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Hep A-Vi (ViATIM / ViVAXIM)

✓ Approved

Sanofi S.A · Vaccine · Vaccine

What is Hep A-Vi?

Hep A-Vi is a vaccine developed by Sanofi S.A. It is approved for therapeutic indications via injectable (others) or intramuscular (im) injection.

Drug Profile

Brand NamesViATIM, ViVAXIM
CompanySanofi S.A
Drug ClassVaccine, Large Molecules
RouteInjectable (Others), Intramuscular (IM) Injection
StatusApproved
Sources: ClinicalTrials.gov, Sanofi S.A

Therapeutic Indications

Hep A-Vi is developed for 2 unique indications across 2 therapeutic areas.

Therapeutic AreaConditionPhase
Infections and infestationsTyphoid fever✓ Approved
Surgical and medical proceduresAntiviral prophylaxis✓ Approved

Related Research Articles

PubMedLivers2026-11-11

Subchronic Exposure to Hexavalent Chromium in Drinking-Water-Induced Sex-Dependent Essential Metal Dyshomeostasis in the Liver, Blood, and Brain of Guinea Pigs.

Delnicki Morgan E ME, Vielee Samuel T ST, Griffin Gabrielle C GC, Meaza Idoia I et al.

Hexavalent chromium [Cr(VI)] is a toxic metal that enters the environment due to natural and anthropogenic processes. The liver is a major target organ of Cr(VI) exposure through drinking water, resulting in an increased risk of exposed individuals developing chronic liver diseases and cancers. Cr(VI) exposure is also associated with neurological dysfunction. Essential metal dyshomeostasis is a well-characterized biomarker of liver and neurological diseases, but the role Cr(VI) plays in altering essential metal levels in both organs is poorly understood. Male and female Hartley guinea pigs were exposed to 0 or 5 mg Cr(VI)/L in drinking water for 90 days. Chromium accumulation and essential metal levels in the liver, blood and brain were analyzed using inductively coupled plasma mass spectrometry. Chromium significantly accumulated in a sex-dependent manner in the livers and blood of guinea pigs given 5 mg Cr(VI)/L in their drinking water, with sex- and region-specific chromium deposition observed in the brain. The livers and blood of female guinea pigs were more vulnerable to Cr(VI) exposure, as evident in the significant chromium accumulation and dyshomeostasis of several essential metals, including hepatic magnesium, zinc and potassium. Conversely, male guinea pigs were more vulnerable to Cr(VI)-induced essential metal dyshomeostasis in the brain, with significant changes in molybdenum and cobalt in nearly half of the 11 brain regions assessed. This study begins the process of establishing a novel model to study Cr(VI)-induced hepatotoxicity, neurotoxicity and organ crosstalk. Overall, Cr(VI) induced sex-dependent essential metal dyshomeostasis in the liver and blood, along with sex- and region-specific essential metal dyshomeostasis in the brain. These results suggest essential metal dyshomeostasis may play an important role in Cr(VI)-induced liver and neurodegenerative diseases, and these effects should guide future mechanistic investigations.

PMID 43011670
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PubMedAnalytical chemistry2026-11-11

Single-Cell ICP-MS Quantification of Intracellular Chromium and Cell-Surface TNFR2 for Assessing Cr(III/VI)-Induced Lung Epithelial Injury and COPD-Relevant Responses.

Lu Xinyi X, Chen Beibei B, He Man M, Hu Bin B

An integrated platform combining droplet microfluidics, lanthanide labeling, and inductively coupled plasma mass spectrometry (ICP-MS) was proposed to quantify intracellular heavy metal and cell-surface protein at single-cell resolution. The workflow performs parallel measurements on homologous single-cell subsets to establish statistical correlations between metal accumulation and functional protein responses. Using tumor necrosis factor receptor 2 (TNFR2) as a model protein, we investigated the effects of atmospheric particulate matter-associated heavy metals on human lung epithelial cells (BEAS-2B). Several heavy metals trigger TNFR2 upregulation, with Cr(VI) exerting the most pronounced effect. The Cr(VI)-induced increase in TNFR2 expression was associated with elevated TNF-α release, higher intracellular ROS, and reduced SOD activity but did not correlate directly with intracellular Cr accumulation, likely due to distinct cellular uptake mechanisms between Cr(III) and Cr(VI). High-concentration Cr(III) exposure, however, led to intracellular Cr enrichment and provoked inflammatory responses. Integration of differential gene expression, TNF-α release, and TNFR2 expression support TNFR2 as a potential indicator of metal-induced oxidative stress, epithelial injury, and COPD-relevant inflammatory responses. This single-cell dual-parameter approach provides a new strategy for linking metal uptake to functional protein responses in environmental toxicology.

PMID 43010549
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PubMedVeterinary research communications2026-11-11

Genomic characterization of a Brazilian multidrug-resistant Klebsiella pneumoniae ST17 isolate associated with bovine mastitis.

da Silva Guilherme Castro Luz GCL, de Moura Souza Rossiane R, Vicente Ana Carolina Paulo ACP, Morgado Sergio Mascarenhas SM et al.

This study presents the genomic and phenotypic characterization of a multidrug-resistant Klebsiella pneumoniae (MDR-Kp) isolate (LC808) obtained from a case of bovine mastitis in Brazil. Antimicrobial susceptibility testing revealed an MDR phenotype, indicating resistance to penicillins, cephalosporins, monobactams, aminoglycosides, tetracyclines, fluoroquinolones, and trimethoprim-sulfamethoxazole. The presence of an extended-spectrum β-lactamase (ESBL) was also confirmed. Whole-genome sequencing identified the isolate as sequence type 17 (ST17) and revealed the presence of the KL127 and O13 loci. The resistome contained genes associated with antimicrobial resistance, including blaCTX-M-15, blaTEM-1, blaSHV-187, and blaOXA-1 (β-lactams); aph(6)-Id, aph(3'')-Ib, aph(3')-Ia, aac(3)-IIe, and aac(6')-Ib10 (aminoglycosides); tet(A) (tetracyclines); qnrB17 (fluoroquinolones); and sul2 (sulfonamides). A class 1 integron carrying dfrA14 was also identified. The virulome included type 1 and type 3 fimbriae, a type VI secretion system, and multiple iron-acquisition systems (fecABCDEIR). Identifying this clinically relevant lineage that carries multiple resistance and virulence determinants highlights the presence of MDR-Kp in bovine mastitis in Brazil. These findings provide the necessary genomic baseline data to support ongoing genomic surveillance of antimicrobial-resistant bacteria in dairy herds within a One Health framework.

PMID 43009713
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PubMedChemical science2026-11-11

Metal-ligand orbital mixing mediates spin-phonon coupling in group VI tetraaryl molecular color centers.

Lee Victor Chang VC, Lee Jaewon J, Park Hong Youl HY, Johnson Dane A DA et al.

Understanding the microscopic mechanisms governing spin-phonon coupling in transition metal complexes is essential for the rational design of molecular qubits with long coherence and relaxation times. Here, we present a comprehensive first-principles study of spin-phonon relaxation in Cr(o-tolyl)4 and Mo(o-tolyl)4 diluted in a diamagnetic Sn(o-tolyl)4 crystal matrix. Our calculations predict a striking two-order-of-magnitude difference in T 1 relaxation times between the two systems, in excellent agreement with experiment. By combining advanced electronic structure theory with lattice dynamical calculations, we reproduce the observed relaxation behavior and uncover the microscopic origin of the enhanced T 1 in Cr(o-tolyl)4. Our analysis reveals that the main difference between the two metal centers is primarily governed by the metal-ligand electronic structure. Greater metal-ligand orbital mixing in the Mo complex, together with its stronger spin-orbit coupling, substantially increase the sensitivity of the zero-field splitting tensor to ligand nuclear motion. This enhanced spin-phonon coupling accelerates spin relaxation and accounts for the shorter T 1 of Mo(o-tolyl)4. Our results establish a direct connection between electronic structure, vibrational coupling, and spin relaxation, providing a microscopic design principle for the development of T 1 relaxation times.

PMID 43011458
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PubMedACS applied materials & interfaces2026-11-11

Phosphate-Functionalized Macroporous Cellulose Sponges for Uranium Recovery from Seawater.

Sekine Yurina Y, Nankawa Takuya T, Sugita Asako A, Konda Miki M et al.

Cellulose-based adsorbents offer a sustainable platform for uranium recovery from seawater, but simple functionalization strategies that enable effective uranium capture under highly competitive marine conditions remain limited. Here, we report a post-phosphorylation strategy for introducing uranium-binding functionality into a preformed freeze-crosslinked carboxymethyl cellulose nanofiber (CMCF) sponge while retaining its interconnected macroporous architecture. Impregnation of the cellulose sponge with NH4H2PO4/urea followed by mild thermal treatment at 120 °C introduced up to 114 ± 18 mg P g-1 sponge. In seawater spiked with 10 mg L-1 U(VI), both nonphosphorylated and phosphorylated CMCF sponges showed similarly high U removal (>96%), largely obscuring the effect of phosphate functionalization. In contrast, a pronounced phosphate-dependent enhancement emerged under realistic seawater conditions: the nonphosphorylated sponge showed negligible U removal from natural seawater, whereas the post-phosphorylated P1-CMCF sponge achieved approximately 99% U removal within 24 h. SEM-EDX and XPS analyses further supported uranium accumulation at phosphate-rich cellulose interfaces and the involvement of phosphate-associated oxygen donor sites in U binding. The captured uranium was nearly quantitatively recovered using 0.1 mol L-1 NaHCO3, and adsorption performance was maintained over three adsorption-desorption cycles. These results demonstrate that simple post-phosphorylation of a preformed macroporous cellulose scaffold provides accessible uranium-binding interfaces while preserving the underlying transport architecture, offering a straightforward route to efficient and regenerable uranium recovery under chemically complex seawater conditions.

PMID 43012362
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PubMedActa neuropathologica communications2026-11-11

Raman spectroscopic identification of biochemical alterations in Alzheimer's disease brain tissue.

Ghazanfarpour Samaneh S, Das Rahul Kumar RK, Ihnatovych Ivanna I, Sule Norbert N et al.

Alzheimer's disease (AD) is a progressive neurodegenerative disorder marked by chronic inflammation, neuronal loss, and continuous decline in memory and cognitive function. Raman Spectroscopy (RS) offers a powerful, label‑free approach for detecting early biochemical alterations in AD by generating highly sensitive molecular fingerprints, which is valuable for identifying subtle changes associated with protein misfolding, lipid dysregulation, and oxidative stress, key processes underlying AD onset and progression. In our study, full‑spectrum RS revealed clear biochemical distinctions between control and AD brain tissues, as well as between Braak IV and Braak VI AD stages. Multivariate analytical methods, including Singular Value Decomposition (SVD) and Linear Discriminant Analysis (LDA), were applied to manage spectral complexity and highlight the principal biochemical contributors to AD pathology. Multiple Raman bands in the 1200-1800 cm-1 region showed increased intensity in AD tissue, including 1296 cm-1 (lipid CH₂ deformation), 1440 cm-1 (lipid/cholesterol deformation), 1554 cm-1 (Amide II), 1585 cm-1 (protein‑folding-related vibrations), and 1640-1680 cm-1 (Amide I). These changes indicate enhanced protein aggregation, loss of ordered secondary structure, and extensive lipid membrane disorganization. Complementary gene‑expression analysis further demonstrated dysregulation of lipid homeostasis in AD, with altered expression of ABCA1, LIPE, CPT1A, PPARA, and SREBP‑1, indicating broad metabolic reprogramming. Together, the coordinated spectral and transcriptional shifts underscore lipid‑metabolic dysfunction as a central feature of AD. By capturing these molecular signatures, RS provides a promising tool for early detection and monitoring of AD progression.

PMID 43010096
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