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insulin glargine (Basalin / Changxiulin / Basugine)

✓ Approved

LG Chem Ltd. · INSR · Recombinant Proteins

What is insulin glargine?

insulin glargine is a recombinant proteins developed by LG Chem Ltd.. It is approved for therapeutic indications via injectable (others) or subcutaneous injection.

Drug Profile

Brand NamesBasalin, Changxiulin, Basugine
CompanyLG Chem Ltd.
Drug ClassRecombinant Proteins, Polypeptide
Molecular TargetINSR
RouteInjectable (Others), Subcutaneous Injection
StatusApproved
Sources: ClinicalTrials.gov, LG Chem Ltd.

Mechanism of Action

Molecular Targets

insulin glargine 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 glargine 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

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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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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PubMedScientific reports2026-07-17

Inhaling high THC cannabis acutely increases inflammation but not insulin sensitivity: a quasi-randomized trial.

Bryan Angela D AD, Skrzynski Carillon J CJ, Yang Jinqiu J, Chrystal Kyle A KA et al.

Cannabis is linked with increased appetite, raising concern about obesity-related disease and type 2 diabetes. Yet data suggest metabolic benefits of cannabis through inflammatory processes and insulin sensitivity. This was a quasi-randomly assigned experimental study comparing acute effects of a CBD-dominant versus THC-dominant versus CBD + THC cannabis flower product. Data were collected from community participants through a mobile pharmacology laboratory and a clinical research center. Participants smoked their assigned pre-rolled cannabis flower cigarette ad libitum. Primary outcomes were IL-10, chemokine MCP-1, a composite of pro-inflammatory cytokines (TNF-α, IL-6, IL-1β, IL-12, IFNG, and IL-4), and insulin sensitivity (Matsuda index). Outcomes were predicted by peak blood levels of THC and CBD immediately after cannabis use. Hypotheses were that inflammation and insulin sensitivity would vary as a function of CBD and THC exposure, and that inflammatory changes would be associated with insulin sensitivity. Participants (n = 108) were 25 to 45 (Mage = 29.7, sd = 5.4), 56.5% Female, and 88.0% white. Mixed effect models indicated a time X peak THC blood level interaction (B = 0.003, SE = 0.001, p = 0.037). As THC blood levels increased, inflammation increased more after acute use. There was a THC X CBD X time interaction on IL-10 (B=-0.001, SE = 0.000, p < 0.001). Higher than average peak blood THC was related to increasing IL-10 over time while lower than average peak THC was related to decreasing IL-10 over time but only at average or lower peak CBD levels. Cannabis use decreased MCP-1 acutely (effect for time: B=-48.757, SE = 15.061, p = 0.002), while there was no effect on the Matsuda Index. Acute cannabis use is associated with increases in both pro- and anti-inflammatory circulating cytokines, but not with insulin sensitivity. Additional research on the possible mediating mechanisms involved in the connection between cannabis use and type 2 diabetes is required.Trial registration: Gov NCT04114903, https://clinicaltrials.gov/study/NCT04114903, Registration date 11/08/2019.

PMID 42463843
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PubMedCase reports in endocrinology2026-07-17

Proinsulinoma Unmasked by Intermittent Fasting: A Case of Endogenous Proinsulinaemic Hypoglycaemia.

O'Brolchain Aongus A, Soosaipillai Gabin G, Pillai Sooraj S, Amer Saima S

We report a 45-year-old man with recurrent fasting and post-prandial hypoglycaemia due to a proinsulin (PI)-secreting pancreatic neuroendocrine tumour (NET). During a supervised fast, plasma glucose fell to 1.8 mmol/L with detectable but low insulin (0.6 μU/L) and C-peptide (range 0.3-0.6 nmol/L). These concentrations did not meet diagnostic thresholds for endogenous hyperinsulinaemia proposed by the Endocrine Society, The North American Neuroendocrine Tumor Society (NANETS), or European Neuroendocrine Tumor Society (ENETS). In contrast, PI was markedly elevated at 33 pmol/L, exceeding all guideline cut-offs (≥5 pmol/L) and establishing PI-mediated hypoglycaemia. Cross-sectional imaging demonstrated a 16-mm arterially enhancing lesion in the pancreatic body, with intense somatostatin receptor expression on DOTATATE PET (SUVmax 18.0) and no evidence of metastatic disease. Histopathology confirmed a Grade 1 pancreatic NET, consistent with a localised proinsulinoma. This case highlights a diagnostic pitfall associated with contemporary insulin immunoassays, which have limited cross-reactivity with PI and may yield deceptively low insulin levels despite clinically significant endogenous hyperinsulinism. Routine measurement of PI during fasting evaluation is essential, particularly when insulin or C-peptide results appear discordant with the clinical phenotype, to avoid delayed diagnosis and facilitate timely curative intervention.

PMID 42466309
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