若生智能
Drug Database
MF

MF-59 (MF59)

✓ Approved

Novartis AG · 小分子 · 小分子

什么是 MF-59？

MF-59 是一种小分子，由Novartis AG研发。该药已获批，用于治疗相关适应症，给药途径：Injectable (Others)。

药物档案

商品名MF59
公司Novartis AG
药物类别小分子
给药途径Injectable (Others)
状态Approved
来源： ClinicalTrials.gov, Novartis AG

治疗适应症

MF-59 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
Surgical and medical proceduresOral appliance application✓ Approved

相关研究文献

PubMedNature neuroscience2026-08-06

Hippocampal CA3 connectomics reveals a gradient of mossy fiber inputs and selective feedforward inhibition onto pyramidal cells.

Zheng Zhihao Z, Park Changjoo C, Hammerschmith Eric W EW, Lu Ran R et al.

The mossy fiber (MF) connections to pyramidal cells in hippocampal CA3 are thought to participate in pattern separation, pattern completion and memory encoding, yet no large-scale neuronal wiring diagram exists for these connections. We assembled a 3D electron microscopy volume (~1 × 1 × 0.1 mm3) from mouse hippocampal CA3. By proofreading and automated segmentation, we reconstructed and classified all soma-containing neurons-including 1,815 pyramidal cells and 229 inhibitory cells-and over 55,000 MF axons. Pyramidal cells receive more numerous MF inputs along a proximodistal gradient. Some distal cells show surprisingly high convergence via relatively small terminals with fewer vesicles. Pyramidal cells share significantly more MF inputs than networks randomized by degree-preserving swap and are better approximated by networks randomized by proximity-preserving swap. We identify a feedforward inhibitory circuit motif from MFs via perisomatic interneurons that selectively target a pyramidal subtype. We demonstrated large-scale mapping across levels in the hippocampus-from circuits to cell types to vesicles. The dataset is shared through Pyr.ai , an online platform for hippocampal connectomics.

PMID 42557444
阅读全文 →
PubMedFrontiers in pharmacology2026-08-06

Ranitidine attenuates myocardial fibrosis by suppressing histamine/H2 receptor signaling and FAK/Src activation.

Yang Liwen L, Zhang Jiexin J, Zhao Jun J, He Meiling M et al.

Myocardial fibrosis (MF) is a pathological process often triggered by chronic inflammation and pressure overload. This study aimed to investigate the therapeutic potential of ranitidine, a histamine H2 receptor antagonist, on MF and explore its underlying mechanisms, focusing on the FAK/Src pathway and inflammatory responses. A mouse model of MF was established by transverse aortic constriction (TAC). Cardiac function was assessed by echocardiography. Histopathological changes, collagen deposition, mast cell infiltration, and the expression of histamine and its H2 receptor were examined. In vitro, NIH/3T3 fibroblasts were stimulated with TGF-β1 to induce fibrotic activation. The effects of ranitidine on collagen synthesis, the expression of fibrotic markers (α-SMA, Collagen I/III), and the phosphorylation of FAK/Src were evaluated. Ranitidine treatment significantly improved TAC-induced cardiac dysfunction and attenuated myocardial fibrosis, as evidenced by reduced collagen deposition. It also markedly decreased mast cell infiltration and the expression of histamine and H2 receptor in cardiac tissues. In TGF-β1-stimulated fibroblasts, ranitidine dose-dependently reduced collagen synthesis, downregulated α-SMA, Collagen I, and Collagen III expression, and suppressed the activation of the FAK/Src pathway. Our findings demonstrate that ranitidine ameliorates pressure overload-induced myocardial fibrosis, likely in association with attenuation of histamine/H2 receptor-related inflammatory responses and reduced FAK/Src activation. This study suggests the repurposing potential of ranitidine for treating MF.

PMID 42558308
阅读全文 →
PubMedFrontiers in immunology2026-08-06

Cellular and molecular aberrations generating new immunotherapeutic approaches in mycosis fungoides and Sézary syndrome: a comprehensive review of literature.

Flechtenmacher Anna Sophia AS, Melchers Susanne S, Nicolay Jan Peter JP

Recent advances in molecular and immunologic profiling have substantially refined the understanding of mycosis fungoides (MF) and Sézary syndrome (SS), the two most prominent subtypes of cutaneous T-cell lymphomas (CTCL). CTCL comprise a heterogeneous group of lymphoid malignancies characterized by clonal proliferation of malignant T-cell with cutaneous tropism. The pathogenesis of MF and SS appears to be driven by convergent oncogenic programs involving dysregulated JAK/STAT, NF-κB, PI3K/AKT/mTOR, and MAPK signaling, epigenetic reprogramming, apoptosis resistance, immune escape, and microenvironmental support. In parallel, altered surface phenotypes and chemokine receptor programs shape tissue tropism across skin, blood, and lymph nodes, while the tumor microenvironment promotes tumor persistence and Th2-skewed immune polarization. These insights have translated into novel targeted and immune-based therapies. This review summarizes current insights into the cell-intrinsic and microenvironmental biology of MF and SS and discusses emerging approaches aimed at achieving more durable and personalized disease control.

PMID 42558889
阅读全文 →
PubMedAllergy2026-08-06

Mycosis Fungoides-Like Atopic Dermatitis Represents a Th22-Dominant Inflammatory Endotype.

Lee Jung Ho JH, Lim Sung Ha SH, Kook Hyungdon H, Kang Seong-Jun SJ et al.

Early-stage mycosis fungoides (MF) often presents diagnostic challenges because of its clinical overlap with atopic dermatitis (AD). In clinical practice, we encountered a subset of patients with severe AD who fulfilled the MF diagnostic criteria yet remained clinically indistinguishable from AD and presented refractoriness to advanced therapies. We termed this ambiguous entity "mycosis fungoides-like AD" (mfAD) and sought to determine whether it represents malignant transformation or a distinct inflammatory endotype of AD. Skin biopsies were obtained from 7 patients with AD and 11 patients with mfAD. We performed paired single-cell RNA sequencing and single-cell T-cell receptor sequencing analyses. Publicly available MF and AD datasets were integrated for comparative analysis. Spatial transcriptomic profiling was used to contextualize single-cell findings within the tissue architecture. Comparative transcriptomic analysis revealed that T cells in mfAD were aligned with those in AD and lacked genomic instability. High-resolution profiling showed that mfAD was characterized by oligoclonal Th22 expansion rather than a single dominant malignant clone. Notably, all patients with mfAD achieved rapid clinical remission with selective JAK1 inhibition, indicating the therapeutic response characteristics of inflammatory dermatoses. Our findings demonstrate that mfAD is not a true malignancy, but rather a Th22-driven inflammatory endotype of AD. These results redefine mfAD as an inflammatory subtype within the AD spectrum, providing a mechanistic explanation for both the "pseudo-monoclonality" that leads to MF misdiagnosis and the failure of dupilumab. This study establishes a rationale for the use of JAK inhibitors in precision medicine for this patient population.

PMID 42560135
阅读全文 →
PubMedFrontiers in allergy2026-08-06

A retrospective study on the effectiveness and safety of the combination of intranasal corticosteroid and intranasal antihistamine in the management of patients with allergic rhinitis.

Monga Anil Kumar AK, Rane Tanmay T, Chinda Monika M, Bhagat Sagar S et al.

The Allergic Rhinitis and Its Impact on Asthma 2025 guideline recommends the combination of intranasal corticosteroid and intranasal antihistamine to be used as first-line treatment for moderate-to-severe allergic rhinitis because of its superior symptom control. This study was conducted to examine real-world evidence regarding the effectiveness and safety of the combination of Mometasone furoate and Azelastine (MF-Az) nasal sprays in Indian patients with allergic rhinitis. This multicentric, retrospective study was carried out across 424 ENT clinics in India. Medical records were scrutinized for information such as medical history, symptoms, clinical results, and adverse events (AEs). The mean change in total nasal symptom scores (TNSS) and total non-nasal symptom scores (TNNSS) from baseline to end of treatment was used to assess effectiveness. Independent EC approval was obtained before initiating the study. The medical records of 4,500 patients with allergic rhinitis from 424 ENT clinics across India were screened. The mean change from baseline TNSS and TNNSS at Day 7 were -1.97 (±2.58) and -1.55 (±2.63), respectively, while those at Day 14 were -3.62 (±3.99) and -2.70 (±3.84), respectively. These changes were statistically significant (p < 0.0001). There was no hospitalization, serious AEs, or treatment discontinuation due to AEs among patients. The study concluded that intranasal MF-Az spray significantly alleviated nasal and non-nasal symptoms and was well tolerated.

PMID 42558569
阅读全文 →
PubMedDiabetes research and clinical practice2026-08-06

Heterogeneous impact of incident type 2 diabetes on six age-related diseases: A 27-Country European Cohort study.

Wu Xiao X, Sha Jiangming J, Zhang Tian T, Gu Yihang Y et al.

Whether type 2 diabetes (T2DM) accelerates age-related disease uniformly across organ systems or selectively in specific domains remains unresolved, as prior evidence comes largely from single-outcome studies. Using SHARE (27 European countries, 2004-2020), we matched incident T2DM cases 1:1 to diabetes-free controls on age, sex, and survey wave, yielding six outcome-specific cohorts (n = 1,589-5,781). We fitted Cox proportional-hazards and Fine-Gray competing-risk models with pre-specified subgroup analyses by age at diagnosis (50-59, 60-69, ≥70 years). Fully adjusted hazard ratios ranged from 1.41 (95% CI 1.23-1.62) for arthritis to 2.34 (1.84-2.97) for stroke. Age at diagnosis modified the associations for heart disease, stroke, cataract, and cancer (P-interaction < 0.05) but not for hypertension (P = 0.071) or arthritis (P = 0.154). The age gradient was steepest for cataract (HR 4.66 at age 50-59 vs. 1.39 at ≥ 70); the diabetes-cancer association disappeared after age 70 (HR 1.01, 95% CI 0.69-1.49). T2DM accelerates age-related disease selectively; excess risk magnitude and its dependence on age at diagnosis differ substantially by outcome. These findings support risk stratification by organ system and diagnosis age rather than uniform comorbidity prevention strategies.

PMID 42556577
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MF-59