Drug Database
RA

rabbit anti-T-lymphocyte immune globulin (Zetbulin)

✓ Approved

Nippon Zoki · Polyclonal Antibodies · Polyclonal Antibodies

What is rabbit anti-T-lymphocyte immune globulin?

rabbit anti-T-lymphocyte immune globulin is a polyclonal antibodies developed by Nippon Zoki. It is approved for therapeutic indications via injectable (others) or intravenous (iv).

Drug Profile

Brand NamesZetbulin
CompanyNippon Zoki
Drug ClassPolyclonal Antibodies, Antibody
RouteInjectable (Others), Intravenous (IV)
StatusApproved
Sources: ClinicalTrials.gov, Nippon Zoki

Therapeutic Indications

rabbit anti-T-lymphocyte immune globulin is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Blood and lymphatic system disordersAplastic anaemia✓ Approved

Related Research Articles

PubMedNature microbiology2026-11-11

Env-specific antibodies promote post-treatment control in SIV-infected macaques.

Singh Vidisha V, Burgess Divine D, Goldy Jordan J, Dashti Amir A et al.

Viral latency reversal was observed in simian immunodeficiency virus (SIV)-infected rhesus macaques receiving antiretroviral therapy (ART), CD8α lymphocyte depletion and N-803 immunotherapy. However, this therapeutic approach did not reduce the viral reservoir size and treatment interruption resulted in rapid virus rebound. Here, to address this shortfall, we used four anti-SIV Env-specific rhesus IgG1 monoclonal antibodies (RhmAbs) that recognize unique targets on the SIV envelope. SIVmac239-infected macaques were treated with ART only (group 1); ART + RhmAbs (group 2); or ART + RhmAbs + CD8α-depletion + N-803 (group 3). Robust latency reversal was only achieved in group 3. Viraemia rebounded in all macaques with similar kinetics after treatment interruption. However, compared with pre-ART viral loads, a greater fold reduction in rebound viraemia was seen in groups 2 and 3 and post-treatment control (PTC) required SIV RhmAbs. CD4+ T cells from macaques with PTC maintained low levels of intact SIV proviruses off ART and expressed increased interferon and decreased TGF-β signalling genes. This antiviral gene expression profile was also observed in CD4+ T cells with lower human immunodeficiency virus (HIV)-DNA content from ART-treated people with HIV. These results suggest that reduced virus production may contribute to PTC following ART interruption and provide a target for immune-based strategies to achieve durable viral control.

PMID 43009538
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PubMedFrontiers in immunology2026-11-11

Molecular mechanisms regulating T-cell receptor signaling and T-cell function.

Kurilin Vasily V VV, Fisher Marina S MS, Sennikov Sergey V SV

The T-cell receptor (TCR) is the central mediator of antigen-specific recognition and a key regulator of T-lymphocyte function. Current evidence indicates that TCR signaling is not a linear cascade but a multilevel dynamic system in which cellular responses are shaped by the combined effects of TCR-CD3 structural organization, spatial receptor distribution, the lipid microenvironment, mechanical forces, kinase and phosphatase activity, co-stimulatory and inhibitory receptors, cellular metabolic state, and the strength and duration of TCR interactions with peptide-MHC (pMHC) complexes. This review summarizes current concepts of the molecular and spatial organization of TCR-CD3; mechanisms of signal initiation involving Lck, CD45, SHP phosphatases, ITAMs, ZAP-70, and the LAT-SLP-76 signalosome; and the coupling of TCR signaling to T-cell metabolic programs. Particular attention is paid to the nonlinear relationship between functional responses, TCR affinity, and target pMHC density; the role of chronic antigenic stimulation in T-cell exhaustion and activation-induced cell death (AICD); and the involvement of NFAT-, TOX-, NR4A-, and TCF1-dependent programs in this process. We also discuss the translational relevance of these mechanisms to antitumor immunotherapy and the restoration of immune tolerance, including immune checkpoint blockade, CAR-T, TCR-T, and TCR-Treg approaches and CD3/TCR-directed T-cell-engager platforms. Finally, we consider the concept of TCR signal tuning, according to which therapeutic efficacy is determined not by maximal receptor signal strength but by an optimal balance between antigen sensitivity, specificity, effector activity, metabolic fitness, and the ability of T cells to retain function under sustained antigenic pressure.

PMID 43011816
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PubMedFrontiers in oncology2026-11-11

Bladder cancer immune microenvironment: immune-cell distribution, disease associations, treatment remodeling, and baseline immune features associated with treatment response and prognosis.

Qin Shaobo S, Yu Xu X, Zuo Shishuai S, He Xiangfei X et al.

Bladder cancer is characterized by substantial heterogeneity in the tumor immune microenvironment (TIME), which influences recurrence, progression, treatment resistance, and responses to Bacillus Calmette-Guérin (BCG), neoadjuvant chemotherapy, immune checkpoint inhibitors, and radiotherapy. This narrative review critically synthesizes evidence on immune-cell distribution, disease-state associations, treatment-associated remodeling, and baseline immune features linked to treatment response and prognosis. Current evidence indicates that the clinical meaning of immune infiltration depends not only on cell abundance but also on localization across histological compartments, functional state, tumor compartment, and therapeutic context. Cytotoxic lymphocyte infiltration may indicate antitumor immune activity when tumor-accessible and functionally active, whereas regulatory T cells, myeloid-derived suppressor cells, and M2-like tumor-associated macrophages often reflect suppressive or treatment-resistant immune states. Treatments can reshape the bladder cancer TIME, but the strength of evidence varies across modalities: BCG has relatively stronger human support for treatment-associated immune changes, whereas evidence for chemotherapy-, immunotherapy-, and radiotherapy-associated remodeling remains more heterogeneous. Baseline or pretreatment immune architecture may provide a more informative basis for biomarker development than single immune-cell markers. Future longitudinal studies with matched pre- and post-treatment specimens are needed to determine whether treatment-induced TIME changes provide additional treatment-response-associated or prognostic information beyond baseline immune features, whereas establishment of predictive utility will require comparative treatment designs with formal biomarker-by-treatment interaction testing.

PMID 43011329
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PubMedNature communications2026-11-11

Integrated multi-omics identifies distinct immune signatures with diagnostic and therapeutic implications in immune checkpoint inhibitor-induced myocarditis.

Zhang Shi-Long SL, Cai Qing-Qing QQ, Zhang Jian J, Liu Yuan Y et al.

Immune checkpoint inhibitor-associated myocarditis (ICI-myocarditis) is a rare but frequently fatal immune-related adverse event. A comprehensive understanding of the cellular and molecular determinants driving ICI-myocarditis is essential for improving diagnostic precision and developing targeted interventions. We delineate the immune landscape of ICI-myocarditis via scRNA-seq, flow cytometry, Olink proteomics, and multiplex cytokine profiling. We demonstrate that high levels of baseline ISG15⁺CD8⁺ T cells are linked to the proinflammatory features of monocytes and in vitro experiments confirm the existence of circulating ISG15⁺CD8⁺ T cells with a high potential to induce cardiomyocyte apoptosis, supporting their pathogenic potential for cardiomyocyte cytotoxicity. Notably, intercellular crosstalk between these subsets is possibly mediated via the CCL2-CCR2 axis, and its blockade attenuated ICI-induced cardiac injury in vivo. Based on the inflammatory signature in ICI-myocarditis, we develop an 8-protein custom panel with promising performance in distinguishing ICI-myocarditis from other ICIs-treated controls. JAK-STAT pathway activation promotes inflammatory programs in both ISG15⁺CD8⁺ T cells and monocytes. Furthermore, JAK-STAT inhibition ameliorates cardiac dysfunction and inflammatory infiltration while enhancing the response to anti-PD-1 therapy in mouse models. In summary, this study implicates immune-pathogenic features of ICI-myocarditis and provides a possible basis for future therapies.

PMID 43009464
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PubMedMedicine2026-11-11

Rapid-onset type 1 diabetes mellitus and diabetic ketoacidosis: A case series of programmed cell death 1 inhibitor-associated endocrine toxicity in China.

Mao Huihui H, Jiang Xuehui X, Huang Xiaowei X, Fang Jingwen J et al.

Immune checkpoint inhibitors (ICIs), including those targeting the programmed cell death 1 (PD-1) receptor, its ligand (PD-L1), and cytotoxic T lymphocyte antigen 4 (CTLA-4), are widely used in treating various cancers. Although generally well-tolerated, ICIs can cause severe immune-related adverse events (irAEs), including endocrine toxicities like hypophysitis, thyroid dysfunction, and adrenal insufficiency. Among these, ICI-induced type 1 diabetes mellitus (T1DM) is a rare but life-threatening irAE. In order to provide a more comprehensive understanding of this condition, we describe 4 cases of PD-1 inhibitor-induced T1DM in Chinese patients. All 4 patients developed diabetic ketoacidosis (DKA) within 1 week of hyperglycemic symptom onset, and 3 were diagnosed with fulminant T1DM. All patients were male, with a mean age of 63 years. The median time from PD-1 inhibitor initiation (sintilimab or camrelizumab) to T1DM diagnosis was 112 days. At onset, the mean blood glucose level was 684 mg/dL, mean glycated hemoglobin (HbA1c) was 8.22%, and mean serum C-peptide level was 0.13 ng/ml. Intravenous insulin was transitioned to subcutaneous insulin in all patients, in addition to receiving fluid resuscitation and corrective electrolyte therapy. All patients eventually discontinued PD-1 inhibitor therapy. Through insulin treatment, their hyperglycemia was effectively controlled. Additionally, all our patients achieved stable disease or partial response in tumor treatment evaluation at T1DM onset. These cases highlight that anti-PD-1 therapy can trigger a rapid and severe form of T1DM. All cancer patients receiving PD-1 inhibitors should undergo close monitoring of blood glucose levels and receive patient education.

PMID 43012797
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PubMedMedicine2026-11-11

Efficacy and influencing factors of rituximab in idiopathic membranous nephropathy: A real-world retrospective study.

Xu Xiaofei X, Zhou Qiwei Q, Li Subo S, Zhang Xiaoru X et al.

This study aims to investigate the efficacy and influencing factors of rituximab (RTX) in the treatment of idiopathic membranous nephropathy (IMN). A total of 46 patients with IMN visited and followed up regularly in our hospital were included in this study. The patients were divided into 2 groups, with 23 patients receiving RTX treatment (RTX group) and 23 patients receiving treatment with cyclophosphamide (CTX group). The clinical data of the patients, including urine examination, blood test, efficacy evaluation results, and adverse events (AEs) were analyzed retrospectively. The changes in clinical and biochemical indicators were compared in RTX groups before and after treatment, and the clinical efficacy and influencing factors of RTX treatment for IMN were evaluated. After 6 months of treatment, in the RTX group, compared to baseline, there was a significant decrease in 24-hour urine protein, total cholesterol, and B lymphocyte count (P < .001, P = .010, P < .001), while albumin (ALB), globulin, and natural killer cells showed a significant increase compared to baseline (P < .001, P < .001, P < .001). After 6 months of treatment, the RTX group showed significantly higher glomerular filtration rate, higher levels of ALB, and higher levels of globulin compared to the CTX group, with statistical significance (P = .042, P = .003, P < .001). Among patients with positive anti-PLA2R antibodies at baseline, the antibody clearance rate at 6 months was significantly higher in the RTX group than in the CTX group (P = .035). By the end of follow-up, the overall remission rates were 91.3% for the RTX group and 87.0% for the CTX group, with no statistically significant difference between the 2 groups (P > .99). A univariate analysis of the correlation between clinical characteristics, laboratory tests, and the efficacy of RTX treatment found that lower baseline 24-hour urine protein levels appeared to be associated with a higher likelihood of achieving remission (P = .035). AEs were observed in 17.4% of RTX-treated patients versus 52.2% of CTX-treated patients (P = .030). RTX appeared to be effective in patients with IMN and was associated with a more favorable safety profile compared with CTX.

PMID 43012768
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