Drug Database
ME

meningococcal vaccine (MCV4, AIM Vaccine)

✓ Approved

AIM Vaccine · Cell-based Therapies · Cell-based Therapies

What is meningococcal vaccine?

meningococcal vaccine is a cell-based therapies developed by AIM Vaccine. It is approved for therapeutic indications via unknown.

Drug Profile

Brand NamesMCV4, AIM Vaccine
CompanyAIM Vaccine
Drug ClassCell-based Therapies, Vaccine
RouteUnknown
StatusApproved
Sources: ClinicalTrials.gov, AIM Vaccine

Therapeutic Indications

meningococcal vaccine is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Infections and infestationsMeningococcal bacteraemia✓ Approved

Related Research Articles

PubMedAdvances in virology2026-09-20

Comparative Sequence Analysis of the Envelope Gene of Kyasanur Forest Disease Virus Vaccine Strain With Currently Circulating Field Strains.

Kaje Keerthi K, Marinaik Chandranaik B CB, Gomes Amitha Reena AR, Rizwan Apsana A et al.

The present study was undertaken with the objective of performing comparative sequence analysis of the envelope (E) gene of Kyasanur forest disease virus (KFDV) vaccine strain P9605 with the circulating field strains. The study was taken up as the currently used KFDV vaccine strain, KFDV P9605, was isolated in the 1960s. For this study, we designed two sets of primers targeting the complete amplification of the E gene of KFDV. The sequencing was performed by the Sanger method, and the deduced sequence of the vaccine virus was deposited in GenBank with accession number PX067005. This sequence obtained for the vaccine virus was aligned and compared with sequences of GenBank-deposited circulating field strains. We also performed comparative sequence analysis of the Kyasanur forest disease (KFD) vaccine seed virus having passaged twice in mouse brain with the vaccine seed virus passaged six times in mouse brain to investigate whether multiple passages in mouse brain will lead to genetic mutation in the immunologically important E gene. The phylogenetic analysis revealed seven amino acid mutations in the field strains at positions A123T, S158N, D178E, D239N, A313S, M429I, and G479A when compared with the vaccine strain. We did not find any mutations at the critical fusogenic segment (residues 98-113) in the E gene of currently circulating field strains compared to the vaccine seed virus. The study found no genetic variations in the E gene of the KFD virus passed two times and passed six times in mouse brain. We performed SWISS-MODEL homology modeling, AlphaFold protein analysis, and Ramachandran plot analysis to study the E protein structures and stability. The observations made in this study suggest slow evolutionary drift and conserved structural stability of the envelope gene of KFDV ever since its emergence 7 decades ago; however, the functional implications of these amino acid substitutions need further studies on their roles in viral infectivity, transmission, and impact on immunity.

PMID 42763584
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PubMedInternational journal of nanomedicine2026-09-20

Biotinylated ε-Polylysine-Cyclodextrin-Coated Mesoporous Silica Nanoparticles for Targeted pH-Responsive Baicalin Delivery.

Liao Rongqiang R, Ruan Yi Y, Zhang Ke K, Liu Maoxia M

Baicalin (BAI) is a natural flavonoid with antitumor potential, but its poor water solubility and low bioavailability limit clinical use. Mesoporous silica nanoparticles are promising drug carriers due to their large surface area and tunable pore structure, yet premature drug leakage remains a key challenge. A multifunctional nanoplatform, designated as BPCD@BAI@BMSN, was constructed to enable efficient baicalin loading, pH-responsive gated release, and biotin-mediated active tumor targeting. A novel biotin-ε-polylysine-cyclodextrin (BPCD) conjugate was synthesized via EDCI/NHS coupling and characterized by NMR and GPC. Hollow mesoporous silica nanoparticles (BMSN) were prepared by the Stöber method, surface-modified with benzothiazole. The BPCD conjugate was coated onto the nanoparticle surface via cyclodextrin-benzothiazole host-guest self-assembly. The resulting nanoparticles were characterized by TEM, DLS, zeta potential, FTIR, and TGA. Drug loading, pH-responsive release, cytotoxicity against SMMC-7721 cells, cellular uptake evaluated by confocal microscopy and flow cytometry, and in vivo antitumor efficacy in nude mice were systematically evaluated. BPCD@BAI@BMSN exhibited near-spherical morphology with a particle size of approximately 200 nm, a positive zeta potential of +10 mV, a drug loading of 19.85%, and an encapsulation efficiency of 89.6%. Cumulative baicalin release reached approximately 62% at pH 5.5, whereas only about 6% was released at pH 7.4, confirming acid-triggered gated release. The blank carrier showed no significant cytotoxicity with cell viability above 95%, while drug-loaded nanoparticles exhibited enhanced cytotoxicity at pH 6.8. Biotin-functionalized nanoparticles demonstrated significantly higher cellular uptake and tumor accumulation compared to non-targeted controls. In vivo, BPCD@BAI@BMSN achieved a tumor growth inhibition rate of 72.5% compared to the control group, with no obvious toxicity to major organs observed during the 21-day treatment period. BPCD@BAI@BMSN integrates high drug loading, pH-responsive supramolecular gating, and active tumor targeting into a single nanoplatform, offering a promising strategy for baicalin delivery with enhanced antitumor efficacy and favorable short-term biosafety.

PMID 42763689
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PubMedEarth, planets, and space : EPS2026-09-20

Estimation of auroral emission altitude in the region of the ISS magnetic footprint during a relativistic electron precipitation event observed by ISS-CALET.

Yanagisawa Kyutaro K, Kataoka Ryuho R, Seki Kanako K, Whiter Daniel D et al.

We report a multi-MeV relativistic electron precipitation (REP) event as observed by the CALorimetric Electron Telescope and the Monitor of All-sky X-ray Image aboard the International Space Station, together with low-cost twin all-sky auroral imagers installed at Athabasca, Canada. We find that visible auroral emissions near the ISS magnetic footprint during REP events are not frequent-observed in only two of 10 conjugate REP events during our survey period from September 2024 to September 2025-and that one case, on 3 May 2025, featured diffuse aurora near the ISS magnetic footprint. Using two independent stereoscopic methods, we estimate the auroral emission height to be ~90 km, which is typically produced by tens-of-keV electron precipitation. Combined with the MeV electron precipitation detected by CALET, such broadband electron precipitation from tens-of-keV to MeV is consistent with the hypothesis of chorus-driven REP events. The emission altitude shows no systematic latitudinal variation, which is not consistent with field-line curvature scattering type energy-dispersed precipitation. The combined space- and ground-based observations contribute to a better understanding of the spatial context of wave-particle interaction associated with the REP events.

PMID 42763453
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PubMedInternational journal of nanomedicine2026-09-20

Engineered Exosomal miRNAs for Post-Stroke Neural Repair: Mechanisms, Delivery Strategies, and Translational Challenges.

Xu Shuangfeng S, Tian Daman D, Wang Zhifeng Z, Yang Jiao J et al.

Functional neurological recovery after ischemic stroke remains a formidable challenge in neuroscience. Exosomes serve as pivotal mediators of intercellular communication, and the microRNAs (miRNAs) they carry, in particular, offer a promising "cell-free therapy" strategy for promoting neurological repair. This review systematically summarizes the multi-target mechanisms by which exosomal miRNAs regulate the neurovascular unit (NVU) and outlines technical strategies to enhance exosomal therapeutic efficacy through targeted modification and engineered cargo loading, with the aim of constructing a smart drug delivery system capable of precise navigation. Following the trajectory of "natural exosomes-engineered exosomes-clinical translation", this review addresses the core scientific question of how to transform exosomal miRNAs from natural messenger molecules with basic reparative activity into an intelligent therapeutic system for precise targeted delivery. It further explores precision exosome treatment models based on the pathological staging of stroke progression, and integrates single-cell, spatial transcriptomic, and multi-omics technologies to decode the "miRNA-cell source-target cell-signaling pathway" regulatory axis, thereby identifying candidate miRNA combinations with translational potential. Finally, this review provides an in-depth analysis of the core challenges in translating such nanotherapeutic strategies from the bench to the bedside, including manufacturing standardization, quality control, and potency assessment, with the aim of providing a theoretical basis for advancing exosomal miRNA therapies from mechanistic studies to precision stroke treatment.

PMID 42763691
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PubMedMolecular cancer2026-09-20

Immune-pressure redistribution in resistance to PD-1/PD-L1 blockade: mechanisms, biomarkers, and therapeutic design.

Wang Xiaodong X, Liu Jiayi J, Hairulajiang Alifujiang A, Wang Junjie J et al.

PD-1/PD-L1 blockade can produce durable tumor control, yet primary, adaptive, and acquired resistance remain common. Existing accounts often catalogue resistance by cellular compartment, obscuring the coordinated nature of tumor adaptation. Here, we introduce immune-pressure redistribution as a treatment-oriented framework that complements cancer immunoediting by asking where therapeutic immune pressure is diverted after checkpoint release. Resistance is organized into three coupled routes: transfer into tumor-intrinsic escape through antigen-presentation loss, interferon-response defects, oncogenic rewiring, and lineage plasticity; weakening through defective priming, terminal T-cell differentiation, compensatory checkpoints, metabolic constraint, and chronic cytokine signaling; and unloading into stromal, vascular, myeloid, regulatory, microbial, and systemic host compartments. We integrate clinically validated mechanisms with emerging evidence, including the temporal duality of interferon-JAK signaling, the role of tumor-draining lymph nodes in sustaining progenitor-exhausted T cells, and the limited translation of TIGIT, IDO1, TGF-β, and CSF-1R targeting. We further propose a biomarker-guided strategy that combines tumor visibility, immune-cell state, spatial architecture, systemic inflammation, and early treatment dynamics to identify the dominant resistance topology. This framework supports topology-matched combinations and adaptive sequencing rather than uniform escalation, with the aim of restoring productive immune pressure while limiting compensatory escape and toxicity.

PMID 42763389
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PubMedInternational journal of toxicology2026-09-20

Drug-drug Interaction Between Alpinetin and Glimepiride and its Potential Mechanism in Rats.

Qin Mengnan M, Zhao Wenwen W, Li Xin X

Given that alpinetin possesses hypoglycemic and cardioprotective properties, it holds potential for co-administration with the antidiabetic agent glimepiride. The aim was to evaluate the impact of alpinetin on the pharmacokinetics and hypoglycemic efficacy of glimepiride, thereby providing a foundation for the development of alpinetin and informing its potential clinical translation. Pharmacokinetic studies were performed in rats following oral administration of glimepiride (1 mg/kg) alone or combined with alpinetin (30 mg/kg). The effect of the combination of glimepiride and alpinetin on blood glucose levels was investigated in a rat model of type 2 diabetes mellitus (T2DM). In vitro experiments were conducted to evaluate the effect of alpinetin on glimepiride metabolic stability and to assess its role on cytochrome P450 2C9 (CYP2C9) activity. Co-administration of glimepiride with alpinetin resulted in significant changes in the pharmacokinetics of glimepiride, as evidenced by an increase in area under the concentration-time curve (AUC), elimination half-life (t1/2), maximum concentration (Cmax), and a decrease in clearance. Glimepiride in combination with alpinetin enhanced the hypoglycemic effect in T2DM rats. Mechanistic studies in liver microsomes revealed that alpinetin improved glimepiride metabolic stability and inhibited CYP2C9 activity. The combination of glimepiride with alpinetin may increase the systemic exposure of glimepiride through inhibition of CYP2C9 activity. This likely contributes to the enhanced hypoglycemic effect observed, but also underscores the need for caution regarding the potential risk of hypoglycemia.

PMID 42763797
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