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human hepatitis B immunoglobulin

✓ Approved

Hualan Biological Engineering Co., Ltd. · Polyclonal Antibodies · Polyclonal Antibodies

What is human hepatitis B immunoglobulin?

human hepatitis B immunoglobulin is a polyclonal antibodies developed by Hualan Biological Engineering Co., Ltd.. It is approved for therapeutic indications via injectable (others) or intramuscular (im) injection.

Drug Profile

CompanyHualan Biological Engineering Co., Ltd.
Drug ClassPolyclonal Antibodies, Antibody
RouteInjectable (Others), Intramuscular (IM) Injection
StatusApproved
Sources: ClinicalTrials.gov, Hualan Biological Engineering Co., Ltd.

Therapeutic Indications

human hepatitis B immunoglobulin is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Infections and infestationsHepatitis B✓ Approved

Related Research Articles

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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PubMedIranian journal of pharmaceutical research : IJPR2026-09-20

Binding of Epimedium Flavonoids to Human Serum Albumin: Insights from Spectroscopic and Molecular Docking Studies.

Wang Na N, Wang Yuwei Y, Yang Yang Y, Dong Lele L et al.

Epimedin A (EA), epimedin B (EB), and epimedin C (EC), major bioactive flavonoids in Epimedium Herba, have diverse pharmacological activities; however, their interactions with human serum albumin (HSA) remain unclear. This study aimed to investigate the binding mechanisms of EA, EB, and EC to HSA. Multispectroscopic techniques, including UV-vis, fluorescence, and synchronous fluorescence spectroscopy, as well as molecular docking and dynamics simulations, were employed under simulated physiological conditions. Fluorescence spectra were recorded at 298, 303, and 310 K, and molecular docking was performed with HSA (PDB ID: 1BKE). All three flavonoids quenched the intrinsic fluorescence of HSA via static quenching, forming 1:1 complexes with binding constants greater than 104 L·mol-1 (EB > EA > EC at 298 K). Thermodynamic analysis indicated spontaneous binding driven by hydrogen bonds and van der Waals forces. Synchronous fluorescence showed no significant microenvironmental changes around Trp and Tyr residues. Molecular docking and dynamics simulations suggested ligand-dependent differences in the preferred binding regions of HSA. These findings provide preliminary in vitro evidence for the binding of epimedin flavonoids to HSA and may inform future pharmacokinetic investigations.

PMID 42763635
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PubMedCureus2026-09-20

Guillain-Barré Syndrome Revealing Coexisting Cervical Spondylotic Myelopathy: A Diagnostic Pitfall.

Boubekri Hatim H, Salah Anass A, Mankar Bennis Najoua N, Khalfaoui Saloua S et al.

Guillain-Barré syndrome (GBS) is an acute inflammatory polyradiculoneuropathy characterized by rapidly progressive weakness and areflexia. Although the diagnosis is usually straightforward, atypical clinical evolution should prompt investigation for concomitant central nervous system pathology. We report the case of a 64-year-old man initially diagnosed with severe GBS based on clinical presentation, cerebrospinal fluid (CSF) analysis, and electroneuromyography (EMNG) findings. Despite partial neurological improvement after intravenous immunoglobulin therapy, the patient later developed cervical pain, brisk reflexes, and a positive Babinski sign. Cervical magnetic resonance imaging (MRI) revealed severe multilevel cervical spondylotic myelopathy (CSM) with spinal cord compression and intramedullary T2 hyperintensity. Surgical decompression was subsequently indicated. This case highlights the importance of reassessing patients with GBS who develop pyramidal signs or atypical neurological findings, as concomitant cervical myelopathy may be overlooked and delay appropriate management.

PMID 42763772
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PubMedGenes & diseases2026-09-20

High-throughput chemical screen identifies epothilone B in modulating inflammatory bowel disease by triggering neutrophil apoptosis.

He Zhenting Z, Deng Ziling Z, Zhang Huan H, Xiang Yiming Y et al.

Inflammatory bowel disease (IBD) is a chronic inflammatory condition of the gastrointestinal tract characterized by a complex interplay of genetic, environmental, and immunological factors. Neutrophils, as a key component of the innate immune system, play a critical role in IBD pathogenesis due to their dysregulated infiltration, impaired apoptosis, and resultant epithelial damage during the disease process. Conventional approaches aimed at suppressing neutrophil activity have achieved only modest clinical efficacy and highlight the need for strategies that recalibrate neutrophil responses without compromising their essential antimicrobial functions. In this study, we employed high-throughput chemical screening using neutrophil-specific transgenic zebrafish larvae to identify compounds capable of modulating neutrophil homeostasis, and subsequently evaluating their efficacy in a dextran sodium sulfate (DSS)-induced IBD model. We identified epothilone B (Epo B), a traditional chemotherapeutic drug, as a potential therapeutic candidate for IBD. Our findings demonstrate that Epo B protects against IBD by promoting intestinal epithelial recovery, alleviating inflammatory responses, and rebalancing the gut microbiota. Mechanistically, Epo B selectively stimulates neutrophil apoptosis by targeting and enhancing Caspase-3 cleavage, thereby inhibiting neutrophilic inflammation. This study underscores the utility of in vivo high-throughput drug screening in IBD and highlights Epo B as a promising candidate for drug repurposing in IBD treatment, offering a novel therapeutic strategy by targeting neutrophil apoptosis.

PMID 42763496
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PubMedAnesthesiology and pain medicine2026-09-20

Effectiveness of Apneic Oxygenation During Induction of General Anesthesia in Children Undergoing Adenotonsillectomy: A Prospective Randomized Controlled Study.

Ragab Safaa Gaber SG, Ali Lotfy Ahmed A, Botros Joseph Makram JM, Hashem Hasnaa Mohsen HM et al.

Children undergoing adenotonsillectomy often have partial airway obstruction due to hypertrophic tonsils and adenoids, increasing their risk of oxygen desaturation during anesthesia induction. This study aimed to evaluate whether apneic oxygenation via nasal cannula prevents oxygen desaturation during tracheal intubation in children aged 3 - 10 years undergoing adenotonsillectomy while assessing its effects on intubation conditions and hemodynamic stability. In this prospective, single-blinded, randomized controlled trial, 140 children scheduled for adenotonsillectomy were allocated to either standard intubation (group A, n = 70) or apneic oxygenation (group B, n = 70; 0.2 L/kg/min via nasal cannula). The primary outcome was the lowest peripheral oxygen saturation (SpO₂) during intubation. Peripheral SpO₂ was significantly lower during intubation in group A (97.40 ± 2.96) than in group B (99.91 ± 0.28) (P < 0.001). Group B also maintained significantly higher SpO₂ immediately after intubation (99.91 ± 0.28%) than group A (97.77 ± 2.24%; P < 0.001). No episodes of desaturation occurred in group B during the procedure (P < 0.001). In group A, 21.43% of patients desaturated to ≤ 95% (P < 0.001). Severe desaturation (SpO₂ < 92%) occurred in 7.14% of controls but was absent in group B (P = 0.023). Intubation time, intubation attempts, and bradycardia rates were comparable between groups (P > 0.05). Apneic oxygenation during intubation in children undergoing adenotonsillectomy effectively prevented desaturation without compromising safety or procedural efficiency.

PMID 42763625
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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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