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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

PubMedMicrobiome2026-11-11

Adjuvant commensal therapy enhances antibiotic efficacy against Staphylococcus aureus.

Chang Chun-Chi CC, Demeter Tomas T, Gómez-Mejia Alejandro A, Barcik Weronika W et al.

Staphylococcus aureus is a common human pathobiont whose nasal colonization represents a major risk factor for subsequent infection. The prevalence of antimicrobial resistance, coupled with antibiotic-induced microbiota perturbation, has rendered S. aureus-associated infections increasingly difficult to treat. Commensal bacteria have emerged as potential modulators of both host immune responses and pathogen pathogenesis; however, whether they can act as therapeutic adjuvants to enhance treatment outcomes in S. aureus-associated infections remains unclear. Here, we assess the efficacy of commensal bacteria as an adjuvant therapeutic strategy. Using A549 Dual™ reporter cells, we demonstrate that commensals and pathobionts elicit distinct activation profiles of NF-κB and interferon regulatory factor (IRF) signaling pathways and differential IL-8 production. In a 3D humanized airway tissue model, D. pigrum significantly enhanced antibiotic-mediated reduction of S. aureus survival relative to antibiotic treatment alone (D. pigrum KPL1914: 37.3% reduction, 95% CI 2.0-72.6%, Padj = 0.0340; D. pigrum AMBR11: 48.1% reduction, 95% CI 2.3-93.9%, Padj = 0.0356), while preserving barrier integrity and augmenting pro-inflammatory cytokine responses. However, the loss of efficacy with heat-killed D. pigrum indicates that viable bacteria and active host- and/or pathobiont-directed interactions are required to mediate its anti-S. aureus effects. Dual RNA-seq transcriptomic analysis revealed enrichment of host inflammatory pathways and reduction of S. aureus pathogenic potential during D. pigrum antibiotic adjuvant treatment in the airway tissue model. Furthermore, co-culture experiments revealed that D. pigrum constrains core metabolic pathways in S. aureus. These findings demonstrate that D. pigrum limits S. aureus through both host immune modulation and direct suppression of bacterial pathogenesis and adaptive fitness, supporting its potential as a microbiota-based therapeutic adjuvant to enhance antibiotic efficacy against S. aureus-associated infections. Video Abstract.

PMID 43010108
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PubMedCell press blue2026-11-11

Cutaneous nonpeptidergic neurons sense extracellular ATP to augment barrier repair and C. albicans host defense.

Edwards Tara N TN, Chen Chien-Sin CS, Cattley Richard T RT, Mehta Isha I et al.

Cutaneous pain-sensing nociceptive neurons can directly recognize pathogen invasion and modulate the resulting host immune response. Neuronal recognition of C. albicans cell wall components is necessary and sufficient for optimal protective local type-17 immune responses. We now report a parallel neuroimmune pathway in which extracellular ATP (eATP) released from C. albicans and keratinocytes activates nonpeptidergic neurons, including Mas-related G protein-coupled receptor D (Mrgprd)-expressing NP1 neurons, through the P2X3 ATP receptor. Ablation of NP1 neurons or P2rx3 increased C. albicans colony-forming units (CFUs), but the induction of type-17 responses was unaffected. Rather, transcriptomic analysis revealed an alteration in genes and pathways associated with barrier repair. P2rx3-/- mice showed increased wound size and transepidermal water loss associated with a delay in barrier repair following C. albicans infection or abrasion. These data identify a neuroimmune circuit where nonpeptidergic neurons sense epidermal damage or infection through eATP and P2X3, resulting in augmented barrier repair and thus host defense.

PMID 43011974
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PubMedFrontiers in immunology2026-11-11

Mechano-metabolic coupling in the tumor microenvironment: from mechanotransduction to protein lactylation and metastatic cascades.

Zhang Wenqing W, Chen Huimei H, Fan Jingying J, He Yingchun Y et al.

Aberrant mechanical signals within the tumor microenvironment (TME)-including increased extracellular matrix stiffness, elevated solid stress, heightened interstitial fluid pressure, and fluid shear stress-have been established as key drivers of malignant tumor progression and metastasis. These physical cues are sensed by mechanoreceptors on the cell membrane (Piezo1, TRP channels, and integrin-FAK complexes), transmitted intracellularly through Rho GTPases and cytoskeletal dynamics, and ultimately reprogram transcriptional programs via nuclear translocation of transcriptional co-activators such as YAP/TAZ. Mechanical signals also drive metabolic reprogramming in tumor cells, particularly enhancing aerobic glycolysis (the Warburg effect), which results in massive lactate accumulation. Landmark discoveries in recent years have revealed that lactate serves as a substrate to drive histone and non-histone lactylation, directly coupling metabolic status with epigenetic regulation. Histone lactylation (e.g., H3K18la, H3K9la) activates pro-metastatic transcriptional programs by remodeling chromatin accessibility, promoting epithelial-mesenchymal transition (EMT), immune evasion, and therapeutic resistance; non-histone lactylation directly modifies cytoskeletal proteins (CFL1, vimentin, TPX2) and transcriptional regulators (Snail, YY1, PRMT1), enhancing the metastatic execution capacity of tumor cells at multiple levels, including cellular mechanical properties, migratory ability, and signal transduction. Importantly, mechanical signals, metabolic reprogramming, and lactylation constitute a mechano-metabolism-lactylation positive feedback loop, forming a self-reinforcing vicious cycle that continuously fuels tumor metastasis. This review systematically outlines the types and mechanotransduction mechanisms of TME mechanical signals, mechanically driven metabolic and transcriptional reprogramming, the multifaceted functions of lactylation in tumor metastasis, and the ultimate execution of the metastatic cascade driven by this positive feedback loop, and discusses potential therapeutic strategies targeting mechanosensitive pathways, metabolic vulnerabilities, and lactylation-modifying enzymes.

PMID 43011729
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PubMedBioscience reports2026-11-11

From genome guardian to immune modulator: the dual faces of DNA-PKcs.

Li Qiang Q, Zhan Pei-Wen PW, Hong Xian X, Qu Ying Y et al.

The DNA-dependent protein kinase catalytic subunit (DNA-PKcs) has long been recognized as a genome guardian, serving as a master regulator of non-homologous end joining (NHEJ), safeguarding genomic integrity and enabling adaptive immunity through V(D)J recombination. Beyond this nuclear function, DNA-PKcs is now increasingly appreciated as a context-dependent immune modulator, acting at the interface between the DNA damage response and inflammatory signaling. This review synthesizes recent advances that redefine DNA-PKcs as a versatile "molecular integrator." We delineate its structural dynamics and multifaceted regulation, and dissect its dual function in the cytoplasm, where it can either potentiate or suppress the cyclic GMP-AMP synthase and stimulator of interferon genes (cGAS-STING) pathway and even initiate STING-independent interferon responses. We further explore how dysregulation of DNA-PKcs underpins a spectrum of pathologies, from immunodeficiency and autoimmunity to cancer and neurodegeneration. Finally, we discuss the translational promise of DNA-PKcs inhibitors, which not only act as classical chemo- and radio-sensitizers but also remodel the tumor microenvironment by activating antitumor immunity. Decoding the context-dependent logic behind these dual faces is therefore paramount for developing novel therapeutics that leverage DNA-PKcs across oncology, autoimmunity, and neurodegeneration.

PMID 43012527
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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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PubMedIndian journal of dermatology2026-11-11

Injections of Autologous Platelet-Rich Plasma into the Facial Skin: Assessing Safety and Influence on the Immune System According to the Routine Laboratory Tests.

Koshkinbayeva Alina R AR, Ogizbayeva Alina V AV, Ponamareva Olga Anatolyevna OA, Omarkulov Bauyrzhan K BK

The purpose of this research was to study the safety of the PRP injections into the facial skin and assess its effect on immune system according to the routine laboratory tests. The research involved 50 women aged 20 to 52 years who received intradermal PRP injections into the facial skin. General examination, complete blood count before the procedure, and 1, 3, and 6 months after it, rheumatoid factor, lupus anticoagulant, and D-dimer in the blood serum before the procedure and 6 months after it were conducted for all the subjects involved in the research. According to the studied indicators of autoimmune diseases (rheumatoid factor and lupus anticoagulant), there were no differences 6 months after the PRP injection procedure (P = 0.139 and P = 0.208, respectively). A small number of patients (6-20%) had a slight increase in lymphocytes (up to a maximum of 47.8%) and monocytes (up to a maximum of 11.4%) in the blood after 1, 3, and 6 months, which tended to normalise over time (P = 0.0001). No undesirable local or systemic reactions after the procedure as well as during the observed period were recorded. An algorithm for laboratory examination of patients before and after the PRP injections into the facial skin was proposed to exclude undesirable adverse reactions after the procedure. The safety research should be continued, taking into account the multiplicity of the procedure and its combination with other cosmetic effects.

PMID 43012010
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