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rituximab (Kikuzubam / PBO326)

✓ Approved

Probiomed · MS4A1 · Monoclonal Antibodies

What is rituximab?

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

Drug Profile

Brand NamesKikuzubam, PBO326
CompanyProbiomed
Drug ClassMonoclonal Antibodies, Antibody
Molecular TargetMS4A1
RouteInjectable (Others), Intracerebral/cerebroventricular Injection, Intravenous (IV), Subcutaneous Injection
StatusApproved
Sources: ClinicalTrials.gov, Probiomed

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)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)Diffuse large B-cell lymphoma✓ Approved
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Non-Hodgkin's lymphoma✓ Approved
Musculoskeletal and connective tissue disordersRheumatoid arthritis✓ Approved

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Related Research Articles

PubMedCureus2026-07-25

Fatal Acute Liver Failure Associated With Presumed Hepatitis B Virus Reactivation During Rituximab Maintenance Therapy: A Case Report.

Tran James J, Zhou Calvin C, Babun Asis A AA, Leung Whinkie W et al.

We report a woman in her 60s with follicular non-Hodgkin lymphoma receiving maintenance rituximab therapy, last administered one month prior to presentation, who developed progressive malaise, jaundice, and acute liver failure. Laboratory evaluation demonstrated severe hepatocellular injury with marked transaminase elevations (alanine aminotransferase: 2,500 U/L; aspartate aminotransferase: 2,400 U/L), hyperbilirubinemia (total bilirubin: 20 mg/dL), and coagulopathy. Hepatitis B virus (HBV) serology demonstrated active infection with elevated hepatitis B surface antigen (HBsAg) and detectable HBV DNA. Baseline HBV screening and antiviral prophylaxis records prior to rituximab initiation were unavailable from the treating institution, limiting the definitive confirmation of pre-existing HBV status. Given the patient's recent rituximab exposure, clinical presentation, and exclusion of alternative etiologies, HBV reactivation was considered the most likely diagnosis. The patient was diagnosed with HBV reactivation associated with rituximab therapy. Despite the initiation of antiviral treatment and aggressive supportive care, her clinical course rapidly deteriorated, complicated by hepatic encephalopathy, acute kidney injury requiring hemodialysis, and hypoxic respiratory failure. She was evaluated for liver transplantation but deemed ineligible due to multiorgan failure and ultimately transitioned to end-of-life care. This case highlights the potentially fatal consequences of HBV reactivation during rituximab therapy and underscores the importance of appropriate screening, prophylaxis, and vigilance in high-risk patients.

PMID 42500753
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PubMedClinical and translational science2026-07-25

Population Pharmacokinetics of Rituximab in Treatment-Naïve Chinese Patients With Diffuse Large B-cell Lymphoma During Induction Therapy: Clinical Implications.

Zhou Wan-Yi WY, Ling Jing J, Guan Meng-Meng MM, Qu Ying Y et al.

This study aimed to establish and validate a population pharmacokinetic model for rituximab during induction therapy in treatment-naive patients with diffuse large B-cell lymphoma, identify covariates affecting key pharmacokinetic parameters, and predict exposure. This retrospective study included newly diagnosed patients receiving rituximab-containing induction regimens. Blood samples were collected before the next dose and after completion of the current dose across different chemotherapy cycles during the induction therapy; plasma concentrations were measured by chemiluminescent immunoassay. A nonlinear mixed-effects model was developed and externally validated. Individual parameters were obtained using empirical Bayesian methods, and first-cycle trough concentrations were predicted. For model building, 45 patients and 115 samples were included; external validation used 12 patients and 28 samples. Rituximab pharmacokinetics were described by a two-compartment model. Representative estimates were: clearance 0.0181 L/h, central volume 8.12 L, intercompartmental clearance 0.0213 L/h, peripheral volume 29.2 L. Albumin-globulin ratio was the final covariate and significantly affected clearance. Validation indicated good stability and predictive performance. Predicted first-cycle trough concentrations were below the reference efficacy threshold, and lower troughs were associated with smaller albumin-globulin ratios. This model quantified the effect of albumin-globulin ratio on clearance and suggests a risk of insufficient rituximab exposure during induction therapy, supporting future individualized dosing and therapeutic drug monitoring.

PMID 42499290
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PubMedBMJ case reports2026-07-25

Serum PLA2R-negative, biopsy-proven PLA2R-positive primary membranous nephropathy in a dichorionic-diamniotic twin pregnancy.

Kansal Abhik A, Meehan Lyra L, MacNeil Metta M, Frawley Natasha N et al.

Primary membranous nephropathy (PMN) in pregnancy is rare and poses significant risks including pre-eclampsia, preterm delivery, low birth weight and fetal death. Anti-phospholipase A2 receptor (PLA2R) antibodies are used to confirm diagnosis.We report a case of biopsy-confirmed PLA2R-positive but seronegative PMN in a woman in her late 20s with a dichorionic-diamniotic twin pregnancy. Initial hypoalbuminaemia was attributed to intercurrent infection but was later recognised as nephrotic syndrome at 20+6 weeks gestation. Renal biopsy at 21 weeks confirmed PMN with positive PLA2R and IgG4 staining, despite negative serum PLA2R antibodies.She was managed with tacrolimus and rituximab, with close monitoring and delivered viable twins via emergency caesarean at 33+3 weeks following premature rupture of membranes. Both maternal disease and neonatal outcomes were favourable. This case highlights the challenges in diagnosing and managing seronegative PMN during pregnancy and supports the role of renal biopsy and rituximab in selected patients.

PMID 42498317
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PubMedFrontiers in neurology2026-07-25

Anti-NMDA-receptor encephalitis and MOGAD associated optic neuritis: a case series.

Parthasarathi Pooja P, Dattilo Michael M, Peragallo Jason J

Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is a well-recognized autoimmune condition that often presents with neuropsychiatric symptoms and seizures. Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) often manifests as optic neuritis and, less frequently, as acute demyelinating encephalomyelitis or transverse myelitis. The co-occurrence of anti-NMDAR encephalitis and MOGAD is becoming increasingly recognized, but clinical series remain limited. We present three patients with anti-NMDAR encephalitis and MOGAD optic neuritis (ON): two men, aged 19 and 26, and one woman, aged 36. Clinical presentations, signs, investigations, and management of each case are discussed. The 26-year-old man presented with altered mental status and concurrent vision loss. The 36-year-old woman presented with altered mental status during the encephalitis episode and developed vision loss 4 months after encephalitis. The 19-year-old man with a prior history of altered mental status, diagnosed with NMDA encephalitis 9 years earlier, presented with headache and vision loss. Abnormal T2/FLAIR lesions in the brain and/or spinal cord during the encephalitis episode and unilateral or bilateral optic nerve enhancement during the optic neuritis episode were detected on brain and orbital magnetic resonance imaging (MRI) in all patients. All patients tested positive for cerebrospinal fluid (CSF) anti-NMDAR antibodies during the encephalitis episode and had positive serum MOG titers during the optic neuritis episode. Each patient presented with bilateral, asymmetrically reduced visual acuity and diminished color vision. One patient exhibited bilateral temporal optic nerve pallor, while two patients had bilateral optic nerve edema. The diagnostic work-up revealed positive serum MOG titers (1:100, 1:10,000, and 1:10,000 in the 36/F, 26/M, and 19/M, respectively). The 36-year-old woman was treated with intravenous (IV) steroids, plasma exchange (PLEX), and rituximab during the encephalitis episode. During the optic neuritis episode, she was treated with IV steroids, IV immunoglobulin (IVIG), and rituximab, followed by long-term rituximab maintenance therapy. The 19-year-old man was treated for encephalitis with IV steroids, IVIG, and rituximab. During his optic neuritis episode, he received IV steroids, IVIG, and tocilizumab, followed by long-term tocilizumab maintenance therapy. The 26-year-old man was treated with IV steroids, PLEX, and rituximab during the acute episode, followed by long-term IVIG maintenance therapy. After achieving 2 years of stability that prompted the discontinuation of IVIG, the patient experienced a MOG-IgG-positive relapse 5 months later. This relapse was marked by a seizure-like episode and the appearance of new lesions on MRI. The acute symptoms resolved after treatment with intravenous steroids and IVIG. Subsequently, the patient was initiated on an indefinite maintenance IVIG regimen. Visual acuity in all patients improved to their baseline levels following treatment. This series highlights the emerging overlap between anti-NMDAR encephalitis and MOGAD optic neuritis. Optic neuritis may occur months to years after encephalitis, underscoring the need for careful monitoring of patients with anti-NMDAR encephalitis who develop new visual symptoms. Dual autoimmunity may represent a distinct phenotype with implications for long-term immunotherapy.

PMID 42500388
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PubMedBlood advances2026-07-25

Long-term outcomes with continuous venetoclax for relapsed chronic lymphocytic leukemia.

McKeague Sean S, Lew Thomas E TE, Lowe Anna A, Lau Lei Shong LS et al.

Venetoclax was first approved for continuous use in relapsed-refractory chronic lymphocytic leukemia (RR CLL), but the efficacy and consequences of very long term BCL2 inhibition are unknown. We describe the frequency, characteristics and outcomes of patients with RR CLL treated with >5 years of continuous venetoclax. Long-term responders (>5 years of continuous therapy without progressive disease [PD]), were identified from a cohort of 86 RR CLL patients treated with continuous venetoclax± rituximab. Landmark analyses at 2 and 5 years assessed association between undetectable measurable residual disease (uMRD; 10-4 peripheral blood flow cytometry) and progression free survival (PFS). Next generation sequencing (NGS) was performed at PD for BCL2 and TP53 mutations. Twenty-nine (33%) patients were long-term responders. Compared to those with PD within 5 years, they were more likely to have mutated IGHV(44% vs. 14%, p =0.029), non-complex-karyotype (89 vs. 50%, p=0.043) and uMRD (79 vs. 30%, p<0.001). At median follow-up of 11.1 years, 76% had ceased venetoclax, mostly due to PD. In a landmark analysis of patients continuing venetoclax beyond 2 years, 5-year PFS was 87% for those with uMRD vs. 45% without (HR1.30, 95% CI 1.12-1.52, p=0.001). BCL2 mutations were detected in 4/8 patients at PD. Grade ≥3 toxicities - including infection (51%), neutropenia (20%) and thrombocytopenia (10%)- occurred at consistent frequency throughout treatment. Long-term responses to continuous venetoclax occur in approximately one third of RR CLL patients. Sustained uMRD confers the most favorable outcome, though all patients show a continuous risk of relapse, infection and cytopenias.

PMID 42498281
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PubMedCureus2026-07-24

Human Herpes Virus 8 (HHV-8)-Associated Multicentric Castleman Disease in an HIV Patient With Severe Immunosuppression: A Diagnostic Challenge.

Birkhamshaw Edmund E, Abbas Ali A, Paing Pyae P, Pillai Anu A et al.

Human herpes virus 8 (HHV-8)-associated multicentric Castleman disease (HHV-8-MCD) is a rare lymphoproliferative disorder that predominantly affects individuals with advanced immunosuppression, especially people living with HIV. The clinical picture frequently overlaps with opportunistic infections, lymphoma, and haemophagocytic lymphohistiocytosis, creating significant diagnostic challenges.  We present a case of a 51-year-old man recently diagnosed with HIV, who developed recurrent pyrexia, profound hyperferritinaemia, cytopenias, rapidly progressive lymphadenopathy, and escalating HHV-8 viraemia. Lymph node biopsy confirmed the diagnosis of HHV-8-positive MCD. Prompt initiation of rituximab and etoposide resulted in complete clinical and radiological remission.  The case highlights the importance of rapid recognition, timely histological confirmation, early initiation of rituximab-based therapy, and multidisciplinary management in HHV-8-MCD.

PMID 42495486
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