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insulin

✓ Approved

MJ Biotech · INSR · Recombinant Proteins

What is insulin?

insulin is a recombinant proteins developed by MJ Biotech. It is approved for therapeutic indications via injectable (others).

Drug Profile

CompanyMJ Biotech
Drug ClassRecombinant Proteins
Molecular TargetINSR
RouteInjectable (Others)
StatusApproved
Sources: ClinicalTrials.gov, MJ Biotech

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 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
InvestigationsGlucose tolerance test abnormal✓ Approved

Related Research Articles

PubMedJournal of microbiological methods2026-08-30

Development of an A7G variant of recombinant human G-CSF for improved fibroblast-mediated wound healing.

Thota Sujani S, Myneni Praveen P, Venkateswarulu T C TC

Recombinant human granulocyte colony-stimulating factor (rh-G-CSF) is useful in tissue regeneration due to its angiogenic and anti-inflammatory actions. The current study focused on the downstream process of A7G mutant rh-G-CSF (m-rh-G-CSF) and the effects of m-rh-G-CSF on human fibroblasts. The m-rh-G-CSF was purified and had 97.24% purity, a final protein concentration of 0.814 g/L and a molecular weight of 18,784 Da. The addition of m-rh-G-CSF significantly elevated the ATP level in the treated cells in a concentration-dependent manner. The maximal ATP level was achieved at a concentration of 2.5 μg/mL and was 89% higher than in the control cells and 13% higher than in reference rh-G-CSF. In the scratch-wound assay, 92.67% and 98.69% wound closure were observed at 24 and 48 h after the addition of m-rh-G-CSF, respectively, compared with 49.93% in control cells at 48 h. These findings support the potential of m-rh-G-CSF as a therapeutic candidate for fibroblast-mediated wound healing.

PMID 42669396
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PubMedPediatric research2026-08-30

A recombinant fragment of human surfactant protein D reduces lung inflammation in preterm lambs.

Castillo-Hernandez Tania F TF, Finkielsztein Ariel A, Bhatt Reena R, Panichi Daniele D et al.

Bronchopulmonary dysplasia (BPD), the major chronic respiratory morbidity in extremely preterm infants, is largely driven by inflammation. Preterm lungs are deficient of surfactant protein D (SP-D), an immunomodulatory protein absent in current commercial surfactant preparations. We hypothesised that using a recombinant fragment of human SP-D (rfhSP-D) as an adjuvant to exogenous surfactant therapy would reduce ventilator-induced inflammation. We utilised a preterm lamb model of ventilator-associated lung injury. Mechanically ventilated preterm lambs were randomised into control and two treated groups, receiving endotracheal surfactant at 15 min post-delivery. Physiological parameters were measured throughout the experiment. Lung tissue was analysed for changes in alveolar architecture and expression levels of pro-inflammatory cytokines. Bronchioalveolar lavage (BAL) was analysed for SP-D concentration, and inflammatory cells. Intratracheal administration of rfhSP-D improved respiratory outcomes, significantly increased airspace and lung compliance in treated groups. Treated lambs also showed a reduction in lung tissue gene expression of inflammatory cytokines and inflammatory cell counts. Intratracheal administration of rfhSP-D did not negatively impact standard surfactant therapy and appeared to complement it. The administration of rfhSP-D as an adjuvant to standard surfactant therapy effectively reduced lung inflammation supporting the potential therapeutic use of rfhSP-D for preterm infants at risk of developing BPD. We have successfully developed and tested a novel recombinant fragment of human surfactant protein D (rfhSP-D) capable of reducing ventilator-associated lung inflammation in a pre-term lamb model. These results suggest rfhSP-D may be a novel potentially useful therapy for Bronchopulmonary dysplasia (BPD) in combination with currently available surfactant replacement therapies and serves as justification for a first in human clinical trial in mechanically ventilated infants. If successful, rfhSP-D could become a therapeutic candidate to mitigate pulmonary inflammation and improve lung outcomes, potentially offering a novel therapeutic avenue in the prevention or management of BPD.

PMID 42668280
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PubMedPhysical chemistry chemical physics : PCCP2026-08-30

Elucidating the electronic origins of a halide-dependent inversion of magnetic anisotropy in tetravalent uranium amidinate complexes.

Näder Adrian A, Hong Boseok B, Fichter Sebastian S, Patzschke Michael M et al.

Recent synthesis and characterization of tetravalent U and Np complexes [AnIVX((S)-PEBA)3] and [AnIVX(iPr2BA)3] (X = F, Cl) bearing the (S,S)-N,N'-bis(1-phenylethyl)benzamidinate ((S)-PEBA) and the N,N'-bis(isopropyl)benzamidinate (iPr2BA) ligands, respectively, have revealed a characteristic inversion of paramagnetic 1H NMR shifts for both [UF(L)3] representatives compared to the [UCl(L)3] compounds. The same effect is not observed for [NpF(L)3] and [NpCl(L)3], with currently no satisfactory explanation for these observations. Using straightforward CASSCF-SOC-NEVPT2 calculations and point-group-optimized geometries, in combination with the Kuprov model approach [G. T. P. Charnock and I. Kuprov, Phys. Chem. Chem. Phys., 2014, 16] for the calculation of pseudo-contact shifts (PCS), the experimentally derived 1H paramagnetic shifts could be reproduced qualitatively and in most cases also quantitatively. The good agreement for most signals allowed for a first evaluation of the contribution of Fermi-contact shifts (FCS) for more strongly deviating data points, which could be supported by unrestricted DFT spin densities and spin populations. To finally gain a deeper understanding as to where the differing magnetic anisotropy for the [UF(L)3] compounds stems from, the magnetic sublevels of the ground atomic multiplet |J,mJ〉 were investigated for all complexes. These revealed that only for the [UF(L)3] compounds a high |mJ〉 (pseudo) doublet showing sufficient isolation is stabilized in the ground state, whose high axiality in the end enables the realization of a prolate χ tensor responsible for the inverse PCS field.

PMID 42669213
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PubMedJournal of extracellular biology2026-08-30

Calpeptin Reduces Extracellular Vesicle Secretion and Induces Anti-Inflammatory Effects but Upregulates HO-1 and Alters Adiponectin Levels in Human Adipocytes.

Matilainen Johanna J, Foster Sanni S, Berg Viivi V, Tampio Janne J et al.

Recent studies have shown that adipose tissue (AT) secretes elevated levels of extracellular vesicles (EVs) in obesity, and these EVs play roles in metabolic diseases. The inhibition of calpains has anti-inflammatory and anti-fibrotic effects on AT in mice and reduces EV secretion in some cell types in vitro. However, its effects on human AT and adipocyte EV secretion remain unexplored. This study aimed to investigate calpeptin's effects on EV-mediated communication and adipocyte function, offering potential insights into therapeutic approaches for metabolic diseases. Human Simpson Golabi Behmel Syndrome (SGBS) preadipocytes were differentiated and treated with calpeptin. EVs were isolated by standard ultracentrifugation, and studied by nanoparticle tracking analysis, electron microscopy, and mass spectrometry. Diverse analyses, including RNA-sequencing, liquid chromatography-mass spectrometry (LC-MS), and confocal microscopy were utilized to study calpeptin's effects on SGBS cells. AT samples from bariatric surgery patients were cultured ex vivo to assess calpeptin's effects on primary AT. We demonstrated for the first time that calpeptin reduces EV secretion in human SGBS adipocytes. Proteomic analyses revealed that calpeptin alters the abundances of proteins related to EV secretory pathways. While reduced EV secretion was accompanied by anti-inflammatory effects, calpeptin also altered insulin signalling pathways and reduced adiponectin expression, suggesting negative effects on adipocyte metabolism. Indeed, LC-MS analyses of cells and EVs revealed that calpeptin altered proteins-both in cells and EVs-that are associated with stress responses. Notably, calpeptin upregulated HO-1 in vitro and in ex vivo AT cultures, indicating induced oxidative stress in adipocytes and AT. While calpeptin shows anti-inflammatory promise in human SGBS adipocytes, its adverse effects on insulin signalling, adiponectin expression, and signs of oxidative stress raise concerns about its therapeutic potential against obesity-related pathologies in humans. Our results highlight the need to understand the broader impact of calpeptin on adipocyte metabolism.

PMID 42668896
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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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PubMedInternational journal for numerical methods in biomedical engineering2026-08-30

Patient-Specific Computational Fluid Dynamics Modeling of Airway Collapse in Infants With Robin Sequence.

Jalori Gautam G, Barbour Michael M, Bindschadler Michael M, Evans Kelly K et al.

Robin Sequence (RS) is a congenital condition in which patients experience dynamic, periodic obstruction or collapse of the upper airway due to an underdeveloped jaw and a posteriorly displaced tongue. Current clinical techniques for evaluating airway obstruction do not provide quantifiable data and fail to account for the dynamic nature of obstruction or collapse. There is no standardized criterion to characterize obstruction or collapse severity. This study presents the first method that extracts airway motion from 4-dimensional computed tomography and performs a patient-specific, moving-mesh computational fluid dynamics (CFD) analysis of RS patients with complete airway collapse or obstruction. To quantify the effects of airway collapse, airflow dynamics are analyzed using both instantaneous metrics (velocity, pressure, and energy dissipation rate) and cycle-averaged metrics (resistive work of breathing). These results are compared between a collapsing airway and its synthetic non-collapsing counterpart. To validate the synthetic non-collapsing case, it is further compared with a patient-specific non-collapsing airway. The results show that, to achieve the same tidal volume, the collapsing case requires significantly greater computed breathing effort (7.55 mJ/cycle) than the synthetic non-collapsing case (3.68 mJ/cycle). The shorter inspiration time due to the collapse leads to a higher inlet velocity, resulting in 1.7 times the maximum velocity during peak inspiration (just prior to collapse) and a 2.7-fold higher pressure drop in the collapsing case compared to the synthetic non-collapsing case. At the onset of collapse, a sharp spike in localized energy dissipation rate is observed due to the abrupt deceleration and dissipation of peak flow velocities. This methodology provides a novel approach to understanding the airflow dynamics of RS patients with airway collapse. It enables quantitative comparison between collapsing and non-collapsing airways, thereby offering the potential to support more informed and objective clinical decision-making.

PMID 42669589
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