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insulin (insulin, HGT / Insuman Implantable / Insuman Comb)

✓ Approved

Sanofi S.A · INSR · 重组蛋白

什么是 insulin？

insulin 是一种重组蛋白，由Sanofi S.A研发。该药已获批，用于治疗相关适应症，给药途径：Injectable (Others)、Intramuscular (IM) Injection、Subcutaneous Injection、Surgical Implantation、Intraperitoneal Injection。

药物档案

商品名insulin, HGT, Insuman Implantable, Insuman Comb
公司Sanofi S.A
药物类别重组蛋白, 多肽类
分子靶点INSR
给药途径Injectable (Others), Intramuscular (IM) Injection, Subcutaneous Injection, Surgical Implantation, Intraperitoneal Injection
状态Approved
来源： ClinicalTrials.gov, Sanofi S.A

作用机制

分子靶点

insulin 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 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

PubMedMetabolites2026-07-27

Insulin Clearance Along the Liver-Kidney Axis: Implications for Insulin Action.

Perdomo Germán G, Cózar-Castellano Irene I, Najjar Sonia M SM

The pleiotropic actions of insulin are mediated by cascades of signaling pathways and are regulated by circulating insulin levels. Under physiologic conditions, insulin levels reflect the balance between pancreatic beta-cell secretion and insulin clearance, which occurs primarily in liver hepatocytes and, to a lesser extent, in kidney proximal tubule cells. Therefore, coordination between insulin secretion and clearance is essential for systemic insulin sensitivity. Whereas insulin secretion is widely investigated, exploring the role of insulin clearance in regulating insulin sensitivity remains limited. This review summarizes the main mechanisms underlying insulin clearance along the liver-kidney axis and discusses how they contribute to metabolic regulation in health and disease.

PMID 42506393
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PubMedBiochimica et biophysica acta. Molecular basis of disease2026-07-27

Beyond apoptosis: Annexin A5 as a multifunctional regulator in the pathophysiology of diabetes and its complications.

Farhan Zamzam Z, Saeed Rania R, Mahgoub Eglal E, Khalique Anila A et al.

Annexin A5 (ANXA5) is a Ca2+-dependent phosphatidylserine (PS)-binding protein classically employed as an apoptosis biomarker. Accumulating evidence now positions ANXA5 as a multifunctional regulator of membrane homeostasis, immunometabolism, and cellular adaptation to metabolic stress across the spectrum of diabetes mellitus (DM). This review synthesizes current mechanistic and translational insights identifying ANXA5 as a candidate molecular determinant of diabetic pathophysiology. Its conserved α-helical architecture and dual-promoter transcriptional regulation enable reversible, high-affinity PS binding and assembly of a two-dimensional (2D) crystalline lattice that underpins its diverse biological functions. In the pancreas, ANXA5 has been shown to inhibit islet amyloid polypeptide (IAPP) aggregation and shields β-cell membranes from amyloid-induced injury; it has also been proposed to modulate mitochondrial Ca2+ homeostasis via VDAC1-associated pathways. In insulin-responsive peripheral tissues, ANXA5 has been hypothesized to modulate insulin signaling fidelity and facilitate glucose uptake through putative IRS-1 interactions and lipid raft stabilization, although direct in vivo validation remains outstanding. In the diabetic endothelium, hyperglycemia-induced dysfunction of acid sphingomyelinase impairs ANXA5-mediated membrane resealing, thereby precipitating Ca2+ overload, inflammasome activation, and a prothrombotic state. Experimental studies further suggest that ANXA5 may promote M2 macrophage polarization and suppress TGF-β/Smad2/3 signaling, indicating potential roles in immunomodulation and fibrosis attenuation. Importantly, distinct disease contexts shape ANXA5 biology: in T2D, glucolipotoxic stress and IAPP aggregation drive ANXA5-dependent protective responses, whereas in T1D, circulating anti-ANXA5 autoantibodies may neutralize membrane-protective functions and amplify vascular injury risk. Emerging translational applications include recombinant ANXA5 (NEXUS) and Diannexin, although prospective clinical validation remains limited. To facilitate interpretation of the literature, we introduce an evidence-grading framework that distinguishes diabetes-validated mechanisms from biologically supported, incompletely validated, and speculative pathways.

PMID 42503360
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PubMedDiabetes research and clinical practice2026-07-27

U-500 regular insulin in automated insulin delivery systems for severe insulin resistance: A single-center retrospective cohort.

Lee David D, Pham Angela Q AQ, Abreu Marconi M

U-500 regular insulin use in automated insulin delivery systems (AIDs) is off-label and minimally studied. In this four-individual cohort, HbA1c remained stable, time below range stayed low, and no diabetic ketoacidosis or severe hypoglycemia occurred, despite lower TIR. These findings provide early clinical experience to inform cautious, individualized off-label use.

PMID 42503314
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PubMedDiabetes, obesity & metabolism2026-07-27

Efficacy and Safety of Once-Weekly Semaglutide 2.0 mg as an Add-On to Dose-Reduced Insulin Glargine versus Dose-Titrated Insulin Glargine in People With Type 2 Diabetes and Overweight (SUSTAIN OPTIMIZE).

Rodbard Helena W HW, Irace Concetta C, Lobo Jevitha J, Makrilakis Konstantinos K et al.

Type 2 diabetes (T2D) management with basal insulin can lead to hypoglycaemia and weight gain. SUSTAIN OPTIMIZE compared once-weekly semaglutide 2.0 mg as add-on to dose-reduced insulin glargine (Sema+IGlarreduced) versus dose-titrated IGlar (IGlartitrated) on glycated haemoglobin (HbA1c), body weight (BW), daily insulin dose, and participant satisfaction. SUSTAIN OPTIMIZE was a 40-week, phase 3b, open-label, randomised study. Adults with T2D, overweight (body mass index ≥ 25 kg/m2), and treatment with basal insulin ≤ 40 units/day were randomised 1:1 into Sema+IGlarreduced or IGlartitrated. The primary endpoint was change in HbA1c using a non-inferiority approach. Secondary endpoints assessed superiority of Sema+IGlarreduced versus IGlartitrated in reducing HbA1c, BW, daily insulin dose, and improving Diabetes Treatment Satisfaction Questionnaire change version (DTSQc) scores. Overall, 573 participants were randomised. Sema+IGlarreduced achieved both non-inferiority and superiority versus IGlartitrated in HbA1c reduction (estimated treatment difference [ETD]: -0.74%; 95% confidence interval [CI95]: -0.90, -0.59) and superiority in BW change (ETD: -8.5 kg; CI95: -9.5, -7.4), relative daily insulin dose change (ETD: -121.9%; CI95: -143.1, -100.6), and DTSQc scores (ETD: 2.6; CI95: 1.6, 3.5) (p < 0.0001 for all endpoints). No new safety concerns were identified. Severe hypoglycaemia was reduced (rate ratio: 0.45; CI95: 0.23, 0.87; p = 0.02), while gastrointestinal events were higher for Sema+IGlarreduced (310 vs. 32 events). Once-weekly subcutaneous semaglutide 2.0 mg as add-on to dose-reduced IGlar achieved superior reductions in HbA1c, BW, and daily insulin dose in people with T2D and overweight, while reducing their risk for severe hypoglycaemia compared to dose-titrated IGlar alone.

PMID 42504064
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PubMedVaccines2026-07-27

Recombinant EHV-1 Vector Expressing Immunodominant Hemagglutinin Protein of Equine Influenza Virus H3N8 (Sub-Lineage Florida Clade 2).

Bera Bidhan Chandra BC, Bernela Manju M, Madhwal Aashwina A, Pradhan Stephanie S SS et al.

Equine herpesvirus type 1 (EHV-1) and equine influenza virus (EIV) are major respiratory pathogens in horses, causing significant economic losses in domesticated horses. Bacterial Artificial Chromosome (BAC) technology can be used to precisely manipulate the EHV-1 genome for the development of live-attenuated vector vaccines. Earlier, our group developed a live-attenuated EHV-1 vaccine by deleting virulence-associated genes using this technology and the mutant EHV-1 has been exploited for expressing foreign gene in the current study. Specifically, in this study, a mutant EHV-1 virus expressing the hemagglutinin (HA) gene of H3N8 EIV (sub-lineage: Florida clade 2) was generated and characterized in vitro. The HA gene of EIV (Florida clade 2) was used for antigen gene cloning. The expression cassette for the HA gene was commercially synthesized and inserted into the backbone of EHV1∆IR6 BAC using an En passant mutagenesis strategy. Recombinant clones were selected using antibiotic selection, PCR, and RFLP. Further, the recombinant virus was regenerated in RK-13 cells via transfection and characterized in vitro for plaque size, growth kinetics and immunofluorescence antibody test (IFAT). PCR and RFLP confirmed the successful insertion of the HA gene into pEHV1∆IR6/gE BAC. The recombinant virus, vEHV1∆IR6/gE-HA(FC2), was successfully rescued in RK13 cells and demonstrated expression of the EIV haemagglutinin proteins by immunofluorescence assay. Although plaque size was reduced in the generated mutant virus in comparison to parental virus, the growth kinetics of the recombinant viruses were comparable to those of vEHV1∆IR6/gE. These findings demonstrate the successful expression of immunodominant hemagglutinin protein of EIV by recombinant EHV-1 and indicate the potential suitability of EHV-1 BAC as a vector platform for foreign gene expression.

PMID 42506671
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PubMedAnnals of medicine2026-07-27

Hypertonic glucose vs insulin-dextrose to prevent hypoglycaemia following treatment for hyperkalaemia (HIGH-K): protocol for a double-blind randomized controlled trial.

Ford Samuel S, La Caze Adam A, Coombes Ian I, Hills Angela A et al.

Hyperkalaemia is a life-threatening electrolyte abnormality commonly managed with intravenous insulin-dextrose therapy (IDT). Although effective, IDT frequently causes hypoglycaemia, particularly in patients without diabetes. Glucose-only therapy, which leverages endogenous insulin production, may offer comparable potassium-lowering effects with reduced hypoglycaemia risk. However, evidence remains limited. The HIGH-K Trial is a single-centre, double-blind, randomised controlled trial in adult, non-diabetic patients presenting to an Australian Emergency Department with hyperkalaemia (>5.5 mmol/L [99 mg/dL]). Ninety-five participants are randomised 1:1 to receive either glucose-only therapy (100 mL 50% dextrose bolus followed by 250 mL 10% dextrose infusion over 2 h) or standard IDT (10 units IV insulin with 25 g dextrose followed by 250 mL saline infusion). The primary safety outcome is the incidence of hypoglycaemia (<3.9 mmol/L [70 mg/dL]) within six hours. The primary non-inferiority outcome is the mean change in serum potassium from baseline to two hours, using a non-inferiority margin of -0.5 mmol/L (-9 mg/dL). Secondary outcomes include severity of hypoglycaemia, rescue insulin requirements, and serum insulin/C-peptide levels. This is the first double-blind, randomised controlled trial to directly compare the safety and biochemical non-inferiority of glucose-only therapy versus standard insulin-dextrose therapy in the emergency department. By utilising a continuous glucose infusion following a bolus, the protocol aims to sustain endogenous insulin release and optimise intracellular potassium shift while preventing hypoglycaemia. If non-inferiority is demonstrated, this approach could provide a safer alternative in high-acuity or resource-limited clinical settings. Results will be disseminated in peer-reviewed journals and at national and international conferences. Findings may inform future research and clinical practice guidelines regarding glucose-only therapy for hyperkalaemia.

PMID 42504062
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