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insulin aspart + insulin aspart protamine

✓ Approved

HEC Pharm · INSR · Recombinant Proteins

What is insulin aspart + insulin aspart protamine?

insulin aspart + insulin aspart protamine is a recombinant proteins developed by HEC Pharm. It is approved for therapeutic indications via unknown.

Drug Profile

CompanyHEC Pharm
Drug ClassRecombinant Proteins
Molecular TargetINSR
RouteUnknown
StatusApproved
Sources: ClinicalTrials.gov, HEC Pharm

Mechanism of Action

Molecular Targets

insulin aspart + insulin aspart protamine 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 aspart + insulin aspart protamine is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
InvestigationsGlucose tolerance test abnormal✓ Approved

Related Research Articles

PubMedDiabetes research and clinical practice2026-08-30

Glycemic and safety outcomes of the insulin-only bionic pancreas in older adults and individuals with impaired awareness of Hypoglycemia: a post hoc analysis of a randomized pivotal trial.

Oktavian Puguh P, Kencono Wungu Citrawati Dyah CD, Amin Indah Mohd IM, Mudjanarko Sony Wibisono SW

Evaluate the efficacy and safety of iLet Bionic Pancreas (BP) in older adults and individuals with impaired awareness of hypoglycemia (IAH). This post hoc analysis used individual participant-level data from the Insulin-Only Bionic Pancreas Pivotal Trial (n = 440; NCT04200313). Eligible participants (n = 96) with type 1 diabetes, aged ≥ 60 years and/or had IAH (Clarke score ≥ 4), were randomized to BP with aspart/lispro (BP-Asp/Lis; n = 45), BP with fast-acting aspart configuration (BP-Fiasp; n = 31), or standard care (SC; n = 20) for 13 weeks. Compared with SC, time-in-range (70-180 mg/dL) significantly increased by 7.49 % (95 % CI: 2.61 to 12.38; ∼1.8 h/day) with BP-Asp/Lis and by 8.28 % (95 % CI: 3.15 to 13.41; ∼2.0 h/day) with BP-Fiasp, driven by reduced hyperglycemia. No significant differences were observed in hypoglycemia exposure. Severe hypoglycemia occurred in four participants (four events) on BP-Asp/Lis and one participant (two events) on SC. One diabetic ketoacidosis event occurred on BP-Fiasp due to an infusion set failure. In high-risk, clinically vulnerable populations, the BP system significantly improved glycemic control while maintaining safety parity with respect to hypoglycemia risk, providing a resilient therapeutic alternative for vulnerable cohorts.

PMID 42669381
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PubMedCureus2026-08-30

Online-Sourced Retatrutide Complicating Impending Diabetic Ketoacidosis in a Patient With Type 1 Diabetes and Concurrent Shigella Gastroenteritis.

Branine Nassim N

Growing public interest in incretin-based therapies for weight loss has been accompanied by increasing availability of research peptides purchasable online. Products may be used without medical assessment or counselling regarding adverse effects, sick-day management or appropriate follow-up. In addition, composition, purity and dosing accuracy may be uncertain. Retatrutide is a novel triple agonist of the glucose-dependent insulinotropic polypeptide, glucagon-like peptide-1 and glucagon receptors currently being investigated for obesity and type 2 diabetes mellitus, but has no established role in type 1 diabetes mellitus. We report a man in his mid-30s with longstanding type 1 diabetes mellitus who presented with severe vomiting, diarrhoea, hyperglycaemia, ketonaemia and acute kidney injury shortly after self-administering an online-purchased product marketed as retatrutide for weight loss. His partner, who had taken the same preparation, also developed gastrointestinal symptoms. Both had also consumed a potential foodborne source of infection. In type 1 diabetes mellitus, where patients remain dependent on exogenous insulin to suppress ketogenesis, gastrointestinal illness may rapidly precipitate ketosis when insulin is omitted and oral intake is reduced. Although diabetic ketoacidosis did not develop, peak ketonaemia reached 4.3 mmol/L in the setting of dehydration and insulin omission, requiring intravenous insulin and fluid replacement. During recovery, recurrent hypoglycaemia required intravenous dextrose and insulin dose adjustment, highlighting challenges of glycaemic management in acutely unwell patients exposed to agents with incretin and glucagon receptor activity. Stool culture subsequently grew Shigella flexneri, introducing diagnostic uncertainty regarding the relative contributions of gastrointestinal infection and retatrutide exposure, and complicating counselling regarding future retatrutide use. While causation cannot be established, the temporal relationship, similar symptoms in another exposed individual, and recognised gastrointestinal adverse-effect profile of retatrutide suggest that exposure may have contributed to symptom severity or amplified the metabolic consequences of infection. This case highlights diagnostic and management challenges created by unregulated research peptides obtained outside healthcare pathways, particularly in patients with type 1 diabetes mellitus where evidence to guide management is limited and clinicians in non-specialist settings may be unfamiliar with these agents. As access expands through online vendors and social media, clinicians should routinely enquire about prescribed and non-prescribed agents when assessing unexplained illness or metabolic decompensation.

PMID 42669023
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PubMedInternational journal of endocrinology2026-08-30

Associations of Five Insulin Resistance-Related Indices With Gout Risk in the 2007-2018 NHANES Cross-Sectional Study.

Yang Kewei K, Yang Kongming K, Liu Yuhan Y, Wang Qin Q et al.

This study investigated the associations between five insulin resistance (IR)-related surrogate indices and gout and compared their associations and discriminative abilities for gout. The indices included the triglyceride-glucose (TyG) index, TyG combined with body mass index (TyG-BMI), lipid accumulation product (LAP), visceral adiposity index (VAI), and metabolic score for insulin resistance (METS-IR). Data from the 2007-2018 National Health and Nutrition Examination Survey (NHANES) were analyzed. Comparisons between the gout and nongout groups were performed using t-tests and chi-square tests. Multivariable logistic regression and subgroup analyses were used to assess the associations. Among 14,582 participants (4.80% with gout), adjusted analyses identified the highest METS-IR quartile as the strongest predictor of gout (adjusted OR = 2.823, 95%CI 1.643-4.851), followed by TyG-BMI (OR = 2.290, 95%CI 1.555-3.373). Restricted cubic splines revealed nonlinear associations of TyG and LAP with gout risk, contrasting with linear trends for TyG-BMI, VAI, and METS-IR. Subgroup analyses suggested that elevated TyG and VAI were positively associated with gout in nondiabetic individuals (interaction p < 0.05). All five IR-related indices showed positive associations with gout, particularly in those with central obesity. These indices showed modest discriminative ability for gout, and further validation is needed.

PMID 42668779
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PubMedPhotodiagnosis and photodynamic therapy2026-08-30

Choroidal microvascular heterogeneity across non-autoimmune type 2 diabetes mellitus subtypes defined by beta-cell function and insulin resistance: a wide-field Swept-Source OCTA study.

Wu Xiaoyan X, Li Qiong Q, Cui Yi Y, Xu Nuo N

To investigate the intergroup differences in choroidal thickness (CT), choroidal vascularity index (CVI), and choroidal vascular volume (CVV) across non-autoimmune type 2 diabetes mellitus (T2DM) subtypes defined by beta-cell function and insulin resistance. This cross-sectional study enrolled 22 healthy controls (22 eyes) and 85 T2DM patients (85 eyes). T2DM patients were categorized into 4 groups using K-means clustering: Severe Insulin-deficient Diabetes (SIDD) =22, Severe Insulin-resistant Diabetes (SIRD)=26, Mild Obesity-related Diabetes (MOD)=16, and Mild Age-related Diabetes (MARD)=21. CT, CVI, CVV were measured by widefield swept-source optical coherence tomography angiography (WSS-OCTA) across three concentric annular regions(0 - 10 mm, 10 - 15 mm, and 15 - 20 mm), subdivided into 12 sectors. Linear mixed-effects and multivariate regression models were constructed to evaluate intergroup differences. Compared with the control group, both CT and CVV decreased significantly in most of the 12 analyzed regions across all T2DM groups, whereas the MOD and SIRD groups exhibited no statistically significant global changes. In contrast, CVI exhibited pronounced spatial and subtype-specific heterogeneity. In the SIDD group, CVI decreased in most regions, with significant reductions in the nasal sector of the 0 - 10 mm annulus (P<0.01]), and in the nasal and inferior sectors of the 10 - 15 mm annulus (P<0.01] and -0.065 (P<0.01). Conversely, the SIRD group demonstrated a widespread increase in CVI, with significant increased in the nasal (P < 0.05), superior (P < 0.05), and temporal (P < 0.05]) sectors of the 15 - 20 mm annulus. Compared with CT and CVV, CVI shows the highest spatial heterogeneity. This indicates that divergent metabolic drivers may exert opposing effects on choroidal vascular remodeling. This subtype-specific characterization enhances our understanding of diabetic choroidopathy pathophysiology and holds potential for guiding personalized screening and therapeutic strategies.

PMID 42669328
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PubMedClinical medicine insights. Case reports2026-08-30

Successful Reversal of Tamoxifen-Associated Weight Gain and Metabolic Dysfunction with Liraglutide in a Breast Cancer Survivor: A Case Report.

Anvarbek Masharibov M, Umarov Doniyor D, Khalbayeva Zarina Z, Smerat Aseel A et al.

Introduction: Adjuvant endocrine therapy for breast cancer - particularly tamoxifen - is commonly associated with weight gain, increased adiposity, and metabolic dysfunction. Lifestyle measures often fail to reverse these effects. Evidence regarding glucagon-like peptide-1 (GLP-1) receptor agonists in this specific context remains limited. Reversal of tamoxifen-associated weight gain with liraglutide has been rarely reported. Case Presentation: A 58-year-old postmenopausal woman with stage IIA, hormone-receptor positive breast cancer experienced marked weight gain after 24 months of tamoxifen therapy, despite diet and exercise. She developed prediabetes, insulin resistance (assessed by Homeostatic Model Assessment of Insulin Resistance [HOMA-IR] 4.9), and dyslipidemia. Liraglutide, a glucagon-like peptide-1 (GLP-1) receptor agonist, was initiated and titrated to 3.0 mg/day. Over 12 months, she lost 18.5 kg, and her metabolic parameters, including HOMA-IR and glycated hemoglobin (HbA1c), normalized. Tamoxifen therapy was continued without adverse effects. Conclusion: This case suggests that liraglutide may reverse substantial tamoxifen-associated weight gain and related metabolic derangements in a breast cancer survivor. The observed improvement exceeded what is typically achieved with lifestyle measures alone. Formal studies are needed to define the role of GLP-1 receptor agonists in managing endocrine therapy-related metabolic complications.

PMID 42668751
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PubMedAging2026-08-30

Human-relevant Ptpn6 mutation alters immune and hepatic functions during aging.

Labrada Beisy Laborit BL, Kumar Amit A, Kolnohuz Alona A, Pineault Marie M et al.

Src homology region 2-containing phosphatase 1 (SHP-1), encoded by the protein tyrosine phosphatase non-receptor type 6 (PTPN6), regulates immune and metabolic signaling pathways. Although its functions in immune cells and insulin-responsive tissues are separately established, its integrative function in immunometabolic regulation remains unclear. A damaging variant in the PTPN6 gene (Ala455Thr) was discovered in a French-Canadian family and found to be the cause of early-onset emphysema. Using mice carrying this whole-body human-relevant mutation, we studied immunometabolic phenotypes across aging. Old mutant mice showed decreased body, liver and adipose tissue weights, improved glucose tolerance, and enhanced hepatic insulin sensitivity. Despite improved metabolic parameters, aged mutant mice developed liver abnormalities, including increased fibrosis and aberrant immune cell infiltration. Transcriptomic and histological analyses revealed an age-associated accumulation of intrahepatic B lymphocytes and macrophages, accompanied by increased SHP-1 protein levels and activation of Signal transducer and activator of transcription 3 (STAT3) signaling. Experiments in primary hepatocytes and old hepatocyte-specific Ptpn6 knockout mice suggest that these alterations are driven by immune rather than intrinsic hepatocyte mechanisms. These findings identify SHP-1 as a critical modulator of liver immune homeostasis during aging and demonstrate that immune cell infiltration contributes to age-related hepatic remodeling under SHP-1 deficiency.

PMID 42669491
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