Drug Database
IN

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

✓ Approved

Novo Nordisk A/S · INSR · Recombinant Proteins

What is insulin Aspart?

insulin Aspart is a recombinant proteins developed by Novo Nordisk A/S. It is approved for therapeutic indications via injectable (others) or subcutaneous injection.

Drug Profile

Brand NamesNovoMix 30 Penfill, NovoMix 30 FlexPen, NovoRapid 30 Mix
CompanyNovo Nordisk A/S
Drug ClassRecombinant Proteins
Molecular TargetINSR
RouteInjectable (Others), Subcutaneous Injection
StatusApproved
Sources: ClinicalTrials.gov, Novo Nordisk A/S

Mechanism of Action

Molecular Targets

insulin Aspart acts on 1 molecular target:

INSRinsulin receptor (CD220, HHF5)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

insulin Aspart is developed for 2 unique indications across 1 therapeutic area.

Therapeutic AreaConditionPhase
Metabolism and nutrition disordersType 2 diabetes mellitus✓ Approved
Metabolism and nutrition disordersType 1 diabetes mellitusPhase I

Related Research Articles

PubMedIranian journal of pharmaceutical research : IJPR2026-09-20

Lyoniresinol Improves Insulin Sensitivity and Induces White-to-Beige Adipose Tissue Conversion in Obese Rats: Associated with JNK/PI3K/mTOR Pathway Modulation.

Lei Wen W, Tripathi Alok A, Hu Shuwen S

Obesity contributes to multiple chronic diseases and remains a critical global health challenge. This study evaluated the therapeutic effects of lyoniresinol on high-fat diet-induced obesity and its underlying molecular mechanisms. Network pharmacology was used to identify potential targets of lyoniresinol in obesity treatment, followed by validation using molecular docking. High-fat diet-induced obese rats received lyoniresinol (30 mg/kg/day) for six weeks. The primary efficacy endpoints were insulin sensitivity, assessed by the oral glucose tolerance test (OGTT), insulin tolerance test (ITT), fasting glucose, and fasting insulin, and adiposity measures, including body weight and regional fat mass. The key secondary endpoint was uncoupling protein 1 (UCP1) expression in adipose tissue, evaluated by Western blotting and immunohistochemistry. Mechanistic validation comprised analysis of the phosphorylation status of c-Jun N-terminal kinase (JNK), phosphatidylinositol 3-kinase (PI3K), and mammalian target of rapamycin (mTOR) by Western blotting. Exploratory assessments included serum lipid profiles, inflammatory cytokines, oxidative stress biomarkers, and histopathological examination. Network pharmacology identified 50 shared targets between lyoniresinol and obesity. Molecular docking indicated favorable binding to JNK, PI3K, and mTOR. For the primary endpoints, lyoniresinol treatment was associated with reduced body weight gain, restored normoglycaemia, enhanced insulin sensitivity, and decreased regional adipose tissue mass. For the key secondary endpoint, UCP1 expression was upregulated, suggesting the browning of white adipose tissue. For the exploratory endpoints, lyoniresinol was associated with improved dyslipidaemia, reduced oxidative stress, suppressed pro-inflammatory cytokines and C-reactive protein (CRP), and attenuated adipocyte hypertrophy. For mechanistic validation, lyoniresinol treatment was associated with suppressed JNK phosphorylation and activation of PI3K/mTOR signaling in adipose tissue, suggesting potential involvement of the JNK/PI3K/mTOR pathway in these effects. Based on the primary efficacy endpoints, lyoniresinol was associated with improved insulin sensitivity and reduced adiposity in obese rats. The key secondary endpoint (UCP1 upregulation) and mechanistic validation (altered JNK/PI3K/mTOR phosphorylation) further support its association with the browning of white adipose tissue. These findings suggest that lyoniresinol may represent a multi-target candidate for further investigation in obesity-related metabolic disorders; however, the precise molecular mechanisms require additional validation.

PMID 42763601
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PubMedCureus2026-09-20

Edinburgh University Solution of Lime (EUSOL) Versus Platelet-Derived Growth Factor Dressing for Wound Contraction in Grade II Wagner Diabetic Foot Ulcers: A Randomized Controlled Trial.

Batool Fizza F, Munawwar Fasiha F, Shaukat Hassan H, Janjua Atif A AA et al.

Background Diabetic foot ulcers remain a leading cause of lower-limb amputation worldwide, and wound management is especially difficult in resource-limited settings where older antiseptic agents such as Edinburgh University Solution of Lime (EUSOL) are still in routine use. This trial compared EUSOL dressing with platelet-derived growth factor (PDGF) dressing for wound contraction in Grade II Wagner diabetic foot ulcers. Methodology In this randomized controlled trial, 120 patients aged 30 to 70 years with Grade II Wagner diabetic foot ulcers were assigned in a 1:1 ratio to daily EUSOL dressing or PDGF dressing applied every fourth day for four weeks after debridement and infection control. Wound healing was defined as a reduction in ulcer area of at least 50% from baseline at four weeks. A multivariate logistic regression model examined treatment group, age, sex, body mass index (BMI), diabetes duration, and antidiabetic therapy as predictors of healing. Results Patients averaged 49.8 ± 10.2 years of age and a BMI of 27.1 ± 3.45 kg/m²; 58.3% were male. Seventy-eight patients (65%) used oral hypoglycemic agents alone, while 42 (35%) required insulin. Seventy-one patients (59.2%) had diabetes for more than 10 years. Wound contraction occurred in 20 of 60 (33.3%) patients on EUSOL versus 44 of 60 (73.3%) on PDGF (P < 0.001). PDGF remained a strong independent predictor of healing on multivariate analysis (adjusted odds ratio (OR) 6.14, 95% confidence interval (CI) 2.69-14.02, P < 0.001), as did insulin therapy (adjusted OR 2.48, 95% CI 1.10-5.59, P = 0.028). Conclusions PDGF dressing produced substantially better wound contraction than EUSOL in Grade II diabetic foot ulcers, an effect that persisted after adjustment for the usual confounders. Insulin use was independently linked to better healing, pointing to glycemic management as a modifiable lever alongside dressing choice. Confirmation in multicenter trials with longer follow-up, blinded outcome assessment, and cost data would strengthen the case for wider adoption of PDGF-based dressings in similar settings.

PMID 42763719
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PubMedCommunications biology2026-09-20

Beyond ER-Golgi trafficking: unconventional protein secretion as a new design frontier for synthetic secretion switches in mammalian cells.

Shi Bingshun B, Qiu Xinyuan X, Jiang Yongheng Y, Cai Jiabo J et al.

Mammalian gene switches enable programmable cell behavior. However, current switches on transcriptional and translational layers require de novo RNA and protein synthesis, and secreted outputs must additionally undergo folding, post-translational processing, and intracellular trafficking, imposing delays that limit rapid extracellular responses. Rapid secretion-control switches instead act on pre-synthesized proteins by controlling retention, trafficking, storage, or release. Most current platforms exploit the classical endoplasmic reticulum (ER)-Golgi pathway, including engineered stimulus-secretion coupling in specialized secretory cells and ER retention, retrieval-signal cleavage, or synchronized trafficking in general mammalian hosts. Although these strategies improve response kinetics, they remain limited by ER dependence, host-cell specificity, cargo compatibility, basal leakage, and post-release transport delays. Here, we review current secretion-control architectures and highlight unconventional protein secretion as an underexplored source of design principles for positioning regulatory control closer to terminal protein export and expanding the architectures available for mammalian secretion control.

PMID 42763312
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PubMedEuropean journal of nutrition2026-09-20

Serum lipidomic profiles associated with Mediterranean diet in overweight and obese breast cancer survivors: an exploratory study.

Lee Jae Hwa JH, Park Ji Seo JS, Park Jin Ju JJ, Lee Ji-Won JW et al.

Among breast cancer (BC) survivors, overweight and obesity increase the risk of recurrence, underscoring the importance of dietary strategies for weight management. The Mediterranean diet (MD) can promote weight loss and reduce lipid levels. Analyzing alterations at the lipid species level can provide more detailed insights into the metabolic benefits associated with the MD. This study aimed to explore lipid remodeling associated with MD adherence in BC survivors through comprehensive lipidomic analysis. This exploratory ancillary study was conducted as non-randomized, non-controlled pre-post intervention analysis of serum samples collected before and after an 8-week MD intervention from 12 overweight or obese BC survivors. Fasting paired serum samples (n = 24) were used to profile lipid species using ultra-high-performance liquid chromatography-tandem mass spectrometry in both positive and negative ionization modes. Multivariate and correlation analyses were used to assess overall lipidomic alterations. Participants were further classified into maintainer or improver subgroups based on changes in their Mediterranean diet score (MDS), and subgroup-specific lipidomic responses to the MD intervention were examined. Participants showed significant reductions in body weight, waist circumference, and clinical triglyceride levels, along with increased quantitative insulin sensitivity check index and MDS following the MD intervention. Forty-three putative lipid species were identified, predominantly characterized by reductions in triacylglycerols (TGs) enriched with saturated fatty acids. TG 16:0_18:0_18:0 and TG 16:0_18:1_24:0 exhibited strong negative correlations with MDS and positive correlations with insulin resistance markers. Significant lipid remodeling was observed only in the maintainer group. In this exploratory study, adherence to an 8-week MD was associated with changes in body composition, metabolic markers, and the serum lipidomic profile in overweight and obese BC survivors. These findings provide preliminary evidence that MD adherence may be associated with lipidomic and metabolic changes in BC survivors, warranting confirmation in larger, controlled studies. http://clinicaltrials.gov , NCT03581630.

PMID 42763329
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PubMedIranian journal of pharmaceutical research : IJPR2026-09-20

ALDH1A3 Inhibition by Prosopis farcta Phytochemicals: A Computational Exploration of a Potential Antidiabetic Mechanism.

Torabi Nilufar N, Taheripak Gholamreza G, Najjar Nabaa N, Nooraniyan Esfehani Mohammad Amin MA et al.

Diabetes mellitus is a chronic condition caused by insufficient insulin secretion or impaired insulin action. Traditionally, pancreatic β-cell loss has been attributed to hyperglycemia-induced apoptosis. However, more recent evidence indicates that β-cells can also undergo dedifferentiation, a process in which they lose their specialized identity and revert to a precursor-like state. ALDH1A3 has been reported as a marker associated with dedifferentiated β-cells in diabetes, making it a potential molecular target for studies of β-cell identity and their redifferentiation. This study aimed to evaluate the potential interactions between phytochemicals in Prosopis farcta root extract and ALDH1A3 using an in silico workflow that included molecular docking, molecular dynamics simulations, and Molecular Mechanics Generalized Born Surface Area (MM-GBSA) analysis. This in silico study evaluated phytochemicals reported in the root extract of Prosopis farcta. The three-dimensional structures of the phytochemicals were downloaded from the PubChem database in SDF format. Molecular docking and molecular dynamics simulations were performed using PyRx and GROMACS, respectively. MM-GBSA analysis was performed using gmx_MMPBSA. Docking analysis suggested that several Prosopis farcta phytochemicals could interact with functionally relevant regions of ALDH1A3, including the retinal- and NAD-binding regions. Among the evaluated compounds, luteolin 7-O-glucoside and luteolin 3'-glucoside exhibited favorable docking scores and stable interaction profiles in subsequent MD and MM-GBSA analyses. These findings suggest that these compounds may form energetically favorable interactions with ALDH1A3. Among the evaluated Prosopis farcta phytochemicals, luteolin 7-O-glucoside and luteolin 3'-glucoside emerged as the most promising computational candidates for further ALDH1A3-focused studies. These findings provide an initial basis for investigating whether interaction with ALDH1A3 may represent a potential mechanism contributing to the reported antidiabetic effects of Prosopis farcta extract and its possible relevance to β-cell dysfunction in diabetes. However, experimental validation is essential to confirm ALDH1A3 inhibition, its effects on β-cell redifferentiation, and antidiabetic potential.

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PubMedClinical ophthalmology (Auckland, N.Z.)2026-09-20

Evidence-Based Clinical Practice Guideline for Diagnosis, Treatment, and Follow-Up of Keratoconus Patients.

Bustamante-Arias Andres A, Rosas-Apraez Andres A, Restrepo Carlos Alberto CA, Lizarazo Martha Isabel MI et al.

Keratoconus is a progressive corneal ectatic disorder characterized by focal stromal thinning and conical protrusion, typically involving the central or paracentral cornea. Disease progression may lead to significant visual impairment and reduced quality of life. Reported global prevalence ranges from 0.17 to 40 cases per 1000 persons, reflecting differences in diagnostic criteria, imaging technologies, and study populations. Early detection, timely intervention, and risk-based follow-up are essential to limit progression and reduce visual morbidity. A systematic literature search did not identify existing clinical practice guidelines for keratoconus diagnosis and management with sufficient methodological quality to support adoption or adaptation. Therefore, a de novo evidence-based clinical practice guideline was developed. The objective was to provide recommendations for timely diagnosis, risk stratification, interventional treatment, and follow-up of pediatric and adult patients with keratoconus, aiming to standardize clinical criteria and support decision-making among healthcare professionals. The guideline was developed through systematic evidence synthesis and the Grading of Recommendations Assessment, Development and Evaluation (GRADE) approach to assess certainty of evidence and strength of recommendations. The evidence base included systematic reviews, diagnostic accuracy studies, randomized clinical trials, and observational studies, according to each clinical question. Recommendations addressed risk factors, diagnostic and staging criteria, progression assessment, corneal cross-linking protocols, intrastromal corneal ring segments, keratoplasty techniques, and individualized follow-up. Most recommendations were conditional, reflecting low or very low certainty of evidence in several domains. This guideline provides a practical framework for standardized keratoconus care while explicitly identifying areas where evidence remains limited and further research is needed.

PMID 42763659
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