often have multiple contraindications and side effects due to their broad immune-suppressing effects. Recently, B-cell-targeting agents, including rituximab, belimumab, as well as telitacicept have shown promising efficacy and reduced side effects in LN treatment. Telitacicept, a novel biological agent, has been approved firstly effective for SLE treatment in China. This review focus on the role of BLYS and APRIL in LN development and progression, alongside clinical data on the targeted therapies of above biologicals.

2025-12-01·JOURNAL OF MEDICAL ECONOMICS

Comparison of utilization and total medicare fee-for-service expenditures for subcutaneous versus intravenous versions of a select group of therapies.

Article

作者: Sarocco, Phillip ; Kardel, Peter ; Maynard, Jason ; Sheetz, Caitlin

INTRODUCTION:

Comparisons of subcutaneous (SC) and intravenous (IV) delivery of biotherapeutics in Europe have revealed differences in cost, convenience, and preference. In the US, claims-based studies comparing SC and IV delivery have been limited. This study compared resource utilization and expenditures between cohorts of patients receiving the same drug by the SC or IV route of administration (ROA) across several indications.

METHODS:

Medicare Fee-For-Service claims were compared between cohorts of patients who received SC- or IV-delivered abatacept, belimumab, daratumumab, infliximab, tocilizumab, trastuzumab/pertuzumab, or vedolizumab. For each drug, utilization rates and healthcare expenditures per service site were compared between ROAs. Observed differences in baseline characteristics were accounted for using Inverse Probability Treatment Weighting models that balanced pre-index differences between ROAs per drug. Each ROA comparison per drug and service site was weighted and conducted independently.

RESULTS:

Across seven drugs, a total sample size of 158,632 (72,820 IV; 85,812 SC) was analyzed. For most comparisons, high-spend sites were utilized at a higher rate for IV administration. In particular, all comparisons revealed more frequent hospital outpatient department utilization for the IV ROA. For five of the seven drugs, SC treatment was associated with lower mean total Medicare expenditures, with savings of up to $56,000 per patient annually. Although three SC treatments had higher medication index spend, the total spend for these drugs across sites was significantly lower for SC delivery.

LIMITATIONS:

Limitations of this study include differences in billing between the SC and IV ROAs, potential treatment selection bias, and the assumption of equivalent efficacy.

CONCLUSIONS:

To our knowledge, this study was the first and largest US Medicare claims analysis, comparing patients receiving SC or IV versions of the same therapeutic across multiple drugs and indications. Findings demonstrated that SC delivery may facilitate reduced resource utilization and expenditures across drugs and disease indications.

333

项与贝利尤单抗相关的新闻（医药）

2025-12-09

·医学界皮肤频道

皮肤红斑狼疮远不止皮肤病！诊疗全攻略来了

*仅供医学专业人士阅读参考皮肤上的自身免疫风暴撰文：易木红斑狼疮（Lupus Erythematosus，LE）是一种临床表现多样的自身免疫性疾病，是一类以皮肤损害为核心表现的自身免疫性疾病，其发病机制涉及遗传易感性、环境触发因素与免疫调节紊乱的复杂交互作用[1]。高达80%的SLE患者会出现皮肤受累，且CLE是约25%患者SLE的首发表现[2]。尽管名为“皮肤”红斑狼疮，但其对患者生活质量的影响深远，尤其在情绪健康和社会功能方面，其负担堪比高血压、2型糖尿病等严重系统性疾病[3]。近期，在JEADV期刊上发表了一篇题为“Update on cutaneous lupus erythematosus pathogenesis, diagnosis and management”的综述文章[4]，本文将根据这篇文章深入探讨CLE的定义与分型、诊断挑战及当前与未来的治疗策略。图1：文献截图 CLE的定义与临床亚型：一幅多样化的皮肤图谱 CLE的本质是机体免疫系统对自身皮肤组织产生异常应答，紫外线（UV）照射是最关键的环境诱因，可诱导角质形成细胞凋亡并释放核抗原，进而激活以Ⅰ型干扰素为核心的免疫放大环路，最终引发局部炎症与组织损伤[5,6]。目前临床最常用的分型为1981年Gilliam与Sontheimer提出的临床病理分类，该分类将CLE特异性皮损分为急性、亚急性、慢性三大类，非特异性皮损则包括血管性与非血管性表现[7]；此外，Dan Lipsker等学者还提出了按皮肤受累层次的分型方案，进一步完善了CLE的分类体系[8]。图2：皮肤红斑狼疮亚型的临床诊断标准[4] 急性皮肤红斑狼疮（Acute CLE，ACLE）：ACLE以突发的皮肤红斑为核心表现，可分为局限性与泛发性两类。局限性ACLE即典型的“蝶形红斑”，对称分布于面颊与鼻梁，皮损无瘢痕形成；泛发性ACLE则表现为全身泛发的斑丘疹，多累及躯干、四肢，且皮损会避开指关节处，部分患者可出现类似多形红斑或重症药疹的表现。ACLE与SLE的关联性极高（>90%），皮损常在SLE系统治疗后好转[7,9]。亚急性皮肤红斑狼疮（Subacute CLE，SCLE）：表现为环状或丘疹鳞屑性皮损，好发于躯干上部、颈部和上肢。约50%的SCLE患者伴发SLE，且光敏感性显著[10]。需特别关注药物诱发的SCLE，常见诱因包括质子泵抑制剂、抗肿瘤坏死因子（TNF）药物等[11]。慢性皮肤红斑狼疮（Chronic CLE，CCLE）：最常见，包含多个亚型：盘状红斑狼疮（Discoid LE, DLE）：为CCLE中最常见类型，表现为附有粘着性鳞屑和毛囊角栓的萎缩性红斑或斑块，愈后常留瘢痕，好发于头颈部。约10%—25%的DLE患者会进展为SLE[12]。冻疮样狼疮（Chilblain LE）：好发于肢端（手指、足趾、鼻尖、耳廓），皮损为疼痛性紫红色斑块或结节，遇冷加重、冬季易溃疡。与SLE关联约为20%—40%[13]。狼疮性脂膜炎（Lupus Panniculitis, LEP）：主要累及皮下脂肪，表现为疼痛性硬结，好发于面部、上肢及臀部，且常合并 DLE 皮损，与SLE关联约为20%—30%[14]。肿胀性狼疮（Lupus Tumidus, LET）：皮损为红斑性浸润斑块，好发于躯干及面部，光敏感发生率 65%～70%，无瘢痕形成，但与SLE关联性最低（<10%）[15]。值得注意的是，有学者提出不同的分类体系，例如基于皮损层次（表皮真皮交界处、真皮、皮下组织）进行分类，或提出“不确定性CLE”的概念[8]，这反映了临床实践中皮损表现的复杂性和早期诊断的挑战。诊断的迷宫：如何从“模仿者”中识别CLE？ CLE的临床表现复杂多样，易与玫瑰痤疮、特发性冻疮、扁平苔藓等多种皮肤病混淆，若误诊可能导致治疗方案偏差，因此需结合临床、病理及免疫检查进行精准鉴别[16,17]。实验室检查：包括抗核抗体（ANA）、抗dsDNA、抗ENA谱（尤其是抗Ro/SSA在SCLE中阳性率高）、补体等，主要用于评估是否伴有SLE。鉴别诊断的挑战：多种皮肤病可酷似CLE，尤其在早期或不典型时。关键的鉴别诊断包括：玫瑰痤疮：同样有面部潮红和光敏感，但常有脓疱、毛细血管扩张，且病理上无界面性皮炎和显著的基底膜增厚。值得注意的是，高达20%的酒渣鼻患者ANA可呈阳性[18]。多形性日光疹（PLE）：同为光线性疾病，但病理上真皮乳头水肿更显著，且通常缺乏CD123阳性的浆细胞样树突状细胞（pDC）浸润[19]。扁平苔藓：尤其当DLE累及头皮或黏膜时需鉴别。组织学上，DLE通常有更显著的毛囊受累、黏蛋白沉积和pDC聚集[20,21]。皮下脂膜炎样T细胞淋巴瘤（SPTCL）：与LEP在临床和病理上极易混淆。SPTCL的病理提示包括非典型淋巴细胞、脂肪组织“镶边”现象及高Ki-67增殖指数[22]。临床中遇到肢端紫癜的SLE患者时，切勿轻易诊断为“狼疮性血管炎”。研究发现，经皮损活检证实，大部分此类病例实为CLE（主要是DLE或冻疮样狼疮），而真正的狼疮性血管炎仅占极少数[23,24]。治疗策略：从基础护肤到精准靶向的阶梯 CLE 的治疗需遵循 “个体化分层” 原则，结合皮损亚型、严重程度、瘢痕风险及是否合并 SLE 制定方案，同时重视基础防护，目前临床已形成“基础防护－一线治疗 - 二线三线治疗 - 生物制剂/新兴疗法” 的阶梯式治疗体系[25,26]。 1 基础与一线治疗一般措施：严格防晒（物理遮挡+广谱防晒霜）是基石。戒烟、补充维生素D（CLE患者常缺乏且维生素D具有光保护作用）同样重要[27-29]。局部治疗：外用强效糖皮质激素或钙调神经磷酸酶抑制剂（如他克莫司），适用于轻度、局限性皮损[30]。全身治疗基石——抗疟药：羟氯喹（HCQ）是系统性治疗的一线选择。若疗效不佳，可换用氯喹或联合奎纳克林，或根据血药浓度调整HCQ剂量[31,32]。有趣的是，近期研究提示，早期启用HCQ可能降低CLE进展为SLE的风险[33]。 2 二线与三线治疗当抗疟药效果不足时，需根据是否伴发SLE选择后续治疗。图3：根据是否存在系统性红斑狼疮伴发情况对皮肤红斑狼疮（CLE）进行治疗管理传统免疫抑制剂：甲氨蝶呤和霉酚酸酯是有效的二线选择，尤其对SCLE和DLE[34]。沙利度胺及其类似物来那度胺疗效显著，但因神经毒性、血栓风险等副作用需谨慎使用[35,36]。氨苯砜对SCLE和DLE有效，且是妊娠期可选药物之一[37]。生物制剂（主要适用于伴发SLE的CLE）：贝利尤单抗：靶向B细胞激活因子（BAFF），可改善SLE整体活动度及部分皮肤黏膜损害[38]。 Anifrolumab：靶向Ⅰ型干扰素受体，在SLE的Ⅲ期试验（TULIP）中显示出快速且显著的皮损改善效果，对包括冻疮样狼疮、LEP在内的多种难治性CLE亚型有效[39-41]。 3 新兴与靶向治疗：未来已来基于对CLE发病机制，尤其是Ⅰ型干扰素通路核心作用的深入理解，一系列新型靶向药物正在研发中[42,43]。靶向浆细胞样树突状细胞（pDC）：如Litifilimab（抗BDCA2）在Ⅱ期试验中显著降低皮损活动度[44]，其Ⅲ期研究正在进行。靶向TLR7/8通路：如Enpatoran，通过抑制TLR7/8信号，在Ⅱ期试验中表现出高应答率[45]。靶向JAK/STAT通路：如德卡伐替尼（TYK2抑制剂）在CLE的Ⅱ期试验中显示出优于安慰剂的疗效[46]。其他靶点：包括靶向IRAK4（如Edecesertib）[47]、通过调节蛋白质降解发挥作用的Iberdomide[48]等，均在临床试验中展现出潜力。结论皮肤红斑狼疮远非简单的“皮肤病”，它是一个涉及复杂免疫失调、具有多种临床表现的疾病实体。准确地分类和细致地鉴别诊断是成功管理的第一步。治疗策略已从传统的抗疟药和免疫抑制剂，迈向以I型干扰素通路为核心的精准靶向时代。随着对疾病机制认识的不断加深和大量新型药物的临床开发，CLE患者正迎来更有效、更安全的治疗前景。临床医生需保持知识更新，为患者提供个体化、分层管理的综合治疗方案。参考文献： [1]Wenzel J, Zahn S, Tüting T. Pathogenesis of cutaneous lupus erythematosus: common and different features in distinct subsets. Lupus. 2010;19(9):1020–8. [2]Yell JA, Mbuagbaw J, Burge SM. Cutaneous manifestations of systemic lupus erythematosus. Br J Dermatol 1996;135:355–62. [3]Bouaziz J D , Barete S , Le Pelletier F ,et al.Cutaneous lesions of the digits in systemic lupus erythematosus: 50 cases[J].lupus, 2007, 16(3):163-167. [4]François Chasset,et al.Update on cutaneous lupus erythematosus pathogenesis, diagnosis and management[J].Journal of the European Academy of Dermatology and VenereologyEarly View.First published: 02 December 2025. [5]Lauffer F, Jargosch M, Krause L, et al. Type I immune response induces keratinocyte necroptosis and is associated with interface dermatitis[J]. J Invest Dermatol, 2018, 138(8):1785-1794. [6]Wenzel J. Cutaneous lupus erythematosus: new insights into pathogenesis and therapeutic strategies[J]. Nat Rev Rheumatol, 2019, 15(9):519-532. [7]Gilliam JN, Sontheimer RD. Distinctive cutaneous subsets in the spectrum of lupus erythematosus[J]. J Am Acad Dermatol, 1981, 4(4):471-475. [8]Lipsker D. The need to revisit the nosology of cutaneous lupus erythematosus: the current terminology and morphologic classification of cutaneous LE: difficult, incomplete and not always applicable[J]. Lupus, 2010,19(9):1047-1049. [9]Biazar C, Sigges J, Patsinakidis N, et al. Cutaneous lupus erythematosus: first multicenter database analysis of 1002 patients from the European Society of Cutaneous Lupus Erythematosus (EUSCLE)[J]. Autoimmun Rev, 2013, 12(3):444-454. [10]R D,Sontheimer,J R,et al.Subacute cutaneous lupus erythematosus: a cutaneous marker for a distinct lupus erythematosus subset.[J].Archives of dermatology, 1979,115(12):1409-15. [11]Kawka L , Mertz P , Chasset F ,et al.Characterization of drug-induced cutaneous lupus: Analysis of 1994 cases using the WHO pharmacovigilance database[J].Autoimmunity Reviews, 2020, 20(1):102705. [12]Callen J P .Chronic cutaneous lupus erythematosus. Clinical, laboratory, therapeutic, and prognostic examination of 62 patients.[J].Archives of Dermatology, 1982, 118(6):412-6. [13]Callen J P .Chronic cutaneous lupus erythematosus. Clinical, laboratory, therapeutic, and prognostic examination of 62 patients.[J].Archives of Dermatology, 1982, 118(6):412-6. [14]Tuffanelli DL. Lupus erythematosus panniculitis (profundus). Arch Dermatol. 1971;103(3):231–42. [15]Kuhn A, Richter-Hintz D, Oslislo C, et al. Lupus erythematosus tumidus—a neglected subset of cutaneous lupus erythematosus: report of 40 cases[J]. Arch Dermatol, 2000, 136(8):1033-1041. [16]Chasset F, Richez C, Martin T, Belot A, Korganow AS, Arnaud L. Rare diseases that mimic systemic lupus erythematosus (lupus mimickers). Joint Bone Spine. 2019;86(2):165–71. [17]Obermoser G, Sontheimer RD, Zelger B. Overview of common, rare and atypical manifestations of cutaneous lupus erythematosus and histopathological correlates. Lupus. 2010;19(9):1050–70. [18]Lazaridou E, Apalla Z, Sotiraki S, Ziakas NG, Fotiadou C, Ioannides D. Clinical and laboratory study of rosacea in northern Greece. J Eur Acad Dermatol Venereol. 2010;24(4):410–4. [19]Wackernagel A, Massone C, Hoefler G, Steinbauer E, Kerl H, Wolf P. Plasmacytoid dendritic cells are absent in skin lesions of polymorphic light eruption. Photodermatol Photoimmunol Photomed. 2007;23(1):24–8. [20]Bolduc C, Sperling LC, Shapiro J. Primary cicatricial alopecia: lymphocytic primary cicatricial alopecias, including chronic cutaneous lupus erythematosus, lichen planopilaris, frontal fibrosing alopecia, and Graham-little syndrome. J Am Acad Dermatol. 2016;75(6):1081–99. [21]Kolivras A, Thompson C. Clusters of CD123+ plasmacytoid dendritic cells help distinguish lupus alopecia from lichen planopilaris.J Am Acad Dermatol. 2016;74(6):1267–9. [22]LeBlanc RE, Tavallaee M, Kim YH, Kim J. Useful parameters for distinguishing subcutaneous panniculitis-like T-cell lymphoma from lupus erythematosus panniculitis. Am J Surg Pathol. 2016;40(6):745–54. [23]Bouaziz JD, Barete S, Le Pelletier F, Amoura Z, Piette JC, Francès C. Cutaneous lesions of the digits in systemic lupus erythematosus: 50 cases. Lupus. 2007;16(3):163–7. [24]Breillat P, Jachiet M, Ditchi Y, Lenormand C, Costedoat-Chalumeau N, Mathian A, et al. Cutaneous vasculitis occurring in the setting of systemic lupus erythematosus: a multicentre cohort study.Rheumatology (Oxford). 2023;62(6):2189–96. [25]O'Kane D, McCourt C, Meggitt S, D'Cruz DP, Orteu CH, Benton E, et al. British Association of Dermatologists guidelines for the management of people with cutaneous lupus erythematosus 2021. Br J Dermatol. 2021;185(6):1112–23. [26]Kuhn A, Aberer E, Bata-Csörgő Z, Caproni M, Dreher A, Frances C, et al. S2k guideline for treatment of cutaneous lupus erythematosus—guided by the European dermatology forum (EDF) in cooperation with the European academy of dermatology and venereology (EADV). J Eur Acad Dermatol Venereol. 2017;31(3):389–404. [27]Scott JF, Das LM, Ahsanuddin S, Qiu Y, Binko AM, Traylor ZP, et al. Oral vitamin D rapidly attenuates inflammation from sunburn: an interventional study. J Invest Dermatol. 2017;137(10):2078–86. [28]Heine G, Lahl A, Müller C, Worm M. Vitamin D deficiency in patients with cutaneous lupus erythematosus is prevalent throughout the year. Br J Dermatol. 2010;163(4):863–5. [29]Cutillas-Marco E, Marquina-Vila A, Grant WB, Vilata-Corell JJ, Morales-Suárez-Varela MM. Vitamin D and cutaneous lupus erythematosus: effect of vitamin D replacement on disease severity. Lupus. 2014;23(7):615–23. [30]Tzung TY, Liu YS, Chang HW. Tacrolimus vs. clobetasol propionate in the treatment of facial cutaneous lupus erythematosus: a randomized, double-blind, bilateral comparison study. Br J Dermatol. 2007;156(1):191–2. [31]Chasset F, Arnaud L, Jachiet M, Monfort JB, Bouaziz JD, Cordoliani F, et al. Changing antimalarial agents after inefficacy or intolerance in patients with cutaneous lupus erythematosus: a multicenter observational study. J Am Acad Dermatol. 2018;78(1):107–114.e1. [32]Chasset F, Arnaud L, Costedoat-Chalumeau N, Zahr N, Bessis D, Francès C. The effect of increasing the dose of hydroxychloroquine (HCQ) in patients with refractory cutaneous lupus erythematosus (CLE): an open-label prospective pilot study. J Am Acad Dermatol. 2016;74(4):693–699.e3. [33]Bar D, Baum S, Segal Z, Barzilai A, Druyan A, Lidar M. Early initiation of hydroxychloroquine in cutaneous lupus erythematosus to prevent progression to systemic lupus erythematosus: a long-term follow-up study. J Am Acad Dermatol. 2025;25:S0190. [34]Keyes E, Jobanputra A, Feng R, Grinnell M, Vazquez T, Diaz D, et al. Comparative responsiveness of cutaneous lupus erythematosuspatients to methotrexate and mycophenolate mofetil: a cohort study. J Am Acad Dermatol. 2022;87(2):447–8. [35]Chasset F, Tounsi T, Cesbron E, Barbaud A, Francès C, Arnaud L. Efficacy and tolerance profile of thalidomide in cutaneous lupus erythematosus: a systematic review and meta-analysis. J Am Acad Dermatol. 2017;78(2):342–50. [36]Aitmehdi R, Arnaud L, Francès C, Senet P, Monfort JB, de Risi Pugliese T, et al. Long-term efficacy and safety outcomes of lenalidomide for cutaneous lupus erythematosus: a multicenter retrospective observational study of 40 patients. J Am Acad Dermatol. 2020;84(4):1171–4. [37]Klebes M, Wutte N, Aberer E. Dapsone as second-line treatment for cutaneous lupus erythematosus? A retrospective analysis of 34 patients and a review of the literature. Dermatology. 2016;232(1):91–6. [38]Manzi S, Sánchez-Guerrero J, Yokogawa N, Wenzel J, Ocran-Appiah JC, Harris JH, et al. The effect of belimumab on mucocutaneous and vasculitis manifestations in patients with systemic lupus erythematosus: a large pooled post hoc analysis. Lupus. 2025;34(7):666–78. [39]Chasset F, Jaume L, Mathian A, Abisror N, Dutheil A, Barbaud A, et al. Rapid efficacy of anifrolumab in refractory cutaneous lupus erythematosus. J Am Acad Dermatol. 2023;89:171–3. [40]Woodbury MJ, Smith KN, Smith JS, Merola JF. Anifrolumab for the treatment of refractory chilblain lupus erythematosus. JAAD Case Rep. 2024;48:69–71. [41]Maeshima K, Abe T, Imada C, Ozaki T, Shibata H. Anifrolumab for refractory lupus erythematosus panniculitis in systemic lupus erythematosus. Rheumatology (Oxford). 2024;63:e115–e117. [42]Lim D, Kleitsch J, Werth VP. Emerging immunotherapeutic strategies for cutaneous lupus erythematosus: an overview of recent phase 2 and 3 clinical trials. Expert Opin Emerg Drugs. 2023;28(4):257–73. [43]Xie L, Lopes Almeida Gomes L, Stone CJ, Faden DF, Werth VP. An update on clinical trials for cutaneous lupus erythematosus. J Dermatol. 2024;51(7):885–94. [44]Werth VP, Furie RA, Romero-Diaz J, Navarra S, Kalunian K, van Vollenhoven RF, et al. Trial of anti-BDCA2 antibody Litifilimab for cutaneous lupus erythematosus. N Engl J Med. 2022;387(4):321–31. [45]Pearson D, Morand E, Wenzel J, Furie R, Dall'Era M, SanchezGuerrero J, et al. Randomized, placebo-controlled phase ii study of Enpatoran, a small molecule toll-like receptor 7/8 inhibitor, in cutaneous lupus erythematosus: results from cohort a. J Rheumatol. 2025;52(1):11–8. [46]Merola JF, Gottlieb AB, Aranow C, Chasset F, Wenzel J, Fiorentino D, et al. POS0781 efficacy and safety of oral deucravacitinib in patients with cutaneous manifestations of lupus erythematosus: results from paisley cle, a global, randomized, placebo-controlled, phase 2 trial. Ann Rheum Dis. 2025;84:940–1. [47]Ammann SE, Cottell JJ, Wright NE, Warr MR, Snyder CA, Bacon EM, et al. Discovery of edecesertib (GS-5718): a potent, selective inhibitor of IRAK4. J Med Chem. 2025;68(11):10619–30. [48]Merrill JT, Werth VP, Furie R, van Vollenhoven R, Dörner T, Petronijevic M, et al. Phase 2 trial of Iberdomide in systemic lupus erythematosus. N Engl J Med. 2022;386(11):1034–45. 责任编辑：大晨 *"医学界"力求所发表内容专业、可靠，但不对内容的准确性做出承诺；请相关各方在采用或以此作为决策依据时另行核查。 ↓↓↓点击「阅读原文」学习更多临床技能

临床研究

2025-12-09

·和祐健康

被这类疾病困扰？国产创新药伏欣奇拜单抗带来新选择！

痛风急性发作时的疼痛的剧烈程度，让很多患者难以忍受，且病情容易反复，长期下来不仅会损伤关节，还可能对心脏、肾脏等器官造成影响。目前我国痛风患者已超 1600万人，不少患者需要长期依靠口服药物缓解症状，但部分药物可能会引起胃肠不适、肝肾损伤等不良反应，还有些患者用药后效果不佳，治疗需求未能得到充分满足。如今，国产创新药「伏欣奇拜单抗」已获批上市，无疑为痛风患者带来了新的治疗选择！ *本文正文为药物科普，不以药品销售为目的。药物为处方药，请在医生指导下使用。 1 什么是国产创新药「伏欣奇拜单抗」？「伏欣奇拜单抗」（商品名：金蓓欣）是我国自主研发的新型生物药，2025 年正式通过国家药品监督管理局批准上市，也是目前国内唯一获批用于治疗急性痛风性关节炎的 1 类创新药。伏欣奇拜单抗是抗 IL-1β 单克隆抗体，并非直接降尿酸药物，其核心作用是：抑制 IL-1β 介导的炎症反应，减少痛风急性发作频率、缓解慢性痛风性关节炎症状（如关节红肿热痛、滑膜炎）。不直接降低血尿酸水平，无法替代降尿酸药物对尿酸盐结晶沉积的 “根源性控制”。图源网络 2 「伏欣奇拜单抗」有什么突出的作用？相比传统痛风治疗药物，「伏欣奇拜单抗」的优势显著，主要体现在以下 4 个方面： 01 长效便捷：一年两针，无需每日用药； 02 快速镇痛：6-72 小时起效，止痛效果与激素相当； 03 大幅降低复发风险：半年内复发风险下降 87%； 04 安全性更优：适合合并慢性病患者。图源网络 3 「伏欣奇拜单抗」有什么突出的优势？机制创新：传统药物多以缓解急性期疼痛为主，无法从根源控制炎症；而「伏欣奇拜单抗」精准作用于痛风炎症的核心因子 IL-1β，减少痛风急性发作频率、缓解慢性痛风性关节炎症状（如关节红肿热痛、滑膜炎）。疗效创新：它是国内首个获批痛风适应症的 IL-1β 单抗，此前同类药物多依赖进口；其 III 期临床数据显示，复发风险降低幅度、药效维持时间均达到国际同类药物先进水平，且基于中国患者的研究数据更贴合国内临床需求。方案创新：传统痛风治疗需要每日服药、定期复诊，患者依从性较差，而 “一年两针” 的长效给药方案，大幅提升了用药便利性，避免因漏服导致病情反复。指南认可：2024 年更新的《中国高尿酸血症与痛风诊疗指南》已纳入「伏欣奇拜单抗」的 III 期临床证据，明确推荐其用于痛风反复发作、常规治疗无效的患者，成为临床权威治疗方案之一。 4 「伏欣奇拜单抗」适用于哪些人群？ 01 对秋水仙碱、非甾体抗炎药等传统药物存在禁忌，或服用后出现不耐受反应的患者； 02 长期使用传统药物治疗，但痛风仍频繁发作，或疼痛无法有效缓解的患者； 03 因合并高血压、糖尿病、骨质疏松等疾病，不适合长期使用激素治疗的患者。 ⚠️需特别注意：活动性感染、结核病患者需慎用；用药前建议接种肺炎/流感疫苗；该药物需在医生指导下进行皮下注射，每次注射间隔不少于8周。痛风并非“忍忍就过”的小病，长期反复的炎症会逐渐损伤关节、心脏、肾脏等重要器官，严重影响生活质量。「伏欣奇拜单抗」的上市，不仅为传统治疗效果不佳、不耐受的患者提供了长效控炎的新选择，也标志着我国痛风治疗进入精准靶向、长效管理的新阶段。如果您或身边的人正被痛风反复困扰，担心传统药物的副作用，或觉得每日服药不便，可咨询风湿免疫科医生，评估是否适合这款国产创新药。需要注意的是，任何药物的使用都需遵循医嘱，具体用药方案需结合个人病情、病史综合判断，切勿自行决定。愿每一位痛风患者都能摆脱疼痛困扰，重拾高质量生活！和祐医院风湿免疫科和祐医院风湿免疫科以“精准诊疗、特色技术、全程守护”为核心理念，专注风湿免疫疾病的前沿诊疗与科研突破，致力于为患者提供与国际接轨的个体化治疗方案。科室聚焦难治性疾病，融合创新技术与多学科协作，打造“少痛苦、高疗效”的诊疗体验，助力患者重获健康生活。目前医院可为患者提供各种免疫相关疾病常用的生物制剂或其他治疗药物，如：痛风性关节炎：伏欣奇拜单抗、多替诺雷等；类风湿关节炎：阿达木单抗、托珠单抗、益赛普、依那西普、乌帕替尼、巴瑞替尼等；强直性脊柱炎：依奇珠单抗、司库奇尤单抗等；系统性红斑狼疮：贝利尤单抗、泰它西普等。专家咨询本文作者>>>风湿免疫科 | 梁碧波（主治医师）本文指导>>>风湿免疫科 | 于清宏（主任医师）（因患者个体存在差异，治疗效果也因人而异，具体请咨询专业医生）

2025-12-09

·聊聊DFPP的那些事

【系统性红斑狼疮（SLE）】2023年ASFA—美国单采学会指南（五十五）

一、基本概述系统性红斑狼疮（SLE）是一种病情异质性强的系统性自身免疫病，约70%患者呈“缓解-复发”交替病程，30%患者病情持续活动（分为长期缓解与持续活动型）。疾病累及多器官系统（如肾脏、血液、皮肤、神经系统等），临床表现复杂，可导致显著的发病率和死亡率。狼疮性肾炎（LN）是SLE的核心并发症，约50%患者以LN为首发表现，其中III/IV+V型LN（尤其是伴肾小球毛细血管内增生、新月体形成或肾功能快速恶化者）预后较差，需强化治疗。二、治疗目标与核心原则SLE治疗需兼顾长期生存、器官功能保护及生活质量提升，核心目标包括：1. 诱导缓解：控制疾病活动，减少器官损伤；2. 维持缓解：预防复发，降低 flare 风险；3. 最小化治疗毒性：平衡免疫抑制强度与感染、并发症风险。儿童SLE治疗原则与成人一致，需根据病情活动度、器官受累程度个体化制定方案。三、常规治疗方案1. 基础药物：● 糖皮质激素：泼尼松等为一线药物，用于快速控制炎症，但长期使用需警惕副作用（如感染、骨质疏松）；● 免疫抑制剂：包括霉酚酸酯、硫唑嘌呤、甲氨蝶呤、环孢素、他克莫司等，用于维持缓解或对激素不耐受者；● 生物制剂：贝利尤单抗（靶向B细胞激活因子BAFF）是首个获批用于SLE的生物制剂，2019年扩展至儿童患者；阿尼鲁单抗（靶向I型干扰素受体）2021年获批用于中重度SLE，需结合SLEDAl评分（>10分提示高疾病活动度）评估。2. 治疗方案选择依据：● SLEDAI评分：通过16项指标评估9个器官系统的活动度，得分越高提示疾病活动度越强；● BILAG指数：按“改善（1）、相同（2）、恶化（3）或新发（4）”分级评估器官受累变化，指导方案调整。四、治疗性血浆置换（TPE）的应用1. 作用机制： TPE通过体外循环去除致病性自身抗体（如抗dsDNA、抗磷脂抗体）、免疫复合物及炎症介质（如补体、细胞因子），短期内快速降低血清中病理成分浓度，理论上可控制疾病活动。2. 疗效争议：● 早期研究：小样本试验显示，TPE联合免疫抑制剂可使74%患者病情改善，13%稳定，13%进展；● 随机对照试验（RCT）：6项针对LN及中枢神经系统受累的RCT显示，TPE+免疫抑制剂组仅18%患者病情改善，且荟萃分析（18项RCT，457例患者）未能证实TPE在LN治疗中的明确获益；● 特殊情况：TPE在血栓性微血管病（TMA）、严重难治性LN（如弥漫性增生性肾炎伴肾功能急剧恶化）及 catastrophic抗磷脂综合征（CAPS）中可能有一定价值，但证据等级有限。3. 技术参数：● 血浆处理量：1-1.5倍血浆容量（TPV）；● 置换液：以白蛋白、血浆为主；● 频率：SLE患者通常隔日或每两日1次，严重病例可增至每周3次。4. 适应症与局限性：● 适应症：目前TPE主要用于SLE合并TMA、CAPS、严重难治性LN（对常规治疗无反应）等情况，作为“挽救性治疗”；● 局限性：缺乏高质量循证证据（多数研究为小样本或病例报告），且TPE可能增加感染、低血压等风险，不推荐作为常规一线治疗。五、疾病活动度评估工具1. SLEDAI（SLE疾病活动指数）：通过16项指标评估9个器官系统的活动度，得分越高提示疾病活动度越强；2. BILAG（英国狼疮评估组指数）：按“改善（1）、相同（2）、恶化（3）或新发（4）”分级评估器官受累变化，指导方案调整。六、研究进展与未来方向1. 生物制剂：除贝利尤单抗、阿尼鲁单抗外，靶向B细胞、I型干扰素通路的新型药物正在临床试验中；2. 个体化治疗：基于基因分型、免疫表型的精准治疗策略逐步探索；3. TPE的再定位：需更多高质量研究明确其在特定亚型（如CAPS、TMA合并SLE）中的价值，未来可能作为“难治性病例的辅助治疗”而非广谱方案。七、结论SLE治疗需以控制疾病活动、保护器官功能为核心，常规方案（激素+免疫抑制剂+生物制剂）为基础，TPE仅作为特定难治性并发症的“挽救性选择”。临床决策需结合SLEDAI、BILAG等评估工具，平衡疗效与安全性，未来需通过精准医学进一步优化治疗策略。

临床研究

100 项与贝利尤单抗相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D03068	贝利尤单抗	L04AA26	DB08879

研发状态

批准上市

10 条最早获批的记录,

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适应症	国家/地区	公司	日期
狼疮性肾炎	欧盟	GlaxoSmithKline Trading Services Ltd.	2011-07-13
狼疮性肾炎	冰岛	GlaxoSmithKline Trading Services Ltd.	2011-07-13
狼疮性肾炎	列支敦士登	GlaxoSmithKline Trading Services Ltd.	2011-07-13
狼疮性肾炎	挪威	GlaxoSmithKline Trading Services Ltd.	2011-07-13
系统性红斑狼疮	美国	GlaxoSmithKline LLC	2011-03-09

未上市

10 条进展最快的记录,

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适应症	最高研发状态	国家/地区	公司	日期
系统性硬皮病	临床3期	美国	GSK Plc	2024-12-12
系统性硬皮病	临床3期	中国	GSK Plc	2024-12-12
系统性硬皮病	临床3期	日本	GSK Plc	2024-12-12
系统性硬皮病	临床3期	阿根廷	GSK Plc	2024-12-12
系统性硬皮病	临床3期	澳大利亚	GlaxoSmithKline (Ireland) Ltd.	2024-12-12
系统性硬皮病	临床3期	比利时	GlaxoSmithKline (Ireland) Ltd.	2024-12-12
系统性硬皮病	临床3期	巴西	GlaxoSmithKline (Ireland) Ltd.	2024-12-12
系统性硬皮病	临床3期	丹麦	GlaxoSmithKline (Ireland) Ltd.	2024-12-12
系统性硬皮病	临床3期	芬兰	GlaxoSmithKline (Ireland) Ltd.	2024-12-12
系统性硬皮病	临床3期	法国	GlaxoSmithKline (Ireland) Ltd.	2024-12-12

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临床结果

适应症

分期

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研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


NCT05917288 (CTgov)	临床1期	系统性红斑狼疮	16	Belimumab (Belimumab 200 mg/mL Every Week)	積衊鏇壓願壓鏇蓋淵糧(製獵糧網衊廠鏇鑰淵範) = 夢鹹廠夢顧築顧淵艱積繭壓襯齋築鹹壓襯艱選 (憲襯齋廠顧窪醖構夢衊, 27.50) 更多	-	2025-11-14
				Belimumab (Belimumab 200 mg/mL Every 10 Days)	蓋鏇淵製廠獵顧築鬱鏇(衊製選鹽構鹽鏇淵網窪) = 襯鑰壓範窪膚網憲艱繭淵襯淵壓糧廠廠壓鏇築 (糧壓鑰獵餘簾齋廠積膚, 17.44) 更多
NCT04515719 (Ann Rheum Dis) 人工标引	临床4期	系统性红斑狼疮	231	BelimumabBelimumab 120 mg + SOC	憲鹹餘繭築糧鹹顧觸蓋(選鏇壓膚築繭構範遞襯) = 鬱艱遞壓襯觸構製衊餘積廠憲製膚繭艱憲範襯 (廠糧築遞窪艱簾選膚築 ) 达到更多	积极	2025-11-06
				Placebo (saline) + SOC	憲鹹餘繭築糧鹹顧觸蓋(選鏇壓膚築繭構範遞襯) = 鹽淵窪鬱選選鹹繭鑰壓積廠憲製膚繭艱憲範襯 (廠糧築遞窪艱簾選膚築 ) 达到更多
NCT04515719 (Pubmed \| Ann Rheum Dis)	临床4期	系统性红斑狼疮	231	Low-dose belimumab	夢鬱鹽糧糧餘衊鬱齋膚(積憲襯積鹹廠遞鹹選積) = 衊顧糧選獵蓋夢艱簾夢繭廠獵築憲夢襯鹹顧窪 (憲淵衊鏇膚築鏇觸艱鹹 ) 更多	积极	2025-11-01
				Placebo (saline)	夢鬱鹽糧糧餘衊鬱齋膚(積憲襯積鹹廠遞鹹選積) = 遞範網構鏇淵鹹衊觸獵繭廠獵築憲夢襯鹹顧窪 (憲淵衊鏇膚築鏇觸艱鹹 ) 更多
NCT04515719 (ACR2025) 人工标引	临床4期	系统性红斑狼疮	231	BelimumabBelimumab 120mg + Standard of Care	簾積範壓憲遞廠遞艱夢(膚夢築蓋觸餘觸鑰選夢) = 艱壓憲鹽遞廠觸網範構繭選膚鑰齋獵艱觸壓簾 (遞鬱觸鏇廠夢廠憲遞觸 ) 达到更多	积极	2025-10-24
				Placebo + Standard of Care	簾積範壓憲遞廠遞艱夢(膚夢築蓋觸餘觸鑰選夢) = 鹽夢糧範襯淵鏇範膚選繭選膚鑰齋獵艱觸壓簾 (遞鬱觸鏇廠夢廠憲遞觸 ) 达到更多
ACR2025	N/A	系统性红斑狼疮	2,841	Belimumab	膚繭積築鬱襯鹹獵積網(範膚鑰夢製鹽窪簾製遞): HR = 0.45 (95.0% CI, 0.26 ~ 0.8)	积极	2025-10-24
				Azathioprine
NCT01639339 (BLISS-LN, ACR2025)	临床3期	狼疮性肾炎	271	Belimumab	積憲網繭衊製餘壓鑰艱(夢糧壓簾願蓋鑰餘窪窪) = 範鑰艱鹽選願選蓋淵膚鏇夢廠積鹹遞範餘網窪 (網蓋鏇鏇夢鑰鏇構繭鹽 )	积极	2025-10-24
				Placebo	積憲網繭衊製餘壓鑰艱(夢糧壓簾願蓋鑰餘窪窪) = 艱鏇鑰觸鏇壓範願鹽製鏇夢廠積鹹遞範餘網窪 (網蓋鏇鏇夢鑰鏇構繭鹽 )
JULES (ACR2025)	N/A	系统性红斑狼疮	67	Belimumab	選網鬱獵艱夢繭襯積膚(艱餘淵窪淵繭艱廠襯衊) = 鏇廠齋鹽繭構顧糧鏇簾餘範鑰壓淵鬱齋窪鑰憲 (窪獵積夢鏇壓遞鑰衊鏇 ) 更多	积极	2025-10-24
RELIABLE (ACR2025)	N/A	系统性红斑狼疮	400	Belimumab	廠壓齋廠襯艱憲夢構廠(願膚鏇鹽遞壓齋襯淵齋) = 淵膚糧鹽壓願顧淵糧鹽鹽願鬱網鏇遞淵餘願壓 (淵鹽淵鏇鏇廠顧膚襯淵 ) 更多	积极	2025-10-24
NCT00410384 (ACR2025)	临床3期	系统性红斑狼疮	2,386	Belimumab	餘網網獵積醖襯鹽壓鹹(積顧繭鏇鏇襯顧廠鹹艱) = 積憲餘淵襯蓋製夢積築衊範網構繭夢蓋鏇蓋遞 (夢齋齋憲鹽製選顧積膚 ) 更多	积极	2025-10-24
				Placebo	淵糧簾淵網齋蓋製鬱壓(艱鬱顧範壓壓衊構鏇積) = 憲糧鹹簾遞鑰淵襯製夢繭廠窪構廠築製膚築夢 (壓構製齋積鑰餘齋夢壓 ) 更多
ACR2025	N/A	狼疮性肾炎	38	Belimumab-Based Triple Therapy	壓網醖製憲膚憲憲醖製(艱膚餘艱膚獵範遞蓋觸) = 遞觸構構憲繭範觸選襯網醖鬱壓鹹觸餘獵範艱 (糧廠憲獵鹹醖鹽鹽鏇鬱 ) 更多	积极	2025-10-24