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rituximab (Usmal / BCD020 / AcellBia)

✓ Approved

Grupo Biotoscana · MS4A1 · 单克隆抗体

什么是 rituximab？

rituximab 是一种单克隆抗体，由Grupo Biotoscana研发。该药已获批，用于治疗相关适应症，给药途径：Injectable (Others)、Intracerebral/cerebroventricular Injection、Intravenous (IV)、Subcutaneous Injection。

药物档案

商品名Usmal, BCD020, AcellBia
公司Grupo Biotoscana
药物类别单克隆抗体, 抗体
分子靶点MS4A1
给药途径Injectable (Others), Intracerebral/cerebroventricular Injection, Intravenous (IV), Subcutaneous Injection
状态Approved
来源： ClinicalTrials.gov, Grupo Biotoscana

作用机制

分子靶点

rituximab 作用于 1 个分子靶点：

MS4A1membrane spanning 4-domains A1 (S7, B1)
需要更深入的分析？Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

rituximab 针对 7 个适应症，涉及 4 个治疗领域。

治疗领域疾病/病症分期
Neoplasms benign, malignant and unspecified (incl cysts and polyps)B-cell lymphoma✓ Approved
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Chronic lymphocytic leukaemia✓ Approved
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Non-Hodgkin's lymphoma✓ Approved
Musculoskeletal and connective tissue disordersRheumatoid arthritis✓ Approved
Vascular disordersMicroscopic polyangiitisPreclinical

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相关研究文献

PubMedInternational journal of clinical oncology2026-06-13

Emerging treatment strategies for newly diagnosed diffuse large B-cell lymphoma.

Miyazaki Kana K

Despite recent progress in improving patient survival, the outcomes in approximately 40% of patients with diffuse large B-cell lymphoma (DLBCL) remain poor. For many years, R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) has been the standard first-line treatment for DLBCL; however, pola-R-CHP (polatuzumab vedotin, rituximab, cyclophosphamide, doxorubicin, and prednisone) has recently emerged as a new treatment option. In parallel, novel molecularly targeted therapies that target signaling pathways, cellular antigens, and epigenetic regulators associated with high-risk DLBCL are in development. Treatment strategies tailored to the cell of origin or to specific molecular subtypes are also being explored using subtype-specific targeted agents. In addition, agents that have demonstrated efficacy in patients with relapsed or refractory DLBCL-such as the anti-CD19 antibody tafasitamab and immunomodulatory drugs such as golcadomide-are currently under investigation for use in newly diagnosed patients. Immunotherapies, including anti-CD19-chimeric antigen receptor-T therapy and CD20×CD3 bispecific antibodies (BsAbs), have significantly improved outcomes in patients with relapsed or refractory disease and are now under evaluation as early-line therapies. BsAbs can enable more flexible treatment strategies, including combination regimens with cytotoxic or chemotherapy-free approaches. This review summarizes recent advances and ongoing trials that are investigating novel therapeutic strategies for newly diagnosed DLBCL that may soon be incorporated into clinical practice.

PMID 42286378
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PubMedArchives of disease in childhood. Education and practice edition2026-06-13

Breaking the heat: managing steroid refractory warm autoimmune haemolytic anaemia.

Clifton Emilie E, McCool Niamh N, Mitchell Bethany B, Mark Catherine C

This article describes a case of warm autoimmune haemolytic anaemia (w-AIHA) in a 16-month-old refractory to first-line treatment. W-AIHA typically responds to systemic corticosteroids. Here, management proved challenging with re-emergence of haemolysis during initial steroid course. Rituximab offered a turning point, demonstrating the utility of targeted anti-CD20 antibody therapy in achieving a sustained haematological response. The patient's clinical course was not without further complications potentially attributable to treatments administered. This paper reviews the management of w-AIHA, beyond steroid therapy, with an additional focus on supportive care measures.

PMID 42285741
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PubMedJournal of the American Academy of Dermatology2026-06-13

Immune Checkpoint Inhibitor-Associated Autoimmune Bullous Disease: A Clinical Review.

Nukaly Houriah Y HY, Barnawi Ghassan G, Thalib Husna Irfan HI, Basamih Khalid Abdulrahman KA et al.

Immune checkpoint inhibitors (ICIs) have markedly advanced oncology by enhancing the immune system's ability to combat malignancies. However, their use is increasingly associated with immune-related adverse events, including immunobullous dermatoses. These disorders, such as bullous pemphigoid, pemphigus vulgaris, linear immunoglobulin A bullous dermatosis, mucous membrane pemphigoid, paraneoplastic pemphigus, dermatitis herpetiformis, and lichen planus pemphigoides present significant diagnostic and therapeutic challenges. This clinical review explores the pathogenesis, clinical presentation, diagnosis, and management strategies of immunobullous dermatoses triggered by ICIs, highlighting the complex relationship between effective cancer treatment and immune regulation. ICI-induced immunobullous dermatoses closely mimic their conventional autoimmune counterparts but often have unique clinical considerations, such as delayed onset, mucosal predilection, and persistence post-discontinuation of medication. Diagnostic evaluation relies on clinical suspicion, histopathology, direct and indirect immunofluorescence, and enzyme-linked immunosorbent assays. Management typically involves corticosteroids and immunosuppressants, with biologics such as rituximab, dupilumab and omalizumab reserved for refractory cases. Decisions regarding the continuation of ICIs require individualized assessment, balancing cancer control with autoimmune toxicity. Dermatologic and oncologic teams must navigate dual priorities of mitigating autoimmune toxicity and preserving oncologic benefit.

PMID 42285257
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PubMedAnnals of the rheumatic diseases2026-06-13

Longitudinal profiling reveals immune dynamics and distinct plasma cell signatures during B-cell depletion in IgG4-related disease.

Kim Hyo Jae HJ, Kim Min-Gang MG, Kim Seongryong S, Kim Mi Hyeon MH et al.

IgG4-related disease (IgG4-RD) is a systemic fibroinflammatory disorder characterised by tissue infiltration of IgG4+ plasma cells, yet the precise roles of B cells remain unclear. This study aimed to characterise the longitudinal immune dynamics in IgG4-RD during B-cell depletion therapy to identify pathogenic cell subsets and specific biomarkers associated with relapse. We performed a longitudinal multiomics analysis on 119 peripheral blood samples from patients with IgG4-RD undergoing rituximab treatment, spanning active, remission, and relapse phases. Integrated single-cell transcriptomics, B-cell receptor (BCR) sequencing, and serum proteomics were performed on matched blood and tissue samples from submandibular gland and lymph nodes, with Sjögren's syndrome and healthy individuals as controls. We identified a previously unrecognised, disease-specific IgG4+ plasma cell subset characterised by aberrant expression of the neuropeptide NMU and highly skewed IGHV1-69 usage. Circulating follicular helper T cells (CD4+Tfh) displayed signatures consistent with chronic antigen stimulation and type 2 immunity. Furthermore, markedly expanded double-negative T cells (dnT) highly expressed IL10, suggesting their involvement in immune regulation and isotype class switching. Longitudinal analysis following B-cell depletion emphasised the reconstitution dynamics of pathogenic plasma cells, furthermore highlighting the concurrent shifts in CD4+Tfh and dnT that mirrored disease remission and relapse, and underscored the amelioration of proinflammatory immune profiles. NMU-expressing IGHV1-69+ plasma cells represent a pathogenic effector population driving IgG4-RD recurrence. These findings establish a mechanistic framework for B-cell depletion and identify specific cellular and molecular biomarkers to improve disease monitoring and relapse prediction in clinical practice.

PMID 42285873
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PubMedPediatric nephrology (Berlin, Germany)2026-06-12

Discontinuation of mycophenolate mofetil as maintenance therapy after rituximab treatment in childhood-onset complicated frequently relapsing or steroid-dependent nephrotic syndrome.

Nada Taishi T, Kamei Koichi K, Sasaki Keigo K, Nishi Kentaro K et al.

Mycophenolate mofetil (MMF) as maintenance therapy after rituximab treatment is effective in preventing relapses in children with complicated frequently relapsing or steroid-dependent nephrotic syndrome. However, once sustained remission has been achieved by MMF, the outcomes and risk of relapse after discontinuing MMF remain unclear. We conducted a two-center, retrospective study of patients with childhood-onset frequently relapsing or steroid-dependent nephrotic syndrome who discontinued MMF because of sustained remission for ≥ 2 years on maintenance MMF after rituximab treatment. Relapse, additional treatment, and risk factors for relapses after MMF discontinuation were analyzed. Sixty patients were enrolled. After tapering or discontinuation of MMF, 35 (58%) patients relapsed, and the median time from tapering to relapse was 276 days. The 50% relapse-free survival was 1.5 years using the Kaplan-Meier method. After relapses, 30 (86%) patients required reinitiation of immunosuppressants or additional rituximab treatment. The history of initial steroid-resistant nephrotic syndrome, relapses < 10 times before the first rituximab treatment with immunosuppressants, and a longer period between the last B-cell recovery and tapering MMF were significantly associated with a lower risk of relapse in a multivariate analysis using the Cox proportional hazards model (all p < 0.05). Discontinuation of MMF may be considered in selected patients with sustained remission after rituximab treatment, particularly those with identified low-risk factors for relapse. The timing of discontinuation should be individualized according to these factors and patient-specific considerations because resumption of immunosuppressants or additional rituximab treatment is frequently required after relapse following MMF discontinuation.

PMID 42283831
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PubMedJournal of clinical medicine2026-06-12

Management of Rituximab-Associated Hypersensitivity Reactions with Successfully Applied Desensitization Protocols: A Clinical Experience of 46 Infusions in 11 Patients.

Candar Ömer Ö, Özkocaman Vildan V, Tülümen Öztürk Raziye R, Ersal Tuba T et al.

Objective: This study aimed to evaluate patients who developed hypersensitivity reactions (HSRs) during rituximab treatment and report the outcomes of desensitization protocols implemented to allow treatment continuation. Methods: We retrospectively reviewed the institutional data of 76 patients who received rituximab therapy at the Adult Hematology Department between January 2022 and September 2023. Among these, 11 patients who experienced immediate hypersensitivity reactions during infusion were analyzed. The overall frequency of rituximab-associated HSRs was 14.47% (11 out of 76 patients). Demographic data, underlying diseases, timing and type of HSRs, and details of the desensitization protocols were recorded. Results: The overall frequency of rituximab-associated HSRs was 14.47% (11 out of 76 patients). Among the 11 patients, eight were male and three were female, with a median age of 56 years (range: 19-72). Eight patients had CD20-positive non-Hodgkin lymphoma (NHL) and three had acute B-lymphoblastic leukemia (B-ALL). HSRs occurred during the first rituximab exposure in nine patients, at the fourth dose in one patient, and at the eighth dose in another. Symptoms included widespread rash, pruritus, flushing, chills, shivering, dyspnea, dysphagia, back pain, dizziness, syncope, and throat discomfort. All the patients were consulted by the Allergy and Immunology Clinic. Based on prick and intradermal test (IDT) results and the planned rituximab dose, desensitization protocols consisting of a three-dilution/12-step and a four-dilution/16-step regimen were prepared. Overall, 46 desensitization procedures were successfully completed in 11 patients. Notably, no severe anaphylactic events or treatment discontinuations due to drug toxicity occurred during the implementation of the protocols. Conclusions: Although the number of patients was limited, our findings indicate that in patients with hematologic malignancies receiving rituximab who develop early HSRs, desensitization represents a safe and effective strategy before considering treatment modification. These results support that, in appropriately selected patients, desensitization protocols are an important approach to continue therapy without interruption while minimizing adverse reactions.

PMID 42279029
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