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anti-hepatitis-B therapy (IMMUNO HBS / UMANBIG / IMMUNOHBS)

✓ Approved

Kedrion · Polyclonal Antibodies · Polyclonal Antibodies

What is anti-hepatitis-B therapy?

anti-hepatitis-B therapy is a polyclonal antibodies developed by Kedrion. It is approved for therapeutic indications via injectable (others) or intramuscular (im) injection or intravenous (iv).

Drug Profile

Brand NamesIMMUNO HBS, UMANBIG, IMMUNOHBS
CompanyKedrion
Drug ClassPolyclonal Antibodies, Antibody
RouteInjectable (Others), Intramuscular (IM) Injection, Intravenous (IV)
StatusApproved
Sources: ClinicalTrials.gov, Kedrion

Therapeutic Indications

anti-hepatitis-B therapy is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Infections and infestationsHepatitis B✓ Approved

Related Research Articles

PubMedMediastinum (Hong Kong, China)2026-09-20

Anti-angiogenic therapy in thymic carcinoma: a narrative review of current evidence and emerging combinations.

Kim Hye Sung HS, Padda Sukhmani K SK

Thymic carcinoma (TC) is a rare and aggressive malignancy with limited systemic treatment options. Although platinum-based chemotherapy has historically been the first-line standard, anti-angiogenic therapy has emerged as an important therapeutic strategy across treatment settings. This review synthesizes current evidence on anti-angiogenic therapies, as monotherapy and in combination with chemotherapy or immunotherapy, and defines their evolving role in TC management. A targeted narrative review was conducted using PubMed/MEDLINE, Embase, Google Scholar, ClinicalTrials.gov, conference proceedings, and reference list screening to identify clinical studies of anti-angiogenic therapy in TC published from January 2000 to January 2026. Anti-angiogenic therapy demonstrates clinical activity across treatment settings in TC. Yet the magnitude and durability of benefit vary by agent, treatment line, and prior vascular endothelial growth factor (VEGF) exposure. In the first-line setting, VEGFR-2 inhibition with ramucirumab combined with platinum-based chemotherapy has achieved encouraging response rates and prolonged progression-free survival (PFS), though findings require cautious interpretation given small sample sizes and early termination of the trials without phase III confirmation. Multikinase inhibitors, such as sunitinib and lenvatinib, provide durable disease control in previously treated patients, with benefit closely linked to maintaining adequate dose intensity. Anti-angiogenic agents combined with immunotherapy have further expanded therapeutic options, particularly in anti-angiogenic-naïve patients; however, superiority over sequential use of these agents is unproven and additive toxicity is substantial. No validated predictive biomarkers currently guide treatment selection or sequencing. Anti-angiogenic therapy has emerged as a clinically active component of TC management across treatment lines and in rational combinations. The evidence base nevertheless rests on small phase II studies without confirmatory phase III data or broad regulatory approval. Future progress will depend on optimizing treatment sequencing, improving toxicity management, and advancing biomarker-driven patient selection through collaborative, multi-institutional efforts.

PMID 42763652
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PubMedCurrent health sciences journal2026-09-20

Evaluating the Role of Exosome Therapy in Reproductive Aging:A Narrative Review of Recent Advancements.

Moghaddam Elham Sadat Alavi ESA, Talebi Hooman Mohammad HM

Exosome therapy shows promise as a non-hormonal treatment to restore ovarian function and combat reproductive aging. This review aims to explore recent advances, mechanisms, and clinical potential of exosome therapy in reproductive aging. This narrative review explored advancements in exosome therapy for reproductive aging through a comprehensive literature search of PubMed, Embase, Google Scholar, and ClinicalKey, covering studies from 2015 to 2025. Using a structured search strategy with relevant MeSH terms and keywords. After applying inclusion and exclusion criteria focused on human studies with therapeutic relevance, 13 articles were selected. Key data were extracted and synthesized to highlight mechanisms, clinical potential, and future directions of exosome-based interventions in ovarian aging. Thirteen human-focused studies were categorized into four themes: ovarian function restoration, exosomal biomarkers, therapeutic roles in reproductive diseases, and clinical applications. Exosomes especially MSC-derived enhanced ovarian regeneration through anti-apoptotic, anti-inflammatory, and metabolic pathways. Age-related changes in exosomal cargo showed strong diagnostic potential. Exosomes also demonstrated therapeutic effects in POI and PCOS and showed promise as low-immunogenic, cell-free nanocarriers for targeted reproductive-aging interventions. Exosome therapy is a promising, non-hormonal option for addressing reproductive aging, with potential for safe and effective clinical use.

PMID 42763769
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PubMedGenes & diseases2026-09-20

LAMA5 pathogenic variant uncovers a novel autoantigen in membranous nephropathy.

Xiao Han H, Yin Hui H, Shi Yulu Y, Zhou Xindi X et al.

Membranous nephropathy is a leading cause of nephrotic syndrome, driven by autoantibodies targeting podocyte antigens. Although antibodies against PLA2R and THSD7A account for the majority of cases, a substantial fraction of patients remain seronegative, implying the existence of additional, unidentified autoantigens. Here, we report the identification of two novel compound heterozygous mutations in LAMA5 encoding Laminin α5, in a pediatric patient with severe nephrotic syndrome. Whole-exome sequencing revealed c.1355A>T (p.N452I) and c.9770A>G (p.N3257S) variants, with structural modeling indicating that p.N452I induces a conformational change in Laminin α5. This altered conformation enhanced its binding to Collagen IV networks, resulting in thickening of the glomerular basement membrane and the creation of a neo-epitope recognized by conformation-specific IgG1/IgG3 autoantibodies. These autoantibodies activated the classical complement pathway, triggering podocyte injury. A knock-in mouse model harboring the Lama5 N457I mutation recapitulated the human phenotype, exhibiting proteinuria, glomerular basement membrane thickening, and glomerular IgG deposits. Notably, rituximab treatment in the patient led to the disappearance of anti-Laminin α5 autoantibodies and sustained clinical remission. Our findings establish Laminin α5 as a novel genetic autoantigen in membranous nephropathy and suggest that screening for anti-Laminin α5 antibodies may help identify patients who could benefit from B-cell-targeted therapies.

PMID 42763546
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PubMedGenes & diseases2026-09-20

Autosomal dominant gain-of-function mutations in LCP1 cause a syndromic neutropenia and immunodeficiency.

Yu Lang L, Zhou Bo B, Liu Wei W, Li Wenhui W et al.

Actin cytoskeleton defects underlie immuno-actinopathies. We identified three patients with heterozygous LCP1 gain-of-function mutations (L362F, A365D) causing activated LCP1-associated immunodeficiency syndrome, characterized by congenital neutropenia, variable combined immunodeficiency, and allergy. Patients' neutrophils show maturation arrest and excessive apoptosis, while T/B cells are reduced and functionally impaired. Patient-derived iPSCs, CRISPR-edited cells, and LCP1+/L362F mice replicate these defects. Mechanistically, mutant LCP1 hyper-bundles F-actin, inducing VDAC1 oligomerization and mitochondrial apoptosis. This study further establishes LCP1 as a regulator of immune cell fate and suggests targeting actin dynamics as therapy.

PMID 42763497
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PubMedCurrent health sciences journal2026-09-20

Cutaneous Tuberculosis in a 22-Day-Old Neonate:A Diagnostic Challenge and Case Report.

Imran Arisha A, Shah Syeda Wareesha Fareeduddin SWF, Shah Syed Abdul Rafayuddin SAR, Rafique Muhammad M et al.

Cutaneous tuberculosis (CTB) is a rare extrapulmonary manifestation of tuberculosis, particularly in neonates. Its diagnosis is often challenging due to non-specific presentations that can mimic common conditions. We report the case of a 22-day-old male neonate who presented to the emergency room with fever and a scalp swelling following a reported fall from bed. Initial assessment suggested a subcutaneous abscess. The patient did not respond to multiple courses of intravenous antibiotics. A blood culture grew Burkholderia species, but targeted therapy also failed. Incision and drainage were performed, and pus GeneXpert testing was positive for Mycobacterium tuberculosis, despite a negative tuberculin skin test and clear chest X-ray. A final diagnosis of cutaneous tuberculosis (tuberculous chancre) was established. Anti-tuberculosis therapy (ATT) was initiated, leading to the complete resolution of the swelling and full recovery. This case underscores the diagnostic challenges of neonatal CTB. It highlights the importance of considering tuberculosis in the differential diagnosis of non-resolving abscesses in infants, especially in endemic areas, and demonstrates the critical role of molecular diagnostics like GeneXpert in achieving a timely diagnosis.

PMID 42763721
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PubMedVirology journal2026-09-20

Regulatory roles of G-quadruplexes and G-quadruplex-binding proteins across the enhancer and promoter of the HBV genome.

He Lina L, Huang Baoyue B, Ma Haiyang H, Wang Lin L et al.

Hepatitis B virus (HBV) infection poses a global threat to human health due to the limited availability of effective treatment options. Recent studies have shown that the structures of G-quadruplex (G4) are related to the pathogenesis of the virus and potential targets for antiviral therapy. G-quadruplex-binding proteins (G4BPs) play a key role in regulating the G4 landscape and its associated functions by anchoring, stabilizing, or unwinding G4 structures. Researchers have actively pursued the identification of G4 structures within the HBV genome, yet a comprehensive, genome-wide analysis revealing their regulatory role and that of G4BPs has remained largely elusive. Consequently, our understanding of the intricate interactions between HBV G4 and G4BPs remains quite limited. Biophysical and molecular biology approaches were employed to investigate HBV G4, focusing on core promoter and enhancer (CP/EN) activities. Mass spectrometry, DNA pull-down, and surface plasmon resonance (SPR) characterized interactions between G4 and G4BPs. Employing the dual luciferase reporter system and HBV infection model, this study utilized binding assays designed for the G4 mutant, alongside overexpression and knockdown experiments, to delve into the regulatory functions of G4 and G4BPs. We identified two functional G4 elements located at positions 1204 and 1732 within the HBV CP/EN regulatory region. Reporter assays containing the CP/EN sequences showed that disruption of either the 1204 or 1732 G4 structure significantly reduced promoter activity. In the HBV 1.3-mer system, disruption of the 1732 G4 markedly decreased HBsAg, HBeAg and HBcAg expression, whereas total HBV RNA and 3.5 kb RNA levels were not significantly affected. Both G4 elements selectively recruited multiple host proteins in vitro, among which the 1732 displayed stronger binding to HNF4A. Functional assays further demonstrated that HNF4A enhanced CP/EN-driven reporter activity in a G4-dependent manner, and stabilization of G4 structures by BRACO-19 further promoted the interaction between G4 and HNF4A. In addition, CNBP, the most highly enriched G4-binding protein, positively regulated HBV antigen and RNA expression; however, CNBP did not enhance CP/EN promoter activity, indicating a regulatory mechanism independent of CP/EN activation. This study reveals that two G4 structures within the HBV CP/EN regulatory region function as structural platforms for host factor recruitment and play distinct roles in regulating viral gene expression. In particular, the 1732 G4 facilitates HNF4A-dependent activation of CP/EN activity, thereby supporting efficient viral protein production, whereas CNBP promotes HBV expression through a CP/EN-independent mechanism.

PMID 42763390
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