Drug Database
IN

insulin (Rinsulin R)

✓ Approved

GeroPharm · INSR · Recombinant Proteins

What is insulin?

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

Drug Profile

Brand NamesRinsulin R
CompanyGeroPharm
Drug ClassRecombinant Proteins
Molecular TargetINSR
RouteInjectable (Others), Intramuscular (IM) Injection, Intravenous (IV), Subcutaneous Injection
StatusApproved
Sources: ClinicalTrials.gov, GeroPharm

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

PubMedBone research2026-07-17

Osteocalcin-dependent and -independent metabolic dysregulation in a mouse model of Osteogenesis imperfecta.

Tauer Josephine T JT, Rauch Frank F, Ferron Mathieu M, Komarova Svetlana V SV

Osteogenesis imperfecta (OI) is a rare bone fragility disorder. Previously, in a severe OI mouse model (Col1a1Jrt/+), a sex- and age-dependent metabolic phenotype was observed, correlating with elevated levels of the bone-derived hormone osteocalcin (OCN). This hormone is known to play a crucial role in managing energy metabolism, including glucose regulation and fat mass. In fact, upon high-fat diet (HFD) exposure, OI mice developed a metabolic syndrome linked to sex and OCN. To assess OCN's role in OI, Col1a1Jrt/+ mice were crossed with OCN-deficient mice (Bglap). Under regular chow and HFD conditions, both OCN-dependent and OCN-independent metabolic alterations were identified. OCN-dependent processes were adipose tissue, liver, and insulin metabolism in a sex-, age-, and diet-dependent manner. OCN-independent traits included the pancreas in juvenile mice, HFD-induced pancreatic insulin levels and glucose intolerance, besides overall growth, fertility, and bone phenotype. Notably, increased juvenile energy expenditure was OCN-independent, while HFD-induced changes were OCN-driven. These findings demonstrate OCN's role in shaping the metabolic phenotype while revealing distinct OCN-independent effects, emphasizing the complex genetic regulation of metabolism in OI.

PMID 42463636
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PubMedSage open pediatrics2026-07-17

Hemophilia and Type 1 Diabetes in a Pediatric Patient: Case Report of an Extremely Rare Association.

Virú-Loza Manuel André MA

Reports on the association between hemophilia and pediatric diabetes are very scarce in the literature, with no more than four worldwide. This report describes the case of a 14-year-old male with severe hemophilia A and type 1 diabetes who was brought to the emergency department due to fever and bruising on his back and jaw following trauma. The patient responded well to plasma-derived factor VIII, drainage, antibiotic therapy, and management with NPH and Regular insulin. There were no problems with the use of subcutaneous insulins during hospitalization. Previously reported cases in the literature describe potential bleeding and bruising associated with devices used for managing pediatric diabetes. However, severe bleeding and bruising that significantly impede diabetes treatment do not appear to be present, although individualized management is still required.

PMID 42466207
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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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PubMedJournal of Alzheimer's disease : JAD2026-07-17

The relationship between low-sodium salt substitutes and cognitive function among middle-aged and older adults: The Chinese Square Dance Cohort.

Zheng Chenchen C, Li Fengping F, Wang Ruhan R, Li Benchao B et al.

BackgroundPrevious studies have indicated that high sodium intake is associated with poorer cognitive function, and low-sodium salt substitutes (LSSS) can reduce sodium intake.ObjectiveWe hypothesized that the use of LSSS is linked to better cognitive performance.MethodsIn this cross-sectional study, participants reported using LSSS or regular salt via questionnaire. Cognitive function was evaluated using Auditory Verbal Learning Test (AVLT), Verbal Fluency Test (VFT), Digit Symbol Substitution Test (DSST), and Trail Making Test-B (TMT-B). Z-scores were utilized to standardize the results, with composite z-score reflecting global cognitive function. Mild cognitive impairment (MCI) was determined by Petersen's criteria, and subclassified into amnestic MCI (aMCI) and non-amnestic MCI (naMCI). Multiple linear regression and logistic regression analyses were performed to assess the associations of the use of LSSS with cognitive function and MCI.ResultsAmong 4201 participants (median age 64 years, 85.91% female), 639 (15.21%) self-reported using LSSS. Compared to those who used regular salt, the use of LSSS was associated with higher composite z-score, VFT, and DSST, with β values (95%CIs) of 0.10 (0.05, 0.15), 0.16 (0.08, 0.24), and 0.17 (0.10, 0.23), respectively. The prevalence of MCI was 8.29% in the LSSS group and 12.80% in the regular salt group, the use of LSSS was related to lower odds of naMCI (OR = 0.63, 95%CI: 0.41, 0.96).ConclusionsOur findings indicate that the use of LSSS was related to better cognitive performance and lower odds of naMCI, suggesting that replacing regular salt with LSSS may be a promising dietary strategy for cognitive aging worthy of further investigation.

PMID 42466706
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