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ustekinumab (Qoyvolma)

✓ Approved

Celltrion, Inc. · IL12B · 单克隆抗体

什么是 ustekinumab？

ustekinumab 是一种单克隆抗体，由Celltrion, Inc.研发。该药已获批，用于治疗相关适应症，给药途径：Injectable (Others)、Intravenous (IV)。

药物档案

商品名Qoyvolma
公司Celltrion, Inc.
药物类别单克隆抗体, 抗体
分子靶点IL12B, IL23A
给药途径Injectable (Others), Intravenous (IV)
状态Approved
来源： ClinicalTrials.gov, Celltrion, Inc.

作用机制

分子靶点

ustekinumab 作用于 2 个分子靶点：

IL12Binterleukin 12B (CLMF2, CLMF)
IL23Ainterleukin 23 subunit alpha (P19, SGRF)
需要更深入的分析？Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

ustekinumab 针对 4 个适应症，涉及 3 个治疗领域。

治疗领域疾病/病症分期
Gastrointestinal disordersColitis ulcerative✓ Approved
Gastrointestinal disordersCrohn's disease✓ Approved
Skin and subcutaneous tissue disordersPsoriasis✓ Approved
Musculoskeletal and connective tissue disordersPsoriatic arthropathy✓ Approved

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Biosimilars in inflammatory bowel disease: from initial uncertainty to clinical normalization.

Argüelles-Arias Federico F, Zabana Yamile Y

Biosimilars have become an integral part of the treatment of inflammatory bowel disease (IBD), evolving from initial uncertainty regarding indication extrapolation and non-medical switching to widespread clinical acceptance. Early concerns focused mainly on the absence of disease-specific evidence and the potential impact of switching on effectiveness, safety, and immunogenicity. Over the past decade, however, extensive real-world evidence and randomized data have consistently supported the use of infliximab and adalimumab biosimilars in both biologic-naïve patients and patients switched from originator products. Recent systematic reviews and meta-analyses further reinforce these findings, showing preserved clinical remission, treatment persistence, inflammatory biomarkers, and immunogenicity after switching. The biosimilar landscape is now expanding to newer therapeutic targets, including ustekinumab, while biosimilar-to-biosimilar and multiple switching is becoming increasingly relevant in routine practice. Nevertheless, scientific interchangeability should not be equated to automatic substitution. Switching decisions should remain clinically supervised and involve gastroenterologists within a multidisciplinary framework, taking into account disease activity, previous response, safety, immunogenicity, and patient preferences. Appropriate communication is also essential to minimize a potential nocebo effect and to avoid unnecessary discontinuation. Biosimilars should therefore be considered fully established biological therapies rather than lower-tier alternatives to originator drugs. Future research should focus less on re-confirming single-switch equivalence and more on unresolved questions, including long-term outcomes after multiple switching, biosimilars of newer therapeutic targets, patient-reported outcomes, treatment persistence, and comparative pharmacoeconomic impact across healthcare systems.

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NOR-1 is an upstream regulator of Ca2+ homeostasis and calmodulin kinase II-dependent arrhythmogenesis.

Vázquez-Sufuentes Paula P, Jiménez-Sábado Verónica V, Ballester-Servera Carme C, Casabella-Ramón Sergi S et al.

Dysregulation of NOR-1 has been reported in cardiovascular diseases associated with altered calcium handling. We therefore investigated how NOR-1 affects calcium homeostasis and arrhythmogenesis to identify the underlying mechanisms. We assessed the expression of NOR-1 and calcium regulatory proteins in myocardial samples from humans and mice that overexpress human NOR-1 in the heart (TgNOR-1). Gene promoter activity was determined by transient co-transfection assays. Calcium imaging, patch-clamp recordings and immunofluorescent labeling was performed in mouse cardiomyocytes. Experimental data were used for mathematical modeling. Arrhythmias were induced in vivo by an epinephrine/caffeine challenge. In human cardiac samples, mRNA levels of genes coding for SERCA2a, CASQ2, TN-C1 and PLB correlated with those of NOR-1, while TgNOR-1 mice exhibited higher cardiac levels of these calcium regulatory proteins than wild-type animals (WT). NOR-1 increased luciferase activity driven by the proximal promoter of both human and mouse genes. Calcium transients were smaller in TgNOR-1 cardiomyocytes while L-type calcium current and SR calcium content were unchanged. Mathematical modeling revealed that more calcium binds to CASQ2 and is released from the SR in TgNOR-1 cardiomyocytes, but the resulting calcium transient is smaller because more calcium is buffered by TN-C1. Furthermore, NOR-1 transgenesis increased the level of reactive oxygen species and CAMKII oxidation, as well as RyR2 phosphorylation at Ser-2814, which led to a higher incidence of calcium waves and afterdepolarizations in resting TgNOR-1 cardiomyocytes. In electrically paced myocytes, NOR-1 transgenesis promoted extra-transients at low frequencies and calcium alternans at high frequencies. Importantly, these derangements in intracellular calcium handling concurred with a dramatic increase in epinephrine/caffeine-induced bidirectional ventricular tachycardia in TgNOR-1 mice. Moreover, the antioxidant N-acetylcysteine and the CAMKII inhibitor KN-93 attenuated arrythmia in TgNOR-1 mice and arrhythmogenic calcium release in isolated myocytes. Our findings highlight NOR-1 as an upstream regulator of CAMKII-oxidation underlying arrhythmia induced by defective calcium homeostasis, pointing to therapies targeting CAMKII as a means to attenuate arrhythmia triggered by pathological upregulation of NOR-1.

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DEL-1 Attenuates Gentamycin-induced Ferroptosis and Apoptosis in Hair Cells Through AMPK/Autophagy-mediated Suppression of ER Stress.

Lim Do Su DS, Ryu Jae Hak JH, Cho Wonjun W, Gwon Hyeon Ji HJ et al.

Developmental endothelial locus-1 (DEL-1), a myokine, has been shown to reduce endoplasmic reticulum (ER) stress in various experimental models. This study aimed to examine the impact of DEL-1 on gentamicin (GT)-induced ototoxicity in cultured hair cell-like cells. The long-term use of GTs for treating infections induces ER stress in the inner ear, leading to hair cell-like death and, as a result, hearing loss. Protein expression was measured via Western blot analysis, and cell viability, caspase 3 activity, and iron levels were assessed. Apoptotic cells were identified via TUNEL staining. GT exposure triggered ferroptosis, apoptosis, and ER stress in HEI-OC1 cells, all of which were reversed by DEL-1 treatment. DEL-1 also promoted AMP-activated protein kinase (AMPK) phosphorylation and autophagy. Inhibition of AMPK with siRNA or 3-methyladenine (3-MA) reduced the protective effects of DEL-1 in the presence of GT. These findings suggest that DEL-1 mitigates ER stress via AMPK/autophagy signaling, reducing ferroptosis and apoptosis in GT-treated hair cell-like cells. These findings indicate that DEL-1, a muscle-secreted protein, may offer a therapeutic strategy for GT-induced hearing loss.

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PubMedBiosensors2026-10-26

GO/Cysteamine-Modified Screen-Printed Carbon Electrode for Square-Wave Anodic Stripping Voltammetric Determination of Cadmium in Fortified Mango and Avocado Digestates.

Lozada Rufino Miguel Angel MA, Zapata Peña Eulogia Isabel EI, Delgado Valdiviezo Gonzalo Manuel GM, Ortiz Castillo Rosa Gisela RG et al.

Cadmium contamination in fruits is a relevant food-safety concern because of its toxicity, environmental persistence, and potential transfer from agricultural soils to edible plant tissues. This study developed a screen-printed carbon electrode modified with graphene oxide and cysteamine (SPCE/GO-cysteamine) to determine Cd(II) by square-wave anodic stripping voltammetry (SWASV). Two surface-modification routes, GO-cysteamine and GO-rGO-cysteamine, and GO concentrations of 0.1, 0.2, and 0.5 mg mL-1 were compared by cyclic voltammetry. The direct GO-cysteamine route at 0.2 mg mL-1 produced the highest CV response among the tested conditions and was selected for Cd(II) determination. Raman spectroscopy FTIR spectroscopy and scanning electron microscopy were used to characterize the graphene-based materials employed during surface optimization. Cd(II) concentrations from 1 to 10 µg L-1 were experimentally evaluated; with a calculated LOQ of 0.74 µg L-1, the entire experimentally evaluated range of 1-10 µg L-1, with a sensitivity of 11.30 µA (µg L-1)-1, R2 = 0.9892, a limit of detection of 0.25 µg L-1 and a limit of quantification of 0.74 µg L-1. Fortified Kent mango and Hass avocado digestates also showed concentration-dependent responses, with R2 values of 0.9799 and 0.9788, respectively, and relative standard deviations below 5%. These results demonstrate the feasibility of the SPCE/GO-cysteamine platform for Cd(II) determination in digested fruit matrices and support its further development as a portable screening approach for food-quality control.

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PubMedCells2026-10-26

Hyperglycemia-Induced Loss of Astrocytic Kir4.1 Is Associated with Increased DNMT1 Activity and Altered AMPK/SIRT1 Signaling.

Colón-Vázquez Jadier J, Hernández-Santiago Yanitza Y, Malpica-Nieves Christian J CJ, Rosado-Rivera Nathaly M NM et al.

The effects of chronic hyperglycemia on CNS, glial homeostasis and Kir4.1 regulation is poorly understood. Elevated blood glucose levels affect polyamine-sensitive inwardly rectifying potassium channels, Kir4.1, in astrocytes and retinal Müller glial cells. These cells regulate extracellular potassium and clear glutamate, processes supported by Kir4.1. Dysregulation of Kir4.1 channels has been implicated in glutamate toxicity, epilepsy, ataxia, and diabetes-induced neurodegeneration. In this study, we used Tandem Mass Tag Proteomic analysis, Pyrosequencing, SDS-PAGE and Western blot analysis, in whole brain and astrocytic primary cultures in hyperglycemic conditions testing DNMT1 and AMPK activities with RG-108, compound C, and AICAR treatments to investigate how hyperglycemia alters Kir4.1 expression in astrocytes and explored two regulatory mechanisms: (i) DNA methylation mediated by DNA methyltransferase 1 (DNMT-1), which uses S-adenosylmethionine (SAM) as a methyl donor, and (ii) metabolic signaling via the AMPK/SIRT-1 cascade. We found that hyperglycemia (25 mM glucose) (i) increased DNMT-1 protein levels in astrocytes by 1.5-2-fold and (ii) decreased AMPK and (iii) SIRT-1 levels, accompanied by a reduction in Kir4.1 protein expression. Pharmacological inhibition of DNMT-1 with RG-108 decreased DNMT-1 levels and restored Kir4.1. Treatment with AICAR, a selective AMPK activator, rescued SIRT-1 and Kir4.1 expression. In summary, hyperglycemia engages dual regulatory pathways: (i) epigenetic via DNMT-1 and (ii) metabolic via AMPK/SIRT-1, which converge on Kir4.1 downregulation in astrocytes. Therefore, both DNMT-1 inhibition and AMPK activation rescued Kir4.1 expression, suggesting functional support for potassium and glutamate homeostasis and membrane potential stability in glia.

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Neuropsychiatric Outcomes Associated With GLP-1 Receptor Agonist Use in Medicare Beneficiaries With Type 2 Diabetes: Variation by Treatment Pattern and Obesity Status.

Baik Seo Hyon SH, Baye Fitsum F, Xian Haotian H, Fung Kin Wah KW et al.

Glucagon-like peptide-1 (GLP-1) receptors are expressed in brain regions governing mood, reward and stress, yet the neuropsychiatric effects of GLP-1 receptor agonist (GLP-1 RA) therapy remain poorly characterized. We estimated associations between GLP-1 RA use and neuropsychiatric disorders and variation by obesity status and treatment pattern. This population-based cohort study used claims data from Medicare enrolees with Type 2 diabetes mellitus. GLP-1 RAs were compared with other second-line glucose-lowering medications and evaluated across four treatment patterns: monotherapy, switch, escalation and augmentation. Eight neuropsychiatric outcomes were examined using 1:1 propensity score-matched, covariate-adjusted stratified Cox regression with time-varying covariates. GLP-1 RA use was associated with a small increase in aggregate psychiatric disorder risk (Hazard Ratio [HR] = 1.04; 95% Confidence Interval: 1.03-1.06; 1.7 excess events/1000 person-years), of uncertain clinical significance given the large cohort size. Risk was elevated for depression (HR = 1.11; 3.0 excess events/1000 person-years) but reduced for substance use disorders (HR = 0.84; 4.1 fewer events/1000 person-years), dementia (HR = 0.87; 2.8 fewer) and suicidal/self-harm (HR = 0.81; 0.4 fewer events/1000 person-years). Associations varied by treatment pattern: monotherapy showed elevated psychiatric (HR = 1.43) and elevated emotional symptom (HR = 1.32) risks; escalation also exhibited elevated psychiatric risk, whereas switch and augmentation demonstrated reduced or null risks. Rather than a uniform class effect, the neuropsychiatric profile of GLP-1 RA appears context-dependent, differing by treatment pattern, obesity status and outcome examined. Elevated risk with monotherapy or escalation may reflect baseline clinical differences rather than pharmacological effect. Reduced risks of substance use disorders, dementia and suicidal/self-harm are reassuring.

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