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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

PubMedBioresource technology2026-07-25

Systematic engineering of Pichia pastoris for high-level production of recombinant human granulocyte-macrophage colony-stimulating factor.

Cheng Zhenzhen Z, Gong Keyu K, Song Yuchao Y, Guo Zhenchang Z et al.

Human granulocyte-macrophage colony-stimulating factor (hCSF2) is a clinically important therapeutic glycoprotein with growing market demand, underscoring the need for efficient recombinant production platforms. To enable high-level production of recombinant hCSF2 (rhCSF2), the Pichia pastoris GS115 strain was systematically engineered through multi-copy integration of the expression cassette, screening for suitable secretory signal peptides, and enhancement of protein folding and transport pathways. The combination of multi-copy integration at multiple genomic loci with the combinatorial use of endogenous and exogenous signal peptides proved critical for improving rhCSF2 titers, while reinforcement of the folding and transport machinery further alleviated the bottleneck of protein throughput. Following high-density fermentation in a 3‑L bioreactor, the optimally engineered strain achieved an rhCSF2 titer of 3.4 g/L-markedly exceeding the highest titer previously reported in yeast hosts by an order of magnitude. Importantly, this engineering strategy was successfully extended to a glycoengineered strain SuperMan5, where it enabled production of rhCSF2 with more homogeneous and humanized N‑glycans and a titer of 4.3 g/L under high‑density fermentation condition. Our work demonstrates that the high-yield production of recombinant human therapeutic glycoproteins bearing homogeneous, humanized N-glycans in engineered yeast offers promising prospects.

PMID 42498019
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PubMedMetabolism: clinical and experimental2026-07-25

Differential mirroring between in vivo insulin secretion and ex vivo islet function in individuals with and without diabetes.

Di Giuseppe Gianfranco G, Gliozzo Giulia G, Carciero Lorenzo L, Puzzangara Maria Carmen MC et al.

Insulin secretion measured in vivo reflects the integrated output of pancreatic islets within a multi-organ regulatory network, whereas ex vivo stimulation of isolated human islets captures intrinsic, islet-autonomous secretory competence. Whether these two levels of β cell function mirror each other in humans remains unclear. We studied 63 individuals undergoing partial pancreatectomy who underwent preoperative OGTT with model-based assessment of β cell function and provided pancreatic tissue for ex vivo islet isolation and glucose stimulation. Ex vivo function was quantified as the stimulation index at 16.7 mmol/L glucose (SI16.7) and related to in vivo indices of insulin secretion. SI16.7 was reduced in islet from people with T2D but showed marked inter-individual variability with overlapping distributions between individuals with and without T2D. In non-diabetic individuals, no significant associations were detected between SI16.7 and OGTT-derived indices. In contrast, in people with T2D, SI16.7 was positively associated with multiple measures of glucose-driven insulin secretion and inversely with potentiation. In multivariable analysis, a composite index of intrinsic glucose-dependent β cell competence remained independently related to SI16.7. These findings indicate that a direct correspondence between systemic β cell function and intrinsic islet secretory capacity emerges only in T2D. This state-dependent alignment suggests that loss of network-mediated regulation may unmasks islet-intrinsic defects, allowing ex vivo islet performance to better reflect in vivo insulin secretion and supporting integrated in vivo-ex vivo phenotyping as a tool for functional stratification of T2D.

PMID 42498076
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PubMedFrontiers in nutrition2026-07-25

Short-term ketogenic diet induces systemic lipidomic remodeling associated with metabolic adaptation in humans.

Park Minkuk M, Yu Jae Sik JS, Jeon Justin Y JY, Oh Hyun-A HA et al.

The ketogenic diet (KD) induces a shift in systemic energy metabolism toward fatty acid oxidation and ketone body production, but its impact on lipid species-level remodeling and insulin sensitivity in humans remains incompletely characterized. We aimed to characterize short-term KD-induced changes in circulating metabolites and lipid profiles and their relationships with insulin sensitivity in healthy adults. Fifteen participants (24-38 years) underwent a 3-day isocaloric KD (75% fat, 20% protein, 5% carbohydrate) under controlled conditions. Serum samples collected before and after the intervention were profiled using metabolomics and lipidomics. KD was associated with increased circulating acylcarnitines, acetyl-L-carnitine, and β-hydroxybutyrate, along with reduced lactate, consistent with enhanced fatty acid oxidation and ketogenesis. Lipidomics showed widespread changes across multiple classes, including lower total triglycerides and shifts toward species with longer acyl chains and higher unsaturation. Ether-linked phospholipids, including plasmalogens, tended to increase, whereas lysophospholipid-to-phospholipid ratios decreased, suggesting altered membrane turnover. Sphingolipid metabolism also appeared to be modulated, with higher sphingomyelin and hexosylceramide levels. Notably, specific lipid species, including phosphatidylethanolamine (16:0/20:5), were correlated with changes in insulin sensitivity indices (QUICKI, HOMA-IR, fasting insulin). Although these associations require validation in larger cohorts, they suggest that lipid species-level remodeling may be linked to short-term metabolic adaptation to KD. These findings highlight lipid species-level remodeling as a key feature of human KD responses and provide a basis for future mechanistic and validation studies.

PMID 42500249
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PubMedComparative biochemistry and physiology. Part D, Genomics & proteomics2026-07-25

Early hepatic protein responses to dietary restriction-refeeding in Japanese quail: A proteomic investigation.

Khalifeh Doha Mohamad DM, Gulyás Gabriella G, Knop Renáta R, Almira Fadella Nur FN et al.

Feed intake and refeeding after nutrient scarcity induce rapid metabolic adaptations in the poultry liver; however, hepatic proteomic recovery pathways in the early hours post-refeeding remain poorly defined. This study aimed to characterize early liver protein signatures in Japanese quail (Coturnix japonica) recovering from nutritional stress under two refeeding conditions. Eighteen 12-week-old male quails (245.20 ± 0.213 g) were assigned to three groups (n = 6): control fed ad libitum (12.13 MJ/kg), 24 h feed deprivation followed by 6 h refeeding, and 24 h low metabolizable energy (6.30 MJ/kg) diet followed by 6 h refeeding. In total, 854 proteins were identified, of which 515 met the filtering criteria. The low metabolizable energy refeeding showed higher abundance of proteins linked to ATP binding and carbohydrate/carboxylic acid metabolism, alongside detoxification-related proteins, while suppressing translation/RNA-binding machinery and antioxidant pathways. Feed-deprived refeeding enriched in oxidative phosphorylation and mitochondrial complex I assembly with reduced cytoplasmic translation, NMD-related components, and sulfur compound metabolism. A direct comparison indicated divergent recovery strategies: low metabolizable energy refeeding mainly reflected oxidoreductase activity and translation initiation, whereas feed-deprived refeeding potentially enriched mitochondrial ATP production and glutathione-based defenses. Our analysis indicate that 6 h of refeeding initiates an early, incomplete recovery toward hepatic homeostasis, with the severity of prior nutritional restriction dictating distinct liver metabolic priorities. Collectively, these findings might provide a preliminary understanding of the hepatic mechanisms involved in recovery from nutrient deprivation and may help in the development of feeding strategies for managing metabolic recovery in poultry. However, these findings should be considered hypothesis-generating pending further validation.

PMID 42497825
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PubMedJournal of environmental sciences (China)2026-07-25

Role of macrophage NLRP3 inflammasome activation in real-ambient particulate matter-induced abnormal hepatic glucose metabolism.

Wu Dong D, Zhang Zhen Z, Chen Sixin S, Chen Haoran H et al.

Evidence regarding the effects of particulate matter (PM) exposure on hepatic glucose metabolism and insulin resistance is limited, and its mechanisms remain unclear. Macrophages, as key regulators of the liver microenvironment, may mediate PM-induced metabolic processes. This study used an individually ventilated cage (IVC)-based real-ambient PM exposure system mouse model, co-cultured macrophages and hepatocytes, and NOD-like receptor protein 3 (Nlrp3)-knockdown model to investigate the impact of macrophages on hepatic insulin resistance (IR) and glucose metabolism under PM exposure. Our findings revealed that glycogen storage was impaired, insulin signaling was suppressed, the mRNA expression of glucose metabolism-related genes was altered, and the number of macrophages increased in the mouse liver after 15 weeks of PM exposure. Additionally, PM exposed mice exhibited reduced glucose tolerance and insulin sensitivity. In the transwell co-culture model, macrophages exposed to PM for 72 h exhibited NLRP3 inflammasome activation and IL-1β release, which were associated with lysosomal damage and cathepsin B release, accompanied by inhibition of insulin signaling and abnormal expression of glucose metabolism-related genes in hepatocytes. In vitro inhibition of NLRP3 and in vivo knockdown of Nlrp3 significantly attenuated these effects of PM exposure. Additionally, IL-1β inhibition improved glucose metabolism abnormalities. These findings reflect specific effects on insulin signaling and glucose metabolism mediated by the NLRP3 inflammasome or IL-1β. These results suggest that PM exposure leading to macrophage NLRP3 inflammasome activation and IL-1β release is an important cause of abnormal hepatic glucose metabolism, providing new insights into the underlying mechanisms of PM-related hepatic glucose metabolism and IR.

PMID 42498412
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PubMedRevista brasileira de ginecologia e obstetricia : revista da Federacao Brasileira das Sociedades de Ginecologia e Obstetricia2026-07-25

Metformin + Insulin vs. Insulin for GDM and T2DM during pregnancy: systematic review and meta-analysis.

Hallack Christiano C, Nogueira Bernardo Vieira BV, Bomfim Maressa M, Meireles Nathália N et al.

Evaluate the effectiveness and safety of adding metformin to insulin (M+I) versus insulin alone for pregnant women with type 2 diabetes mellitus (T2DM) or gestational diabetes mellitus (GDM), focusing on stillbirth as the primary outcome. PubMed, Embase, and Cochrane Central were searched. No date limits. Last search: January 2025. Randomized clinical trials including women with T2DM or GDM were eligible. Trials restricted to type 1 diabetes were excluded. Two reviewers extracted maternal and neonatal outcomes and assessed risk of bias with the Cochrane RoB 2 tool. Evidence certainty was graded using GRADE. Data were pooled with random-effects models and reported as risk ratios (RRs) or mean differences (MDs) with 95% confidence intervals. Nine RCTs (2,420 women) were included, most with GDM and some with T2DM. Moderate-quality evidence indicated reduced stillbirth risk with M+I (6 RCTs, 2,196 participants; RR 0.36, 95% CI 0.14-0.90; NNT 111). Low-quality evidence suggested lower risks of gestational hypertension (4 RCTs; RR 0.68, 95% CI 0.48-0.97) and neonatal hypoglycemia (7 RCTs; RR 0.49, 95% CI 0.30-0.80). No significant differences were found for cesarean section, preterm delivery, or other neonatal outcomes. Heterogeneity, baseline imbalances, and small samples limited certainty. M+I may reduce stillbirth and some adverse outcomes compared with insulin alone, but most evidence remains low certainty. Further high-quality RCTs are needed.Registered in PROSPERO: CRD42024617330.

PMID 42500179
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