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

PubMedComprehensive Physiology2026-05-30

Photobiomodulation Alleviates Insulin Resistance Induced by Intermittent Hypoxia, Through Preservation of Adipose Tissue Insulin Signaling and Reduction of Hepatic Oxidative Stress in Mice.

Paradis Stéphanie S, Blachot-Minassian Britanny B, Bouyon Sophie S, Boutin Antoine A et al.

Chronic intermittent hypoxia (IH), a hallmark of obstructive sleep apnea (OSA), contributes to metabolic diseases and enhances associated cardiovascular (CV) complications through oxidative stress and metabolic alterations. We hypothesize that photobiomodulation (PBM), a non-invasive low-level laser therapy, prevents IH-induced insulin resistance (IR), by preserving insulin signalization and reducing oxidative stress in insulin-sensitive organs. Male C57BL/6J mice were randomized in 4 groups, submitted to either 2-weeks IH (21%-5% FiO2, 60 s cycle, 8 h/day) or normoxia (N), with or without PBM (630 nm, 5 J/cm2, 32 mW, 120 s, 5 days/week). At day 11, insulin sensitivity was assessed by insulin tolerance test. Then, canonical insulin signaling pathway was explored by western-blot, and oxidative stress was assessed by measurement of enzymatic activity, O2·- content, and lipid and protein oxidation in liver, gastrocnemius (GC) muscle, and epididymal white adipose tissue (eWAT). IH induces systemic IR, impairs insulin signaling in liver and eWAT, and increases hepatic O2·- content, while pro/anti-oxidant enzyme activities were unchanged. Interestingly, in IH group only, PBM significantly improves systemic insulin sensitivity, prevents eWAT insulin signaling alteration and decreases hepatic O2·- content. PBM alleviates systemic insulin resistance, restores eWAT insulin signaling, and limits hepatic oxidative stress induced by IH. By enhancing insulin sensitivity, PBM could be proposed as a new therapeutic strategy against OSA-associated metabolic comorbidities.

PMID 42216497
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PubMedMetabolism: clinical and experimental2026-05-30

Hepatic TGFβ1 signaling impairs insulin sensitivity via inducing insulin receptor substrate 1 degradation.

Ai Weiqi W, Pan Quan Q, Shen Zheng Z, Yang Wanbao W et al.

Obesity is associated with insulin resistance, a major risk factor for type 2 diabetes (T2D), yet the underlying mechanisms remain incompletely defined. We hypothesized that elevated transforming growth factor beta 1 (TGFβ1) level is associated with impaired insulin sensitivity. Using primary hepatocytes, and mouse models with hepatic TGFβ1 overexpression or hepatic TGFβ1 signaling disruption, we examined the impact of TGFβ1 signaling on hepatic insulin signaling and glucose metabolism. We performed bulk RNA sequencing of liver samples identify potential mediator of obesity-induced insulin resistance. Immunoprecipitation, in vitro kinase assay, and mass-spec assay were used to explore the mechanisms underlying TGFβ1-induced insulin receptor substrate (IRS1) degradation. We further evaluated the therapeutic potential of targeting TGFβ1 signaling to improve glycemic control using the TGFβ1 signaling inhibitor LY2157299. Prolonged TGFβ1 exposure markedly reduced IRS1 protein abundance and impaired insulin-stimulated Akt activation in hepatocytes. Hepatic TGFβ1 overexpression exacerbated insulin resistance, whereas hepatic TGFβ1 signaling disruption improved insulin sensitivity by increasing IRS1 protein abundance. Mechanistically, TGFβ1 signaling increased Cullin 7 (CUL7) expression and promoted IRS1 phosphorylation at serine 685, leading to ubiquitin-dependent IRS1 degradation. Pharmacological inhibition of TGFβ1 signaling by LY2157299 improved insulin sensitivity in both lean and diabetic db/db mice. These findings identify TGFβ1 as a key driver of hepatic insulin resistance by promoting CUL7-dependent IRS1 degradation, establishing a mechanistic link between obesity-associated cytokine signaling and impaired insulin action and highlighting the TGFβ1-CUL7-IRS1 axis as a potential therapeutic target for T2D.

PMID 42214482
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PubMedResearch in veterinary science2026-05-30

Assessment of insulin sensitivity and blood pepsinogen values in dairy herds with high risk for displaced abomasum.

Hirakawa-Ueno Kie K, Makino Kotaro K, Fukumori Rika R, Tharwat Mohamed M et al.

This study evaluated insulin sensitivity and serum pepsinogen in dairy cows from herds with high and low risk for displaced abomasum (DA) across different lactation stages. Blood samples and body condition scores (BCS) were collected from 235 clinically healthy cows on five farms in Hokkaido, Japan, including two high-DA farms (≥4%) and three DA-free farms. Cows from high-DA farms consistently exhibited lower values of the revised quantitative insulin sensitivity check index and quantitative insulin sensitivity check index, along with higher values of homeostatic model assessment, indicating reduced insulin sensitivity. These cows also had higher BCS and elevated circulating insulin concentrations, particularly during the dry period and late lactation. In contrast, serum pepsinogen values remained within the normal range and did not differ significantly between groups, suggesting no apparent abomasal mucosal damage. These findings indicate that cows in the high-DA farms experience a prolonged negative energy balance from early lactation to mid lactation, which may contribute to persistent insulin resistance and increased susceptibility to DA. The results may highlight the importance of metabolic management, rather than abomasal pathogenesis, in preventing DA in high-risk farms.

PMID 42214273
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PubMedActa paediatrica (Oslo, Norway : 1992)2026-05-30

Pubertal Timing Associates With Cardiometabolic Markers During Puberty and in Young Adulthood.

Nummela Saga S, Pahkala Katja K, Karppinen Sinikka S, Toppari Jorma J et al.

To study how pubertal timing associates with cardiometabolic measures in puberty and young adulthood. Cardiovascular risk factors, anthropometry and pubertal development were regularly studied in STRIP study subjects until age 26 years. The study participants were divided into tertiles (early, average, and late) according to the age at the beginning of breast/testicular growth, menarche in females, and end of testicular growth in males. Differences in cardiometabolic variables between tertiles were analysed using one-way ANOVA. Earlier breast development was associated with higher body mass index (BMI), waist circumference (WC), and blood pressure (BP) in adulthood compared to the late group. Earlier age at menarche was associated with higher BMI and WC in adulthood. Earlier beginning of testicular enlargement was associated with higher insulin and insulin resistance at 26 years when compared to the late group. Earlier end of testicular growth tended to have higher insulin values and insulin resistance at 26 years than the average group. Early pubertal development in females is associated with higher BMI and WC. In males, early pubertal development is associated with increased insulin levels and insulin resistance. More research is needed to study whether these metabolic differences build up a cumulative burden.

PMID 42216495
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PubMedThe Journal of biological chemistry2026-05-30

Cell type-specific expression and subcellular localization of the human insulin upstream open reading frame (INSU) protein in pancreatic β-cells.

Liu Qing-Rong QR, Zhu Min M, Hartnell Lisa M LM, Tian Jane J et al.

INSU was evolutionarily selected in human and chimp genomes by deletion of the 16 bp in INS 5'UTR regions present in other primate species that do not contain the upstream open-reading-frame (uORF). We now aim to identify the islet cell type in which INSU is produced, its subcellular distribution, and its response to stress in human islets. To do this, we developed an INSU specific rabbit polyclonal antibody, and we employed immunohistochemistry (IHC), immunofluorescence (IF), and immuno-gold labelling with electron microscopy (EM) technologies. We used LC-MS/MS-based Selected Reaction Monitoring (SRM) proteomic assay to quantify INSU in islets, plasma and cerebral spinal fluid (CSF). Unlike mature insulin, INSU levels were unchanged in plasma and CSF two hours after continuous intravenous glucose infusion. The INSU immunohistochemistry signal partially overlapped with that of insulin and was more intensely polarized in β-cells in islets. INSU was not present in α-, δ-, ε-, or PP-cells. Dual IF and immuno-gold EM showed that INSU was present in immature insulin granules and crinosomes, but there was little to none present in mature secretory granules, implying INSU involvement in quality control of β-cells.

PMID 42214675
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PubMedAmerican journal of perinatology2026-05-30

Is fetal sex associated with maternal diabetes 10-14 years after delivery?

Field Christine C, Wu Jiqiang J, Scholtens Denise D, Lowe William W et al.

We examined the association between fetal sex and the risk of maternal prediabetes or diabetes 10-14 years after delivery. Secondarily, we assessed whether this association varied by GDM status and whether measures of maternal insulin sensitivity and resistance varied by fetal sex. This is a secondary analysis from the prospective, international Hyperglycemia and Adverse Pregnancy Outcome Follow-Up Study (HAPO FUS). The exposure was assigned fetal sex at birth (female as the reference). The primary outcome was prediabetes or diabetes assessed 10-14 years after the index pregnancy. The effect modifier was GDM per the International Association of Diabetes and Pregnancy Study Group criteria. Modified Poisson regression models were used and adjusted for baseline covariates at enrollment and time from enrollment to follow-up. We secondarily assessed whether the association between fetal sex and prediabetes or diabetes varied by GDM and whether maternal insulin sensitivity at pregnancy enrollment and insulin resistance at 10-14 year follow-up differed by fetal sex. Of 4,609 individuals in the analytic sample, 48.9% of infants were assigned female sex at birth, which was 47.1% with GDM and 49.2% without GDM (p=0.3). At a median 11.6 years after delivery, 22.4% postpartum individuals developed prediabetes and 2.9% developed diabetes. The risk of prediabetes or diabetes did not differ by fetal sex (female vs. male: 24.7 vs. 24.6%; adjusted risk ratio, aRR: 1.00, 95% CI: 0.89, 1.12). This association was similar regardless of GDM status (interaction p=0.6). There was no association between fetal sex and insulin sensitivity at enrollment or insulin resistance at follow-up. In the prospective HAPO FUS cohort, there was no association between fetal sex and the risk of maternal prediabetes or diabetes 10-14 years after delivery. Further research is needed to better understand the possible impact of fetal sex on peripartum glucose homeostasis.

PMID 42214436
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