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RH

Rho(D) Immune Globulin

✓ Approved

CSL Limited · Polyclonal Antibodies · Polyclonal Antibodies

What is Rho(D) Immune Globulin?

Rho(D) Immune Globulin is a polyclonal antibodies developed by CSL Limited. It is approved for therapeutic indications via injectable (others) or intravenous (iv).

Drug Profile

CompanyCSL Limited
Drug ClassPolyclonal Antibodies, Antibody
RouteInjectable (Others), Intravenous (IV)
StatusApproved
Sources: ClinicalTrials.gov, CSL Limited

Therapeutic Indications

Rho(D) Immune Globulin is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Congenital, familial and genetic disordersRhesus haemolytic disease of newborn✓ Approved

Related Research Articles

PubMedJournal of translational medicine2026-07-17

Systemic immune profiling of heterologous versus homologous boosting of COVID-19 vaccination.

Han Xu X, Jiang Hudachuan H, Zheng Hui H, Jin Pengfei P et al.

Compared with homologous boosting, heterologous boosting with a different COVID-19 vaccine following priming generates stronger antibody responses against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) as well as variants, particularly for inactivated COVID-19 vaccine(CoronaVac). However, it is still unclear about the potential immune enhancement mechanism underlying heterologous boosting. In this study, we isolated spike protein binding-specific monoclonal antibodies at day 180 post a homologous booster with CoronaVac or a heterologous booster with Ad5-nCoV based on two-dose of CoronaVac using the single B cell sorting platform. Subsequently, we verified their neutralization activity to SARS-CoV-2 variants, germline gene sequences and affinity kinetics targeting SARS-CoV-2 NTD/RBD/S1. Additionally, we conducted an in-depth analysis of the immunological response characteristics, by integrating single-cell RNA/V(D)J sequencing(scRNA/ V(D)J-seq). Our study demonstrated that heterologous boosting with Ad5-nCoV elicited more mature B cells with higher affinity and activated more abundant immune-related pathways compared to the homologous boosting with CoronaVac. In addition, Ad5-nCoV boosting expanded unique clonal types of B and T cells, whereas CoronaVac boosting led to a small-sized clonal expansion. Furthermore, the utilization of germlines associated with neutralizing antibody were preferentially enriched in recipients with Ad5-nCoV boosting. Above all, our study gives insights for elaborating the systemic immune landscape of heterologous-boosting COVID-19 immunization by the novel single B cell sorting platform and scRNA/V(D)J-seq technology. NCT04892459.

PMID 42464341
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PubMedXi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology2026-07-17

[To explore the immune landscape of lung adenocarcinoma patients with draining lymph nodes based on single cell sequencing].

Shi Tingwei T, Li Wen W, Fan Zhiliang Z, Liu Hanshen H et al.

Objective To explore the immune landscape of patients with lung adenocarcinoma with drainage lymph nodes by single-cell sequencing technology. Methods The lung cancer single cell dataset (GSE277742) was obtained from the Gene Expression Omnibus (GEO) database of the National Center for Biotechnology Information (NCBI). The dataset included intrathoracic DLN from 18 patients with pathologically confirmed lymph node metastasis and 4 control patients without evidence of metastasis. R language was used for data quality control, dimensionality reduction clustering, cell subgroup annotation and cell communication analysis to identify key cell subsets and screen differentially expressed genes. Kaplan-Meier survival analysis was performed using the TCGA database. Results Single cell sequencing analysis showed that the proportion of CD8+ T cells in patients with draining lymph nodes was significantly higher, among which cyclin-dependent kinase 6(CDK6), cyclin D3(CCND3), CCNH, cyclin-dependent kinase inhibitor 2A/B/D(CDKN2A/B/D) and retinoblastoma transcriptional corepressor 1(RB1) were highly expressed. TCGA database analysis showed that the expression of genes related to the BIOCARTA_CELLCYCLE_PATHWAY pathway was significantly different between tumor and normal samples, and was related to survival. Conclusion Several key genes differentially expressed in the draining lymph nodes of patients with lung adenocarcinoma are screened by bioinformatics methods, which provides a new perspective for further analysis of the regulatory mechanism of the immune microenvironment of lung adenocarcinoma with draining lymph nodes.

PMID 42463311
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PubMedJournal of human immunity2026-07-17

Implementing calculated globulin screening for immunodeficiencies: The benefits and challenges.

Jolles Stephen S, Poli Cecilia C, Rider Nicholas L NL, Negritu Gabriela G et al.

There is a need for pragmatic and cost-effective methodologies to facilitate earlier diagnosis of patients with primary and secondary immunodeficiencies, who often experience diagnostic delays that impact their quality of life, morbidity, and mortality. This review article will consider the utility of calculated globulin (CG) as a simple and unbiased screening tool for immunodeficiencies. We review literature indicating that CG can serve as an inexpensive and routinely performed proxy for immunoglobulin levels due to their established correlation. We also set out a workflow for the implementation of CG into clinical practice and discuss optimal approaches to embedding into laboratory reporting systems, and integration of AI approaches could expedite diagnoses. Finally, we discuss the challenges and pitfalls of CG screening, including the need for established CG cutoffs/action values across different patient age cohorts. Collaboration among biochemistry and immunology laboratories, clinicians, and patient organizations will be required to manage the logistics of effective broader implementation of CG screening into clinical practice.

PMID 42466166
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PubMedFrontiers in immunology2026-07-17

Immunological coagulation dual axis stratification identifies ultra high-risk phenotypes in systemic sclerosis.

Zhao Yaqi Y, An Yan Y, Yang Qingrui Q, Ma Zhenzhen Z

Systemic sclerosis is a heterogeneous autoimmune disease characterized by complex interplay among immune activation, inflammation, coagulation, and fibrinolysis. This study aimed to construct a comprehensive immune-inflammation-coagulation-fibrinolysis (IICF) network and to evaluate its topological features and prognostic value across distinct organ involvement phenotypes. A total of 287 patients with systemic sclerosis were retrospectively enrolled, including 166 with isolated SSc, 85 with concomitant interstitial lung disease (ILD), 18 with pulmonary hypertension (PH), and 18 with both ILD and PH. Twelve composite indices encompassing IICF pathways were calculated. LASSO-Cox regression was employed to build a multi-index prognostic score, K-means clustering was performed to identify molecular endotypes, and patients were stratified using optimal cut-off values of the Systemic Immune-Inflammation Index (SII) and the D-dimer-to-Platelet Ratio (DPR) for dual-axis survival analysis. Immune-coagulation dual-axis stratification revealed that patients with concurrent elevation of both SII and DPR had a 7.41-fold higher mortality risk than those with dual-low levels (HR 7.41, 95% CI 2.09-26.30, P = 0.002), whereas elevation of either index alone did not reach statistical significance. K-means clustering identified three IICF molecular endotypes, which showed incomplete concordance with the presence of ILD or PH. The multi-index prognostic score yielded an area under the curve of 0.747 for mortality prediction, surpassing the Prognostic Nutritional Index (0.693) and the Neutrophil-to-Lymphocyte Ratio (0.675). Adverse outcomes in systemic sclerosis are driven by systemic network disequilibrium rather than isolated pathway aberrations, with synergistic interplay between immune activation and coagulation dysregulation representing a pivotal mechanism. IICF-based dual-axis stratification and multi-index scoring provide a quantifiable approach for precision phenotyping and may inform stratified therapeutic decision-making.

PMID 42465738
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PubMedCell reports. Medicine2026-07-17

Evolution of SPP1+ cavity macrophage-mediated immunotherapy resistance in peritoneal metastasis of colorectal cancer.

Dai Xiaomeng X, Lai Chunyu C, Hong Libing L, Jin Yuzhi Y et al.

The immunometabolic basis of therapy-resistant colorectal cancer (CRC) peritoneal carcinomatosis with malignant ascites remains poorly defined. Here, we profile ascites immune cells from 20 patients across treatment-naive, chemo/targeted therapy-refractory, and immune checkpoint blockade (ICB)/adoptive T cell therapy (ACT)-resistant CRC. Single-cell RNA sequencing identifies SPP1+ cavity macrophages as drivers of CD8+ T cell dysfunction. Proteomic profiling of 36 patients confirms SPP1 enrichment in ICB/ACT-resistant peritoneal metastases. Mechanistically, SPP1 sustains an M2-like program via PPARγ activation and lipid uptake. SPP1 deficiency reduces PPARγ ligand precursors, triggering NF-κB-driven macrophage reprogramming and reversing CD8+ T cell suppression. Supplementation with 15 d-PGJ2 and fatty acids restores the M2 phenotype. In vivo, macrophage-specific SPP1 knockout enhances cytotoxic T lymphocyte infiltration and ICB efficacy, while SPP1 neutralization overcomes ICB resistance and augments ACT efficacy. Thus, SPP1+ cavity macrophages are central immunometabolic regulators, and SPP1 inhibition represents a promising strategy to overcome immunotherapy resistance in this lethal disease.

PMID 42462726
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PubMedJournal of translational medicine2026-07-17

The NLRP3 inflammasome in gastrointestinal malignancies: molecular mechanisms, regulatory networks, and therapeutic opportunities.

Cai Lei L, Deng Wenzhi W, Liu Bang B, Wang Jin J et al.

The NLRP3 inflammasome is a key inflammatory sensing platform in the innate immune system. It integrates pathogen-associated molecular patterns, damage-associated molecular patterns, and diverse cellular stress signals. Once activated, it promotes caspase-1 activation, maturation and release of IL-1β and IL-18, and gasdermin D-mediated pyroptosis. Through these processes, the NLRP3 inflammasome contributes to inflammatory responses and the maintenance of tissue homeostasis. Increasing evidence has shown that the NLRP3 inflammasome plays a critical but complex role in the initiation and progression of gastrointestinal malignancies. In esophageal cancer, gastric cancer, and colorectal cancer, NLRP3 activity can be regulated by microbial infection, bile acid stimulation, environmental carcinogens, gut dysbiosis, metabolic abnormalities, mitochondrial dysfunction, reactive oxygen species accumulation, and treatment-induced stress. Sustained or aberrant NLRP3 activation may promote chronic inflammation, epithelial barrier disruption, IL-1β-mediated myeloid cell recruitment, immunosuppressive microenvironment formation, tumor invasion and metastasis, and therapeutic resistance. In contrast, under specific therapeutic conditions, NLRP3-mediated pyroptosis in tumor cells can enhance antigen release, activate antitumor immunity, and improve the efficacy of chemotherapy, radiotherapy, and immune checkpoint inhibitors. Therefore, the function of the NLRP3 inflammasome in gastrointestinal tumors is highly dependent on cell type, disease stage, inflammatory intensity, immune composition, and treatment context. This review summarizes the molecular mechanisms of NLRP3 inflammasome activation, its tumor-promoting and tumor-suppressive roles in gastrointestinal malignancies, its relationship with immune checkpoint inhibitor response, and emerging therapeutic strategies targeting this pathway. The NLRP3 inflammasome is not simply a tumor-promoting or tumor-suppressive factor in gastrointestinal malignancies. Instead, its biological effects are highly context dependent. Precise modulation of NLRP3, rather than simple inhibition or activation, may provide new opportunities for individualized treatment of gastrointestinal cancers. Future studies should define the cellular source, activation state, downstream effector profile, and immune context of NLRP3 signaling to guide rational therapeutic application.

PMID 42464297
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