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

PubMedThe Journal of pharmacy technology : jPT : official publication of the Association of Pharmacy Technicians2026-10-15

Evaluation of Chromium Picolinate Supplementation and Insulin Requirements in Critically Ill Adults With Type 2 Diabetes Mellitus.

Tomika Alvin A, Finnell Corey C, Yann Reesie R, Bui Phuoc Tyler PT

Chromium picolinate has been studied as an adjunct to improve glycemic indices in ambulatory type 2 diabetes mellitus, but its role in critically ill patients is unknown. To evaluate whether chromium picolinate supplementation was associated with reduced insulin requirements without worsening glycemic control in critically ill adults with type 2 diabetes mellitus. We conducted a single-center retrospective pre-post cohort study of adult intensive care unit patients with type 2 diabetes mellitus or hemoglobin A1c ≥6.5% who received insulin and at least 4 consecutive chromium picolinate doses between July 2022 and January 2023. Patients served as their own controls during 24-hour pre- and post-chromium periods. The primary outcome was change in total daily insulin dose. Secondary outcomes included proportion of measured glucose values within 140 to 180 mg/dL, acute kidney injury, hypoglycemia, and exploratory Sequential Organ Failure Assessment-2 change. Among 91 screened patients, 45 met the inclusion criteria. Median total daily insulin dose decreased from 76.3 U/d (interquartile range [IQR], 40.1-96.9) before chromium to 40.0 U/d (IQR, 20.5-65.6) after chromium; the Hodges-Lehmann paired difference was -23.0 U/d (95% CI, -33.25 to -14.25; P < .0001). Proportion of measured glucose values within target did not differ significantly. No post-intervention hypoglycemia was observed, and 2 patients met the study-defined acute kidney injury criterion. Interpretation is limited by the retrospective design and absence of a concurrent control group. Chromium picolinate supplementation was associated with lower insulin requirements without worsening glycemic control. These hypothesis-generating findings require confirmation in prospective controlled studies.

PMID 42876873
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PubMedFrontiers in endocrinology2026-10-15

Diabetes in Cushing's disease: age, hypercortisolism, central adiposity, and β-cell stress as determinants of glycaemia.

Witek Przemysław P, Kwiatkowski Jakub J, Witek Joanna J, Szamotulska Katarzyna K et al.

Diabetes is a frequent complication of Cushing's disease, but metabolic differences between normal glucose tolerance, prediabetes, and diabetes remain incompletely characterised. We aimed to characterise glucose metabolism across these groups, assess abnormalities in patients with normal glucose tolerance, and identify clinical, hormonal, and body-composition factors associated with glycaemia. Cross-sectional analysis of a prospective cohort with matched healthy controls. The study included 50 patients with Cushing's disease and 52 age- and sex-matched healthy controls who underwent detailed metabolic phenotyping, including multi-timepoint oral glucose tolerance testing with assessment of insulin sensitivity and β-cell compensatory function, and body composition analysis by dual-energy X-ray absorptiometry. Forward stepwise linear regression was performed separately in each group to identify variables independently associated with HbA1c. Glucose metabolism disturbances affected 68% of patients with Cushing's disease, including prediabetes in 42% and diabetes in 26%, with most diabetes cases previously undiagnosed. Even patients with normal glucose tolerance showed lower insulin sensitivity and enhanced β-cell secretory activity compared with healthy controls. Prediabetes was characterised mainly by lower insulin sensitivity with preserved β-cell compensation, whereas diabetes was associated with a reduced insulin-to-glucose AUC ratio without significantly lower insulin sensitivity than in prediabetes. In Cushing's disease, age, morning cortisol, waist-to-hip ratio, and proinsulin were independently associated with HbA1c, explaining 59.5% of its variance; in controls, only age and BMI were associated with HbA1c. BMI was not significantly correlated with HbA1c in Cushing's disease, whereas trunk fat percentage was positively associated with HbA1c. In Cushing's disease, reduced insulin sensitivity with preserved β-cell compensation is detectable even in patients with normal glucose tolerance, whereas overt diabetes is characterised by impaired β-cell compensation without significantly lower insulin sensitivity than in prediabetes. Age, morning cortisol, waist-to-hip ratio, and proinsulin are independently associated with HbA1c. Central fat distribution may be more closely related to glycaemia than BMI.

PMID 42876832
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PubMedImmunological reviews2026-10-15

Oxidative Stress, Post-Translational Modifications, and Type 1 Diabetes Pathogenesis.

Winstead Colleen J CJ, Hodel Miki M, Tse Hubert M HM

Type 1 diabetes (T1D) is an organ-specific autoimmune disease that destroys insulin-producing beta-cells. Insulin is a vital hormone for regulating glycemia that often undergoes post-translational modifications during processing from pre-proinsulin to biologically active insulin. While necessary for proper glucose homeostasis, insulin is also an autoantigen recognized by autoreactive T cells in T1D. Cellular stress pathways including endoplasmic reticulum stress and oxidative stress mediated by an increase in reactive oxygen species (ROS) synthesis and/or a concomitant decrease in antioxidant function can further drive post-translational modifications of various autoantigens in T1D including insulin. Innate immune-derived ROS generation is an essential frontline defense against microbial infections, but ROS can also function as signaling intermediates to properly stimulate T cell responses. Oxidative stress-induced post-translational modifications are thought to trigger autoreactive T cells in T1D by generating novel neoepitopes, eliciting epitope spreading, or enhancing autoantigen interactions with antigen-presenting cells. With the current technology, detecting post-translationally modified proteins is challenging. In this review, we will explore the role of ROS and other post-translational modifications involved in T1D. We will also discuss islet transplantation strategies being used for patients with T1D including novel cell sources for beta-cell replacement and management of oxidative stress after transplantation.

PMID 42876362
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PubMedPhysiologia plantarum2026-10-15

Sodium Hydrosulfide Delays Postharvest Softening of Sand Pear Fruit in Association With Altered Ethylene Production and Cell Wall Metabolism.

Gao Jie J, Ren Hai-Ying HY, Wang Peng-Yuan PY, Wang Chun-Lei CL et al.

Sodium hydrosulfide (NaHS), a hydrogen sulfide donor, has been reported to regulate postharvest senescence and quality maintenance in horticultural crops. However, its role in sand pear softening and the underlying physiological basis remain unclear. Mature fruits of the climacteric sand pear cultivar "Sucui No. 1" were treated with NaHS and stored at 20°C to evaluate its effects on postharvest quality, ethylene production, cell wall metabolism, and softening-related gene expression. Treatment with 1 mmol L-1 NaHS delayed firmness loss and reduced ethylene production, with limited effects on fruit color, weight loss, and total soluble solids during storage. NaHS-treated fruit retained significantly higher firmness than control fruit from Day 15 onward, with the largest difference between treatments being 3.25 N on Day 15. NaHS-treated fruit retained higher levels of cellulose, hemicellulose, covalently soluble pectin, and ionically soluble pectin, and accumulated less water-soluble pectin, indicating delayed cell wall polysaccharide disassembly. Consistently, NaHS suppressed the activities of several cell wall-modifying enzymes, including cellulase, β-glucosidase, xyloglucan endotransglucosylase/hydrolase, polygalacturonase, and pectin methylesterase. RNA sequencing and qRT-PCR analyzes showed that NaHS modulated the expression of genes associated with cell wall remodeling, ethylene biosynthesis, sulfur-related metabolism, and transcriptional regulation, particularly during the early-to-middle storage stage. Transient silencing assays further indicated that the XTH gene (gene11051) was associated with cellulose-hemicellulose remodeling, whereas the two PME genes (gene26382 and gene8920) were associated with pectin solubilization. These results suggest that the delay in postharvest softening following NaHS treatment was associated with coordinated changes in ethylene production and cell wall disassembly.

PMID 42875954
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PubMedCell death & disease2026-10-15

Mesenchymal stromal cells immunosuppress osteoarthritis synovial fluid modulated monocytes via IL-6 and CCL2.

Rasti Mozhgan M, Barazandeh Aida Feiz AF, Nouri Shahrzad S, Robb Kevin P KP et al.

Mesenchymal stromal cell (MSC) interactions with monocytes/macrophages are central to their therapeutic effects in knee osteoarthritis (KOA); however, mechanisms of these interactions are not fully understood. We hypothesize that MSC soluble factors, particularly interleukin-6 (IL-6) and C-C motif chemokine ligand (CCL2) modulate monocytes in KOA environment. Using healthy donor CD14+ monocytes exposed to KOA synovial fluid (SF) in the presence or absence of marrow-derived MSC(M) directly or conditioned medium (CM), we evaluated cell surface markers and signaling via signal transducer and activator of transcription (STAT3), nuclear factor kappa-light-chain-enhancer of activated B (NF-κB) and c-Jun Terminal Kinase (JNK); functional responses were measured by secretion of tumor necrosis factor (TNF) and IL-1, and by phagocytosis of pHrodo Red E-coli. CD14+ monocytes demonstrated a mixed phenotype in KOA SF with increased CD163, CD206, and unchanged HLA-DR, CD86 marker expression. This was accompanied by activated STAT3, JNK, and NF-κB signaling. TNF and IL-1 secreted levels were unchanged, but phagocytosis was impaired, indicative of a net dysfunctional repair phenotype and functionality. CD14+ monocytes in KOA SF were hyporesponsive to additional lipopolysaccharide re-challenge, based on TNF and IL-1 secretion. Addition of MSC(M) to KOA SF programmed CD14+ monocytes resolved the dysfunctional phenotype and functionality, with significant increases in CD163, CD206; significant reductions in HLA-DR and CD86 expression; this was accompanied by significantly increased activated STAT3 and decreased activated JNK and NF-κB. TNF and IL-1 secretion were also significantly reduced, and phagocytic capacity restored. Blocking IL-6, or to a lesser extent, CCL2, partially abrogated MSC(M) soluble factor effects. MSC(M) experienced apoptosis in KOA SF; however, apoptotic bodies did not fully recapitulate MSC(M) soluble factor effects. IL-6, CCL2, other soluble factors and apoptotic bodies from MSC(M) secretome mitigate the dysfunctional effects of KOA SF on CD14+ monocytes resulting in immunosuppressed phenotype and functionality.

PMID 42875435
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PubMedProtein science : a publication of the Protein Society2026-10-15

A generalizable method for the purification and biophysical characterization of bacterial membrane receptors.

Bosetto Federico F, Zacharopoulou Maria M, Bycroft Mark M, Kish Monika M et al.

Membrane-embedded bacterial receptors are challenging to express and purify in soluble form, yet their isolated domains are essential tools for structural and ligand-discovery studies. Pseudomonas aeruginosa relies on the TonB-dependent heme receptor HasR for iron acquisition, a process central to its pathogenicity. Here, we report a robust strategy for the recombinant expression, purification, and biophysical characterization of the two soluble HasR domains directly involved in heme uptake: the N-terminal plug and the Secretin/TonB short N-terminal domain. Each domain was expressed individually in Escherichia coli and purified to homogeneity, adopting well-folded conformations as confirmed by circular dichroism, NMR spectroscopy, and mass spectrometry. We then engineered a fusion construct containing both domains and systematically evaluated multiple solubilization tags. A GST-His dual-affinity strategy enabled efficient purification of the construct, whereas His6-tag alone resulted in insoluble protein and HLT-tag fusions suffered from non-specific proteolysis. Biophysical analyses revealed that the Secretin/TonB short N-terminal domain remains stably folded within the fusion construct, while the N-terminal plug domain becomes partially disordered, a finding further supported by hydrogen/deuterium exchange mass spectrometry. Together, these results establish a generalizable workflow for producing soluble receptor domains from membrane proteins and provide validated HasR constructs suitable for downstream ligand-screening applications, including aptamer and nanobody discovery.

PMID 42876396
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