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rituximab (Rituxirel / Toritz)

✓ Approved

Reliance Life Sciences Private Limited · MS4A1 · Monoclonal Antibodies

What is rituximab?

rituximab is a monoclonal antibodies developed by Reliance Life Sciences Private Limited. It is approved for therapeutic indications via injectable (others) or intracerebral/cerebroventricular injection or intravenous (iv) or subcutaneous injection.

Drug Profile

Brand NamesRituxirel, Toritz
CompanyReliance Life Sciences Private Limited
Drug ClassMonoclonal Antibodies, Antibody
Molecular TargetMS4A1
RouteInjectable (Others), Intracerebral/cerebroventricular Injection, Intravenous (IV), Subcutaneous Injection
StatusApproved
Sources: ClinicalTrials.gov, Reliance Life Sciences Private Limited

Mechanism of Action

Molecular Targets

rituximab acts on 1 molecular target:

MS4A1membrane spanning 4-domains A1 (S7, B1)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

rituximab is developed for 8 unique indications across 4 therapeutic areas.

Therapeutic AreaConditionPhase
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Non-Hodgkin's lymphoma✓ Approved
Musculoskeletal and connective tissue disordersRheumatoid arthritis✓ Approved
Neoplasms benign, malignant and unspecified (incl cysts and polyps)B-cell lymphomaPreclinical
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Chronic lymphocytic leukaemiaPreclinical
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Mantle cell lymphomaPreclinical

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Related Research Articles

PubMedAngewandte Chemie (International ed. in English)2026-08-25

Expansion Microscopy Reveals the Spatial Association of Therapeutic Antibody-Receptor Complexes With Cholesterol-Rich Membrane Domains.

Wen Gang G, Seifert Nicole N, Eiring Patrick P, Meyer Johanna J et al.

Understanding the complex interplay between therapeutic monoclonal antibodies (mAbs) and target receptors within the plasma membrane is essential for improving immunotherapy efficacy. However, direct visualization of lipid nanodomains remains challenging due to their nanoscale dimensions and dynamic behavior. Here, we combine expansion microscopy (ExM) with a fluorescent perfringolysin O domain-4 probe to map cholesterol-rich nanodomains in the membrane of whole intact cells with a spatial resolution approaching ∼40 nm on a confocal setup. We demonstrate that cholesterol-rich domains predominantly localize to actin-supported membrane protrusions in COS-7 cells. We directly visualize how the binding of therapeutic mAbs rituximab (RTX) and daratumumab (DARA) redistributes CD20 and CD38 on lymphoma and multiple myeloma cells, respectively, into cholesterol-rich nanodomains. Accumulation of receptor/mAb complexes within lipid nanodomains creates Fc fragment-dense regions that enhance signal transduction, apoptotic signaling, and complement-dependent cytotoxicity. Furthermore, RTX binding induces pronounced B-cell polarization and accumulation of CD20/RTX complexes in cholesterol-rich membrane nanodomains, whereas CD38/DARA complexes exhibit a more homogeneous membrane distribution indicating that mAb binding-induced receptor reorganization occurs in a cell-type- and receptor-dependent manner at the nanoscale. Our results show how ExM can be used advantageously to improve our understanding of the complex interplay of mAbs and lipid nanodomains.

PMID 42638193
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PubMedCurrent rheumatology reviews2026-08-24

Efficacy and Safety of Rituximab in Patients with Active Rheumatoid Arthritis: Results of a Lebanese National Multicenter Observational Study.

Uthman Imad I, El Hasbani Georges G, Attoui Said S, Merheb Georges G et al.

This study aims to evaluate changes in disease activity and safety of the combination of rituximab and methotrexate in patients with active rheumatoid arthritis (RA) in routine clinical practice in a developing country. This is a national, multicenter, descriptive, longitudinal cohort study of adults with active RA who are eligible to receive rituximab following an inadequate response to a single cycle of anti-tumor necrosis factor (anti-TNF) therapy. The study included baseline and follow-up visits whereby demographics, medical history, and clinical data were collected. 77 patients were included in the study (women: 79.2%; mean age: 51.84 ± 13.19 years). The most common extra-articular manifestations were the presence of rheumatoid nodules (n=13; 16.9%). The mean baseline disease activity score (DAS28) was 5.48 ± 1.23. Descriptive DAS28 mean scores decreased to 3.31 ± 1.16 at the end of the follow-up period compared to the baseline. The majority of the adverse events were non-serious, with few being related to medication. The study showed a descriptive improvement in disease activity scores among RA patients treated with rituximab in combination with methotrexate. The results were consistent with findings from multi-country studies, and the combination was well tolerated. Rituximab in combination with methotrexate demonstrated a clear reduction in DAS28 scores and was well tolerated in patients with RA who had failed a single course of anti-TNF therapy in routine clinical practice in Lebanon, a developing country. However, due to complete-case analysis and the lack of a control arm, these longitudinal trends should be interpreted with caution regarding absolute clinical efficacy.

PMID 42634567
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PubMedEJHaem2026-08-24

Complement-Dominant Relapse of Mixed Autoimmune Hemolytic Anemia After Rituximab Response.

Tomigaki Naru N, Kakiuchi Seiji S, Sakamoto Akimasa A, Fujioka Shutaro S et al.

Mixed autoimmune hemolytic anemia (AIHA) may show temporal shifts in its predominant effector mechanism. We serially assessed clinical course, direct antiglobulin test (DAT) specificity, cold agglutinin activity, complement markers, marrow findings, and immunofixation after rituximab response. During winter relapse, the previously identified κ-restricted CD20-positive population was no longer detectable by marrow flow cytometry. Hemolysis was cold-reactive and complement-dominant. Hemoglobin increased without transfusion after sutimlimab, with C4 recovery and total hemolytic complement activity (CH50) suppression despite persistent cold agglutinin activity. Immunofixation later identified IgG-κ and IgM-κ monoclonal proteins. Serial reassessment may identify complement-mediated relapse in mixed AIHA. Trial Registration: The authors have confirmed clinical trial registration is not needed for this submission.

PMID 42634707
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PubMedBMJ case reports2026-08-24

Idiopathic fibrosing mediastinitis mimicking malignancy: when imaging deceives.

Jethani Varuna V, Venkatesh Mohan M, Singh Yogesh Preet YP, Sharma Kartika K

Woman in her 30s presented with dry cough and shortness of breath since 8 months and swelling of the face and lower limbs since 2 months. Imaging revealed a fluorodeoxyglucose-avid mediastinal mass encasing the superior vena cava and right pulmonary artery, raising a strong suspicion for malignancy. Investigations, including extensive serological testing, bronchoscopy with endobronchial ultrasound lymph node sampling and thoracoscopic biopsy, excluded secondary causes. Histopathology demonstrated dense fibrocollagenous tissue with lymphoplasmacytic infiltrates, confirming idiopathic fibrosing mediastinitis. She showed minimal response to corticosteroids and tamoxifen but exhibited substantial clinical and radiological improvement following rituximab therapy. This highlights the diagnostic complexity of idiopathic fibrosing mediastinitis and supports the emerging role of B-cell-directed immunotherapy in refractory cases.

PMID 42637505
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PubMedCureus2026-08-24

Severe Warm Autoimmune Hemolytic Anemia With Profound Anemia Requiring Multimodal Immunosuppressive Therapy.

Awada Helena H, Chawla Rohan R, Shepherd Yanicka Y, Bondy Cameron C et al.

Warm autoimmune hemolytic anemia (wAIHA) is an uncommon but potentially life-threatening autoimmune disorder characterized by immunoglobulin G (IgG)-mediated destruction of erythrocytes. Secondary wAIHA frequently occurs in association with systemic autoimmune diseases, particularly systemic lupus erythematosus (SLE), while Sjögren syndrome represents a less common but recognized association. Fulminant presentations with profound anemia remain rare and require prompt diagnosis, aggressive immunosuppressive therapy, and multidisciplinary management. We present the case of a 25-year-old woman with a history of reported Sjögren syndrome, Hashimoto thyroiditis, and clinical and serologic features concerning for evolving SLE who developed rapidly progressive direct antiglobulin test (DAT)-positive wAIHA. Despite receiving five units of packed red blood cells (PRBCs) at an outside hospital, her hemoglobin continued to decline after transfer, reaching a nadir of 3.2 g/dL. Laboratory evaluation demonstrated marked hemolysis with reticulocytosis, elevated lactate dehydrogenase, indirect hyperbilirubinemia, undetectable haptoglobin, spherocytes on peripheral smear, and a DAT positive for both IgG and complement (C3). The hospital course was further complicated by thrombocytopenia and severe splenomegaly, raising concern for autoimmune overlap syndrome and possible Evans syndrome. She was successfully treated with pulse-dose intravenous methylprednisolone, intravenous immunoglobulin (IVIG), folic acid supplementation, and transfusion support. Rheumatologic evaluation revealed positive antinuclear antibody (ANA), anti-SSA, antiphospholipid, and anti-thyroid peroxidase antibodies, prompting initiation of hydroxychloroquine. Hemolysis resolved rapidly with normalization of bilirubin, recovery of platelet count, and sustained improvement in hemoglobin, allowing transition to an oral prednisone taper without requiring rituximab or splenectomy. This case highlights that wAIHA may represent the initial manifestation of evolving systemic autoimmune disease and should be considered in young patients presenting with profound hemolytic anemia. Early recognition, aggressive first-line immunosuppressive therapy, timely transfusion support, and multidisciplinary collaboration can be lifesaving and may achieve complete hematologic recovery without the need for second-line biologic therapy.

PMID 42634647
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PubMedCureus2026-08-24

Pediatric Post-COVID-19 Neuromyelitis Optica Spectrum Disorder: A Case Report.

Espinel-Porras Julieth Bibiana JB, Arenas Laura Daniela LD, Mora-Bautista Victor Manuel VM

Neuromyelitis optica spectrum disorder (NMOSD) is a rare autoimmune astrocytopathy affecting the central nervous system, particularly the optic nerves and spinal cord. Post-infectious triggers, including SARS-CoV-2 (COVID-19), have been increasingly recognized as potential catalysts for this immune-mediated condition. We report the case of a nine-year-old boy who developed AQP4-IgG-positive NMOSD following confirmed SARS-CoV-2 infection. The patient's clinical onset began 1.5 months prior to admission with a seven-day episode of intractable vomiting, indicative of area postrema syndrome (APS). He subsequently presented with a 20-day history of progressive gait weakness, dysarthria, and complex ocular and cranial nerve deficits. Neurological examination revealed a right one-and-a-half syndrome, bilateral sixth cranial nerve paresis, left peripheral facial paresis, profound bulbar dysfunction (including a weak gag reflex and bilateral 12th nerve paresis), lower limb weakness (4/5), gait ataxia, and bilateral extensor plantar responses. Magnetic resonance imaging (MRI) demonstrated extensive central nervous system involvement. Brain MRI revealed typical hyperintense lesions in the periventricular white matter, thalamic-hypothalamic area, midbrain, medulla, and area postrema, alongside bilateral retrobulbar optic nerve enhancement. Spinal imaging confirmed longitudinally extensive transverse myelitis (LETM) spanning the C1-C6 and T2-T6 levels, featuring central gray matter involvement (H-sign) extending into the lateral columns. Cerebrospinal fluid was largely unremarkable. Serological testing confirmed the diagnosis with positive aquaporin-4 (AQP4)-IgG antibodies (cell-based assay (CBA)), positive antinuclear antibodies (ANAs) (1:80), and positive COVID-19 IgG antibodies, while anti-MOG antibodies were negative. Acute targeted immunotherapy was initiated with high-dose intravenous methylprednisolone (30 mg/kg/day for five days). While this achieved complete resolution of his gait abnormalities, visual impairment persisted. He subsequently underwent five sessions of therapeutic plasmapheresis as rescue therapy, resulting in full visual and neurological recovery. The patient was discharged on a maintenance regimen of oral azathioprine (2 mg/kg/day) and biannual intravenous rituximab. A four-month follow-up MRI confirmed dramatic radiologic improvement, with complete resolution of the spinal cord abnormalities. This pediatric case highlights post-COVID-19 NMOSD as a severe but highly treatable neurological emergency. It underscores the critical need for rapid diagnosis through detailed clinical recognition (including preceding APS), advanced radiographic imaging, and targeted serologic evaluation, as well as the efficacy of plasmapheresis for steroid-refractory symptoms to prevent irreversible disability.

PMID 42634781
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