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IN

insulin (Oralgen, Generex / insulin, RapidMist / Oralgen)

✓ Approved

Eli Lilly · INSR · Polypeptide

What is insulin?

insulin is a polypeptide developed by Eli Lilly. It is approved for therapeutic indications via oral (po) or sublingual (sl)/oral transmucosal.

Drug Profile

Brand NamesOralgen, Generex, insulin, RapidMist, Oralgen
CompanyEli Lilly
Drug ClassPolypeptide
Molecular TargetINSR
RouteOral (PO), Sublingual (SL)/Oral Transmucosal
StatusApproved
Sources: ClinicalTrials.gov, Eli Lilly

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 3 unique indications across 1 therapeutic area.

Therapeutic AreaConditionPhase
Metabolism and nutrition disordersType 1 diabetes mellitus✓ Approved
Metabolism and nutrition disordersType 2 diabetes mellitus✓ Approved
Metabolism and nutrition disordersGlucose tolerance impairedPhase II

Related Research Articles

PubMedEpilepsy & behavior : E&B2026-07-17

Caregiver preferences and training needs in the administration of rescue medication for prolonged convulsive seizures in children and adolescents with epilepsy: Results from a multinational survey.

Vigevano Federico F, Arzimanoglou Alexis A, Auvin Stéphane S, Kaindl Angela M AM et al.

This multinational survey explored caregivers' preferences and training needs regarding the administration of rescue medication for prolonged convulsive seizures in children and adolescents with epilepsy across 7 European countries. A total of 68 caregivers of children with epilepsy (aged 6 months to 18 years) who had experienced a prolonged convulsive seizure in the past 12 months completed an anonymous survey in 2024. The survey assessed caregiver preferences and satisfaction with buccal, nasal, or rectal rescue medication, quality of life (QoL), valued medication attributes, and training experience. Intranasal formulations were not consistently available across countries during the study period. Most caregivers (80.9%) preferred buccal over rectal or nasal administration, and satisfaction was higher among users of buccal midazolam compared with rectal diazepam. This preference aligned with a positive impact on patients' and caregivers' QoL. Caregivers rated ease of administration as the most important attribute of rescue medication (mean: 4.8/5), followed by effectiveness in stopping seizures (mean: 4.1/5). Despite their critical role, 44.1% had received no specific training; among those trained, 62.2% preferred face-to-face sessions. Training satisfaction was higher among caregivers who administered buccal midazolam (mean: 8.3/10; standard deviation [SD]: 2.4) compared with those using rectal diazepam (mean: 5.3/10; SD: 3.3). This survey underscores a strong caregiver preference for buccal midazolam in pediatric out-of-hospital settings. However, caregiver training remains a substantial unmet need, and standardized programs could improve preparedness for managing prolonged seizures. These findings reinforce the importance of integrating caregiver perspectives to optimize emergency pediatric epilepsy care.

PMID 42462388
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PubMedDiabetes technology & therapeutics2026-07-17

Evaluation of an Objective Measure of Mealtime Insulin Administration Frequency in Emerging Adults with Type 1 Diabetes.

Pierce Jessica S JS, Clements Mark A MA, Lockee Brent B, Patton Susana R SR

Objective measures of self-management are critical for understanding glycemic outcomes in individuals with type 1 diabetes (T1D). The mealtime insulin bolus score (BOLUS), derived from insulin pump data, is a validated indicator of mealtime insulin engagement in pediatric T1D populations, but its validity in emerging adults (EA) is unknown. We examined associations between BOLUS scores and glycemic outcomes (HbA1c and continuous glucose monitoring metrics) in 347 EA with T1D (ages 18-22). Higher BOLUS scores were associated with lower HbA1c (r = -0.24, P < 0.001), greater time in range (r = 0.23, P < 0.001), and lower time above range (r = -0.23, P < 0.001). The mean BOLUS score (1.17) was substantially lower than the previously reported mean pediatric BOLUS score. Findings support the validity of BOLUS as an objective behavioral measure in EA with T1D and highlight reduced mealtime insulin engagement during this developmental period.

PMID 42466753
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PubMedmedRxiv : the preprint server for health sciences2026-07-17

Coffee Intake is Associated with Improved Insulin Sensitivity and Lower Visceral Adiposity: Evidence from Biomarker and Genetic Analysis.

Sevilla-González Magdalena M, Wang Xingyan X, Yun Huan H, Mei Zhendong Z et al.

Higher coffee intake has been associated with lower risk of type 2 diabetes (T2D), but the underlying biological pathways remain incompletely understood. To examine associations of coffee intake with insulin sensitivity, adiposity, and T2D risk, and assess whether coffee intake modifies associations between pathway-specific genetic susceptibility and incident T2D. Cross-sectional analyses among 806 participants without T2D in the VITamin D and OmegA-3 TriaL (VITAL) clinical sub-cohort, who underwent repeated dietary assessment, clinical phenotyping, and dual-energy X-ray absorptiometry imaging at baseline and year-2. Prospective analyses among 333,053 UK Biobank participants without T2D at baseline who had dietary and genetic data and were followed for a median of 13.3 years. Coffee intake assessed by food frequency questionnaires. In UK Biobank, 12 pathway-specific polygenic scores (pPS) representing distinct T2D pathophysiological mechanisms were evaluated. The primary outcomes, in VITAL, were HbA1c, oral glucose tolerance test-derived measures of glucose response and insulin sensitivity, β-cell function, and overall, truncal, and visceral adiposity; in UK Biobank, was incident T2D. In VITAL, higher coffee intake was associated with higher insulin sensitivity (standardized β per cup/day, 0.046; P = .004) and lower visceral adipose tissue mass (β, -0.047; P = .006), after adjusting for demographic, lifestyle, and clinical factors, including body mass index. In UK Biobank, higher coffee intake was associated with lower T2D incidence (hazard ratio per cup/day, 0.96; 95% CI, 0.95-0.97), lower triglyceride-to-HDL cholesterol ratio (β,-0.01; P = 2.51 × 10^-19), and lower visceral adipose tissue mass (β, -0.01; P = 4.28 × 10^-9). Associations of 3 pPS related to insulin resistance and fat distribution with incident T2D were attenuated among participants consuming higher amount of coffee than among non-consumers (P for interaction < .0043). Higher coffee intake was associated with greater insulin sensitivity, lower visceral adiposity, and lower risk of T2D. Together with the attenuation of associations between pathway-specific genetic susceptibility and T2D risk among higher coffee consumers, these findings suggest that insulin resistance and visceral adiposity-related pathways may contribute to the association between coffee intake and T2D risk. Question: Is coffee intake associated with specific insulin sensitivity and adiposity markers, and type 2 diabetes risk, and does it modify associations between pathway-specific genetic susceptibility and type 2 diabetes?Findings: In analyses repeated dietary, clinical, and imaging phenotyping in 806 VITAL participants and prospective data from 333,053 UK Biobank participants, higher coffee intake was associated with greater insulin sensitivity, lower visceral adiposity, and lower type 2 diabetes risk. Higher coffee intake also attenuated associations of three pathway-specific polygenic scores related to insulin resistance and fat distribution with type 2 diabetes risk.Meaning: These findings suggest that pathways related to insulin sensitivity and visceral adiposity may contribute to the associations between coffee intake and lower type 2 diabetes risk.

PMID 42465876
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PubMedbioRxiv : the preprint server for biology2026-07-17

Hepatic stearoyl-CoA desaturase deficiency ameliorates hyperglycemia through bile acid signaling in an insulin-independent manner.

Kalyesubula Mugagga M, Kim Daehan D, Kim Woo Sung WS, Wicker Nicole B NB et al.

Hyperglycemia in Type 1 Diabetes (T1D) is managed almost exclusively via exogenous insulin therapy, an approach restricted by significant glycemic fluctuations, long-term side effects such as weight gain, and high economic burden. Identifying physiological pathways capable of clearing blood glucose independent of insulin is therefore of paramount clinical importance. Here, we demonstrate that liver-specific stearoyl-CoA desaturase-1 (SCD1) deficiency protects against diabetic hyperglycemia and hepatic steatosis in an insulin-independent manner. SCD1 ablation decreases cellular oleate availability, altering lipid flux and redirecting excess cholesterol into alternative biosynthetic pathways. This redirection drives a 2-fold elevation in hepatic bile acids and a striking 10-fold increase in plasma bile acids, predominantly characterized by the accumulation of taurocholic acid. This shifted bile acid pool stimulates the expression of glucose transporter 1 ( Glut1 ) in the liver via activation of the nuclear hormone receptor FXR, facilitating basal glucose clearance in the absence of insulin. Genetic deletion models show that while the hepatokine FGF21 serves as a partial mediator of this phenotype, the local bile acid-FXR axis remains a sufficient driver of systemic glucose clearance. Finally, we show that dietary oleate supplementation completely reverses this protective phenotype, turning down Glut1 expression and restoring overt diabetes. Together, our findings uncover a novel bile acid-FXR-Glut1 signaling axis triggered by SCD1 inhibition, offering a framework for insulin-independent glycemic control. Here, we demonstrate that liver-specific stearoyl-CoA desaturase-1 (Scd1) deficiency protects against diabetic hyperglycemia and hepatic steatosis in an insulin-independent manner. Mechanistically, Scd1 ablation redirects excess cholesterol into bile synthesis, predominantly characterized by an increase in liver and plasma taurocholic acid. These shifted bile acids stimulate hepatic glucose transporter 1 ( Glut1 ) expression via the farnesoid X receptor (FXR) activation to facilitate basal glucose clearance. While the hepatokine FGF21 acts as a partial systemic mediator, the local bile acid-Fxr axis remains a sufficient driver of clearance, a protective phenotype completely reversed by dietary oleate supplementation.

PMID 42465393
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PubMedCase reports in pediatrics2026-07-17

Incidental Detection of Acute Leukemia During Genetic Evaluation of Neurodevelopmental Disorder in a Pediatric Clinic: A Case Report.

Jones Stephen G SG

A previously healthy 5-year-old boy presented to pediatric neurology for evaluation of recurrent migraine headaches with associated anxiety. Neurologic imaging was unremarkable, but clinical features consistent with autism spectrum disorder were noted. As part of standard-of-care ASD evaluation, SNP chromosomal microarray (CMA) on peripheral blood revealed a hypodiploid genome (∼35 chromosomes), suspicious for leukemia. Prompt notification led to repeat blood testing showing ∼30% circulating blasts. A diagnosis of acute leukemia was made, and constitutional CMA on buccal DNA showed a normal diploid male karyotype. This case illustrates the potential for ASD genetic testing to yield critical, incidental systemic findings and underscores the importance of rapid follow-up and interdisciplinary care.

PMID 42466354
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PubMedbioRxiv : the preprint server for biology2026-07-17

Gene model for the ortholog of raptor in Drosophila grimshawi.

Lieser Bethany C BC, Lose Bailey B, Kiser Cole A CA, Butterfield Sydney S et al.

Gene model for the ortholog of raptor in the D. grimshawi May 2011 (Agencourt dgri_caf1/DgriCAF1) Genome Assembly (GenBank Accession: GCA_000005155.1) of Drosophila grimshawi . This ortholog was characterized as part of a developing dataset to study the evolution of the Insulin/insulin-like growth factor signaling pathway (IIS) across the genus Drosophila using the Genomics Education Partnership gene annotation protocol for Course-based Undergraduate Research Experiences.

PMID 42465446
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