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alpha-1 proteinase (Trypsone / Trypsan)

✓ Approved

Grifols, S.A. · SERPINA1

什么是 alpha-1 proteinase？

alpha-1 proteinase 是一种治疗药物，由Grifols, S.A.研发。该药已获批，用于治疗相关适应症，给药途径：Injectable (Others)、Intravenous (IV)。

药物档案

商品名Trypsone, Trypsan
公司Grifols, S.A.
分子靶点SERPINA1
给药途径Injectable (Others), Intravenous (IV)
状态Approved
来源： ClinicalTrials.gov, Grifols, S.A.

作用机制

分子靶点

alpha-1 proteinase 作用于 1 个分子靶点：

SERPINA1serpin family A member 1 (PRO2275, nNIF)
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

alpha-1 proteinase 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
Congenital, familial and genetic disordersCongenital emphysema✓ Approved

相关研究文献

PubMedTransplantation2026-10-27

Combination of Serum Leucine-rich Alpha-2-Glycoprotein 1 and Citrulline as Biomarkers of Graft Monitoring and Response to Antirejection Treatment in Intestinal Transplantation.

Matsuura Toshiharu T, Toriigahara Yukihiro Y, Maeda Shohei S, Takahashi Yoshiaki Y et al.

Intestinal transplantation (ITx) has the highest rejection rate among solid organ transplantations. Nevertheless, convenient, reliable, and noninvasive biomarkers for rejection surveillance are lacking. Leucine-rich alpha-2-glycoprotein 1 (LRG-1) has been developed as a new serum biomarker of disease activity in numerous gastrointestinal inflammatory pathologies. Therefore, this study aimed to evaluate the utility of serum LRG-1 as a biomarker for predicting post-ITx rejection, using citrulline as a known marker. Serum LRG-1 (n = 77) and citrulline (n = 64) samples were obtained from 5 post-ITx patients. We analyzed the correlation between these serum levels and the "villi appearance, erythema, capillary network, crypt widening, and heterogeneity (VENCH)" score according to the endoscopic findings of the intestinal graft evaluated on the same day as serum sample collection, as well as histopathological diagnosis. We observed a negative correlation between serum LRG-1 and citrulline levels. LRG-1 values in the VENCH score ≥4 group were significantly higher than those in the VENCH <4 group (P < 0.0001). The area under the curve of the citrulline/LRG-1 (C/L) ratio for detecting endoscopic abnormalities was 0.896 (sensitivity: 0.87; specificity: 0.89). In addition, LRG-1 values in the pathological rejection group were significantly higher than those in the nonrejection group (P < 0.0001). The area under the curve of the C/L ratio for detecting rejection was 0.992 (sensitivity: 1.0; specificity: 0.94). The present data support the hypothesis that LRG-1 is an attractive noninvasive biomarker of rejection after ITx, especially as an indicator, such as the C/L ratio. Routine serum LRG-1 monitoring may help to reduce the frequency of invasive endoscopic surveillance.

PMID 42934206
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PubMedPharmaceuticals (Basel, Switzerland)2026-10-27

Niosomal Mexiletine Attenuates Rotenone-Induced Parkinsonism via Modulation of the circDLGAP4/miR-134-5p/p-CREB Axis and Restoration of Mitochondrial-Autophagic Homeostasis.

Raafat Eman M EM, Alanazi Fares Farhan FF, Alanazi Sarah Khalifah SK, Mansour Yara E YE et al.

Background: Parkinson's disease (PD) is distinguished by progressive dopaminergic degeneration driven by the convergence of oxidative stress, neuroinflammation, mitochondrial dysfunction, and impaired autophagy. Mexiletine (Mexil), which has demonstrated antioxidant properties, has not been systematically investigated yet for its potential to mitigate mitochondrial-dysfunction-related neurodegeneration in PD. Using an integrated computational and experimental approach, we characterized, for the first time, the neuroprotective mechanisms of Mexil's action against rotenone (Rot)-induced Parkinsonism and employed niosomes as a nanocarrier platform to enhance mexil delivery and augment its neuroprotective potential in a Parkinson's disease model. Methods: Molecular docking identified candidate molecular targets underlying niosomal Mexil's neuroprotective potential. Sprague-Dawley male rats were assigned to control, Rot, and Rot plus niosomal Mexil (30 and 50 mg/kg) groups. Motor performance was evaluated, while dopaminergic degeneration, oxidative stress, neuroinflammation, mitochondrial dysfunction, and autophagy were assessed biochemically, histopathologically, and immunohistochemically. Results: Docking revealed promising interactions between Mexil and both phosphorylated cAMP response element-binding protein (p-CREB) and alpha-synuclein, with binding scores of -5.2 and -4.9 kcal/mol, respectively. Niosomal Mexil improved motor function, restored dopamine and tyrosine hydroxylase levels, and curtailed alpha-synuclein accumulation. Most notably, niosomal Mexil engaged a previously unexplored circular RNA DLGAP4/microRNA-134-5p/p-CREB axis, promoted mitochondrial biogenesis via the phosphorylated AMP-activated protein kinase (p-AMPK)/peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α)/sirtuin-1 (SIRT-1) pathway, and rebalanced mitochondrial dynamics. These changes were accompanied by restored autophagic axis and suppressed oxidative stress and inflammation. Conclusions: Niosomal Mexil confers neuroprotection against Rot-induced Parkinsonism by orchestrating oxidative, mitochondrial, autophagic, and inflammatory pathways, positioning it as a mechanistically novel disease-modifying candidate warranting further preclinical evaluation in PD.

PMID 42943351
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PubMedFood science & nutrition2026-10-27

XuanBi Mitigates Rheumatoid Arthritis via Regulation of ECM-Receptor Interactions and IL-17 Signaling: Insights From Integrated Proteomic and Pharmacological Analyses.

Zhu Hao H, Pan Zhenfeng Z, Lu Ying Y, Xia Ping P et al.

Plant-derived polyphenols possess broad anti-inflammatory activities and may benefit chronic inflammatory diseases. XuanBi is a traditional Chinese medicine formula containing orally absorbable polyphenolic constituents and is used to treat rheumatoid arthritis (RA). This study investigated its absorbable components and potential mechanisms associated with synovial inflammatory hyperplasia. XuanBi was evaluated in collagen-induced arthritis (CIA) rats and rheumatoid arthritis synovial fibroblasts (RASFs). Constituents in the decoction and rat serum were characterized by high-performance liquid chromatography coupled with quadrupole-Orbitrap mass spectrometry (HPLC-Q-Orbitrap-MS). Predicted targets were intersected with synovial differentially expressed proteins (DEPs), followed by network pharmacology, Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses, and experimental validation. Twenty-six absorbable constituents were identified, including catechin, quercetin, baicalein, and wogonin, together with 14 candidate proteins associated with RA synovial pathology. Enrichment analysis implicated extracellular matrix (ECM)-receptor interaction, focal adhesion, and interleukin-17 (IL-17) signaling. Medium- and high-dose XuanBi reduced joint swelling, synovial hyperplasia, and inflammatory infiltration in CIA rats. In RASFs, XuanBi inhibited proliferation, migration, and invasion. It also downregulated fibronectin 1 (FN1) and caveolin 1 (CAV1), reduced phosphorylation of SRC, focal adhesion kinase (FAK), and FYN, decreased integrin alpha 2b (ITGA2B)+/integrin beta 1 (ITGB1)+ cells, and reduced interleukin-1 beta (IL-1β), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), matrix metallopeptidase 3 (MMP3), and matrix metallopeptidase 9 (MMP9). Overall, XuanBi exerted anti-inflammatory and anti-synovial-hyperplasia effects in experimental RA, accompanied by changes in proteins associated with these pathways, supporting the potential involvement of these pathways and warranting further mechanistic and clinical investigation.

PMID 42936092
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PubMedMicroorganisms2026-10-27

HIV-1 Infection Alters Post-Transcriptional Processing of HTLV-1 RNA in MT-2 Cells.

Liu Haoting H, Wei Shuanglong S, Han Jingwan J, Li Hanping H et al.

Human T-lymphotropic virus type 1 (HTLV-1) gene expression is extensively regulated at the post-transcriptional level, but how human immunodeficiency virus type 1 (HIV-1) infection affects the processing of HTLV-1 RNA remains unclear. Here, we combined reverse transcription quantitative PCR (RT-qPCR) with Oxford Nanopore direct RNA sequencing (ONT DRS) to characterize HTLV-1 RNA levels, alternative splicing, poly(A)-tail length, and RNA modifications in HIV-1-infected MT-2 cells. HIV-1 infection did not significantly alter total HTLV-1 RNA levels but was associated with changes in HTLV-1 RNA processing. D1-A8 splicing became predominant, and the proportion of p21rex transcripts increased from 29.45% to 82.07% of total HTLV-1 transcripts. Poly(A)-tail changes were transcript-specific, with longer tails in env and shorter tails in p21rex, HBZ, and unannotated transcripts. HIV-1 infection also altered N6-methyladenosine (m6A), 5-methylcytidine (m5C), and pseudouridine (Ψ) modifications, with more extensive changes in m5C and Ψ than in m6A. Demethylation mediated by alpha-ketoglutarate-dependent dioxygenase AlkB homolog 5 (ALKBH5) further supported the assignment of nucleotides 7011, 7357, and 7691 as m6A modification sites. Together, these findings demonstrate that HIV-1 infection alters the post-transcriptional regulation of HTLV-1 RNA despite stable total HTLV-1 RNA levels.

PMID 42943598
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PubMedRSC advances2026-10-27

Radiopharmaceuticals and theranostics: reshaping cancer diagnosis and therapy with targeted radionuclides.

Zulfiqar Humaira H, Waqas Muhammad M, Ali Ijaz I

The theranostic paradigm, combining molecular diagnosis and targeted radionuclide therapy in a single platform, has revolutionized precision oncology. Radiopharmaceutical theranostics enables targeted visualization, characterization, and treatment of malignancies through tumor-associated molecular targets, including prostate-specific membrane antigen (PSMA), somatostatin receptors (SSTR), and fibroblast activation protein (FAP). The approvals of 177Lu-DOTATATE (Lutathera®) for GEP-NETs and 177Lu-PSMA-617 (Pluvicto®) for mCRPC are groundbreaking advances that have triggered exponential growth in the field: the VISION study showed a 38% reduction in the risk of death with 177Lu-PSMA-617, and NETTER-1 a 79% reduction in the risk of progression with 177Lu-DOTATATE in midgut NETs. Beyond beta emitters, targeted alpha therapy (TAT) with actinium-225, radium-223, and lead-212 is emerging as a powerful strategy to overcome beta-particle resistance, as the high linear energy transfer of alpha particles delivers greater cytotoxicity even in radioresistant tumors. Novel targets such as FAP, CXCR4, HER2, and gastrin-releasing peptide receptor (GRPR) are further diversifying the theranostic armamentarium across malignancies. This review synthesizes the current status of the field, spanning the radiobiology of targeted radionuclide therapy, clinical evidence from pivotal and ongoing trials, alpha-emitting radioisotopes, next-generation radioligands, the growing role of AI-enabled personalized dosimetry, and combination therapies with immunotherapy, PARP inhibitors, and androgen-receptor pathway inhibitors. We also address current challenges heterogeneous target expression, dose-limiting toxicities, radionuclide supply-chain constraints, and the regulatory framework as well as future directions poised to expand the theranostic paradigm to a broader range of cancers.

PMID 42936734
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PubMedInternational journal of molecular sciences2026-10-27

Prophylactic ALA Administration Attenuates Liver and Lung Injury in CLP-Induced Sepsis in Mice Through CSE/H2S Dependent Pathways.

Shahid Aqsa A, Scott-Thomas Amy A, Chambers Stephen S, Miller Andrew A et al.

Sepsis is a life-threatening syndrome characterized by a dysregulated host immune response to infection. Sepsis development usually results in organ dysfunction and multiple organ failure, including the liver and lungs. Alpha-lipoic acid (ALA) is a well-known anti-inflammatory agent. However, its effects on the endogenous cystathionine γ-lyase/hydrogen sulfide (CSE/H2S) pathway during cecal ligation and puncture (CLP)-induced sepsis remain unclear. In this study, the protective effects of ALA in wild-type (WT) and CSE knockout (CSE-/-) mice were investigated. Mice were randomly divided into six experimental groups, including (a) WT sham (b) CSE-/- sham (c) WT CLP (d) CSE-/- CLP (e) WT CLP + ALA.P and (f) CSE-/- CLP + ALA.P (n = 8 in each group). ALA (100 mg/kg) was administered intraperitoneally one hour before CLP surgery. Eight hours after CLP induction, mice were euthanized, and blood, liver and lung tissues were collected. Body weight changes, proinflammatory cytokine and chemokine concentrations (including tumor necrosis factor-alpha (TNF-α), monocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein-2 alpha (MIP-2α), myeloperoxidase (MPO) activity, histopathological changes, plasma H2S concentrations, and CSE expression in the liver and lung were measured. Severe liver and lung damage was characterized by markedly increased levels of MCP-1, MIP-2 α, TNF-α, and myeloperoxidase (MPO) activity, compared to WT sham control and CSE-/- groups (p < 0.0001). WT CLP-induced septic mice showed liver and lung injury as evidenced by hepatocyte swelling and ballooning degeneration with liver sinusoidal congestion, as well as pulmonary intra-alveolar and interstitial edema associated with thickening of alveolar septa and leucocyte infiltration, as compared to WT sham control and CSE-/- groups (p < 0.001). The WT-CLP group also showed a significant increase in hepatic and pulmonary expression of the H2S-producing enzyme (CSE) with elevated levels of plasma H2S concentrations, as compared to the WT sham group (p < 0.0001). Prophylactic ALA administration markedly improved these changes in the WT group. ALA also significantly decreased plasma H2S concentrations and hepatic and pulmonary CSE expression as compared to the WT CLP group (p < 0.01). However, ALA administration did not confer additional significant protective effects in CSE-/- mice, which supports the hypothesis that the effects of ALA are mediated through the modulation of the CSE/H2S pathway. In conclusion, this is the first experimental evidence showing that ALA prevents sepsis-associated organ injury at least partly by the downregulation of hepatic and pulmonary cystathionine γ-lyase expression.

PMID 42942108
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