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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

PubMedChildren (Basel, Switzerland)2026-10-27

Pediatric Anaphylaxis in a Tertiary Pediatric Emergency Department: Observation Duration and Biphasic Reactions.

Ayar Murat M, Demir Şule Ş, Şahin Cihangir C, Çağlar Aykut A

Background/Objectives: Biphasic reactions are an important consideration during post-treatment observation of children with anaphylaxis; however, real-world pediatric data on observation practices and the timing of these reactions remain limited. This study aimed to describe the clinical characteristics, management practices, observation duration, and occurrence of biphasic reactions among children presenting with anaphylaxis to a tertiary pediatric emergency department (PED). Methods: This single-center retrospective observational study included children aged 0-18 years who presented with anaphylaxis to a tertiary PED between January 2014 and December 2024. Potential cases identified through ICD-10 codes and PED intramuscular adrenaline administration records were reviewed to confirm the diagnosis according to established criteria. Demographic and clinical characteristics, suspected triggers, treatments, observation duration, and biphasic reactions were evaluated. Results: Seventy anaphylaxis episodes in 68 patients were analyzed. The median age was 93.5 months (IQR, 50-156). Food (32.9%) and insect stings (28.6%) were the most common suspected triggers, followed by drug/vaccine-related triggers (18.6%) and allergen immunotherapy (11.4%). Adrenaline was administered in 94.3% of episodes, and intravenous fluid therapy in 50.0%. Central nervous system involvement and age-adjusted hypotension were more frequent among episodes receiving intravenous fluid therapy (p = 0.004 and p < 0.001, respectively). The median PED observation duration was 5.5 h (IQR, 2-8). Biphasic reactions occurred in three episodes (4.3%), all within three hours after initial symptom resolution. Conclusions: In this tertiary PED cohort, adrenaline administration was frequent, and biphasic reactions were uncommon and occurred during the early observation period. Given the small number of biphasic reactions, these findings should be interpreted as descriptive and are insufficient to determine the optimal observation duration.

PMID 42940653
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PubMedLife (Basel, Switzerland)2026-10-27

Metabolic Dysfunction-Associated Steatotic Liver Disease and Steatohepatitis (MASLD/MASH) and Cardiovascular Risk: Emerging Therapeutic Strategies at the Interface of Liver and Cardiometabolic Disease.

Boutari Chrysoula C, Charalampidis Konstantinos K, Sideras Lazaros L, Sinakos Emmanouil E et al.

Metabolic dysfunction-associated steatotic liver disease (MASLD) and its progressive form, metabolic dysfunction-associated steatohepatitis (MASH), are increasingly recognized as systemic cardiometabolic disorders rather than isolated liver diseases. Cardiovascular disease (CVD) represents the leading cause of mortality in patients with MASLD/MASH, highlighting the need for therapeutic strategies that address both hepatic and cardiovascular risk. MASLD/MASH and CVD are connected through a network of interdependent mechanisms, including adipose tissue dysfunction, insulin resistance, altered insulin-glucagon signaling, atherogenic dyslipidemia, lipotoxicity, mitochondrial and endoplasmic reticulum stress, innate immune activation, chronic inflammation, endothelial dysfunction, thrombogenic signaling, and dysregulated hepatokine and adipokine pathways. These mechanisms provide potential therapeutic entry points across the liver-adipose tissue-vascular axis. Lifestyle modification and conventional cardiometabolic therapies remain foundational, while several pharmacological agents increasingly target specific components of this network. We summarize the mechanistic rationale and clinical evidence for emerging therapies, including glucagon-like peptide-1 receptor agonists, dual incretin agonists, fibroblast growth factor 21 analogs, thyroid hormone receptor-β agonists, peroxisome proliferator-activated receptor agonists, and agents targeting de novo lipogenesis. We further discuss why residual metabolic, inflammatory, and fibrogenic activity may limit monotherapy and how mechanism-based combination therapy could improve efficacy while mitigating treatment-related metabolic liabilities. Finally, we outline future priorities, including biomarker-guided patient selection, longitudinal noninvasive monitoring, integrated hepatic-cardiovascular trial endpoints, adaptive combination strategies, and development of therapies targeting immune, fibrogenic, and inter-organ signaling pathways.

PMID 42942242
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PubMedMetabolites2026-10-27

Lactate-Driven Biphasic Reprogramming of Macrophage Immune Responses.

Guo Qingshuang Q, Ren Pan P, He Lanqi L, Gao Jiaying J et al.

Lactate is a metabolic substrate, an extracellular signaling molecule, and a precursor for protein lactylation, with diverse effects on macrophage immunity. Evidence from infection, tissue injury, efferocytosis, and cancer indicates that lactate-associated pathways can amplify inflammation, support resolution and tissue repair, or sustain immune suppression. These outcomes depend on the timing, cellular source and compartment, chemical formulation and pH, transport and receptor engagement, and the chemistry and targets of lactylation. In this narrative review, we critically synthesize the biochemical foundations of lactate metabolism and lactyl-group donation and examine the mechanisms underlying these distinct macrophage responses. We distinguish model-specific biphasic responses from a universal sequence of early inflammation followed by resolution, and separate reparative programs from impaired antimicrobial or antitumor immunity. We also evaluate evidence for histone and non-histone lactylation, emphasizing the limits of metabolic perturbations and chromatin associations for establishing site-specific causality. This framework identifies experimental variables that should be controlled and supports context-selective investigation of lactate-related therapeutic targets in inflammatory diseases and cancer.

PMID 42941263
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PubMedInternational journal of molecular sciences2026-10-27

Insulin Intensification and Simplification Strategies in Patients with Type 2 Diabetes and Overweight or Obesity: A Scoping Review.

Chua Chew Huey CH, Chong Wei Lim WL, Zaman Huri Hasniza H

Overweight and obesity complicate insulin treatment in adults with type 2 diabetes mellitus (T2DM), requiring consideration of glycaemic control, insulin requirements, body weight, and treatment burden. This scoping review mapped insulin treatment modification (ITM) strategies, synthesised their reported outcomes, and identified evidence gaps among insulin-treated adults with T2DM and overweight or obesity. Five electronic databases were searched following Preferred Reporting Items for Systematic Reviews and Meta-Analyses extension for Scoping Reviews (PRISMA-ScR) and updated Joanna Briggs Institute methodological guidance. Thirty-three studies were classified into four ITM domains: add-on therapy to insulin, switching to advanced insulin formulations, simplifying complex insulin regimens with adjunctive therapy, and switching to fixed-ratio combinations. Intensification was generally studied in patients with higher baseline glycated haemoglobin or insulin requirements, whereas simplification was more often evaluated in those receiving complex insulin regimens. Insulin-dominant intensification generally increased total daily insulin dose, while intensification incorporating Glucagon-Like Peptide-1 Receptor Agonists (GLP-1RAs) or Sodium-Glucose Cotransporter-2 Inhibitors (SGLT2i) commonly reduced insulin requirements and body weight. Simplification generally reduced insulin requirements and/or injection burden while maintaining or improving glycaemic control, with weight reduction frequently reported. Direct comparisons and obesity-specific subgroup analyses were limited. Intensification and simplification should therefore be considered complementary rather than opposing approaches, with outcomes influenced by therapeutic components and patient characteristics.

PMID 42941823
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PubMedDiabetes/metabolism research and reviews2026-10-27

A Novel Paradigm for Adult-Onset Type 1 Diabetes: Once-Weekly Basal Insulin and SGLT-2 Inhibition to Harness Residual β-Cell Function.

Pozzilli Paolo P, Leslie Richard David RD

Type 1 diabetes (T1D) in adults is characterised by a less aggressive disease course than in children. Most patients retain preserved C-peptide (> 0 . 2 nmol/L) and some of them benefit from a protracted phase without the need for insulin. Here, we propose a hypothesis-generating therapeutic paradigm with once-weekly basal insulin combined with an SGLT2 inhibitor (SGLT2is) as initial therapy in T1D patients with preserved C-peptide. Once-weekly basal insulin, approved in Europe and now also in the US, confirm comparable HbA1c reductions to insulin degludec or glargine, albeit always alongside prandial insulin. SGLT2is, approved as adjuncts in T1D in select regions, can control prandial peaks without boluses. No trials have tested the combination of weekly insulin with SGLT2is in adult T1D patients. Nonetheless, the rationale is robust especially in adults with C-peptide > 0·2 nmol/L. In this respect, we urge proof-of-concept trials of 12-months randomised studies in adults ≥ 18 years, to evaluate this combination.

PMID 42937021
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PubMedJournal of hypertension2026-10-27

Insulin resistance in the adipose tissue is associated with cardiac mortality: the Hiroshima study on glucose metabolism and cardiovascular diseases.

Sasaki Nobuo N, Ueno Yoshitaka Y, Ozono Ryoji R, Nakano Yukiko Y et al.

Insulin resistance is a fundamental pathophysiology of cardiovascular disease. This study aimed to investigate the association of adipose tissue insulin resistance with cardiac and cerebrovascular mortality in comparison with hepatic and skeletal muscle insulin resistance. This retrospective cohort study enrolled 12 306 participants (mean age, 64.5 years; female, 49.9%) who underwent a general health checkup in Hiroshima City between January 1982 and March 2003. Based on the median values of adipose insulin resistance index (Adipo-IR), homeostasis model assessment of insulin resistance (HOMA-IR), and Matsuda index, participants were divided into high and low insulin resistance groups in adipose tissue, liver, and skeletal muscle, respectively. Over a median 15.6-year follow-up period, 1001 cardiac and 629 cerebrovascular deaths occurred. Multivariate Cox proportional hazards regression analysis revealed that the hazard ratio (HR) for cardiac mortality was higher in the high Adipo-IR group than in the low Adipo-IR group (1.20 [95% confidence interval, 1.05-1.38]), whereas the HR for cerebrovascular mortality did not differ. In the stratified analyses, a significantly increased HR for cardiac mortality was observed in participants without antihypertensive or antihyperlipidemic medications in the high Adipo-IR group. HOMA-IR and the Matsuda index were also associated with cardiac mortality; however, these associations were not significant after adjusting for glycemic status. The association between insulin resistance in various tissues and cardiac mortality has been clarified. An increased risk of cardiac mortality was associated with insulin resistance in adipose tissue, independent of glycemic status.

PMID 42937097
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