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human normal immunoglobulin G (NPB01)

✓ Approved

Nihon Pharmaceutical · Polyclonal Antibodies · Polyclonal Antibodies

What is human normal immunoglobulin G?

human normal immunoglobulin G is a polyclonal antibodies developed by Nihon Pharmaceutical. It is approved for therapeutic indications via injectable (others) or intravenous (iv).

Drug Profile

Brand NamesNPB01
CompanyNihon Pharmaceutical
Drug ClassPolyclonal Antibodies, Antibody
RouteInjectable (Others), Intravenous (IV)
StatusApproved
Sources: ClinicalTrials.gov, Nihon Pharmaceutical

Therapeutic Indications

human normal immunoglobulin G is developed for 11 unique indications across 5 therapeutic areas.

Therapeutic AreaConditionPhase
Skin and subcutaneous tissue disordersErythema multiforme✓ Approved
Nervous system disordersGuillain-Barre syndrome✓ Approved
Skin and subcutaneous tissue disordersPemphigoid✓ Approved
Skin and subcutaneous tissue disordersPemphigus✓ Approved
Infections and infestationsSalmonellosis✓ Approved

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Related Research Articles

PubMedbioRxiv : the preprint server for biology2026-07-17

Allosteric disulfide control of ligand binding and endocytosis of KIR2DL4, the natural killer cell receptor for HLA-G.

Rajagopalan Sumati S, Chiu Joyce J, Chaurasia Priyanka P, Lu Jinghua J et al.

Human Leukocyte Antigen (HLA)-G is selectively expressed by fetal trophoblast cells that invade maternal tissue and encounter maternal natural killer (NK) cells early in pregnancy. In NK cells, the endosomal receptor KIR2DL4 responds to soluble HLA-G by inducing a broad transcriptional program to support placental development. Structural features of KIR2DL4 that control ligand binding and endocytosis are unclear. Random mutagenesis revealed that three cysteines in the first immunoglobulin domain of KIR2DL4 regulate endocytosis and uptake of HLA-G. We found that the atypical Cys10-Cys28 disulfide bond observed in the KIR2DL4 crystal structure is an allosteric disulfide with potential to switch to a conventional Cys28-Cys74 bond. KIR2DL4 in human cells exists in both disulfide-bonded states, as shown by mass spectrometry analysis. The Cys10-Cys28 bond in a Cys74Ser KIR2DL4 mutant was reduced by protein disulfide isomerase (PDI) in vitro. Inhibition of PDI prevented HLA-G uptake by KIR2DL4 in both transfected 293T cells and primary NK cells. Mutants in the Cys10-Cys28 configuration endocytosed spontaneously but did not bind HLA-G. Conversely, KIR2DL4 with a Cys28-Cys74 bond was at the plasma membrane and responded to soluble HLA-G by endocytosis and transcription of the interferon stimulated gene IFI44L , like wild-type cells. A purified Cys10Leu KIR2DL4 mutant, which exhibited a reduced tendency to oligomerize, bound HLA-G in a peptide dependent manner with an affinity in the low micromolar range. Disulfide switching from the Cys10-Cys28 to the Cys28-Cys74 form correlated with a distant allosteric change, as predicted by AlphaFold, that could reorient a D0 domain loop to facilitate HLA-G binding. Thus, conversion from an inactive state to an HLA-G binding form regulates KIR2DL4 cellular localization and function to promote fetal development.

PMID 42465296
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PubMedEuropean journal of case reports in internal medicine2026-07-17

Isolated Cytomegalovirus Optic Neuritis in an Immunocompetent Patient.

Petrakis Vasileios V, Aggelopoulou Christina C, Tartanis Georgios G, Tsakaldimi Soultana S et al.

Cytomegalovirus (CMV) typically causes asymptomatic or mild, self-limiting infections in immunocompetent individuals. Severe end-organ disease, particularly isolated central nervous system or ocular involvement, is associated with significant immunosuppression. Isolated optic neuritis due to CMV in a healthy, immunocompetent host is a rare clinical entity, which can lead to delayed diagnosis and potential vision loss. We report a rare case of a previously healthy 25-year-old male who presented with a 3-day history of intermittent right retrobulbar pain and was found to have early bilateral optic disc oedema. Best-corrected visual acuity was 9/10 in the right eye, with normal colour vision and no relative afferent pupillary defect. An extensive neurological, immunological, and infectious disease workup was negative for autoimmune and demyelinating conditions. However, serological testing revealed positive immunoglobulin M and immunoglobulin G titres for CMV. Concurrent polymerase chain reaction (PCR) testing detected CMV viremia in both blood and cerebrospinal fluid (CSF), confirming an active CMV infection with central nervous system involvement. The patient was treated with high-dose intravenous corticosteroids and systemic antiviral therapy with valganciclovir leading to a complete clinical and anatomical recovery and no clinical relapse during the follow-up period. This case highlights that severe CMV neuroretinal manifestations can occur in strictly immunocompetent patients. Prompt molecular diagnostic testing, specifically CSF and blood PCR, is crucial when atypical optic neuritis is encountered. A combined regimen of antiviral therapy and high-dose corticosteroids represents a highly effective, organ-saving approach for managing CMV-induced optic neuritis. Cytomegalovirus must be included in the differential diagnosis of acute optic neuritis and bilateral optic disc oedema, even in young, strictly immunocompetent patients without concurrent retinitis or prior immunosuppression.The utilization of polymerase chain reaction to detect viral copies in both blood and cerebrospinal fluid is essential for confirming active systemic and central nervous system viral involvement.The management of viral optic neuritis may necessitate a dual pharmacological strategy. High-dose corticosteroids are crucial to rapidly suppress tissue-damaging inflammation behind an intact blood-brain barrier, while systemic antiviral therapy is required to eradicate the underlying viral load and prevent clinical relapse.

PMID 42466218
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PubMedInternational journal of cancer2026-07-17

Survival Outcomes Associated With Short-Acting Versus Long-Acting G-CSF Use During First-Line Chemoimmunotherapy for Advanced Lung Cancer: A Retrospective Study.

Xiong Yanjuan Y, Guo Wenjing W, Ma Chenxi C, Ren Xiubao X et al.

While granulocyte colony-stimulating factor (G-CSF) is used to prevent and treat chemotherapy-induced neutropenia, it also regulates key immune cells and may therefore affect the efficacy of immunotherapy. Short-acting and long-acting G-CSF have similar efficacy in managing neutropenia, but they differ in effects on immune cells. However, the overall impact of G-CSF and its different formulations on survival in advanced lung cancer patients receiving chemoimmunotherapy remains unclear. This retrospective study enrolled patients with advanced primary lung cancer receiving first-line chemoimmunotherapy at Tianjin Medical University Cancer Institute and Hospital. The primary outcome was overall survival (OS). Inverse probability of treatment weighting (IPTW) was used to balance heterogeneity between groups. Kaplan Meier and Cox models were used to estimate OS and progression-free survival (PFS). Among 606 patients, 308 developed neutropenia and received G-CSF support (pegylated recombinant human G-CSF [PEG-rhG-CSF]: 183; recombinant human G-CSF [rhG-CSF]: 125); 298 without neutropenia received no G-CSF. After IPTW, no significant differences in PFS and OS were observed between G-CSF group and non-G-CSF group. Patients receiving rhG-CSF had significantly improved OS (42.6 vs. 28.2 months, p = 0.041) and PFS (15.4 vs. 9.4 months, p < 0.001) than those receiving PEG-rhG-CSF. Multivariable analysis confirmed rhG-CSF as a favorable independent prognostic factor for both PFS and OS. Among patients with advanced primary lung cancer receiving first-line chemoimmunotherapy, G-CSF support effectively abrogates the adverse survival impact of chemotherapy-induced neutropenia. Moreover, rhG-CSF was associated with improved clinical outcomes versus PEG-rhG-CSF. Prospective randomized trials are required to validate these findings and guide clinical practice.

PMID 42463467
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PubMedCase reports in nephrology2026-07-17

A Rare Diagnostic Dilemma of P-ANCA/MPO Positive Crescentic Glomerulonephritis in an Immunosuppressed Lupus Patient.

Elrefy Omar O, Carpenter Sweta S, Saini Manu M, Balasubramanian Manjula M et al.

Perinuclear antineutrophil cytoplasmic antibodies (P-ANCAs) and myeloperoxidase (MPO) antibodies are detected in 15%-25% of lupus nephritis patients, but systemic lupus erythematosus (SLE)/ANCA-associated vasculitis (AAV) overlap syndrome is rare, occurring in approximately 2% of cases. We present a 57-year-old woman with SLE and antiphospholipid syndrome (APS) on belimumab, hydroxychloroquine, and prednisone, who presented with acute ischemic stroke requiring thrombectomy and rapidly progressive renal failure (creatinine rising from 1.1 to 5.2 mg/dL) with nephrotic-range proteinuria (8.6 g/g). P-ANCA titer was > 1:640 with MPO positivity, while anti-dsDNA, C3, and C4 were normal. Kidney biopsy revealed crescentic glomerulonephritis with neutrophil-rich infiltrates and immune complex deposits on electron microscopy but without "full house" immunofluorescence, favoring SLE/AAV overlap rather than isolated lupus nephritis flare. Treatment with methylprednisolone, rituximab, and anticoagulation resulted in significant renal recovery (creatinine 1.7 mg/dL, proteinuria 4.4 g/g). This case highlights the importance of ANCA testing in SLE patients with unexplained rapidly progressive glomerulonephritis, as early recognition of overlap syndrome carries distinct therapeutic implications, including the use of rituximab-based regimens targeting both disease processes.

PMID 42465798
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PubMedModern rheumatology case reports2026-07-17

Persistent parvovirus B19 infection in an older patient with rheumatoid arthritis receiving immunosuppressive therapy: A case report and literature review.

Oyama Masako M, Yoshida Yusuke Y, Yoshida Tetsumi T, Kobayashi Hiroki H et al.

An 84-year-old man with rheumatoid arthritis undergoing treatment with methotrexate presented with fever, general fatigue, and appetite loss. He had a 3-month history of unexplained normocytic anaemia with reticulocytopenia. Bone marrow examination revealed erythroid hypoplasia with giant pro-erythroblasts, leading to a diagnosis of parvovirus B19 infection. In this case, intravenous immunoglobulin therapy improved the patient's anaemia and systemic symptoms. Six months after the treatment, parvovirus B19 DNA remained detectable using polymerase chain reaction; however, the viral load had markedly decreased, indicating a favourable virological response. Twenty cases of parvovirus B19 infection in older adults (aged ≥65 years) were identified in the literature. Immunocompromised older patients frequently develop persistent parvovirus B19 infections that require treatment with intravenous immunoglobulin therapy, whereas persistent infections are not observed in immunocompetent older individuals. Therefore, this case suggests that clinicians should be aware of persistent parvovirus B19 infection in older immunosuppressed patients who develop unexplained anaemia with reticulocytopenia. Moreover, intravenous immunoglobulin therapy may be considered as an effective therapeutic option for persistent parvovirus B19 infection in immunocompromised patients.

PMID 42466599
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PubMedHandbook of experimental pharmacology2026-07-17

TAAR Immunopharmacology.

Magnesa Anna A, Pacini Andrea A, Rutigliano Grazia G

Trace amine-associated receptors (TAARs) were originally identified as G protein-coupled receptors involved in monoaminergic signaling within the central nervous system. However, accumulating evidence indicates that TAARs, particularly TAAR1 and TAAR2, are also expressed in the immune system, including circulating leukocytes, lymphocytes, macrophages, and microglia. This chapter reviews current evidence regarding TAAR expression, functional pharmacology, and potential translational relevance within the immune system.Expression studies support a predominant TAAR1/TAAR2 pattern across both innate and adaptive immune-cell populations. Functional studies indicate that TAAR signaling can modulate inflammatory responses through chemotaxis, cytokine production, and immunoglobulin secretion. However, these effects are highly context-dependent, preventing a simple classification of TAAR signaling as either pro-inflammatory or anti-inflammatory.The chapter also discusses the emerging role of TAAR signaling in the pathophysiology of diseases, including inflammatory bowel disease, methamphetamine-associated immune dysfunction during HIV infection, multiple sclerosis, Parkinson's disease, fibromyalgia, and hematological malignancies.Despite growing interest in TAAR immunopharmacology, the current evidence remains largely preclinical and methodologically heterogeneous. Major limitations include incomplete protein-level validation, reliance on immortalized cell lines or mixed-cell populations, species-specific pharmacology of available ligands, and limited understanding of physiological trace amine signaling under basal conditions. Further integrative studies will be required to clarify TAAR pathophysiological significance and determine whether TAAR-targeted strategies may have translational relevance in immune-mediated disorders.

PMID 42463873
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