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Ypeginterferon alpha-2b (PegBeron)

✓ Approved

Xiamen Amoytop Biotech Co.ltd · 重组蛋白 · 重组蛋白

什么是 Ypeginterferon alpha-2b?

Ypeginterferon alpha-2b 是一种重组蛋白,由Xiamen Amoytop Biotech Co.ltd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PegBeron
公司Xiamen Amoytop Biotech Co.ltd
药物类别重组蛋白
给药途径Injectable (Others), Subcutaneous Injection
状态Approved

治疗适应症

Ypeginterferon alpha-2b 针对 3 个适应症,涉及 2 个治疗领域。

治疗领域疾病/病症分期
Infections and infestationsHepatitis B✓ Approved
Infections and infestationsHepatitis C✓ Approved
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Essential thrombocythaemiaPhase II

相关研究文献

PubMedHepatology (Baltimore, Md.)2026-10-26

A phase 2b/3 trial of saroglitazar in primary biliary cholangitis.

Vuppalanchi Raj R, Villamil Alejandra A, Yilmaz Yusuf Y, Idilman Ramazan R et al.

Saroglitazar, a dual PPAR alpha/gamma agonist, improved serum alkaline phosphatase (ALP) levels in patients with primary biliary cholangitis (PBC) in a phase 2a clinical trial. EPICS-III is a phase 2b/3 adaptive, double-blind, randomized controlled trial in patients with PBC who had an inadequate response to or were intolerant of ursodeoxycholic acid (UDCA). In phase 2b, 37 participants received placebo or saroglitazar magnesium 1 or 2 mg for 16 weeks. Saroglitazar magnesium 1 mg (0.97 mg of saroglitazar) was selected for phase 3, which randomized 148 patients to saroglitazar (n=97) or placebo (n=51) for 52 weeks. The primary endpoint was biochemical response at week 52, defined as ALP <1.67 x ULN with ≥15% reduction from baseline and total bilirubin below ULN; the key secondary endpoint was ALP normalization. Baseline characteristics in the phase 3 efficacy population were comparable except for higher baseline ALP and other liver biochemistries in the saroglitazar group. Biochemical response was achieved in 56.7% versus 9.8% with placebo (difference, 48.0%; 95% CI, 35.3 to 60.8; p<0.001). Among participants with baseline ALP ≤3xULN, biochemical response rates were 79.0% versus 14.3%, and 83.1% versus 14.7% in the per-protocol analysis. ALP normalization occurred in 8.2% with saroglitazar versus 0% with placebo (difference, 8.5%; 95% CI, 2.9 to 14; p=0.016). Among participants with baseline 5-D Itch score ≥12, the week-24 treatment difference was -3.2 points (95% CI, -5.66 to -0.82) but was not maintained at week 52. Adverse events occurred in 81.1% with saroglitazar versus 90.5% with placebo, and serious adverse events occurred in 6.3% and 11.1%, respectively. Saroglitazar 0.97 mg significantly improved biochemical response and ALP normalization and was well tolerated over 52 weeks.

PMID 42929426
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PubMedJournal of biochemical and molecular toxicology2026-10-26

Theranekron Attenuates Inflammation, Oxidative Stress Index, and Apoptosis in Lipopolysaccharide-Induced Cardiovascular Toxicity: Association With Hypoxia-Inducible Factor-1 Alpha-Related Gene Expression.

Savran Mehtap M, Asci Halil H, Imeci Orhan O, Oguzlar Furkan Cagri FC et al.

This study aimed to evaluate the possible protective effects of Theranekron, an extract derived from Tarantula cubensis venom, on cardiovascular damage induced by lipopolysaccharide (LPS) in an experimental rat model. A total of 32 male Wistar Albino rats were randomly divided into 4 groups: Control, Lipopolysaccharide, Lipopolysaccharide plus Theranekron, and Theranekron alone. Lipopolysaccharide administration caused pronounced histopathological changes in the heart and aorta, including endothelial sloughing, hyperemia, hemorrhage, and infiltration of inflammatory cells. These pathological findings were accompanied by elevated oxidative stress markers, increased tumor necrosis factor-alpha and inducible nitric oxide synthase immunoreactivity, and increased caspase-3 immunoreactivity. Additionally, genes associated with the hypoxia-inducible factor-1 alpha (HIF-1α) pathway-such as interleukin 6, signal transducer and activator of transcription 3 (STAT3), and vascular endothelial growth factor-were significantly upregulated in the lipopolysaccharide group. Theranekron pretreatment was associated with partial attenuation of oxidative stress imbalance, of inflammatory and apoptotic immunoreactivity, and of the upregulation of HIF-1α-related transcripts. Overall, these findings suggest that Theranekron may offer partial protection against early LPS-induced cardiovascular injury.

PMID 42929009
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PubMedHepatology (Baltimore, Md.)2026-10-26

Phase 1b study of miricorilant in patients with presumed metabolic dysfunction-associated steatohepatitis (MASH).

Alkhouri Naim N, Rudraraju Madhavi M, Leibowitz Mark M, Jenders Robert A RA et al.

Miricorilant, an oral nonsteroidal selective glucocorticoid receptor modulator, is being investigated as a therapy that modulates hepatic cortisol activity in patients with metabolic dysfunction-associated steatohepatitis (MASH). This phase 1b study evaluated miricorilant's efficacy and safety. Seventy patients with presumed MASH received oral miricorilant daily (30-150 mg) or intermittent (100-200 mg once, twice, or thrice weekly) dosing regimens for 12 or 24 weeks. Across dosing regimens, reductions in relative liver fat content (LFC) ranged from 10.1% to 76.6%. Improvements in MASH liver function markers and the enhanced liver fibrosis (ELF) score were observed across regimens. Treatment-emergent adverse events (TEAE) leading to drug interruption/discontinuation occurred in 12.9% of patients (n=9) each; most were due to aminotransferase elevations during an excessively rapid drop in LFC (up to 70.2% at week 6) and in patients receiving daily dosing. Intermittent dosing enabled more patients to complete 12 weeks of treatment without discontinuation due to TEAEs. Intermittent dosing with miricorilant 100 mg twice weekly had the best benefit-risk profile; this cohort demonstrated a mean LFC reduction of 28.2% at week 12, with a corresponding decline in liver enzymes (ALT, -3.8 U/L; AST, -6.0 U/L). Patients in this cohort also had numerical improvement in lipid profiles, glycemic markers, and fibrosis biomarkers. Intermittent miricorilant dosing of 100 mg twice weekly achieved meaningful reductions in LFC and improved liver health markers with a favorable safety profile. This regimen is being evaluated in the phase 2b MONARCH study (NCT06108219).

PMID 42929711
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PubMedEcology2026-10-26

Community history modifies how plant diversity shapes beta multifunctionality.

He Yan Y, Yang Rui R, Mao Lingfeng L

Research on ecosystem multifunctionality (EMF) has mainly quantified the magnitude of multiple functions within local communities (alpha multifunctionality [alpha-EMF]), whereas less is known about variation in function profiles among communities (beta multifunctionality [beta-EMF]). We asked how plant diversity affects variation in ecosystem function profiles among communities and whether this relationship depends on community history. We analyzed 5-year means of six ecosystem functions from 240 subplots in the DELTa-BEF, short for DEterminants of Long-Term Biodiversity Effects on Ecosystem Functioning Experiment, comparing new communities without experimental plant or soil history, resown communities retaining soil history, and old communities with continuous plant and soil histories. We adapted a variance-based beta diversity framework to quantify beta-EMF and partition it into local contributions to beta multifunctionality (LCBM) and function contributions to beta multifunctionality (FCBM). Plant diversity increased alpha-EMF in all treatments, with stronger increases in resown and old than in new communities. Richness was not detectably related to LCBM in new communities but was associated with lower LCBM in resown communities and higher LCBM in old communities, with the clearest contrast between the resown and old treatments. Leaf area index contributed more to beta-EMF than expected under equal contributions (20.2%), whereas basal respiration contributed less (13.2%); the other four functions did not differ from the equal-contribution expectation. Thus, similar gains in local multifunctionality can be accompanied by contrasting patterns of spatial functional heterogeneity, depending on community history. Partitioning beta-EMF into local and function contributions provides a practical way to identify which communities and functions contribute to spatial heterogeneity.

PMID 42928695
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PubMedJournal of materials chemistry. B2026-10-26

Alpha-mangostin combined with doxorubicin-loaded hydrogel for the treatment of ovarian cancer.

Liu Xia X, Zhou Wenjie W, Chen Lezong L, Wang Yue Y et al.

Ovarian cancer is one of the most prevalent malignancies of the female reproductive system and a gynecological malignancy with a high mortality rate. Alpha-mangostin is a xanthone derivative with anticancer activity that can increase the sensitivity of ovarian cancer cells to doxorubicin, and the combination of the two drugs exerts a synergistic therapeutic effect. However, the poor solubility of α-mangostin limits its application. To solve this problem, we prepared an α-mangostin nanoformulation via self-assembly using the film dispersion method. The formulation had a uniform particle size of approximately 58 nm, a stable nanostructure and good water solubility. Hydrogels, as good thermosensitive drug delivery systems, enable sustained and controlled release of drugs. Accordingly, we utilized the synergistic efficacy of the α-mangostin nanoformulation combined with doxorubicin and used a thermosensitive hydrogel carrier to jointly treat ovarian cancer. In vitro, the combined treatment achieved better effects than either drug alone in inducing ovarian cancer cell apoptosis, inhibiting ovarian cancer cell proliferation, and inducing cell cycle arrest. In vivo, this composite formulation effectively inhibited tumor growth by inducing ovarian cancer cell apoptosis, inhibiting tumor cell proliferation, and suppressing tumor angiogenesis, and effectively inhibited ascites formation, achieving a better antitumor effect than either drug alone. In summary, the composite hydrogel co-loaded with α-mangostin nanoformulation and doxorubicin represents a promising and effective strategy for the treatment of ovarian cancer.

PMID 42929270
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PubMedAutophagy2026-10-26

AKT1-phosphorylated TERT assembles a FOXO3-MYC transcriptional complex that drives ERphagy and proteostasis in post-mitotic RPE.

Babu Vishnu Suresh VS, Ghosh Sayan S, Bammidi Sridhar S, Jiwon Ryu R et al.

The retinal pigment epithelium (RPE) sustains lifelong proteostasis under chronic stress, yet how post-mitotic cells activate macroautophagy/autophagy when canonical kinase pathways suppress it remains unresolved. Here we demonstrate that AKT1 (protein kinase B alpha), drives autophagy through a non-canonical transcriptional mechanism triggered by isoform imbalance. In RPE and age-related macular degeneration (AMD) models, AKT2 (protein kinase B beta) hyperactivation destabilizes MTORC2 (mechanistic target of rapamycin complex 2) and engages RPS6KB/S6K (ribosomal protein S6 kinase beta) -mediated IRS-1 (insulin Receptor Substrate 1) inhibition, creating a feedforward autophagic arrest. Compensatory AKT1 activation via MTORC2 phosphorylates TERT (telomerase reverse transcriptase) at serine 824, driving nuclear translocation that is independent of telomere maintenance. In the nucleus, TERT assembles with FOXO3 (forkhead Box O3) and MYC (MYC proto-oncogene, bHLH transcription factor) into a tripartite transcriptional complex that occupies the EIF2AK3/PERK promoter (eukaryotic translation initiation factor 2-alpha kinase 3/ protein kinase R-like endoplasmic reticulum kinase), enabling EIF2AK3 transcriptional activation. This activity converts the unfolded protein response from pro-apoptotic to cytoprotective: EIF2AK3-ATF4 (activating transcription factor 4) signaling promotes core autophagy machinery biogenesis and selective ERphagy through the receptors TEX264 (testis expressed 264) and CCPG1(cell cycle progression 1), which prevents pathological EIF2AK3 clustering and preserves tubular ER architecture in diseased RPE. Using C. elegans phosphorylation-deficient mutants, mouse models and AMD patient iPSC-RPE, we establish that AKT1-mediated TERT phosphorylation is an evolutionarily conserved prerequisite for FOXO/DAF-16 nuclear function and lysosomal homeostasis in post-mitotic cells, offering therapeutic potential through targeted pharmacologic inhibition of AKT2.Abbreviations: ACTB: actin, beta; AKT1: AKT serine/threonine kinase 1; AKT2: AKT serine/threonine kinase 2; ALP: autophagy-lysosomal pathway; AMD: age-related macular degeneration, ATF4: activating transcription factor 4; ATG3: autophagy related 3; ATG4B: autophagy related 4B cysteine peptidase; ATG7: autophagy related 7; CCPG1: cell cycle progression 1; CFH: complement factor H; C57BL/6J: C57 black 6J; DMSO: dimethyl sulfoxide; MYC: MYC proto-oncogene, bHLH transcription factor; EIF2A/eIF2α: eukaryotic translation initiation factor 2A; EIF2AK3/PERK: eukaryotic translation initiation factor 2 alpha kinase 3; ER: endoplasmic reticulum; ERN1/IRE-1α: endoplasmic reticulum to nucleus signaling 1; ERphagy: endoplasmic reticulum-selective autophagy; FOXO1: forkhead box O1; FOXO3: forkhead box O3; iPSC-RPE: induced pluripotent stem cell-derived retinal pigment epithelium; ITGB1/integrin β1: integrin subunit beta 1; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MAPKAP1/SIN1: MAPK associated protein 1; MTOR: mechanistic target of rapamycin kinase; MTORC1: MTOR complex 1; MTORC2: MTOR complex 2; PBS: phosphate-buffered saline; PI3K: phosphoinositide 3-kinase; RICTOR: RPTOR independent companion of MTOR complex 2; RPE: retinal pigment epithelium; RPTOR: regulatory associated protein of MTOR complex 1; SQSTM1/p62: sequestosome 1; TERT: telomerase reverse transcriptase; TEX264: testis expressed 264, ER-phagy receptor; UPR: unfolded protein response; VCL: vinculin; WT: wild type.

PMID 42929416
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