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AN

anti-tetanus immunoglobulin (Tetglob)

✓ Approved

Bharat Serums and Vaccines Limited · therapeutic agent

What is anti-tetanus immunoglobulin?

anti-tetanus immunoglobulin is a therapeutic agent developed by Bharat Serums and Vaccines Limited. It is approved for therapeutic indications via injectable (others) or intramuscular (im) injection.

Drug Profile

Brand NamesTetglob
CompanyBharat Serums and Vaccines Limited
RouteInjectable (Others), Intramuscular (IM) Injection
StatusApproved

Therapeutic Indications

anti-tetanus immunoglobulin is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Infections and infestationsTetanus✓ 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.

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.

PubMedIn vitro models2026-09-20

A flow cytometry-based assay system for the in vitro screening of anti-steatotic compounds.

Deshmukh Kajal K, Malladi Navya N, Banerjee Sanjay K SK

The rising prevalence of MASLD and the absence of approved therapies highlight the need for reliable, quantifiable in vitro assays to screen compounds targeting hepatic lipid accumulation. Current methods are often semi-quantitative and lack sensitivity. This study aimed to develop and validate a flow cytometry-based assay using HepG2 cells to assess lipid accumulation, a key early marker of hepatic steatosis and toxicity. Steatosis was induced using varying concentrations of oleic acid (0-800 μM) for 12-48 h. Lipid accumulation was quantified using Nile Red staining and flow cytometry. The data were compared with two other conventional methods, the absorbance/fluorescence-based and the image-based systems. The developed assay system was tested against various clinically used drugs known to have anti-hepatosteatosis properties. Compared to the conventional methods, Oleic acid-induced fat accumulation, measured by flow cytometry in the hepatocyte-specific HepG2 cell line, was observed to be dose-dependent and time-dependent, with significant lipid accumulation at 400 μM oleic acid after 24 h. The assay was validated using known anti-steatotic drugs, where Saroglitazar, Pioglitazone, Empagliflozin, and Atorvastatin significantly reduced lipid accumulation in HepG2 cells. Further, the sensitivity of the assay was checked by calculating the IC₅₀ values, where Saroglitazar and Triacsin C showed IC₅₀ values of 0.16 μM and 0.15 μM, respectively. This study successfully developed a flow cytometry-based in vitro assay using HepG2 cells to screen drugs against MASLD. The present flow cytometry assay is a human cell-based and animal-free system that offers a sensitive, accurate, and high-throughput platform for evaluating anti-steatotic compounds, with clear advantages over conventional methods for early-stage drug discovery. The online version contains supplementary material available at https://doi.org/10.1007/s44164-026-00110-4.

PubMedIn vitro models2026-09-20

Anti-biofilm and anti-virulence properties of Ricinus communis and Catharanthus roseus leaves against Pseudomonas aeruginosa PAO1.

Gebaly Eman El EE, Taha Mostafa N MN, Ashour Hossam M HM, Khairalla Ahmed S AS

Pseudomonas aeruginosa remains a major concern in clinical microbiology owing to its intrinsic multidrug resistance and its elaborate regulatory networks that enable evasion of host immune responses, particularly through robust biofilm development and the secretion of diverse virulence factors. These pathogenic behaviors are tightly governed by quorum-sensing (QS) systems, prompting increasing interest in exploiting plant-derived compounds as potential anti-virulence therapeutics. In this study, leaf extracts from Ricinus communis and Catharanthus roseus were examined for their capacity to modulate biofilm formation and QS-regulated virulence gene expression in the P. aeruginosa PAO1 strain. The production of key virulence factors was evaluated using multiple standardized assays, including the crystal violet binding assay (biofilm), azocasein assay (protease), chloroform-HCl extraction (pyocyanin), and the orcinol assay (rhamnolipids), while gene expression was quantified via quantitative real-time polymerase chain reaction (qPCR). The findings indicated that the extracts, rich in tannins and flavonoids, did not affect the planktonic growth of PAO1; however, both significantly (P < 0.05) suppressed biofilm formation and attenuated the production of pyocyanin, protease, and rhamnolipids. Additionally, qPCR analysis revealed pronounced downregulation of central QS regulatory genes, lasI, lasR, and rhlR, highlighting the potential of these phytochemicals to disrupt quorum-sensing-mediated pathogenicity.

PubMedAsian Pacific journal of allergy and immunology2026-09-20

Type 2-interferon imbalance in allergic barrier disease: An asthma-centered, cross-disease perspective.

Rao Shenghong S, Li Shumei S, Shen Haoyue H, Jin Tengchuan T

Allergic diseases are typically regarded as type 2 inflammatory disorders driven by interleukin-4, interleukin-5, and interleukin-13, which mediate immunoglobulin E class switching, eosinophilic inflammation, mucus hypersecretion, pruritus, tissue remodeling, and epithelial barrier dysfunction. However, type 2 cytokine activity alone does not fully account for variations in exacerbation risk, susceptibility to infections, comorbidities, or responses to biologic therapy. This narrative review proposes an asthma-centered type 2-interferon imbalance framework and discusses its cautious, disease-specific extension to atopic dermatitis, chronic rhinosinusitis with nasal polyps, eosinophilic esophagitis, and food allergy. The model emphasizes that, particularly in asthma, allergic barrier inflammation arises and persists in injured tissues where excessive type 2 inflammation may coexist with impaired interferon-mediated host defense. Evidence is strongest in asthma, where deficiencies in type I and type III interferon responses are linked to rhinovirus susceptibility, delayed viral clearance, and recurrent exacerbations. In other allergic diseases, interferon dysfunction appears more variable, reflecting differences in tissue context, disease stage, and environmental exposure. In asthma, and potentially in selected allergic barrier diseases, persistent inflammation may result from a cycle of epithelial injury, alarmin release, cytokine amplification, impaired antiviral defense, ongoing exposure, and incomplete tissue repair. These mechanisms provide a rationale for tiered intervention, including blockade of upstream epithelial alarmins, inhibition of downstream type 2 effector pathways, and selected investigational approaches aimed at restoring mucosal host defense.

PubMedCase reports in critical care2026-09-20

Pan-Neurofascin Antibody-Associated Nodopathy: A Critical Guillain-Barré Syndrome Mimic in the Differential Diagnosis-Report of Two Cases.

Nemethova Andrea A, De Ridder Willem W, Baar Ingrid I, Alonso-Jimenez Alicia A

Guillain-Barré syndrome (GBS) is an acute autoimmune polyradiculoneuropathy typically characterized by an ascending sensorimotor deficit with potential involvement of bulbar and respiratory muscles that may necessitate intensive care admission and mechanical ventilation. Standard treatment includes supportive care, management of complications such as weakness, immobility, respiratory failure, autonomic dysfunction and pain, along with early initiation of immunotherapy-either intravenous immunoglobulin (IVIg) or plasma exchange (PE). However, lack of significant clinical improvement following immunotherapy should prompt consideration of alternative diagnoses, including pan-neurofascin antibody-positive autoimmune nodopathy (panNF + AN). In this report, we present two patients presenting with a severe GBS-like neuropathy. Initial treatment with IVIg resulted in either no response or only transient, mild improvement, followed by rapid clinical deterioration to near-complete tetraplegia, respiratory failure, and autonomic and cranial nerve involvement. Both patients were unresponsive to further treatment with a second course of IVIg, PE and corticosteroids. Subsequent diagnostic evaluation revealed the presence of pan-neurofascin antibodies, confirming panNF + AN. This prompted initiation of treatment with rituximab, which resulted in sustained and complete clinical recovery in both cases. A transient or mild clinical response-or an initial lack of response-to standard GBS-treatment followed by rapid and severe deterioration in cases initially presenting as GBS should be considered a red flag warranting evaluation for AN-associated antibodies. Recognition of this important GBS mimic is critical, as it requires an alternative treatment approach with rituximab, which has been associated excellent clinical outcomes.

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