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human insulin (Biohulin)

✓ Approved

Novo Nordisk A/S · INSR · Small Molecule

What is human insulin?

human insulin is a small molecule developed by Novo Nordisk A/S. It is approved for therapeutic indications.

Drug Profile

Brand NamesBiohulin
CompanyNovo Nordisk A/S
Drug ClassSmall Molecule, Polypeptide
Molecular TargetINSR
StatusApproved
Sources: ClinicalTrials.gov, Novo Nordisk A/S

Mechanism of Action

Molecular Targets

human 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

human insulin is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
InvestigationsGlucose tolerance test abnormal✓ Approved

Related Research Articles

PubMedJournal of biophotonics2026-09-19

Enhancement of Harvested Islet Functionality Through Photostimulation.

Fowlds Kelli K, Darden Carly M CM, Lawrence Michael C MC, Cho Michael M

Allogeneic islet transplantation is a promising treatment for Type I diabetes, but its success is limited by islet loss during isolation, purification, and engraftment, resulting in variable long-term insulin independence. Our previous studies demonstrated that photobiomodulation (PBM) significantly enhances insulin and glucagon secretion in pancreatic cells, likely through modulation of ATP production and calcium signaling pathways involved in hormone release. Building on these mechanistic findings, we investigated whether PBM could similarly improve the functionality of whole islets before transplantation. Mouse islets were isolated by pancreatectomy, cultured ex vivo, and treated daily with PBM for 7 days. Fluorescence imaging and functional assays were used to assess insulin expression and secretion. PBM significantly enhanced insulin secretion, with an approximately twofold increase observed after 3 days of treatment. These findings support PBM as a promising, noninvasive approach for improving islet function before transplantation.

PMID 42760903
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PubMedJournal of ovarian research2026-09-19

Hypothalamic Epac2/AKT/GnRH signalling is associated with metformin-responsive neuroendocrine improvement in a PCOS model.

Guo Na N, Li Hongyun H, He Jinhong J, Zhou Huanhuan H et al.

Polycystic ovary syndrome (PCOS) is a complex endocrine-metabolic disorder characterised by hypothalamic-pituitary-gonadal (HPG) axis dysfunction and pathological gonadotropin-releasing hormone (GnRH) hypersecretion. While metformin demonstrates therapeutic efficacy in PCOS, its potential neuroendocrine mechanisms remain incompletely understood. This study aimed to investigate the involvement of hypothalamic signalling in metformin-responsive neuroendocrine regulation in PCOS. Letrozole-induced PCOS rat models were treated with metformin to assess reproductive and metabolic outcomes. Data-independent acquisition (DIA) proteomics of hypothalamic tissue was performed to identify dysregulated pathways, followed by network analysis to explore candidate regulatory nodes. Mechanistic investigations were conducted in glucosamine-induced insulin-resistant GT1-7 GnRH neurons using pharmacological modulation and siRNA knockdown. In vivo functional relevance was examined using AAV-mediated Epac2 knockdown in the mouse arcuate nucleus. Metformin improved metabolic and reproductive abnormalities in PCOS rats, including insulin resistance, GnRH/LH hypersecretion, estrous cyclicity disruption, and ovarian morphological alterations. Hypothalamic proteomic and network analyses suggested that metformin-responsive changes were associated with insulin and cAMP-related signalling pathways. In GT1-7 neurons, metformin increased Epac2 expression, restored AKT signalling, and reduced GnRH overproduction under insulin-resistant conditions. Hypothalamic Epac2 knockdown reduced AKT signalling and was associated with systemic insulin resistance, increased GnRH/LH secretion, and preliminary supportive ovarian morphological observations, consistent with a functional contribution of Epac2 to reproductive-metabolic regulation. These findings support the involvement of hypothalamic Epac2/AKT/GnRH signalling in metformin-responsive neuroendocrine regulation in PCOS. Further studies are required to determine the relative contributions of central and peripheral mechanisms.

PMID 42760541
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PubMedActa neuropathologica communications2026-09-19

Experimental induction of myelin damage in post-mortem human brain slice cultures.

Meijns Niels Reinder Coenraad NRC, Muñoz González Gema G, Stolker Sabine S, T Hart Bert B et al.

The mechanisms that drive myelin damage as seen in demyelinating disorders such as multiple sclerosis remain incompletely understood. Much of our current knowledge is derived from animal models, but interspecies differences limit their relevance in the context of human pathology and could explain why various promising therapies failed during clinical translation. Human post-mortem organotypic brain slice cultures provide a unique platform to study human myelin biology, as they preserve genetic, cytoarchitectural, pathological and species-specific context. Here, we evaluated myelin integrity in a human post-mortem organotypic brain slice culture model and experimentally induced focal myelin damage. Human post-mortem organotypic brain slice cultures retain key features throughout the culturing period, but exhibit gradual cellular and myelin loss over time. Myelin fibres within the white matter remain detectable and display preserved structural and chemical integrity up to 13 days in vitro, as indicated by the conserved ultrastructure, paranodal and nodal organization, and stable myelin spectroscopic signature. Topical delivery of lysophosphatidylcholine using cryogel scaffolds enables focal drug administration throughout the full depth of the slice with minimal diffusion into surrounding tissue and induces localized demyelination. Similar focal application of β-scorpion toxin Cn2, a Nav1.6 channel agonist, induces subtle myelin destabilization. Overall, our results demonstrate human post-mortem organotypic brain slice culture model as an adequate platform for studying myelin damage in a human context.

PMID 42760561
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PubMedbioRxiv : the preprint server for biology2026-09-19

Electrophysiological dissociation of human posterior cingulate cortex contributions to value- and memory-based decision-making.

Koslov Seth R SR, Rey Hernan G HG, Heilbronner Sarah R SR, Provenza Nicole R NR et al.

The human posterior cingulate cortex (PCC) is routinely implicated in cognition and disease, yet its specific functional contributions remain unclear. Historically, human neuroimaging has linked the region to episodic memory and the default mode network, while a distinct non-human primate electrophysiology literature has focused on economic decision-making. Integrating anatomical evidence with these literatures, it has recently been proposed that this divergence reflects subregional organization, with dorsal PCC as a potential convergence site for value-based and memory-based decisions. Here, we recorded local field potentials (LFPs) and single units from human PCC while the same participants performed matched value- and memory-based decision tasks. LFPs in dorsal but not ventral PCC showed sustained engagement across both tasks, with risk sensitivity emerging only after the decision. In contrast, single-unit activity was more temporally circumscribed and could be grouped into response profiles active before or after the decision. Dorsal but not ventral PCC engagement further extended to memory encoding, recognition, and confidence judgments. Together, these findings reveal a consistent functional dissociation, identifying dorsal PCC as a domain-general interface between evaluative and mnemonic systems. In doing so, they align human and non-human primate accounts of PCC function and help orient future targeted studies of its role in cognition and disease.

PMID 42760980
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PubMedNature computational science2026-09-19

Large language models as human proxies.

Karetnikov Nikita N, Rahwan Iyad I, Svetinovic Davor D

The idea of computationally approximating human behavior is being reshaped by the emergence of large language models (LLMs). Although LLMs do not explain the mechanisms of human behavior, they can potentially stand in for humans-giving rise to new applied and scientific uses. Here we analyze research from multiple disciplines that explicitly or implicitly use LLMs as human proxies and organize them into four roles: believable agents, task agents, experimental subjects and silicon samples. By comparing the roles, we show that similarity to humans is not a single feature: each supports a different scientific claim and requires its own validity criteria.

PMID 42760398
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PubMedActa veterinaria Scandinavica2026-09-19

Treatment, monitoring, and euthanasia in canine diabetes mellitus - a questionnaire-based survey among veterinarians in Norway.

Nerhagen Sivert S, Eriksen Esben Østergaard EØ, Amundstad Jo J, Anfinsen Kristin Paaske KP

Canine diabetes mellitus (DM) is a relatively common endocrinopathy, and it requires dedication and commitment from an owner to care for a diabetic pet. This study aimed to describe treatment and monitoring habits, perceived owner and veterinary concerns when treating and monitoring a diabetic dog, as well as triggers for and risk of euthanasia in diabetic dogs among Norwegian veterinarians. A questionnaire was designed and made available online. A total of 125 veterinarians completed the survey. According to the data collected, the cumulative incidence risk for treatment initiation was 71.6% (95% CI 63.2, 80.6), suggesting that the respondents started most of the diabetic dogs seen in their practice on treatment. The majority of the respondents reported that all female entire diabetic dogs were neutered near the time of diagnosis. Main veterinary treatment concerns identified were difficulties in achieving rapid and adequate control. Main respondent-perceived owner concerns were cost and injecting their diabetic dog. About 60% of respondents had never used a continuous glucose monitor. Of respondents having used such monitors, half had experienced owners changing the insulin dose themselves, without consulting a veterinarian. Nearly one third of the veterinarians recalled that issues related to monitoring contributed directly to euthanasia of a diabetic dog in their care. The estimated one month and one year cumulative risk of euthanasia in dogs started on insulin therapy found in our study were 11.5% (95% CI 8.3, 14.6) and 26.9% (95% CI 22.0, 31.8), respectively. In our study population, respondents working in large cities were more likely to report a high probability of starting treatment than respondents in small cities and rural areas. Respondents in small cities and rural areas were also more likely to report medium and high risk of euthanasia compared to respondents in large cities, respectively. Veterinary-perceived owner triggers for euthanasia were dogs' quality of life, monitoring, and owners' lifestyle changes. For the respondents themselves, comorbidities were the leading factor reported for recommending euthanasia. This questionnaire-based study describes perceived treatment concerns, and reasons for and estimates of euthanasia risk in dogs with DM, based on the experiences of veterinary practitioners working in Norway. The results highlight important aspects of the treatment and monitoring of dogs with DM, as well as triggers for euthanasia. Further investigations into the aspects identified could be useful to improve the overall care for diabetic dogs.

PMID 42760569
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