若生智能
Drug Database
IN

interferon beta-1b (Infibeta)

✓ Approved

Generium Pharmaceutical · 重组蛋白 · 重组蛋白

什么是 interferon beta-1b？

interferon beta-1b 是一种重组蛋白，由Generium Pharmaceutical研发。该药已获批，用于治疗相关适应症，给药途径：Injectable (Others)、Subcutaneous Injection。

药物档案

商品名Infibeta
公司Generium Pharmaceutical
药物类别重组蛋白
给药途径Injectable (Others), Subcutaneous Injection
状态Approved
来源： ClinicalTrials.gov, Generium Pharmaceutical

治疗适应症

interferon beta-1b 针对 1 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Nervous system disordersMultiple sclerosis✓ Approved

相关研究文献

PubMedCurrent oncology (Toronto, Ont.)2026-07-27

Interleukin-1β Gene (IL-1B) rs16944 (-511 C > T) Promoter Polymorphism Is Associated with Cutaneous Melanoma Susceptibility, Stage, and Anatomical Localization in a Northern Italian Case-Control Study.

Cauci Sabina S, Buligan Cinzia C, Nacci Patrizia P, Petris Gianluca G et al.

Immunity plays critical roles in cutaneous melanoma. We investigated the association between the pro-inflammatory interleukin-1β gene (IL-1B) rs16944 (-511 C > T) promoter single nucleotide polymorphism (SNP) and cutaneous melanoma susceptibility and clinical features. This observational case-control study included 133 patients with cutaneous melanoma and 900 healthy controls from Northeastern Italy. The rs16944 C > T polymorphism was determined by genomic DNA restriction fragment analysis. The IL-1B rs16944 C allele (OR = 1.44, p = 0.014) and CC genotype (OR = 1.48, p = 0.037) were associated with modestly higher odds of melanoma. Among melanoma patients, the CC genotype was associated with Stage I disease (OR = 2.45, p = 0.016) and Breslow thickness ≤ 0.75 mm (OR = 2.27, p = 0.049), whereas it was less frequent in Stage IV melanoma (OR = 0.37, p = 0.029). The CT genotype was associated with Stage IV melanoma (OR = 3.03, p = 0.014) and with lower-limb (OR = 2.45, p = 0.038) and lower-extremity (OR = 3.09, p = 0.005) melanoma. These divergent associations are exploratory and do not establish disease trajectory or a functional effect of rs16944; mechanistic interpretation remains uncertain because IL-1β expression or activity was not measured in this cohort. To our knowledge, this is the first report of an association between a genetic polymorphism and lower-limb/lower-extremity melanoma. These exploratory findings require confirmation in independent cohorts.

PMID 42505240
阅读全文 →
PubMedProtein & cell2026-07-27

CRISPR screening identifies GNPTAB as a noncanonical STING activator driving cellular senescence.

Yin Jian J, Gao Yizhou Y, Jing Yaobin Y, Jiang Xiaoyu X et al.

Cellular senescence is accompanied by profound lysosomal alterations, yet whether lysosome-associated factors actively drive aging remains unclear. Through a focused CRISPR/Cas9 screen in human mesenchymal progenitor cells (hMPCs), we identified N-acetylglucosamine-1-phosphotransferase subunits alpha and beta (GNPTAB), an enzyme responsible for lysosomal hydrolase targeting, as a potent regulator of cellular senescence. Genetic ablation of GNPTAB attenuated senescence, whereas its overexpression accelerated senescence. This pro-senescent function occurred independently of GNPTAB's canonical enzymatic role. Instead, GNPTAB binds to the innate immune adaptor stimulator of interferon genes (STING) via a specific interface (E1119), leading to activation of STING and its downstream TANK-binding kinase 1 (TBK1), as well as pro-inflammatory gene expression. A STING-binding-deficient GNPTAB mutant (E1119A) preserved canonical lysosomal functions but failed to induce senescence, while STING depletion abolished GNPTAB-driven senescence. Together, these findings uncover a new signaling pathway wherein GNPTAB engages STING to facilitate its activation, nominating this interface as a potential target for mitigating age-related cellular dysfunction.

PMID 42505080
阅读全文 →
PubMedAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026-07-27

Synthetic Toll-Like Receptors for Control of Innate Immunity With Far-Red Light.

Leopold Anna V AV, Verkhusha Vladislav V VV

Toll-like receptors (TLRs) are single-pass transmembrane proteins that initiate innate immune responses through recognition of pathogen-associated molecular patterns, including lipopolysaccharide, flagellin, and microbial nucleic acids. In mammals, TLRs are expressed in both immune and non-immune cells, where they activate cytokine expression through the myeloid differentiation primary response 88 (MyD88) signaling pathway and subsequently engage the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) or interferon regulatory factor 3 / interferon regulatory factor 7 (IRF3/IRF7) pathways. To enable optical control of TLR function, the extracellular domains of several homodimeric TLRs, including TLR3, TLR4, and TLR5, are replaced with the photosensory core module of the bacterial phytochrome DrBphP. The resulting chimeric receptors activate the NF-κB and IRF3/IRF7 pathways in mammalian cells in a far-red-light-dependent manner. The MyD88 pathway is further reprogrammed to induce caspase activation instead of cytokine production, thereby creating a synthetic system that links TLR stimulation to caspase signaling. This strategy establishes a versatile optogenetic platform for far-red-light control of innate immune and cell death pathways.

PMID 42504985
阅读全文 →
PubMedJournal of vestibular research : equilibrium & orientation2026-07-27

High beta activity tracks disease state in persistent postural-perceptual dizziness: A longitudinal quantitative EEG study.

Kim Suk Jae SJ, Kim Chi-Hun CH, Ryoo Sookyung S, Hwang Jaechun J et al.

BackgroundPersistent postural-perceptual dizziness (PPPD) is a chronic vestibular disorder lacking objective tools for monitoring disease activity. Quantitative electroencephalography (qEEG) has identified cortical hyperexcitability in migraine, but whether analogous patterns exist in PPPD and reverse with treatment is unknown. We investigated high beta (25-30 Hz) activity as a state-dependent biomarker for PPPD.MethodsThis retrospective longitudinal study analyzed 19-channel resting-state qEEG from 163 unmedicated PPPD patients, 86 healthy controls (HC), and 67 vestibular migraine (VM) patients as a dizzy control group at a specialized neurology clinic. Absolute power was z-score normalized against an age-adjusted reference database. The primary outcome was the number of electrodes with high beta absolute power z-score > +1.96; the continuous mean high beta z-score served as a confirmatory outcome. Patients were followed through pharmacotherapy, with qEEG repeated at follow-up (n = 107) and at relapse after discontinuation (n = 23).ResultsHigh beta electrode counts were graded across groups and highest in PPPD (median: HC 2 [IQR 0-4], VM 7 [3-13], PPPD 16 [12-18]; all pairwise p < 0.001), discriminating PPPD from HC with an AUC of 0.956 (OR = 1.53 per electrode; 95% CI 1.38-1.69); the continuous mean z-score yielded a comparable AUC (0.948). Within PPPD, high beta count was not confounded by age, sex, comorbid migraine, or anxiety (all p > 0.30). Marked responders (n = 76) showed near-normalization of high beta electrode count (17 → 2.5; Cohen's d = 2.58), whereas partial responders (n = 31) showed smaller reductions (15 → 11; p < 0.001). Clinical improvement correlated with reduction in high beta electrode count (ρ = 0.509; p < 0.001). Relapse after discontinuation produced a V-shaped trajectory (n = 23; 15 → 2 → 13).ConclusionsOn qEEG, high beta-trans-diagnostic but most pronounced in PPPD-represents a promising state-dependent biomarker. Its cross-sectional elevation versus controls establishes it as a valid marker, while its differential reduction with treatment and V-shaped relapse trajectory support its potential as a clinically accessible metric for within-subject monitoring of disease activity in PPPD. These findings warrant multicenter, prospective validation.

PMID 42503621
阅读全文 →
PubMedJournal of agricultural and food chemistry2026-07-27

Discovery and Engineering of a Plant Glycosyltransferase for Efficient Benzylisoquinoline Alkaloid Glycosylation.

Song Jun J, Qin Yutong Y, Jin Lu L, Han Liang L et al.

Benzylisoquinoline alkaloids (BIAs) hold broad pharmaceutical potential, yet poor water solubility and low bioavailability limit their application. Glycosylation improves these properties, but glycosyltransferases (GTs) efficiently catalyzing diverse BIAs remain scarce. Here, we identify UGT74AN1 from Asclepias curassavica, capable of glycosylating various BIAs. Structure-guided semirational engineering yielded the double mutant UGT74AN1M2, exhibiting a 341-fold increase in catalytic efficiency. Molecular dynamics simulations revealed that these mutations widen the substrate channel and strengthen binding. To overcome UDP-glucose dependency, we designed the fusion enzyme AtSuSy-L12-UGT74AN1M2 via the iMARS platform, enabling in situ UDP-glucose generation coupled with highly efficient BIA glycosylation. Consequently, the synthesized dihydrojatrorrhizine-3-O-β-d-glucoside (1b) demonstrated superior antitumor activity compared to its aglycone through stronger proliferation inhibition and apoptosis induction. This work provides an efficient enzymatic toolkit for green BIA glycoside synthesis and identifies promising candidates for drug development.

PMID 42505063
阅读全文 →
PubMedMetabolites2026-07-27

GABA Regulates Ca2+ Oscillations and Synchronization in Pancreatic Beta Cells.

Grubelnik Vladimir V, Marhl Marko M

Gamma-aminobutyric acid (GABA) is increasingly recognized as an important modulator of pancreatic beta-cell function, but the mechanisms by which it regulates intracellular Ca2+ oscillations and coordinated beta-cell activity remain insufficiently understood. The aim of this study was to investigate how GABA influences the amplitude, frequency, phase adjustment, entrainment, and synchronization of beta-cell Ca2+ oscillations. We developed a reduced ATP-Ca2+ oscillation model, based on established beta-cell oscillatory frameworks, and coupled it to the GABA-shunt subsystem derived from our previously established Dual Anaplerotic Model. The model incorporates explicit dynamics of cytosolic Ca2+, endoplasmic reticulum Ca2+, ATP, and a regulatory variable controlling Ca2+ influx, while the interstitial GABA signal is represented as a delayed feedback signal acting on cellular excitability. Single-cell and two-cell simulations were performed to analyze GABA-dependent oscillatory regulation and intercellular coupling. The model reproduced key experimental observations under both control and GABA-deficient conditions, including reduced Ca2+-oscillation amplitude and a prolonged oscillation period when GABA production was suppressed. Mechanistically, GABA affected single-cell oscillations through two complementary pathways: metabolically, by modulating ATP production through PEP-related and TCA-related contributions linked to the GABA shunt, and as an interstitial/paracrine signal, by adjusting the phase of Ca2+ influx through fast and delayed inhibitory feedback. In the reduced two-cell model, delayed interstitial GABA signaling could phase-lock non-identical oscillators over finite ranges of parameter mismatch. When included as an additional weak effective term, electrical coupling broadened these ranges, consistent with a complementary interaction between GABA-mediated phase adjustment and established electrical coupling. GABA acts as a dual regulator of beta-cell dynamics, linking intracellular metabolism to Ca2+-oscillation patterning and promoting coordinated activity through intercellular phase adjustment. The model provides a mechanistic framework connecting GABA metabolism, ATP dynamics, Ca2+ signaling, and beta-cell synchronization in pancreatic islets.

PMID 42506415
阅读全文 →

注册免费账户还可查看另外 9996 篇文献

免费注册查看全部文献 →

了解更多interferon beta-1b