若生智能
Drug Database
IN

interferon (DS Sumiferon / Humoferon / Sumiferon)

✓ Approved

Pacific Pharmaceuticals · IFNAR2

什么是 interferon？

interferon 是一种治疗药物，由Pacific Pharmaceuticals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、Subcutaneous Injection。

药物档案

商品名DS Sumiferon, Humoferon, Sumiferon
公司Pacific Pharmaceuticals
分子靶点IFNAR2
给药途径Injectable (Others), Intramuscular (IM) Injection, Subcutaneous Injection
状态Approved
来源： ClinicalTrials.gov, Pacific Pharmaceuticals

作用机制

分子靶点

interferon 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

interferon 针对 9 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
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Respiratory papilloma✓ Approved
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Chronic myeloid leukaemia✓ Approved
Infections and infestationsHepatitis B✓ Approved
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Plasma cell myeloma✓ Approved

注册免费账户还可查看另外 4 个适应症

免费注册查看全部适应症 →

相关研究文献

PubMedMilitary medicine2026-08-06

Comparison Between Reverse Transcription Droplet Digital and Quantitative Polymerase Chain Reactions for the Determination of Viral RNA Copy Numbers in COVID-19 Patient Plasma.

Chen Hua-Wei HW, Sugiharto Victor A VA, Simons Mark P MP, Jenkins Sarah A SA

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is the causative agent of coronavirus disease 2019 (COVID-19). Studies have shown the association of viral RNAemia with the severity of COVID-19 and poor patient outcomes. Here, we compared 2 reverse transcription PCR assays: droplet digital PCR (ddPCR) and quantitative PCR (qPCR), in determining the viral RNA copy numbers in patient plasma. A total of 229 plasma samples collected on days 0, 1, 4, 7, and 28 (when available) from 33 COVID-19 ICU patients were analyzed. RNA was extracted from samples using the MagNA Pure 96 DNA and Viral NA small volume kit (Roche Diagnostic) on the MagNA Pure 96 platform with 100 mL starting and elution volumes. For ddPCR, the quantification of viral RNA copies was performed using a SARS-CoV-2 ddPCR kit (Bio-Rad Laboratories Inc.) following the manufacturer's instruction. For qPCR, the quantification of viral RNA copies was determined using the CDC 2019-Novel Coronavirus real-time RT-PCR diagnostic panel on an Applied Biosystems 7500 Fast Dx real-time PCR system with a set of known copy-positive controls as standard. Our results showed that not all patients had detectable viral RNA in their plasma samples by both methods, with only 23 (70%) and 31 (94%) patients having detectable viral RNA by ddPCR and qPCR, respectively. The qPCR detected viral RNA amplicons of both N1 and N2 targets in 87 specimens, and when these N1 and N2 copy numbers were averaged, the median was 447.7 copies/mL of plasma with a range of 56.8 to 192,495.5 copies/mL of plasma. The ddPCR detected viral RNA amplicons in 64 specimens, the median was 173.4 copies/mL of plasma with a range of 39.7-108,326.6 copies/mL of plasma when the N1 and N2 copy numbers were averaged. Both ddPCR and qPCR methods can detect viral RNA in plasma samples from severe COVID-19 patients. The qPCR was able to detect more positive specimens, suggesting higher sensitivity compared to the ddPCR method.

PMID 42560228
阅读全文 →
PubMedImmunometabolism (Cobham, Surrey)2026-08-06

Mitochondrial reactive oxygen species regulate HIF-1α stabilization and methylglyoxal accumulation in classically activated mouse macrophages.

Prantner Daniel D, Watson Mark A MA, Brand Martin D MD, Paton Jules C JC et al.

The economic and medical burden of sepsis worldwide underscores the need for novel therapeutics. Early sepsis involves dramatic metabolic changes. Classically activated macrophages, stimulated with lipopolysaccharide and interferon-γ, shift their metabolism to glycolysis. The reactive glycolytic metabolite, methylglyoxal, accumulates and has been associated with adverse outcomes in sepsis. We previously demonstrated that hypoxia-inducing factor-1α (HIF-1α) contributes to methylglyoxal accumulation. Treatment with lipopolysaccharide or interferon-γ individually stabilized HIF-1α protein; however, co-stimulation with both lipopolysaccharide and interferon-γ accelerated HIF-1α stabilization, implying a shared upstream mediator. Therefore, we sought to characterize mechanisms underlying methylglyoxal accumulation. Quantitative polymerase chain reaction and immunoblotting were used to analyze HIF-1α expression in classically activated primary mouse macrophages. Nos2 expression was induced by lipopolysaccharide or interferon-γ and markedly enhanced by combined treatment, possibly linking inducible nitric oxide synthase (iNOS) activity to HIF-1α stabilization. Inhibiting iNOS with l-NG-Nitro arginine methyl ester (l-NAME) reduced HIF-1α stabilization in a dose-dependent manner. Mitochondrial reactive oxygen species (mROS), generated following nitric oxide inhibition of cytochrome oxidase, similarly contributed to HIF-1α stabilization, as shown by the effects of suppressors of ROS production by mitochondrial complex I (S1QEL1.1) and III (S3QEL1.2) and the compartment-specific antioxidant Mito-TEMPO. Blocking mROS also decreased Il1b, Il6, and Cxcl10 expression in activated macrophages, supporting a broader impact on inflammation. Additionally, S1QEL1.1 treatment reduced accumulation of methylglyoxal. These data support a model in which nitric oxide-mediated mitochondrial dysfunction increases mROS, promoting HIF-1α stabilization and methylglyoxal accumulation, thereby shaping macrophage inflammatory responses. Thus, targeting mROS may offer a therapeutic strategy to improve sepsis outcomes.

PMID 42559272
阅读全文 →
PubMedExperimental hematology2026-08-06

cGAS-STING signaling in acute myeloid leukemia: biology, pathophysiology and therapeutic implications.

Bhowmik Satyaki S, Ghosh Subhadeep S, Sengupta Amitava A

The 'cyclic GMP-AMP synthase-Stimulator of interferon genes' (cGAS-STING) pathway is a key component of the innate immune machinery, that detects the presence of cytosolic dsDNA and initiates type I interferon-driven inflammation, resulting in downstream immune responses. In cancer, aberrant activation or suppression of this signaling pathway connects genomic instability with immune surveillance, causing context-dependent outcomes that can either augment antitumor immunity or promote tumor progression. This paradox can be exemplified using acute myeloid leukemia (AML), a genetically and clinically heterogeneous hematologic malignancy with poor long-term survival, as a model disease. Emerging evidence indicates that cGAS-STING signaling plays multifaceted roles in AML pathogenesis, influencing leukemic cell survival, stemness, inflammatory signaling, and interactions with the immune microenvironment. Genetic and epigenetic alterations common in AML engage the cGAS-STING axis to drive chronic inflammatory states, clonal expansion, and leukemic transformation, while acute or therapeutic activation of STING can improve anti-leukemic immunity. Pharmacologic STING activation promotes dendritic cell maturation, type I interferon production, and cytotoxic T cell and NK cell responses, and can synergize with hypomethylating agents, PARP inhibitors, immune checkpoint blockade, and nanoparticle-based delivery systems. This review highlights current understanding of cGAS-STING biology, its contentious roles in cancer, and its specific functions in AML, highlighting therapeutic opportunities, caveats and challenges. We discuss how the delicate balance between acute and chronic STING signaling in the setting of underlying genetic regulation and immune landscape can play critical role in determining clinical outcome, positioning cGAS-STING as a promising therapeutic target and biomarker of sterile inflammation in AML. Teaser Abstract: In this review article, we have discussed how the delicate balance between acute and chronic STING signaling in the setting of underlying genetic regulation and immune landscape can play critical role in determining clinical outcome, positioning cGAS-STING as a promising therapeutic target and biomarker of sterile inflammation in acute myeloid leukemia.

PMID 42556702
阅读全文 →
PubMedThe British journal of social psychology2026-08-06

National identity as both cure and curse: The effects of three facets of national identification on post-traumatic stress (PTS) symptoms in wartime Ukraine.

Bilewicz Michał M, Wypych Michał M, Płoszaj Adam A, Gromova Anna A et al.

The social cure hypothesis proposes that national identification can be beneficial to the well-being and mental health of ingroup members. However, research has also identified a social curse phenomenon in which identification can exacerbate distress and undermine recovery after trauma. We propose that these seemingly paradoxical phenomena arise from the effects of different dimensions of identification. To test this approach, we examined the context of the ongoing Russian invasion of Ukraine, as the actions of Russian troops, bombings, and the loss of homes and relatives are all sources of trauma for Ukrainians. Our research hypothesised that ingroup ties and ingroup affect would serve as protective factors, while identity centrality would serve as a risk factor for post-traumatic stress (PTS) symptoms. Using two studies conducted among Ukrainians living in Ukraine (N1 = 1012) and Ukrainian refugees in Poland (N2 = 381), we consistently found that identity centrality was positively associated with PTS symptoms. In addition, Study 2 provided evidence for the protective role of ingroup ties and affect. These findings clarify how specific dimensions of national identification may function as either a 'social cure' or a 'social curse' during ongoing conflict, with important implications for mental health interventions for war-affected populations.

PMID 42557849
阅读全文 →
PubMedBlood2026-08-06

Recipient Endothelial IRF1 mediates IFNγ-driven tissue tolerance in mouse models of acute Graft-versus-Host Disease.

Neidemire-Colley Lotus L, Kumar Rathan R, Garfinkle Elizabeth Ar EA, Steere Camryn C et al.

Recipient endothelial cells (ECs) actively respond to inflammation during allogeneic hematopoietic cell transplant (allo-HCT), yet mechanisms by which ECs influence acute graft-versus-host-disease (GVHD) pathology remain incompletely defined. Single cell RNA-sequencing of ECs isolated from a GVHD target organ, the liver, showed rapid, subset-specific transcriptional reprogramming after allo-HCT, with induction of canonical interferon-γ (IFNγ)-inducible genes including interferon regulatory factor 1 (IRF1), MHC II, and PD-L1 in lymphatic ECs (LECs). In allo-HCT recipients, circulating IFNγ peaked on day 4 (early), decreased but remained elevated at day 14 (late), and declined by day 21, with a concordant induction of IRF1+ LECs in the liver and GI tract. IFNγ neutralization with anti-IFNγ monoclonal antibody at either early or late time points attenuated IRF1⁺MHCII⁺PD-L1⁺ LEC activation. Notably, early donor T cell expansion was IFNγ-independent, whereas late IFNγ blockade selectively impaired donor Treg, but not Th1, expansion, leading to accelerated GVHD. Using in vitro LEC-CD4 T cell co-cultures and allo-HCT in Irf1-/- bone marrow chimera recipients, we show that recipient ECs that cannot mediate IFNγ-IRF1 signaling exhibit reduced activation and apoptosis, but also have impaired Treg expansion, increased donor Th1/Treg ratios, and worsened GVHD severity. Finally, pharmacological JAK inhibition in allo-HCT recipient mice spares IRF1+ LECs and Tregs while reducing pathogenic Th1 cells, correlating with reduced GVHD severity and improved survival. Our findings identify a role for the lymphatic endothelial IFNγ-IRF1 axis in regulating early vascular remodeling, donor T cell mediated tolerance, underscoring a potential "goldilocks" level of pathway activation required to improve post-transplant outcomes.

PMID 42550771
阅读全文 →
PubMedFrontiers in immunology2026-08-06

Targeted therapy against recurrent anti-synthetase syndrome associated interstitial lung disease after bilateral lung transplantation guided by transcriptomic analyses: a case-based study.

Wang Shiyao S, Shi Qingya Q, Xu Wenxiu W, Li Haibo H et al.

Anti-synthetase syndrome (ASS) associated interstitial lung disease (ILD) usually responds to immunosuppressive therapy, but recurrence is common. We report a 58-year-old man with ASS-ILD who developed recurrent ILD within one year after bilateral lung transplantation (LTx). Despite triple immunosuppression (glucocorticoids, tacrolimus, mycophenolate mofetil), systemic inflammation persisted. This case represents an in vivo model of ASS-ILD recurrence, warranting further investigation into underlying mechanisms and novel therapeutic strategies. Peripheral blood mononuclear cells (PBMCs) were collected at 56 and 84 weeks post-transplant for single-cell RNA sequencing (scRNA-seq), while lung tissue was analyzed via spatial transcriptomics. Control data came from five naïve ASS-ILD patients and two clinically stable connective tissue disease associated ILD (CTD-ILD) patients post-LTx. Differential gene expression and pathway enrichment analyses were performed to identify therapeutic targets. Exploratory PBMC scRNA-seq analysis suggested enrichment of interferon-, interleukin- and JAK-STAT-related signaling programs in circulating monocytes and neutrophils. Based on this immune activation profile, a multidrug treatment adjustment was implemented, including short-term glucocorticoid augmentation, replacement of mycophenolate mofetil with Janus kinase inhibitor tofacitinib, and replacement of tacrolimus with cyclosporine A. Following treatment adjustment, systemic inflammatory markers declined and interstitial lesions in both lungs were markedly alleviated on imaging. Subsequent spatial transcriptomic analysis of lung tissue revealed persistent interferon-related signaling and identified pro-fibrotic transcriptional programs in alveolar macrophages and transitional type II alveolar cells. Functional enrichment suggested a potential association between systemic inflammatory activation and localized fibrotic remodeling within the lung microenvironment. This case illustrates the potential utility of scRNA-seq and spatial transcriptomics for characterizing immune-related transcriptional programs in recurrent ASS-ILD after LTx. Transcriptomic profiling informed therapeutic decision-making in this complex clinical setting, and clinical improvement was observed following treatment adjustment. These findings generate exploratory insights into potential therapeutic targets in recurrent ASS-ILD.

PMID 42558891
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