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insulin glargine (Galactus / Glaricon / Basalog)

✓ Approved

Mylan · INSR · Recombinant Proteins

What is insulin glargine?

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

Drug Profile

Brand NamesGalactus, Glaricon, Basalog
CompanyMylan
Drug ClassRecombinant Proteins, Polypeptide
Molecular TargetINSR
RouteInjectable (Others), Subcutaneous Injection
StatusApproved
Sources: ClinicalTrials.gov, Mylan

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

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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PubMedMolecular genetics & genomic medicine2026-10-15

The First Case of Digenic MODY Diabetes Involving Compound Heterozygosity of Three Variants in the PDX1 and HNF1B Genes.

Płonka-Stępień Magdalena M, Szopa Magdalena M, Zawada Magdalena M, Malecki Maciej T MT

We report a rare case of digenic MODY. In 2016, at age 15, the patient was diagnosed with type 1 diabetes and began insulin therapy. After discrepancies in her glycaemic control were observed, an extensive differential diagnosis was conducted. In 2024, genetic testing confirmed monogenic diabetes, allowing for tailored treatment of the patient. The initial diagnosis was type 1 diabetes, later revised to MODY after Sanger screening. Genetic testing detected c.293C>T, p.Ala98Val in the HNF1A gene, which was initially misinterpreted as a variant causing Maturity Onset Diabetes of the Young (MODY), an autosomal dominant monogenic diabetes. Eventually, next-generation sequencing (NGS) revealed three heterozygous variants in the MODY genes: HNF1B and PDX1. The HNF1B and PDX1 genes are transcription factors responsible for pancreas development and insulin gene transcription. Two variants located very close to each other in the PDX1 gene were identified: c.694G>A, p.Gly232Ser and c.697G>T, p.Glu233Ter. The first causes an amino acid change, while the latter leads to an early termination codon. The third variant, c.827_828insT, p.Gly277ArgfsTer17, was found in the HNF1B gene, resulting in a premature STOP codon and a truncated nonsense protein product. This is the first report of a patient with a double MODY variant resulting in early protein termination. Overall, the available evidence suggests that all variants may be pathogenic. The variants' severity and likely digenic nature matched the proband's diabetes presentation, which didn't respond to oral agents and required insulin. Neither parent nor brother, each with a detected variant in a single gene, has developed diabetes. However, renal cysts were discovered in the mother and brother, and the father was diagnosed with prediabetes. This case highlights the severe presentation of likely digenic MODY, similar to type 1 diabetes. As NGS use increases, more patients like these are expected to be identified.

PMID 42876335
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PubMedFrontiers in endocrinology2026-10-15

Age-specific association between remnant cholesterol and insulin resistance in women with polyendocrine metabolic ovarian syndrome.

Yu Chiyuan C, Sun Zhonghua Z, Wu Qinyao Q, Zhou Zhiyi Z et al.

Insulin resistance (IR) is a major metabolic feature in women with polyendocrine metabolic ovarian syndrome (PMOS). Remnant cholesterol (RC), which reflects the cholesterol burden of triglyceride-rich remnant lipoproteins (TRLs), may capture lipid disturbances related to insulin-resistant dyslipidemia. Whether RC is linked to IR in women with PMOS remains unclear. This study enrolled 617 women with PMOS. Participants were grouped according to natural-log-transformed remnant cholesterol (lnRC) quartiles. Adjusted odds ratios (ORs) for IR were estimated using multivariable logistic regression models, and restricted cubic splines (RCS) were fitted to characterize the potential dose-response patterns. Multiplicative and additive interaction analyses were performed to evaluate the interaction between age and lnRC. Discrimination of IR by lnRC was assessed using receiver operating characteristic (ROC) curve, and age-specific estimates were compared using DeLong's test. Integrated discrimination improvement (IDI) and net reclassification improvement (NRI) were calculated to assess whether lnRC added information beyond the base model. Higher lnRC levels were significantly associated with increased odds of IR (Q4 vs. Q1: odds ratio [OR] = 3.11, 95% confidence interval [CI]: 1.57-6.14, P = 0.001). This relationship was stronger in women aged < 30 years than in those aged ≥ 30 years (OR: 2.01 vs. 1.13, P for interaction = 0.046). A multiplicative interaction between age and lnRC was also observed for IR (OR = 0.438, 95% CI: 0.197-0.977, P = 0.044). Exploratory age-stratified ROC analysis showed that the area under the curve (AUC) of lnRC for IR discrimination was higher among women aged <30 years than among those aged ≥30 years (0.654 vs. 0.523, DeLong P = 0.024). Adding lnRC to the base model improved risk reclassification and discrimination (NRI = 0.381, 95% CI: 0.165-0.597, P = 0.001; IDI = 0.025, 95% CI: 0.007-0.0439, P = 0.005). This study indicates that the lnRC-IR association was stronger in women aged <30 years, and a multiplicative interaction between lnRC and age group was observed. These findings suggest that RC may provide complementary information for metabolic assessment in younger women with PMOS and support its further evaluation as a readily calculable lipid marker.

PMID 42876462
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PubMedFrontiers in endocrinology2026-10-15

Types 1 diabetes mellitus and Graves' disease in Sanjad-Sakati syndrome: a case report in Saudi Arabia.

Almasri Ghada G, Almubayedh Alaa Ahmed AA, Zaitoun Maryam M, Almutairi Nawal N et al.

Sanjad-Sakati syndrome (SSS) is a rare autosomal recessive disorder caused by TBCE gene variants and characterized by congenital hypoparathyroidism, severe growth retardation, developmental delay, and dysmorphic features. We report a nine-year-old Saudi boy with genetically confirmed SSS due to a homozygous 12-bp deletion in exon 3 of the TBCE gene (c.155_166del12bp; p.S52_G55del), who presented with hypocalcemic convulsions at three weeks of age. At three years, he developed type 1 diabetes mellitus (T1DM) with profound insulin deficiency and positive anti-islet cell and anti-GAD-65 antibodies. At four years, he developed Graves' disease, confirmed by hyperthyroidism, positive TSH receptor antibodies, and increased thyroid vascularity, followed by hypothyroidism requiring levothyroxine. Severe bilateral medullary nephrocalcinosis was also identified. This case highlights the unusual coexistence of TBCE-related SSS, autoimmune T1DM, and Graves' disease, raising the possibility of potential immune dysregulation, although causality cannot be established. Longitudinal endocrine surveillance, particularly of thyroid function, may be warranted in patients with SSS.

PMID 42876469
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