Drug Database
AN

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

PubMedCureus2026-07-25

Fatal Acute Liver Failure Associated With Presumed Hepatitis B Virus Reactivation During Rituximab Maintenance Therapy: A Case Report.

Tran James J, Zhou Calvin C, Babun Asis A AA, Leung Whinkie W et al.

We report a woman in her 60s with follicular non-Hodgkin lymphoma receiving maintenance rituximab therapy, last administered one month prior to presentation, who developed progressive malaise, jaundice, and acute liver failure. Laboratory evaluation demonstrated severe hepatocellular injury with marked transaminase elevations (alanine aminotransferase: 2,500 U/L; aspartate aminotransferase: 2,400 U/L), hyperbilirubinemia (total bilirubin: 20 mg/dL), and coagulopathy. Hepatitis B virus (HBV) serology demonstrated active infection with elevated hepatitis B surface antigen (HBsAg) and detectable HBV DNA. Baseline HBV screening and antiviral prophylaxis records prior to rituximab initiation were unavailable from the treating institution, limiting the definitive confirmation of pre-existing HBV status. Given the patient's recent rituximab exposure, clinical presentation, and exclusion of alternative etiologies, HBV reactivation was considered the most likely diagnosis. The patient was diagnosed with HBV reactivation associated with rituximab therapy. Despite the initiation of antiviral treatment and aggressive supportive care, her clinical course rapidly deteriorated, complicated by hepatic encephalopathy, acute kidney injury requiring hemodialysis, and hypoxic respiratory failure. She was evaluated for liver transplantation but deemed ineligible due to multiorgan failure and ultimately transitioned to end-of-life care. This case highlights the potentially fatal consequences of HBV reactivation during rituximab therapy and underscores the importance of appropriate screening, prophylaxis, and vigilance in high-risk patients.

PMID 42500753
Read full article →
PubMedOpen forum infectious diseases2026-07-25

Prevalence of Hepatitis B Coinfection in People With HIV by Birth-Year Cohort.

Lee So Jeong SJ, Verinumbe Tarfa T, Lesko Catherine R CR, Fojo Anthony A et al.

Availability of the hepatitis B virus (HBV) vaccine in the United States since 1982 and recommendations for universal/catch-up vaccination of infants and children since the 1990s may be associated with lower HBV prevalence among people with human immunodeficiency virus (HIV; PWH) born after 1980. Active HBV infection prevalence, defined as the proportion of patients with a positive hepatitis B surface antigen result, was assessed among PWH at entry into a clinical cohort. Patients were categorized into birth-year cohorts of 1940-1959, 1960-1979, or 1980-1999 and then further dichotomized into pre- and post-1980 birth-year cohorts. Log binomial regression was used to assess the association of birth-year cohort with hepatitis B surface antigen positivity, adjusting for race/ethnicity, HIV infection risk factor, baseline HIV viral load and CD4+ cell count, HBV active therapy, and year of/age at cohort entry. Among 5598 PWH, most were male (67%) and Black (77%), with a mean age (SD) of 39.7 (9.6) years at cohort entry. Approximately a third of the participants (30%) identified as men who have sex with men, and 39% reported a history of injection drug use. At cohort entry, the majority had a CD4+ cell count <350/µL and a viral load >1000 copies/mL. The HBV prevalence was 6.7% overall but varied by birth-year cohort: 6.2% for 1940-1959, 7.9% for 1960-1979, and 2.6% for 1980-1999. The risk of HBV infection was lower in the post-1980 than in the pre-1980 cohort (adjusted prevalence ratio, 0.19 [95% confidence interval, .09- .42]). PWH born after 1980 had a lower prevalence of HBV coinfection than those born before 1980, supporting the potential impact of universal childhood HBV vaccination.

PMID 42500124
Read full article →
PubMedArchives of virology2026-07-25

HBV PreS/S gene mutations in patients with chronic hepatitis B.

Çakal Bülent B, Çavuş Bilger B, Atasoy Alp A, Bulakçı Mesut M et al.

Variants in the hepatitis B virus (HBV) PreS/S gene have been suggested to contribute to the development of progressive liver disease. This study aimed to evaluate the association between HBV PreS/S variations and liver histopathology in patients with chronic hepatitis B. A total of 109 patients under clinical follow-up for chronic hepatitis B were included. The HBV PreS/S gene was amplified by PCR and sequenced using the Sanger method. Amino acid substitutions, nonsense mutations, and deletions were analyzed in relation to liver fibrosis stage. Overall, 58 of 389 amino acid sites (14.9%) in the HBV PreS/S gene showed substitutions, with the highest mutation rate observed in the PreS2 region (27.27%). Mutations L54P (PreS1), F130L/S (PreS2), and S207R/N/I/T and I208T (S gene) were significantly more frequent in patients with advanced fibrosis (F ≥ 3) (p < 0.05). Multivariable analysis identified S207R/N/I/T as an independent risk factor for liver fibrosis. Patients with PreS2 mutations had higher fibrosis scores (p < 0.05). The S207R/N/I/T mutation in the C-terminal region of the HBV S protein is independently associated with liver fibrosis, while PreS2 mutations may contribute to fibrosis progression in chronic hepatitis B.

PMID 42498832
Read full article →
PubMedHealth science reports2026-07-25

Improvement in the Microbiological Diagnosis of Hepatitis D on the Mediterranean Coast of Southeastern Spain: A Repeated Cross-Sectional Survey.

Ventero Maria Paz MP, Tyshkovska Iryna I, Castillo-Sanchez Jose Carlos JC, Reus Sergio S et al.

Hepatitis D virus (HDV) remains underdiagnosed, and universal screening of HBsAg-positive patients is recommended. We assessed changes in HDV diagnostic capacity across public hospitals in the Valencian Community, Spain. Repeated cross-sectional surveys were conducted in 2024 and 2025. Analyses included the 19 hospitals participating in both years and evaluated anti-HDV testing, HDV RNA detection, reflex testing, and clinician notification. Anti-HDV testing increased from 84.2% to 94.7%, HDV RNA testing from 68.4% to 84.2%, reflex testing from 43.8% to 77.8% (p = 0.04), and direct clinician communication from 75.0% to 83.3%. Improvements were most marked in hospitals with fewer than 500 beds, where anti-HDV testing rose from 78.6% to 92.9% and HDV RNA testing from 57.1% to 78.6%. HDV diagnostic capacity improved substantially, particularly in smaller hospitals. Further organizational measures are needed to achieve universal double-reflex testing and timely communication of positive results.

PMID 42499788
Read full article →
PubMedJPGN reports2026-07-25

Itching for a diagnosis: Dysesthesias as an atypical presentation of Wilson disease in an adolescent-Case report.

Mosher Tierra L R TLR, Hicks John J, Mysore Krupa R KR

Wilson disease (WD) is an autosomal recessive disorder of hepatic copper metabolism with varied clinical presentations. We describe a 15-year-old male referred for elevated aminotransferases, burning facial pruritis, scalp dysesthesias, and chronic bilateral lower extremity edema. Initial workup showed low-normal ceruloplasmin, hypergammaglobulinemia, positive antinuclear antibody (ANA) and anti-smooth muscle antibody, and liver biopsy compatible with autoimmune hepatitis (AIH) (simplified AIH score = 6). Lack of response to prednisone therapy for probable AIH prompted further testing. Moreover, 24-h urine copper was 1285 µg (normal 15-60 µg/24 h), ceruloplasmin was 9 mg/dL (initially 18 mg/dL), Kayser-Fleischer rings were appreciated, and elevated liver copper quantification. ATP7B gene testing revealed two heterozygous pathogenic variations in two different genes. Initiation of copper chelation therapy led to the resolution of symptoms and normalization of aminotransferases in 8 weeks. This case underscores the need for timely WD evaluation in patients with atypical presentations.

PMID 42499713
Read full article →
PubMedJHEP reports : innovation in hepatology2026-07-25

Fate of hepatitis D virus-specific CD8+ T cells during bulevirtide monotherapy in patients with chronic hepatitis delta☆.

Oberhardt Valerie V, Degasperi Elisabetta E, Maas Michelle M, Borghi Marta M et al.

Bulevirtide reduces viremia in chronic hepatitis D virus (HDV) infection, but long-term treatment is required in most patients to prevent relapse. Sustained treatment responses may be fostered by therapy-induced amelioration of HDV-specific CD8+ T-cell responses that are exhausted due to high viremia and antigen loads during chronic HDV infection. We therefore studied the effect of bulevirtide monotherapy on HDV-specific CD8+ T-cell repertoire, phenotype, and functionality. 28 HDV-infected cirrhotic patients starting bulevirtide treatment were followed for 40-120 weeks on treatment. HLA-class-I typing and HDV sequencing was performed. HDV-specific CD8+ T cells were analyzed longitudinally using optimal epitopes and overlapping peptides spanning the L-HDAg. Ex vivo high-dimensional flow cytometry analysis of peptide/HLA class I tetramer+ CD8+ T cells was performed longitudinally in selected patients. In 42% of patients, an HDV-specific CD8+ T-cell response was detectable at baseline, but did not substantially increase during treatment. Importantly, a large majority of HDV-specific CD8+ T-cell responses targeted viral epitopes with sequence variations consistent with viral escape mutations. Only one HLA-B*35-restricted HDV-specific CD8+ T-cell epitope was conserved and continuously targeted throughout therapy. HDV-specific CD8+ T cells targeting this conserved epitope displayed a predominant terminally exhausted phenotype at baseline that shifted longitudinally to a memory-like phenotype with suppression of HDV load. Albeit based on small patient numbers, antiviral treatment with bulevirtide could ameliorate exhausted HDV-specific CD8+ T cells targeting conserved HDV epitopes. However, as the majority of HDV-specific CD8+ T-cell responses target escaped viral epitopes, this does not translate to a substantial improvement in overall HDV-specific CD8+ T-cell immunity. Our findings may explain in part why long-term bulevirtide treatment is required to prevent viral relapse.

PMID 42498134
Read full article →

+9996 more articles available with a free account

Sign up free to view all articles →

Ask about anti-hepatitis-B therapy