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LY

lyophilized hepatitis-B human immunoglobulin

✓ Approved

Tonrol Bio-Pharmaceutical · Polyclonal Antibodies · Polyclonal Antibodies

What is lyophilized hepatitis-B human immunoglobulin?

lyophilized hepatitis-B human immunoglobulin is a polyclonal antibodies developed by Tonrol Bio-Pharmaceutical. It is approved for therapeutic indications via injectable (others) or intravenous (iv).

Drug Profile

CompanyTonrol Bio-Pharmaceutical
Drug ClassPolyclonal Antibodies, Vaccine, Antibody
RouteInjectable (Others), Intravenous (IV)
StatusApproved

Therapeutic Indications

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

Therapeutic AreaConditionPhase
Infections and infestationsHepatitis B✓ Approved

Related Research Articles

PubMedJPMA. The Journal of the Pakistan Medical Association2026-06-09

Healthcare Related Factors Associated with Mono-Infection and Co-Infection of Bloodborne Viruses in Lasbela and Quetta, Baluchistan.

Rasheed Nida N, Karim Mehtab M, Ali Syeda Tabeena ST

To determine the frequency of human immunodeficiency virus, hepatitis B virus and hepatitis C virus infection, and to compare the prevalence and risk factors of mono-infection versus co-infection. The comparative, cross-sectional study was conducted in selected hospitals in Lasbela and Quetta districts of Balochistan, Pakistan, from November 2022 to April 2023, and comprised patients of either gender aged ≥18 years visiting the participating hospitals. The patients were screened using an immunochromatographic test kit, and were divided into mono-infected with human immunodeficiency virus group 1, mono-infected with hepatitis C virus group 2, mono-infected with hepatitis B virus group 3, co-infected with two or three viruses group 4, and healthy controls group 5. Factors associated with co-infection versus mono-infection of blood-borne viruses were identified. Data was analysed using SPSS 21. Of the 1992 subjects, 1043(52.4%) were females, 949(47.60%) were males, and 864(43.4%) were aged 30-44 years. Of the total, 75(3.8%) subjects were in group 1, 175(8.8%) in group 2, 88(4.4%) in group 3, 79(4%) in group 4, and 1,575(79.1%) in control group 5. In group 4, 27(34.1%) subjects had human immunodeficiency virus and hepatitis B virus, followed by 26(32.9%) having hepatitis B virus and hepatitis C virus, 17(21.5%) having human immunodeficiency virus and hepatitis C virus, and 9(11.3%) having triple infection. Among other findings, history of surgical procedures, male gender and rural residence were significantly associated with co-infection (p<0.05). Strengthening infection control practices in district hospitals, expanding vaccination coverage, incorporating supplementary testing methods, and promoting community awareness campaigns about safe injection and transfusion practices are to control the risk of life-threatening virus in the community.

PubMedSaudi journal of kidney diseases and transplantation : an official publication of the Saudi Center for Organ Transplantation, Saudi Arabia2026-06-09

"Seroprevalence and Associated Factors of Hepatitis B, Hepatitis C, and Human Immunodeficiency Virus Among Haemodialysis Patients in Morocco.

Bidarne Lahcen L, Kharbach Ahmed A, Razine Rachid R, Mechita Nada Bennani NB et al.

Haemodialysis patients are especially vulnerable to blood-borne viral infections because of repeated exposure to invasive procedures and the dialysis care environment. This study aimed to determine the HBV-positive status of hepatitis B virus, hepatitis C virus, and human immunodeficiency virus among haemodialysis patients and to identify factors associated with HBV seropositivity. A cross-sectional analytical study was conducted among haemodialysis patients in Morocco. A total of 305 haemodialysis patients were included. Sociodemographic, clinical, and serological data were collected using a structured form. Serological status for HBV, HCV, and HIV was assessed by ELISA and confirmed using specific confirmatory assays. Statistical analysis used: Univariate and multivariable logistic regression analyses were performed to identify factors associated with HBV seropositivity. Odds ratios (ORs) with 95% confidence intervals (CIs) were estimated, and statistical significance was set at p < 0.05. The overall seroprevalence was 2.62% for HBV, 0.33% for HCV, and 0.66% for HIV. Multivariable analysis showed that use of an arteriovenous fistula and complete HBV vaccination (3-4 doses) were significantly associated with lower odds of HBV infection (OR = 0.012, 95% CI: 0.010-0.286, p = 0.007; OR = 0.008, 95% CI: 0.000-0.511, p = 0.023, respectively). In contrast, longer haemodialysis duration was significantly associated with increased HBV seropositivity (OR = 1.036, 95% CI: 1.012-1.061, p = 0.004). Despite the low prevalence of HBV, HCV, and HIV, prevention, surveillance, and strengthened vaccination strategies remain necessary in haemodialysis settings.

PubMedChinese medical journal2026-06-09

Anti-PD-1 monoclonal antibody suppresses hepatitis B virus in patients with hepatocellular carcinoma.

Zhao Chuanhua C, Zhang Yanqiao Y, Wang Gang G, Chen Weiqing W et al.

PubMedHemaSphere2026-06-09

Lamin B1 safeguards the B cell genome and shapes lymphoma outcome.

Filipsky Filip F, Chapman Katarina B KB, Bloehdorn Johannes J, Maiques Oscar O et al.

Lamin B1 is a structural component of the nuclear lamina that participates in genome organization and transcriptional control. During adaptive immune responses, B lymphocytes in germinal centers (GCs) undergo clonal expansion and programmed DNA damage at immunoglobulin loci, while simultaneously downregulating Lamin B1. Likewise, Lamin B1 downregulation has been observed in GC-derived lymphomas and myeloid malignancies, yet the functional consequences of Lamin B1 loss during B cell development remain poorly understood. Here, we used in vivo and in vitro B cell models of conditional hypomorphic Lamin B1 expression, which showed elevated DNA damage and disrupted transcriptional profiles. Using sBLISS (in situ labeling and sequencing of double-strand breaks), we identified nonrandom double-strand break hotspots in both mouse and human GC B cells depleted of Lamin B1. These breaks are preferentially located near transcriptional start sites (TSSs) and regulatory elements that control translation and mRNA fate, suggesting Lamin B1 has a role in protecting regulatory genomic regions. Moreover, low LMNB1 expression is associated with poor clinical outcomes in patients with diffuse large B-cell lymphoma (DLBCL). Together, this study reveals a crucial role for Lamin B1 in preserving genomic stability in B cells, underscoring its impact on the pathogenesis of B cell-derived malignancies.

PubMedAnnals of clinical and laboratory science2026-06-09

Letter to the Editor: Detection of Chlamydia trachomatis Immunoglobulin E Antibody in Human Sera.

Smith-Norowitz Tamar A TA, Abdelmajid Haram H, Klein Elliot E, Joks Rauno R et al.

PubMedArchives of microbiology2026-06-09

GATA2 promotes hepatitis B virus-associated hepatocellular carcinoma development by regulating AURKA.

Di Liang L, Guo Qingliang Q, Zhao Xiaofei X, Ding Jing J

Hepatitis B virus (HBV)-associated hepatocellular carcinoma (HCC) refers to liver cancer caused by chronic HBV infection and is the leading cause of liver cancer globally. Although aurora kinase A (AURKA) has been reported to be highly expressed in HBV-associated HCC, its specific mechanisms of action remain unclear. Through bioinformatics analysis (Gene Expression Omnibus (GEO)) and experimental validation (Western blot), the expression levels of AURKA, hepatitis B virus X protein (HBX), and GATA binding protein 2 (GATA2) were assessed. A HepG2.2.15 cell model was established. Functional assays (colony formation, flow cytometry, mouse xenograft tumor model) and mechanistic studies (dual-luciferase reporter assay, JASPAR database analysis, and chromatin immunoprecipitation (ChIP)) were conducted to investigate the mechanism of AURKA in HBV-associated HCC. Bioinformatics analysis identified AURKA as a core gene in HBV- associated HCC. AURKA was highly expressed in HBV-associated HCC. Knockdown of AURKA inhibited the proliferation of HepG2.2.15 cells, induced apoptosis, and reduced the protein level of the autophagy substrate P62 as well as the ratio of the autophagy marker LC3BII/LC3BI. By forming a complex with GATA2, HBX enhanced the transcriptional activity of the AURKA promoter, thereby promoting the malignant phenotypes of HepG2.2.15 cells. Additionally, in vivo experiments demonstrated that knockdown of GATA2 inhibited tumor growth. In conclusion, GATA2-regulated AURKA promotes the development of HBV-associated HCC, underscoring its potential as a therapeutic target.

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