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Hep A-Vi (ViATIM / ViVAXIM)

✓ Approved

Sanofi S.A · 疫苗 · 疫苗

什么是 Hep A-Vi？

Hep A-Vi 是一种疫苗，由Sanofi S.A研发。该药已获批，用于治疗相关适应症，给药途径：Injectable (Others)、Intramuscular (IM) Injection。

药物档案

商品名ViATIM, ViVAXIM
公司Sanofi S.A
药物类别疫苗, 大分子
给药途径Injectable (Others), Intramuscular (IM) Injection
状态Approved
来源： ClinicalTrials.gov, Sanofi S.A

治疗适应症

Hep A-Vi 针对 2 个适应症，涉及 2 个治疗领域。

治疗领域疾病/病症分期
Infections and infestationsTyphoid fever✓ Approved
Surgical and medical proceduresAntiviral prophylaxis✓ Approved

相关研究文献

PubMedJournal of translational medicine2026-10-26

In vitro bioactivity profile-driven discovery of drug synergies in hepatocellular carcinoma.

Xu Tuan T, Xu Miao M, Ngan Deborah K DK, Zhao Tongan T et al.

Combination therapy is a central strategy to overcome drug resistance in hepatocellular carcinoma (HCC), yet systematic identification of synergistic combinations is constrained by the combinatorial search space. We developed a data-driven workflow to integrate two orthogonal single-agent resources for 244 drugs, including cell viability profiles across 11 liver cancer cell lines and bioactivity signatures across 1,925 biochemical and cell-based assays. We calculated the correlation of the bioactivity profiles between each drug pair yielding 821 high-confidence combinations involving 190 unique drugs, from which eight anchors and a 125-drug library were selected by frequency-guided prioritization. Fixed-concentration screening of 992 anchor-library combinations in the Hep 3B2.1-7 cell line yielded 89 combinations with potency enhancement. Panobinostat showed the largest potency gains when combined with briciclib or thiocolchicine (69.5-fold and 81.1-fold lower IC₅₀, respectively). Matrix-based screening of these two representative combinations across 11 cell lines revealed pronounced concentration- and context-dependence. At optimal dose pairs, strong synergy was observed in Hep 3B2.1-7 (Zero Interaction Potency (ZIP) = 40.80 ± 4.22 with 58.53 ± 6.54% inhibition), whereas antagonism was observed in some cellular backgrounds. This label-free integration strategy reduces the experimental burden for hypothesis-driven combination discovery and provides context-specific preclinical leads for follow-up evaluation in HCC.

PMID 42928229
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PubMedInorganic chemistry2026-10-26

Dimerization Pathway, Structure, and Acidity of Binuclear Mo(VI) Species in Aqueous Solution from First-Principles Molecular Dynamics.

He Mengjia M, Zhang Yingchun Y, Lu Xiancai X

Understanding the early condensation of aqueous Mo(VI) species is important for improving polyoxomolybdate speciation models, particularly in the highly acidic environments relevant to high-level liquid waste (HLLW) processes. Here, we carried out first-principles molecular dynamics (FPMD) simulations to investigate the dimerization of monomeric MoO(OH)3(H2O)2+ and characterize the structure and acidity of the resulting binuclear species. Constrained molecular dynamics simulations show that dimerization is initiated by a hydroxyl-hydroxyl H-bonded precursor formed between two monomers, followed by proton transfer, nascent water formation, dissociation, and μ2-oxo bridge formation. The overall free energy change (-19.2 kcal/mol) indicates that the dimer [Mo2O3(OH)4(H2O)4]2+ is thermodynamically stable. For this dimer, each Mo center adopts a distorted octahedral coordination environment with one terminal oxo ligand, one μ2-oxo bridge, two hydroxyl groups, and two coordinated water molecules. pKa calculations using the FPMD-based vertical energy gap method further indicate that deprotonation preferentially occurs at the hydroxyl groups rather than at the coordinated water. These results suggest hydroxyl-assisted dehydration as a key elementary step in Mo(VI) dimerization and provide a molecular basis for understanding the early growth of polyoxomolybdate clusters in aqueous solution.

PMID 42929627
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PubMedMicrobial biotechnology2026-10-26

Adaptive Laboratory Evolution Rewires Pseudomonas putida for Resource-Efficient Acetate Assimilation.

Gurdo Nicolás N, Srinivasan Aparajitha A, Tagliani Tommaso T, Filbig Melanie M et al.

Acetate is an attractive renewable two-carbon substrate for microbial biotechnology, but toxicity limits growth and carbon-use efficiency at process-relevant concentrations. Here, we used adaptive laboratory evolution to improve acetate tolerance in a genome-reduced strain of Pseudomonas putida and combined whole-genome sequencing, quantitative physiology, reverse engineering, transcriptomics, proteomics and 13C-acetate fluxomics to resolve the underlying adaptation mechanisms. Evolution under increasing acetate concentrations selected recurrent mutations in gacA and fabB, which encode a global response regulator and a fatty acid biosynthesis enzyme, respectively. Reverse engineering of these mutations recapitulated most of the evolved phenotype, including shorter lag phase and substantially higher biomass yield from acetate. Multi-omic analyses showed repression of type VI secretion systems, carbohydrate storage functions, fatty acid metabolism and oxidative stress-associated proteins, indicating resource reallocation away from costly stress and non-essential programs. Fluxomics further revealed reduced carbon cycling and increased glyoxylate shunt flux, consistent with improved acetate-carbon retention in biomass. These results establish acetate tolerance in P. putida as a resource-efficiency phenotype and identify gacA and fabB as actionable targets for acetate-based bioproduction.

PMID 42929247
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PubMedInternational journal of nanomedicine2026-10-26

Nanotechnology-Enabled Immunotherapy for Colorectal Cancer: Overcoming the "Cold" Tumor Microenvironment in Microsatellite-Stable Disease.

Xu Jiayu J, Yu Jiankang J, Liu Gang G, Zhang Hao H et al.

Immune checkpoint inhibitors (ICIs) have transformed the management of mismatch repair-deficient/microsatellite instability-high (dMMR/MSI-H) colorectal cancer (CRC), yet the ~95% of patients with mismatch repair-proficient/microsatellite-stable (pMMR/MSS) disease derive little benefit owing to an immunologically "cold" tumor microenvironment (TME), poor T-cell infiltration, myeloid dominance, TGF-β-enriched stroma, and the systemically immunosuppressive milieu imposed by hepatic metastases. Clinically tested combinations-multikinase inhibitor plus anti-PD-1, Fc-enhanced dual checkpoint blockade, chemotherapy- or antiangiogenic-ICI regimens-have so far produced modest, largely non-durable response rates that are further attenuated in liver-metastatic disease, motivating approaches that pharmacologically remodel the TME rather than only release checkpoint restraint. To provide an evidence-stratified synthesis of nanotechnology-enabled immunotherapy in CRC that explicitly separates (a) clinically established evidence, (b) strategies under early-phase clinical investigation, and (c) concepts that remain preclinical or are extrapolated from other tumor types, and to derive from this appraisal a biomarker-enriched translational research agenda. Narrative, integrative (non-systematic) review. PubMed, Embase, Web of Science, ClinicalTrials.gov, and ASCO/ESMO/AACR proceedings were searched from January 2010 through April 2026. Each strategy was appraised according to the highest available level of evidence, the tumor type and model system in which the evidence was generated, and its demonstrated CRC specificity. In current clinical practice, nanomedicine in CRC is essentially limited to nanoparticle-formulated cytotoxics exploited for pharmacokinetic advantage (e.g. liposomal irinotecan), whereas nano-enabled immunotherapy is confined to a small number of early-phase trials-most notably lipid nanoparticle (LNP)-formulated individualized neoantigen mRNA vaccines in ctDNA-positive resected CRC and hafnium-oxide nanoparticle radioenhancers-none of which has yet demonstrated a progression-free or overall survival benefit in MSS CRC. Against this background we critically appraise six classes of strategy: (i) LNP-based mRNA neoantigen vaccines; (ii) polymeric and inorganic nanocarriers for STING and TLR agonists; (iii) tumor-associated macrophage-repolarizing nanoparticles; (iv) nano-radiosensitizers and photothermal/photodynamic platforms priming immunogenic cell death; (v) nano-formulated checkpoint inhibitor delivery; and (vi) locoregional nano-strategies directed at hepatic metastasis-specific immunosuppression. For categories (ii)-(vi) the supporting evidence is predominantly murine (largely subcutaneous CT26/MC38 models) or extrapolated from immunologically "hot" tumors such as melanoma and non-small-cell lung cancer, in which both the underlying biology and the checkpoint backbone differ materially from MSS CRC. Recurrent translational barriers include low, highly heterogeneous nanoparticle accumulation in human tumors, dense TGF-β-rich stroma and elevated interstitial pressure, mononuclear phagocyte system clearance, liver-metastasis-specific tolerance that subcutaneous models do not reproduce, unresolved manufacturing/CMC and regulatory pathways, and the absence of validated pharmacodynamic biomarkers of intratumoral immune conversion. Nanotechnology offers a mechanistically coherent and experimentally testable-but at present clinically unproven-set of strategies for converting "cold" MSS CRC into immune-responsive disease. We therefore position nano-enabled immunotherapy as a research priority rather than an imminent standard of care, and argue that its clinical value can only be established through biomarker-enriched, paired-biopsy early-phase trials with pharmacodynamic endpoints of immune conversion and prospective stratification by metastatic site (particularly hepatic involvement) and consensus molecular subtype. This is a narrative rather than systematic review; it is therefore subject to selection and publication bias, and much of the evidence synthesized is preclinical and of limited direct translational certainty.

PMID 42928874
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PubMedBiosensors2026-10-26

A Graphene Quantum-Dot Electrometer Array for Sub-Micrometre Imaging of Interfacial Charge Layers in Cryofixed Cells: A Design Analysis.

Celebi Cem C, Ludwig Stefan S, Siddiki Afif A

We analyse, as a design study, a cryogenic sensor that images the electrostatic stray field of a vitrified biological cell with an array of gate-defined quantum dots in gapped bilayer graphene. No device has been fabricated and no transport data are reported. The sensor is a Coulomb-blockade electrometer: each dot converts the offset charge induced on it by the sample into a shift in its resonance, and the steepness of that resonance-a property of the discrete density of states rather than of the device area-sets the gain, so that sensitivity is not lost as the element is made smaller. For a 50 nm dot at 4.2 K we estimate a charge sensitivity of order 10-2 e/√Hz for a charge 50 nm away, limited by an assumed 1/f offset-charge noise; this is a calculated, not a measured, figure. Because a vitrified sample is electroneutral beyond the Debye length, the sensor does not see net charge but the frozen interfacial dipole layers, whose dipole density equals the permittivity times the potential step across each layer. The measured quantity is therefore a band-limited map of lateral variations in the interfacial potential within about 100 nm of the sensor; a laterally uniform layer is invisible. In this map the membrane potential enters with a weight β = Cmt/εwε0 ≈ 0.07 relative to the surface potential of the glycocalyx, so the sensor is primarily a surface-potential imager and only secondarily, through a calibration we specify, a membrane-potential probe. A 10 mV surface-potential contrast at a period of 250 nm exceeds the 1 ms detection limit by a factor of about 4-13, and the 8 × 8 array at 250 nm pitch resolves periods of 250-300 nm. We give the device geometry, the plunge-freezing protocol, the controls and the inversion procedure, and list what remains to be measured.

PMID 42930134
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PubMedBiosensors2026-10-26

A Portable UV-LED Dual-Nafion Microfluidic Platform for Label-Free Trace Protein Preconcentration and Absorbance Detection.

Shih Yi-Jia YJ, Chen Yu-Sheng YS, Jen Chun-Ping CP

Sensitive label-free detection of low-abundance proteins requires both effective on-chip preconcentration and a compact, low-noise optical readout for use outside conventional laboratories. Here, we present a portable UV-LED dual-Nafion microfluidic platform that integrates a 280 nm UV-LED, a chromium-coated slot collimator, a dual-Nafion ion concentration polarization (ICP) preconcentrator, and a miniature spectrometer within a 3D-printed enclosure. The symmetric dual-Nafion geometry on a UV-transparent quartz substrate confines the ICP enrichment zone to a fixed 120 × 500 µm interrogation window, enabling spatially stable, label-free on-chip absorbance monitoring at 280 nm. Using bovine serum albumin (BSA) as a model protein, the platform showed a linear absorbance response over 0-60 µM (R2 = 0.9933) and a static-loading limit of detection of 0.91 µM. Under a 30 V bias in 0.3 mM phosphate-buffered saline, representative 60 min experiments produced apparent enrichment factors of approximately 41, 4.5 × 103, and 1.6 × 104 at initial BSA concentrations of 1 µM, 10 nM, and 1 nM, respectively. At 10 pM, a reproducible, voltage-dependent absorbance increase was detected with three independent chips, whereas the 0 V and BSA-free controls remained below the detection threshold. The platform provides a practical approach for label-free trace-protein analysis and a potential upstream module for biomarker-specific assays.

PMID 42930138
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