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rhIFN-alpha (ReliFeron)

✓ Approved

Reliance Life Sciences Private Limited · IFNAR2 · 重组蛋白

什么是 rhIFN-alpha?

rhIFN-alpha 是一种重组蛋白,由Reliance Life Sciences Private Limited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、Intravenous (IV)、Subcutaneous Injection。

药物档案

商品名ReliFeron
公司Reliance Life Sciences Private Limited
药物类别重组蛋白
分子靶点IFNAR2
给药途径Injectable (Others), Intramuscular (IM) Injection, Intravenous (IV), Subcutaneous Injection
状态Approved

作用机制

分子靶点

rhIFN-alpha 作用于 1 个分子靶点:

IFNAR2interferon alpha and beta receptor subunit 2 (IFNARB, IFN-alpha-REC)
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

rhIFN-alpha 针对 8 个适应症,涉及 2 个治疗领域。

治疗领域疾病/病症分期
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Hairy cell leukaemia✓ Approved
Infections and infestationsHepatitis B✓ Approved
Infections and infestationsHepatitis C✓ Approved
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Kaposi's sarcoma✓ Approved
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Non-Hodgkin's lymphoma✓ Approved

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相关研究文献

PubMedClinical case reports2026-08-05

Alpha-Mannosidosis in a 3.5-Year-Old Girl: A Case Report.

Bonilla Fornes Samuel S, Mendez Perez Maria Pilar MP, Torres Diaz Marta M, Sanchez Gutierrez Maria Eugenia ME et al.

Alpha-mannosidosis is a rare lysosomal storage disease caused by a deficiency of the enzyme alpha-mannosidase. It manifests as a continuous spectrum of signs and symptoms characterized by dysmorphic features, skeletal abnormalities, delayed psychomotor and speech development, impaired hearing, and psychiatric involvement. When suspected, alpha-mannosidosis must be confirmed by biochemical and molecular testing, namely, assessment of blood levels of alpha-mannosidase in leukocytes or fibroblasts and Sanger or next-generation sequencing of the MAN2B1 gene. The disease must be diagnosed and treatment started as quickly as possible, since the long-term prognosis for untreated patients is very poor. Enzyme replacement therapy (ERT, human recombinant alpha-mannosidase) has replaced allogeneic stem cell transplant as the mainstay of therapy, thus improving disease-related outcomes with, for example, reduced serum oligosaccharide levels, greater functional capacity, and improved quality of life, all with a good safety profile. We report the seventh case of alpha-mannosidosis in Spain. The patient was a 3.5-year-old girl assessed in the clinical genetics department for developmental delay and marked dysmorphic features (trigonocephaly, exophthalmos, hypertelorism, and a flat nasal bridge). Radiography revealed shortening and thickening of the long bones, as well as metopic and coronal synostosis. Craniosynostosis was treated with surgery. Assessment of alpha-mannosidase revealed complete absence of enzymatic activity. Genetic analysis revealed the homozygous pathogenic variant of MAN2B1, c.2248C>T, which is associated with alpha-mannosidosis. ERT is the only currently available pharmacological option for treating children with mild-to-moderate alpha-mannosidosis. Without ERT, patients' quality of life would be impaired, and their prognosis would worsen significantly.

PMID 42553539
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PubMedTherapeutic advances in rare disease2026-08-05

First bone marrow transplantation for mucopolysaccharidosis type I in Vietnam: a case report.

Nguyen-Ngoc-Quynh Le L, Can-Thi-Bich Ngoc N, Dang-Anh Duong D, Dang-Thi Ha H et al.

Mucopolysaccharidosis type I (MPS-I) is an inherited lysosomal storage disorder characterized by alpha-L-iduronidase deficiency, leading to progressive multi-organ damage and fatal complications. Early treatment is crucial to improve outcomes, particularly in patients with severe phenotypes. We present the first case of successful allogeneic bone marrow transplantation (BMT) for MPS-I in Vietnam. A 10-month-old girl experienced coarse facial features, congenital dermal melanocytosis spots, kyphoscoliosis developmental delay. Laboratory analyses revealed reduced alpha-L-iduronidase activity and elevated urinary glycosaminoglycans, genetic mutations identified two heterozygous mutations in the IDUA gene, confirmed the diagnosis of MPS-I. At 3 years old, she underwent allogeneic BMT from an HLA-matched sibling donor following conditioning regimen with busulfan, cyclophosphamide, antithymocyte globulin. Neutrophil engraftment was achieved on day +24, and platelet engrafted on day +32. The post-transplant course was complicated by respiratory deterioration requiring 5 days of mechanical ventilation, which was promptly managed and resolved. No graft-versus-host disease occurred. Post-transplant chimerism showed 95.77% donor-derived cells on day +30 and remained stable at 100% from 2 months. The patient demonstrated improvement in clinical symptoms, accompanied by alpha-L-iduronidase activity returned to normal range, urinary glycosaminoglycan levels decreased and remained stable during follow-up. At 12 months, she demonstrated complete immune reconstitution. This case suggests that allogeneic BMT may be a therapeutic approach for patients with MPS-I in resource-limited settings.

PMID 42553443
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PubMedMolecular pharmaceutics2026-08-05

Macropa-Based 225Ac-Labeled RGD Peptides for Targeted Alpha Therapy.

Echigo Hiroaki H, Munekane Masayuki M, Fuchigami Takeshi T, Mishiro Kenji K et al.

Macropa has formed more stable complexes with 225Ac, although DOTA has been extensively used as a chelator for 225Ac. This study aimed to design and synthesize two novel 225Ac-labeled RGD peptides, [225Ac]Ac-Macropa-c(RGDyK) ([225Ac]1) and [225Ac]Ac-Macropa-[c(RGDyK)]2 ([225Ac]2), and to evaluate their potential for targeted alpha therapy (TAT) of glioblastoma. Further, whether combination therapy with homoarginine (hArg), a modulator of lysosomal function, could further improve therapeutic efficacy was investigated. In Colon-26 cells, [225Ac]2 demonstrated significantly higher cellular uptake and cytotoxicity than [225Ac]1. In Colon-26 tumor-bearing mice, [225Ac]2 exhibited higher tumor accumulation and significant tumor growth inhibition. In GL261 glioblastoma cells, [225Ac]2 showed comparable cellular uptake to that in Colon-26 cells, and combination with hArg in vitro improved its cytotoxicity. However, no significant difference in therapeutic efficacy was observed between the hArg-treated and control groups in the orthotopic GL261 glioblastoma mouse model. The results of this study indicate the potential of 225Ac-labeled RGD peptides incorporating Macropa as a chelator as promising agents for TAT. However, the further optimization of combination strategies and pharmacokinetics is required.

PMID 42554513
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PubMedFrontiers in oncology2026-08-05

Impact of high-fat Western diet on chronic lymphocytic leukemia disease progression and gut microbiome profile in Eµ-TCL1 mice.

Skupa Sydney A SA, Hernandez Jordan B JB, Smith Audrey L AL, Drengler Erin M EM et al.

The composition and function of the gut microbiome have been shown to contribute to both health and disease. One of the most powerful modulators of microbial composition and function is diet. Using the Eµ-TCL1 murine model of B-cell chronic lymphocytic leukemia (CLL), we assigned male and female mice to a high-fat, high-carbohydrate Western diet (HF) or standard chow (CH) diet. Mice consuming a HF diet had significantly shorter survival than those consuming a CH diet, irrespective of sex. We also observed a significant increase in splenic involvement by CLL in the HF diet-fed mice at time of sacrifice. Mice receiving the HF diet demonstrated immediate and profound effects on the gut microbiome, marked by reduced alpha diversity and significantly different community composition as measured by beta diversity. A larger change in alpha diversity between the pre-CLL engraftment (F1) and 4-weeks post-engraftment (F3) assessment significantly correlated with higher disease burden at week 4 (p = 0.009, r = 0.406) and worse survival (p = 0.001, r = -0.492). Notably, there was a sustained increase in Akkermansia muciniphila and Bacteroidetes thetaiotaomicron in HF diet-fed mice, coupled with a corresponding increase in microbiome functional pathways related to arginine and histidine biosynthesis, chitin degradation, and nucleotide biosynthesis. Collectively our data provides evidence of the profound and sustained impact of a high-fat Western diet on the gut microbiome community and CLL pathogenesis in the Eµ-TCL1 murine model of CLL.

PMID 42553064
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PubMedFrontiers in cellular and infection microbiology2026-08-05

Systematic review of gut microbiota structural characteristics in patients with ischemic stroke.

Tang Rong R, Xu Ying Y, Zhou Yu Y, Yang Dixiao D et al.

Emerging evidence implicates the gut microbiota (GM) in the pathogenesis of ischemic stroke (IS). However, systematic evaluations synthesizing evidence on microbial shifts, functional alterations, and clinical correlations are lacking. This study aimed to comprehensively analyze GM characteristics in IS patients versus healthy controls (HC). A systematic search of PubMed, Web of Science, and Embase was conducted from inception to April 2025. Observational studies comparing GM in IS patients and HC were included. Data on alpha/beta diversity, relative microbial abundance (phylum to species), predicted functional pathways, and microbiota-clinical indicator correlations were extracted. A narrative synthesis summarized the direction and consistency of reported findings. Twenty-four studies involving 1,957 participants (1,159 IS, 798 HC) were included. The qualitative synthesis revealed no consistent differences in alpha diversity indices between IS and HC, while significant beta diversity separation was frequently reported (18/22 studies). At the phylum level, an increased relative abundance of Proteobacteria and a decreased abundance of Firmicutes were the most consistent findings in IS patients. Key genera frequently enriched in IS included Lactobacillus, Streptococcus, and Parabacteroides, while Faecalibacterium, Agathobacter, and Blautia were commonly depleted. LEfSe analysis confirmed these discriminative taxa. Predicted functional analysis suggested enrichment of pro-inflammatory pathways (e.g., lipopolysaccharide biosynthesis) and depletion of metabolic and neuroprotective pathways in IS. Clinically, Faecalibacterium abundance correlated negatively with NIHSS and mRS scores, while Lactobacillus and Streptococcus showed positive correlations with stroke severity and inflammatory markers. Ischemic stroke is associated with distinct gut microbial dysbiosis characterized by a pro-inflammatory, opportunistic pathogen-enriched, and butyrate-producer-depleted profile. These alterations correlate with disease severity and are linked to predicted disruptions in microbial metabolic functions. However, whether this dysbiosis is a cause, consequence, or exacerbating factor of IS remains to be determined. The gut microbiota may serve as a potential biomarker and therapeutic target in ischemic stroke. https://www.crd.york.ac.uk/PROSPERO/view/CRD420251117510, identifier CRD420251117510.

PMID 42553205
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PubMedCancer management and research2026-08-05

Astragalin Suppresses Colorectal Carcinogenesis by Targeting Proliferation, Oxidative Stress, and Inflammation.

Shareef Suhayla Hamad SH, Nanakaly Haween Toufiq HT, Ahmed Salam Adil SA, Gheni Noor Ali NA et al.

Colorectal cancer (CRC) is a leading cause of cancer-related death worldwide. This study evaluated astragalin's (AST) anti-proliferative and chemopreventive effects on CRC. AST's effects were assessed in vitro on Caco-2 and HT-29 cells and in vivo on azoxymethane (AOM)-induced aberrant crypt foci (ACF) in rats. Rats received AST (50 or 100 mg/kg, 60 days) or 5-fluorouracil (5-FU) (35 mg/kg, 5 days). AST inhibited Caco-2 and HT-29 cell growth (IC50: 20.15-34.50 µg/mL). In AOM-induced rats, AST reduced ACF formation, improved colon histology, downregulated β-catenin, and upregulated Bax. AST also enhanced superoxide dismutase (SOD) and catalase (CAT) activities, reduced malondialdehyde (MDA) levels, and modulated tumor necrosis factor alpha (TNF-α), interlukin-6 (IL-6), and IL-10 levels. AST demonstrated chemopreventive activity against CRC by exerting antiproliferative, antioxidant, and anti-inflammatory effects, supporting its potential as a therapeutic agent.

PMID 42553650
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