Drug Database
IN

insulin (Monotard MC / Novolin L / Human Monotard)

✓ Approved

Novo Nordisk A/S · INSR · Recombinant Proteins

What is insulin?

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

Drug Profile

Brand NamesMonotard MC, Novolin L, Human Monotard
CompanyNovo Nordisk A/S
Drug ClassRecombinant Proteins, Polypeptide
Molecular TargetINSR
RouteInjectable (Others), Intramuscular (IM) Injection, Subcutaneous Injection
StatusApproved
Sources: ClinicalTrials.gov, Novo Nordisk A/S

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

PubMedSignal transduction and targeted therapy2026-08-25

Zinc accumulation in macrophages exacerbates metabolic dysfunction-associated steatotic liver disease progression.

Zhou Jiahui J, Wang Xinhui X, Liu Wen-Yue WY, Yu Yingying Y et al.

Metabolic dysfunction-associated steatotic liver disease (MASLD) affects over 1 billion people globally, yet the role of trace elements in its progression remains poorly defined. Here, we identify "macrophage zinc trapping" (i.e., selective zinc accumulation in hepatic macrophages despite systemic zinc depletion) as a critical driver of MASLD. In a cohort of 1069 individuals with MASLD, we found that serum zinc levels were inversely correlated with the disease severity. In a mouse model of MASLD, the hepatic macrophages are marked by zinc accumulation. Macrophage-specific depletion of the zinc exporter Slc30a1 in mice recapitulates human MASLD pathology. In macrophage-specific Slc30a1-deficient mice, trapped zinc activates the Ire1α-Xbp1s pathway, which on the one hand stimulates IL-1β secretion to alter hepatocyte lipid metabolism via IL-1β signaling, and on the other hand enhances direct lipid transfer from macrophages to hepatocytes, thereby synergistically exacerbating steatosis. Notably, treatment with Ire1α inhibitors (4μ8C and STF-083010) or IL-1β blockade (clinically approved anti-IL-1β antibodies) reverse established steatosis, inflammation, and fibrosis in preclinical mouse models. This work redefines the role of zinc in MASLD, shifting the paradigm from systemic deficiency to cell-specific sequestration. It reveals that zinc accumulation in macrophages exacerbates hepatocyte lipid accumulation through both fatty acid transflux and inflammation-driven metabolic reprogramming, uncovering novel therapeutic targets and a clinically actionable biomarker.

PMID 42637722
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PubMedNature communications2026-08-25

Electronically coupled Co single atoms with Co-Pd alloy catalyst for high-performance rechargeable hydrazine-assisted Zn-Air batteries.

Ren Lijuan L, Hu Xiuli X, Wang Shuyu S, Shi Jiaqi J et al.

Zinc-air batteries are promising devices for use in safe and cost-effective energy storage applications. However, their practical utility is hindered by sluggish oxygen evolution and oxygen reduction reactions. We show that hybridizing electronically coupled Co single atoms and a CoPd alloy within a three-dimensional macroporous N-doped carbon (CoPd/Co@3D NC) enables high-performance N2H4-assisted zinc-air batteries, where the oxygen evolution reaction is replaced with the thermodynamically more favorable hydrazine oxidation reaction. Experimental and theoretical data reveal that electronic coupling between the Co single atoms and the CoPd alloy mutually modifies their electronic structures, which, in turn, weakens oxygen adsorption on the Co single atoms and enhances N2H4 adsorption on the Pd sites. The electronic-coupling effect accelerates the rate-limiting steps of the oxygen evolution and hydrazine oxidation reactions. Consequently, N2H4-assisted zinc-air batteries employing CoPd/Co@3D NC exhibit a small charging/discharging voltage gap of 0.52 V at 100 mA cm-2, a peak specific power of 151 mW cm-2, and a specific capacity of 810 mAh g-1 at 10 mA cm-2; these values are competitive when compared to those exhibited by conventional zinc-air batteries.

PMID 42637716
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PubMedDiabetic medicine : a journal of the British Diabetic Association2026-08-25

Evaluating EndoC βH5 pseudoislets as a model for human islet transplantation.

Daniels Gatward Lydia F LF, Blackstone Whines William T WT, Hong Tzu-Wen TW, Sullivan Rosie R et al.

The EndoC βH5 cell line represents a promising human β-cell model for preclinical diabetes research. Indeed, EndoC βH5 cells aggregate into islet-like organoids, secrete insulin in a glucose-dependent manner, and express a variety of β-cell functional markers. However, EndoC βH5 cell survival and functionality in vivo have not yet been investigated. Here, we have transplanted EndoC βH5 pseudoislets under the kidney capsule in SCID mice and analysed their capacity to regulate whole body blood glucose concentrations. EndoC βH5 pseudoislets were formed in agar microwells. Oxygen consumption rate and glucose-stimulated insulin secretion were quantified in vitro. After 31 days, groups of 1000 EndoC βH5 pseudoislets were transplanted under the kidney capsule in SCID mice. To selectively ablate endogenous β-cells, streptozotocin was administered 1 month after transplantation, and EndoC βH5 graft function was analysed through quantification of blood glucose and human plasma insulin. EndoC βH5 pseudoislets exhibited glucose-induced insulin secretion at 15 days, which was maintained at 31 days of culture. Human insulin was detectable in mouse plasma at 1 week post-transplantation. Despite this, streptozotocin administration led to overt diabetes in transplant recipients. EndoC βH5 pseudoislets secrete insulin in a glucose-responsive manner in vitro, remain viable in vivo, and secrete insulin. Despite this, transplantation of 1000 pseudoislets is not sufficient to maintain glycaemia when endogenous β-cells are destroyed. Nonetheless, EndoC βH5 pseudoislets represent a useful tool for preclinical islet transplantation studies where graft control of systemic glycaemia is not a requirement.

PMID 42638372
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PubMedKansas journal of medicine2026-08-25

Elevated Circulating Fibroblast Growth Factor 21 in Lean Type 2 Diabetes: Evidence of Metabolic Dysregulation in the Absence of Adiposity.

Nafea Sarah S, Siddique Nasir N, Abdulqadir Seemal S, Noe Hsu Myat HM et al.

Lean type 2 diabetes mellitus (T2DM) is a form of diabetes that develops in persons with normal Body Mass Index (BMI) and considerable metabolic impairment. High levels of Fibroblast Growth Factor-21 (FGF21) can indicate disrupted metabolic signaling in this group. The study aimed to assess circulating FGF21 levels in lean T2DM and to examine their association with insulin resistance and hepatic steatosis, both biomarkers of metabolic dysregulation. This cross-sectional study included 425 lean adults (body mass index 18.5-22.9 kg/m2), comprising 200 lean T2DM patients and 225 non-diabetic controls. An enzyme-linked immunosorbent assay (ELISA) was used to measure serum FGF21 levels. Insulin resistance was assessed using the Homeostatic Model Assessment of Insulin Resistance (HOMA-IR), and ultrasonography was used to evaluate hepatic steatosis. Lean T2DM patients had significantly higher levels of glycated hemoglobin (HbA1c), homeostatic model assessment of insulin resistance (HOMA-IR), fasting glucose, fasting insulin, low-density lipoprotein (LDL) cholesterol, aspartate aminotransferase (AST), and total cholesterol, while high-density lipoprotein (HDL) cholesterol was lower than non-diabetic controls (all p <0.001). In multivariable analyses of the lean T2DM cohort, serum FGF21 was independently associated with HOMA-IR (β = 0.775, p <0.001) and hepatic steatosis (OR, 1.02; 95% CI, 1.01-1.03). Circulating FGF21 levels are elevated in lean T2DM and may reflect compensatory upregulation or altered FGF21 signaling rather than confirmed tissue-level resistance. FGF21 was an independent predictor of insulin resistance and hepatic steatosis, suggesting its potential as a biomarker of metabolic dysfunction in the normal-BMI group.

PMID 42639604
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PubMedmicroPublication biology2026-08-25

Gene model for the ortholog of gfzf in Drosophila cardini.

Lowry Brianna B, Chialvo Pablo P, Scott Chialvo Clare C

We developed a gene model for the GST-containing FLYWCH zinc-finger protein ortholog ( gfzf ) in the ASM1890373v1 Genome Assembly (GenBank Accession: GCA_018903735.1 ) of Drosophila cardini . This ortholog was characterized as part of a developing dataset for a comparative study of detoxification gene family evolution in the immigrans - tripunctata radiation of the genus Drosophila using an adapted Genomics Education Partnership gene annotation protocol for Course-based Undergraduate Research Experiences.

PMID 42639331
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PubMedPolish archives of internal medicine2026-08-25

Links of BMP4, BMPR1A and GREM1 expression in subcutaneous and visceral adipose tissue with metabolic syndrome and their regulation by insulin and weight loss.

Dobrzycka Marta M, Stefanowicz Magdalena M, Matulewicz Natalia N, Nikołajuk Agnieszka A et al.

PMID 42639863
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