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insulin Aspart (NovoMix 30 Penfill / NovoMix 30 FlexPen / NovoRapid 30 Mix)

✓ Approved

Novo Nordisk A/S · INSR · 重组蛋白

什么是 insulin Aspart？

insulin Aspart 是一种重组蛋白，由Novo Nordisk A/S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NovoMix 30 Penfill, NovoMix 30 FlexPen, NovoRapid 30 Mix
公司Novo Nordisk A/S
药物类别重组蛋白
分子靶点INSR
给药途径Injectable (Others), Subcutaneous Injection
状态Approved
来源： ClinicalTrials.gov, Novo Nordisk A/S

作用机制

分子靶点

insulin Aspart 作用于 1 个分子靶点：

INSRinsulin receptor (CD220, HHF5)
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

insulin Aspart 针对 2 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Metabolism and nutrition disordersType 2 diabetes mellitus✓ Approved
Metabolism and nutrition disordersType 1 diabetes mellitusPhase I

相关研究文献

PubMedFrontiers in endocrinology2026-09-11

A case report of young-onset type 2 diabetes patient with severe metabolic dysregulation carrying an LRP6 variant.

Xiang Dan D, Yuan Li L, Liao Shuaiju S, Wang Yangtian Y

The global epidemic of type 2 diabetes mellitus (T2D), along with its rising prevalence among younger populations, raises substantial public health concerns; severe hypertriglyceridemia (sHTG) is a major risk factor for acute pancreatitis. Insulin resistance in T2D often coincides with dyslipidemia, contributing to lipotoxicity, and insulin-resistant states may be linked to specific genetic variants. This report presents a 27-year-old man with poor glycemic control, recurrent dizziness, extreme hypertriglyceridemia (TG > 37.87 mmol/L), insulin resistance, pancreatic fat infiltration, and early-stage diabetic nephropathy. Despite a family history of T2D, his clinical presentation far exceeded that of typical T2D. High-throughput sequencing revealed a heterozygous LRP6 variant (c.3107A>G, p.Asn1036Ser). Multidisciplinary treatment-incorporating acute-phase plasma exchange, ω-3 fatty acid ethyl ester 90, inclisiran, subcutaneous insulin aspart pump therapy, metformin, insulin icodec, finerenone, and Huangkui capsules-led to improvements in the patient's metabolic indicators. This case report describes a patient with type 2 diabetes mellitus presenting with extreme metabolic disorders, in whom a variant in the LRP6 gene was detected. Although the variant co-occurs with the observed phenotype, its pathogenicity cannot currently be established in the absence of functional validation. This case emphasizes that genetic variant screening should be considered in patients with unexplained severe metabolic disturbances, particularly those with early-onset disease. This case also provides a foundation for future functional studies and genetic confirmation.

PMID 42723884
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PubMedPlant communications2026-09-11

De novo Genes in Plants: Origins, Mechanisms, and Functional Implications.

Zuo Zhihao Z, Chen Rujia R, Lu Yue Y, Yang Zefeng Z

De novo genes originate from previously non-coding genomic regions. They provide an important source of lineage-specific innovation. In plants, these genes may contribute to adaptation, trait diversity and crop evolution. This review summarizes recent progress in plant de novo gene research. It first discusses major routes of gene birth, including transcription-first, open reading frame (ORF)-first and concurrent models. It also examines how nascent loci acquire regulatory control and enter existing biological networks. The review then summarizes their evolutionary features, including weak early constraint, rapid molecular change, restricted expression and structural refinement. It further discusses plant de novo genes involved in stress responses, seed germination, kernel dehydration, subspecies divergence, reproductive isolation and floral scent diversification. Current methods for identifying de novo genes remain limited by rapid sequence evolution, genome annotation quality, polyploidy and transposable elements. Whole-genome synteny alignment, multi-omics evidence and machine-learning approaches can improve candidate discovery. However, each method has important limitations. Finally, this review highlights key future questions in functional validation, latent coding potential in long non-coding RNAs, epigenetic activation, regulatory-network integration and crop improvement. These perspectives clarify how de novo genes shape plant adaptation and how they may be used in precision breeding and synthetic biology.

PMID 42723285
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PubMedPhysics in medicine and biology2026-09-11

A biphasic spatiotemporal non-homologous end joining model coupled with Monte Carlo DNA damage data for chromosome aberration prediction.

Zhao Man M, Wu Jianan J, Huang Guomin G, Zheng Chunling C et al.

Objective.This study extends a DNA damage simulation package to incorporate a biphasic spatiotemporal non-homologous end joining (NHEJ) repair framework. The aim is to predict radiation induced chromosome aberrations for various beam qualities and dose rates from an independent parameter set.Approach.A biphasic NHEJ kinetic model, characterized by fast and slow components with experimentally constrained repair rate constants (λf= 2.48 h-1andλs= 0.408 h-1) and slow portion (ηDSB= 19%), was coupled to a DNA end diffusion process (D= 0.1 μm2h-1). DNA damage data from Monte Carlo-based biophysical program was used as input, while different types of chromosome aberrations were generated as output. The extended framework was benchmarked against chromosome aberration measurements in human fibroblasts under acuteγ-rays,αparticles, and chronic low dose-rateγ-ray irradiations. All parameters were obtained from independent measurements without fitting to chromosome aberration data. Model performance was evaluated using the coefficient of determination (R2).Main Results.For acuteγ-rays andαparticles, the proposed model reproduced the dose-response curves of dicentrics and interstitial deletions with reasonable accuracy, while larger deviations were observed for rings and terminal deletions. The corresponding total-aberrationR2were 0.973 and 0.947. Notably, the inclusion of spatiotemporal repair dynamics substantially improved agreement of rings and terminal deletions forα-particles compared to a pure distance-dependent model. Simulations of chronicγ-ray irradiations reproduced total aberration yields at 6.3 cGy h-1withR2= 0.968, while the 2.8 cGy h-1case exhibited notable deviation withR2= - 0.517. Sensitivity analyses suggested model stability and robustness with all sensitivity coefficients remaining below 1.3.Significance.By integrating spatial diffusion and biphasic repair kinetics, the proposed model provides a quantitative link between microdosimetric energy deposition and macroscopic chromosome aberrations. The approach offers a foundation for mechanistic modeling of relative biological effectiveness in particle therapy.

PMID 42723441
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PubMedChembiochem : a European journal of chemical biology2026-09-11

A De Novo Peptide That Induces Axonal Growth Through TrkB Activation.

Maini Rumit R, Tamada Kota K, Fukuda Kunihiro K, Takumi Toru T et al.

Brain-derived neurotrophic factor (BDNF) and its receptor, tropomyosin-related kinase B (TrkB), are key regulators of neuronal survival and synaptic plasticity. Impaired BDNF-TrkB signaling is strongly implicated in neurodegenerative and neuropsychiatric disorders, including Alzheimer's disease and major depressive disorder. However, the clinical use of BDNF is limited by poor pharmacokinetics and low tissue stability, highlighting the need for alternative TrkB agonists. Many previously reported agonists have shown inconsistent or indirect TrkB activation, raising concerns about their mechanism of action. In this study, we employed the random nonstandard peptides integrated discovery (RaPID) system to identify de novo macrocyclic peptide ligands that bind the extracellular domain of TrkB with high affinity and selectivity. One of the peptides was turned into a dimeric peptide, diTrbL3, which induced TrkB autophosphorylation and activated canonical downstream pathways, including ERK1/2 and AKT, without detectable cross-activation of other receptor tyrosine kinases. Functionally, diTrbL3 promoted axonal elongation and upregulated activity-dependent immediate early genes in primary hippocampal neurons. These findings establish diTrbL3 as a potent de novo TrkB agonist and highlight RaPID-derived macrocyclic peptides as a promising class of BDNF mimetics for targeting TrkB-dependent signaling in neurological disease.

PMID 42723246
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PubMedTranslational cancer research2026-09-11

Association between primary tumor surgery and survival in patients with de novo stage IV triple-negative breast cancer with visceral metastases: a SEER-based propensity score-matched study.

Yue Ruizhe R, Wang Zheng Z, Zhang Hao H

The role of primary tumor surgery in patients with de novo stage IV triple-negative breast cancer (TNBC) with visceral metastases remains controversial. This study investigated the association between primary tumor surgery and survival outcomes in this high-risk population. Female patients diagnosed with de novo stage IV TNBC with liver, lung, and/or brain metastases between 2010 and 2020 were identified from the Surveillance, Epidemiology, and End Results (SEER) database. Overall survival (OS) and breast cancer-specific survival (BCSS) were compared between patients who underwent primary tumor surgery and those who did not. Propensity score matching (PSM), Kaplan-Meier analysis, Cox regression, subgroup analysis, robust sensitivity analysis, and restricted mean survival time (RMST) analysis were performed. A total of 1,827 patients were included, of whom 543 underwent primary tumor surgery and 1,284 did not. After 1:1 PSM, 507 matched pairs were generated. After matching, the median OS was 15 months in the surgery group and 9 months in the non-surgery group, while the median BCSS was 15 months and 10 months, respectively. In multivariable Cox analysis, primary tumor surgery was independently associated with longer OS [hazard ratio (HR) =0.532, 95% confidence interval (CI): 0.462-0.612, P<0.001] and BCSS (HR =0.544, 95% CI: 0.470-0.629, P<0.001). These associations remained stable in robust Cox sensitivity analyses. RMST analyses at 24 and 36 months further supported the robustness of the observed survival association. Primary tumor surgery was associated with longer OS and BCSS in patients with de novo stage IV TNBC with visceral metastases. This observed association may partly reflect patient selection, underlying health status, metastatic burden, and response to systemic therapy. Therefore, these findings should be interpreted as hypothesis-generating real-world evidence rather than definitive evidence of a causal treatment benefit. Individualized surgical decision-making should be based on careful patient selection and multidisciplinary evaluation.

PMID 42724824
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PubMedF1000Research2026-09-11

Green Tea and Decaffeinated Light Roasted Green Coffee Extract Combination Improved Cardiac Insulin Resistance through Free Fatty Acids and Adiponectin/FAS Pathways Amelioration in Metabolic Syndrome Rat Model.

Lukitasari Mifetika M, Rohman Mohammad Saifur MS, Nugroho Dwi Adi DA, Nur Kholis Mukhamad M et al.

Insulin resistance has been independently associated with cardiac diseases. Free fatty acids (FFAs) are known to induce cardiac insulin resistance via low-grade inflammation. Therefore, lowering FFA levels may improve cardiac insulin resistance. This study investigated the effects of a combination of green tea and decaffeinated light-roasted green coffee extract on free fatty acid-induced cardiac insulin resistance by modulating the adiponectin/FAS pathways. This study used 25 male Sprague-Dawley rats. Metabolic syndrome (MS) was induced using a high-fat, high-sucrose (HFHS) diet and a low-dose streptozotocin (STZ) injection, while a normal chow (NC) diet served as the healthy control. The MS rats were treated for 9 weeks with green tea (300 mg/kg b.w.), decaffeinated light-roasted green coffee (200 mg/kg b.w.), or a combination of both extracts. The experimental subjects were divided into five groups: 1) MS (HFHS diet + STZ), 2) NC (normal chow), 3) GT (green tea extract), 4) GC (decaffeinated light-roasted green coffee extract), and 5) CM (combination of both extracts). Adiponectin and HOMA-IR levels were analysed using ELISA, while the gene expression of Adipo-R1, FAS, PI3K, PDK1, Akt, and GLUT4 was measured using RT-PCR. The combination of green tea and decaffeinated light-roasted green coffee demonstrated synergistic effects in reducing FFA levels. The adiponectin/FAS pathways were attenuated in the CM group. Furthermore, the combination therapy improved cardiac insulin resistance marker expressions, including IRS-1/2, PI3K, PDK1, Akt, and GLUT4. The combination of green tea and decaffeinated light-roasted green coffee extract improved cardiac insulin resistance more effectively than the administration of either extract alone, by reducing FFA levels through the modulation of the adiponectin/FAS pathways.

PMID 42723777
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