Drug Database
IN

insulin (Univia / rh Insulin / Insulin R)

✓ Approved

Bayer AG · INSR · Recombinant Proteins

What is insulin?

insulin is a recombinant proteins developed by Bayer AG. It is approved for therapeutic indications via injectable (others) or intravenous (iv) or subcutaneous injection.

Drug Profile

Brand NamesUnivia, rh Insulin, Insulin R
CompanyBayer AG
Drug ClassRecombinant Proteins, Polypeptide
Molecular TargetINSR
RouteInjectable (Others), Intravenous (IV), Subcutaneous Injection
StatusApproved
Sources: ClinicalTrials.gov, Bayer AG

Mechanism of Action

Molecular Targets

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

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

Related Research Articles

PubMedFrontiers in cell and developmental biology2026-07-25

Gut microbiota-derived metabolites and EVs-mediated signaling in type 2 diabetes mellitus.

Chen Xi-Peng XP, Xu Jia-Qi JQ, Zhang Nan-Nan NN, Huang Qiang Q et al.

Type 2 diabetes mellitus is characterized by systemic insulin resistance, chronic low-grade inflammation, and progressive metabolic dysfunction. Increasing evidence identifies the gut microbiota as a central regulator of host immunometabolism through a diet-microbiota-host axis. Gut microbiota-derived metabolites, including short-chain fatty acids, bile acids, branched-chain amino acids, and trimethylamine N-oxide, integrate endocrine signaling, intracellular metabolic pathways, and inflammatory responses across intestinal and systemic compartments, thereby shaping glucose homeostasis and metabolic balance. Diet acts as an upstream determinant by modulating microbial composition and metabolic activity. Beyond soluble metabolites, extracellular vesicles have emerged as an additional mode of intercellular communication. Vesicles derived from diet or microbiota carry bioactive cargos such as proteins, lipids, and small RNAs, enabling the transfer of functional signals that may influence both microbial ecology and host immunometabolic processes. This review summarizes metabolite-dependent and vesicle-mediated signaling pathways and highlights how these interconnected mechanisms position the gut microbiota as a signaling hub linking dietary inputs to host cellular regulation. This framework provides a conceptual basis for microbiota-targeted strategies in the prevention and treatment of type 2 diabetes.

PMID 42499706
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PubMedJournal of environmental sciences (China)2026-07-25

Role of macrophage NLRP3 inflammasome activation in real-ambient particulate matter-induced abnormal hepatic glucose metabolism.

Wu Dong D, Zhang Zhen Z, Chen Sixin S, Chen Haoran H et al.

Evidence regarding the effects of particulate matter (PM) exposure on hepatic glucose metabolism and insulin resistance is limited, and its mechanisms remain unclear. Macrophages, as key regulators of the liver microenvironment, may mediate PM-induced metabolic processes. This study used an individually ventilated cage (IVC)-based real-ambient PM exposure system mouse model, co-cultured macrophages and hepatocytes, and NOD-like receptor protein 3 (Nlrp3)-knockdown model to investigate the impact of macrophages on hepatic insulin resistance (IR) and glucose metabolism under PM exposure. Our findings revealed that glycogen storage was impaired, insulin signaling was suppressed, the mRNA expression of glucose metabolism-related genes was altered, and the number of macrophages increased in the mouse liver after 15 weeks of PM exposure. Additionally, PM exposed mice exhibited reduced glucose tolerance and insulin sensitivity. In the transwell co-culture model, macrophages exposed to PM for 72 h exhibited NLRP3 inflammasome activation and IL-1β release, which were associated with lysosomal damage and cathepsin B release, accompanied by inhibition of insulin signaling and abnormal expression of glucose metabolism-related genes in hepatocytes. In vitro inhibition of NLRP3 and in vivo knockdown of Nlrp3 significantly attenuated these effects of PM exposure. Additionally, IL-1β inhibition improved glucose metabolism abnormalities. These findings reflect specific effects on insulin signaling and glucose metabolism mediated by the NLRP3 inflammasome or IL-1β. These results suggest that PM exposure leading to macrophage NLRP3 inflammasome activation and IL-1β release is an important cause of abnormal hepatic glucose metabolism, providing new insights into the underlying mechanisms of PM-related hepatic glucose metabolism and IR.

PMID 42498412
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PubMedRevista brasileira de ginecologia e obstetricia : revista da Federacao Brasileira das Sociedades de Ginecologia e Obstetricia2026-07-25

Metformin + Insulin vs. Insulin for GDM and T2DM during pregnancy: systematic review and meta-analysis.

Hallack Christiano C, Nogueira Bernardo Vieira BV, Bomfim Maressa M, Meireles Nathália N et al.

Evaluate the effectiveness and safety of adding metformin to insulin (M+I) versus insulin alone for pregnant women with type 2 diabetes mellitus (T2DM) or gestational diabetes mellitus (GDM), focusing on stillbirth as the primary outcome. PubMed, Embase, and Cochrane Central were searched. No date limits. Last search: January 2025. Randomized clinical trials including women with T2DM or GDM were eligible. Trials restricted to type 1 diabetes were excluded. Two reviewers extracted maternal and neonatal outcomes and assessed risk of bias with the Cochrane RoB 2 tool. Evidence certainty was graded using GRADE. Data were pooled with random-effects models and reported as risk ratios (RRs) or mean differences (MDs) with 95% confidence intervals. Nine RCTs (2,420 women) were included, most with GDM and some with T2DM. Moderate-quality evidence indicated reduced stillbirth risk with M+I (6 RCTs, 2,196 participants; RR 0.36, 95% CI 0.14-0.90; NNT 111). Low-quality evidence suggested lower risks of gestational hypertension (4 RCTs; RR 0.68, 95% CI 0.48-0.97) and neonatal hypoglycemia (7 RCTs; RR 0.49, 95% CI 0.30-0.80). No significant differences were found for cesarean section, preterm delivery, or other neonatal outcomes. Heterogeneity, baseline imbalances, and small samples limited certainty. M+I may reduce stillbirth and some adverse outcomes compared with insulin alone, but most evidence remains low certainty. Further high-quality RCTs are needed.Registered in PROSPERO: CRD42024617330.

PMID 42500179
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PubMedMetabolism: clinical and experimental2026-07-25

Differential mirroring between in vivo insulin secretion and ex vivo islet function in individuals with and without diabetes.

Di Giuseppe Gianfranco G, Gliozzo Giulia G, Carciero Lorenzo L, Puzzangara Maria Carmen MC et al.

Insulin secretion measured in vivo reflects the integrated output of pancreatic islets within a multi-organ regulatory network, whereas ex vivo stimulation of isolated human islets captures intrinsic, islet-autonomous secretory competence. Whether these two levels of β cell function mirror each other in humans remains unclear. We studied 63 individuals undergoing partial pancreatectomy who underwent preoperative OGTT with model-based assessment of β cell function and provided pancreatic tissue for ex vivo islet isolation and glucose stimulation. Ex vivo function was quantified as the stimulation index at 16.7 mmol/L glucose (SI16.7) and related to in vivo indices of insulin secretion. SI16.7 was reduced in islet from people with T2D but showed marked inter-individual variability with overlapping distributions between individuals with and without T2D. In non-diabetic individuals, no significant associations were detected between SI16.7 and OGTT-derived indices. In contrast, in people with T2D, SI16.7 was positively associated with multiple measures of glucose-driven insulin secretion and inversely with potentiation. In multivariable analysis, a composite index of intrinsic glucose-dependent β cell competence remained independently related to SI16.7. These findings indicate that a direct correspondence between systemic β cell function and intrinsic islet secretory capacity emerges only in T2D. This state-dependent alignment suggests that loss of network-mediated regulation may unmasks islet-intrinsic defects, allowing ex vivo islet performance to better reflect in vivo insulin secretion and supporting integrated in vivo-ex vivo phenotyping as a tool for functional stratification of T2D.

PMID 42498076
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PubMedMedicine2026-07-25

Perioperative nursing care for a patient undergoing image-guided planned autologous islet transplantation after total pancreatectomy: A case report.

Yang Jianwen J, Qi Xuefeng X, Xu Qin Q, Qian Weiming W

Total pancreatectomy (TP) often leads to insulin-deficient diabetes, including unstable "brittle diabetes." Autologous islet transplantation during or after TP can prevent or treat diabetes by reinfusing functional islets into the portal vein. This case report details the perioperative nursing strategies for a patient undergoing image-guided planned autologous islet transplantation following TP. A 64-year-old male with pancreatic cancer, type 2 diabetes, and hypertension underwent TP and initial autologous islet transplantation but required a second transplantation due to poor graft function. Preoperatively, he exhibited fluctuating blood glucose (8.9-14.5 mmol/L) and anxiety about surgical outcomes. The patient was diagnosed with recurrent pancreatic cancer post-TP and chemotherapy, compounded by insulin-dependent diabetes and suboptimal islet function necessitating secondary transplantation. A multidisciplinary approach included meticulous preoperative islet quality control, intraoperative portal vein catheterization under ultrasound guidance, and dynamic monitoring of portal pressure. Postoperative care featured anticoagulation (heparin/low-molecular-weight heparin), glycemic management via insulin micropump, and thromboprophylaxis using intermittent pneumatic compression. Psychological support and preoperative education alleviated patient anxiety. Posttransplantation, blood glucose stabilized (3.9-7.7 mmol/L), enabling discontinuation of exogenous insulin. The patient was discharged on day 18 without complications such as thrombosis or hemorrhage. Multidisciplinary collaboration, tailored nursing interventions, and rigorous complication prevention ensured successful outcomes. This case highlights the critical role of structured perioperative care in achieving insulin independence after complex islet transplantation.

PMID 42499104
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PubMedMolecular and cellular endocrinology2026-07-25

Gut Microbiota Contributes to Protection Against High-Fat Diet- Induced Insulin Resistance in iNOS Knockout Mice.

Zanotto Tamires M TM, Santos Andrey A, Vecina Juliana F JF, Quaresma Paula G F PGF et al.

Inducible nitric oxide synthase (iNOS) is activated in obesity and is involved in the regulation of cellular pathways, including the unfolded protein response and insulin signaling. We previously showed that iNOS deficiency is associated with reduced obesity-induced insulin resistance (IR), particularly in skeletal muscle, in iNOS knockout (iNOS KO) mice fed a high-fat diet (HFD). However, the mechanisms underlying protection against HFD-induced IR in iNOS KO mice remain incompletely understood. Several studies have reported associations between gut microbiota composition and metabolic outcomes, including body weight regulation and insulin resistance, with differences observed between lean and obese subjects. However, the potential contribution of the gut microbiota to the metabolic phenotype observed in iNOS KO mice has not been fully investigated. To address this question, we assessed glucose homeostasis, adipose tissue inflammation, gut microbiota composition, and intestinal barrier integrity. Fecal microbiota transfer (FMT) experiments were also performed between HFD-fed iNOS KO and C57BL/6J mice in both directions. HFD-fed iNOS KO mice exhibited reduced adipose tissue inflammation, characterized by decreased numbers of mast cells and pro-inflammatory M1 macrophages, together with increased numbers of anti-inflammatory M2 macrophages, compared with HFD-fed C57BL/6J mice. The gut microbiota profile of HFD-fed iNOS KO mice was associated with increased expression of genes related to intestinal tight junction integrity. Fecal microbiota transfer from HFD-fed iNOS KO mice was associated with improved glucose tolerance, enhanced insulin sensitivity, and increased expression of genes related to intestinal tight junction integrity in recipient mice. These findings suggest that gut microbiota contributes, at least in part, to the protection against HFD-induced IR in iNOS KO mice and support the potential of targeting gut microbiota as a therapeutic strategy to improve metabolic disturbances.

PMID 42498211
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