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insulin aspart

✓ Approved

Jilin Huisheng Biopharmaceutical · INSR · 重组蛋白

什么是 insulin aspart？

insulin aspart 是一种重组蛋白，由Jilin Huisheng Biopharmaceutical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

公司Jilin Huisheng Biopharmaceutical
药物类别重组蛋白
分子靶点INSR
给药途径Injectable (Others)
状态Approved
来源： ClinicalTrials.gov, Jilin Huisheng Biopharmaceutical

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 1 diabetes mellitus✓ Approved
Metabolism and nutrition disordersType 2 diabetes mellitus✓ Approved

相关研究文献

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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PubMedPolymers2026-10-27

Solution Versus Suspension: How Does the Pharmaceutical Form of Insulin Shape the Mechanical Properties and Release Kinetics of a Carbopol® Ultrez™ 10/Sodium Alginate Hybrid Hydrogel with a Molecular-Docking Rationale for Diffusion-Controlled Delivery.

Ostróżka-Cieślik Aneta A, Ramachandran Sowmya S, Marczak Wojciech W

This study aimed to determine how insulin's pharmaceutical form governs release from a topical matrix and to provide a molecular-level rationale for the observed behavior. A hybrid hydrogel of Carbopol® Ultrez™ 10 and sodium alginate (1:2) was loaded with human insulin in two clinically distinct forms: a soluble solution (Actrapid®) and an isophane/NPH suspension (Insulatard®). Insulin release from the CU10:SA (1:2) hybrid hydrogel is continuous, without any sudden surge in release (the so-called *burst* effect), and follows diffusion according to Fick's law. The soluble formulation released more insulin than the suspension, although the two profiles were similar in shape (f1 = 13.39; f2 = 97.54). The two CU10/SA insulin hydrogels were pseudoplastic fluids with pronounced shear-stress hysteresis and did not differ in hardness, cohesiveness, adhesiveness, or elasticity. Two rheological models, including the Carreau-Yasuda (CY) model and Santesarti's shear rate-based model (SRB), described the recorded shear stress vs. shear rate curves fairly well. To explore this behavior at the molecular level, cavity-guided blind docking (CB-Dock2/AutoDock Vina) was performed on both the insulin monomer and the assembled zinc hexamer, using deprotonated oligomer models of the polymers. The alginate and Carbopol fragments converged on a single B-chain surface patch, where a carboxylate-Arg-B22 salt bridge supported by hydrogen bonding appeared to be the main anchoring motif, with weak docking scores (-4.5 to -4.9 kcal/mol on the insulin monomer) indicative of reversible physisorption rather than tight binding; the same patch was also engaged on the hexamer, which suggests that the proposed interaction motif does not depend on the insulin association state. These docking results are hypothesis-generating and complement, rather than prove, the experimental findings. The greater release of soluble insulin is attributed mainly to its pharmaceutical form, since the larger, less mobile protamine-zinc microcrystals of NPH insulin are likely to be more strongly entrapped in the matrix, rather than to differences in interaction chemistry. Together, the results link interaction chemistry, formulation state, and diffusion-controlled release.

PMID 42942577
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PubMedPreventive nutrition and food science2026-10-27

Gut Microbiota as a Mechanistic Nexus between Type 2 Diabetes and Alzheimer's Disease: Insulin Resistance, Neuroinflammation, and Functional Food Strategies.

Bae Yun-Jung YJ, Daily James W JW, Park Sunmin S

Type 2 diabetes mellitus (T2DM) and Alzheimer's disease (AD) share substantial pathological overlap, including brain-specific insulin resistance driven by impaired insulin receptor substrate-1/phosphoinositide 3-kinase/protein kinase B signaling, glycogen synthase kinase-3β dysregulation, tau hyperphosphorylation, and amyloid-β accumulation. Brain-insulin resistance is a key mechanistic link between peripheral metabolic dysfunction and neurodegeneration, although the upstream regulatory pathways remain incompletely defined. Gastrointestinal depletion of butyrate-producing microbial taxa and enrichment of pro-inflammatory genera have been independently documented in T2DM and AD. Gut microbiota dysbiosis propagates insulin resistance through at least five pathways: short-chain fatty acid depletion, lipopolysaccharide (LPS)-mediated endotoxemia, bile acid dysregulation, tryptophan-kynurenine imbalance, and vagus nerve disruption. Critically, LPS translocation and kynurenine-driven neurotoxicity propagate AD-relevant neuroinflammation independently of peripheral metabolic dysfunction, implicating a bidirectional gut-brain mechanism. These risks are amplified in Asian populations, who exhibit a lower pancreatic β-cell mass and attenuated insulin secretion that confer disproportionate vulnerability to glucotoxic cycling and its neurological complications. Such a population-specific dimension remains largely absent from reviews. Against this backdrop, traditional Asian fermented foods (chungkookjang, kimchi, and natto) and plant-derived functional ingredients (Eucommia ulmoides, gooseberry, and black garlic) have a preclinical capacity to restore microbial balance, attenuate insulin resistance, and exert neuroprotection. This review integrates these strands into a unified mechanistic and translational framework, positioning gut microbiota modulation through culturally grounded dietary strategies as a tractable approach to reducing the converging burdens of T2DM and AD in Asians.

PMID 42935632
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PubMednpj metabolic health and disease2026-10-27

Multifaceted role of genetic and epigenetic architecture of glucose homeostasis and diabetes.

Khokhar Manoj M

Glucose homeostasis depends on coordinated genetic and epigenetic regulation of pancreatic beta-cells, insulin-sensitive tissues, and neuroendocrine circuits. This review synthesises evidence from over 600 GWAS loci and the primary literature published between 2008 and 2026, and emerging single-cell functional genomics, CRISPR-based perturbation screens, deep-learning variant-effect predictors (DeepSEA, Enformer, AlphaGenome), and polygenic risk frameworks to explain insulin secretion, insulin signalling, and diabetes susceptibility, converting GWAS associations into mechanistic insight and genotype-guided precision therapies.

PMID 42934248
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