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insulin (Rinsulin R)

✓ Approved

GeroPharm · INSR · 重组蛋白

什么是 insulin？

insulin 是一种重组蛋白，由GeroPharm研发。该药已获批，用于治疗相关适应症，给药途径：Injectable (Others)、Intramuscular (IM) Injection、Intravenous (IV)、Subcutaneous Injection。

药物档案

商品名Rinsulin R
公司GeroPharm
药物类别重组蛋白
分子靶点INSR
给药途径Injectable (Others), Intramuscular (IM) Injection, Intravenous (IV), Subcutaneous Injection
状态Approved
来源： ClinicalTrials.gov, GeroPharm

作用机制

分子靶点

insulin 作用于 1 个分子靶点：

INSRinsulin receptor (CD220, HHF5)
需要更深入的分析？Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

insulin 针对 2 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Metabolism and nutrition disordersType 1 diabetes mellitus✓ Approved
Metabolism and nutrition disordersType 2 diabetes mellitus✓ Approved

相关研究文献

PubMedJournal of cellular and molecular medicine2026-06-13

Insulin Signalling-Inducible IFITM1 Promotes Multiple Myeloma Progression and Bortezomib Resistance.

Lim Ji-Young JY, Kim Yeojin Y, Park Sung-Soo SS, Lee Jungyeon J et al.

Insulin substantially promotes the growth of malignant cells that overexpress the insulin receptor (INSR), and insulin excess has been recognised as a cancer-promoting factor in patients. Interferon-induced transmembrane protein 1 (IFITM1) is also overexpressed in various cancers. In this study, we investigate the association between insulin signalling-induced IFITM1 expression and multiple myeloma (MM) aggressiveness. We observed that expression of both INSR and IFITM1 was significantly elevated in symptomatic MM patients compared with those with monoclonal gammopathy of undetermined significance (MGUS) and smouldering MM (SMM). Notably, IFITM1-but not INSR-expression correlated with prognosis following autologous stem cell transplantation and bortezomib-based induction therapy. Further analysis revealed that IFITM1 expression in bone marrow plasma cells was associated with the concentrations of insulin and insulin-like growth factor 2 (IGF-II) in the bone marrow microenvironment. Insulin and IGF-II enhanced MM cell proliferation through IFITM1 upregulation, whereas suppression of IFITM1 abrogated the proliferative effects of these ligands. Moreover, insulin and IGF-II attenuated apoptosis and the inhibition of cell migration induced by the proteasome inhibitors (PIs) bortezomib and carfilzomib, and these effects were reversed by IFITM1 knockdown. The ability of insulin to reduce bortezomib-induced apoptosis and G2/M phase cell cycle arrest was likewise dependent on IFITM1 expression. Collectively, these findings suggest that insulin-induced IFITM1 plays a pivotal role in MM progression and resistance to bortezomib, highlighting IFITM1 as a potential prognostic biomarker and therapeutic target.

PMID 42286874
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PubMedFood and chemical toxicology : an international journal published for the British Industrial Biological Research Association2026-06-13

Bisphenol S induces hepatic steatosis and insulin resistance through AMPK inhibition and endoplasmic reticulum stress.

Sepúlveda-Fragoso Vinicius V, Dos Reis Emanuelle Barreto EB, de Souza Carvalho Laureano Thais T, Stockler-Pinto Milena Barcza MB et al.

Bisphenol S (BPS), a common substitute for bisphenol A, has emerged as a widespread environmental contaminant, yet its metabolic effects remain poorly understood. Increasing evidence links BPS exposure to metabolic dysfunction-associated steatotic liver disease (MASLD), although the underlying mechanisms are unclear. Here, we investigated the metabolic effects of chronic BPS exposure (4, 25, and 50 μg/kg/day for 12 weeks) in C57BL/6 mice and evaluated its impact on human Huh-7 hepatocytes. In vivo, exposure to 25 μg/kg/day exhibited obesogenic potential, while all doses induced insulin resistance and promoted hepatic micro- and macrovesicular steatosis. BPS triggered endoplasmic reticulum (ER) stress and suppressed AMP-activated protein kinase (AMPK) phosphorylation, disrupting hepatic lipid and glucose metabolism. Consistently, BPS exposure in Huh-7 cells induced ER stress, reduced AMPK activity, and impaired insulin-stimulated Akt phosphorylation, indicating decreased insulin sensitivity. Notably, pharmacological activation of AMPK attenuated BPS-induced inhibition of insulin signaling, identifying AMPK as a key mediator of BPS-driven metabolic dysfunction in hepatocytes. Collectively, these findings demonstrate that BPS promotes hepatic steatosis and insulin resistance by activating ER stress and inhibiting AMPK, highlighting BPS as a potential environmental contributor to MASLD and related metabolic disorders.

PMID 42285293
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PubMedChinese journal of natural medicines2026-06-13

Nuciferine ameliorates cognitive impairment and insulin resistance in T2DM by targeting the insulin receptor and activating PI3K/AKT signaling.

Zheng Miao M, Wang Can C, Liu Jiayi J, Xia Yi Y et al.

Insulin resistance is a hallmark of type 2 diabetes (T2DM) and can increase the risk of cognitive impairment, including Alzheimer's disease. Nuciferine, an alkaloid derived from lotus leaves, shows neuroprotective effects. This study investigated nuciferine's protective role in T2DM-induced cognitive impairment (T2DM-CI) and its mechanisms. Mouse models were created using high-fat diets and streptozotocin, along with high glucose-induced HT-22 cells. Nuciferine reduced blood glucose, improved cognitive function, and mitigated glial cell activation, neuron and synapse loss in T2DM mice. It enhanced insulin signaling by increasing protein levels of IR, IRS1, and IGF-1R, reversing PI3K and AKT phosphorylation, inhibiting GSK3β activity, and reducing hyperphosphorylated Tau in HT-22 cells and T2DM mice. mRNA levels of these molecules matched their protein levels. Further studies revealed that nuciferine directly interacts with IR, knocking out IR abolished its effects on the PI3K/AKT pathway. Thus, nuciferine activates the PI3K/AKT pathway via IR, improving insulin resistance and slowing T2DM-CI progression.

PMID 42285687
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PubMedInternational journal of pharmaceutics2026-06-13

A dual-microneedle system for integrated continuous glucose monitoring and feedback insulin delivery.

Zhao Kangxun K, Niu Yangguang Y, Cao Xiaoping X, Ma Tianqi T et al.

Effective precision diabetes management requires seamless integration of continuous glucose monitoring and therapeutic intervention. In this study, we present a novel dual-microneedle regulatory system, which combines a biosensing microneedle for real-time interstitial glucose monitoring and a therapeutic microneedle for precise transdermal insulin delivery. The biosensing microneedle utilizes glucose oxidase-functionalized electrodes for continuous glucose sensing (demonstrating a broad linear range of 1-34 mM and a limit of detection of 0.4 mM), while the therapeutic microneedle employs electroosmotic flow to regulate insulin infusion through hollow channels under a constant 5 V voltage. This integrated system was demonstrated to provide accurate glycemic control in diabetic Wistar rat models (achieving a 55 % blood glucose reduction within 144 min and demonstrating high clinical accuracy with 88 % of points in Zone A of the Clarke Error Grid), successfully merging continuous glucose monitoring with on-demand insulin delivery. The proposed system demonstrates a solid proof-of-concept for physically segregated closed-loop regulation, paving the way for the development of miniaturized, wearable artificial pancreas platforms for more effective diabetes management.

PMID 42285381
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PubMedJournal of applied toxicology : JAT2026-06-13

Epirubicin Alters Pancreatic Autophagy and Insulin Synthesis Through a Zinc-Dependent Mechanism.

Afşar Ebru E, Eranıl Işıl I

Epirubicin (EPI) can cause metabolic side effects, including chemotherapy-related diabetes, partly through oxidative stress that disrupts zinc (Zn) homeostasis and impairs autophagy. This study investigated the effects of EPI on Zn regulation and autophagy in the pancreas, as well as the modulatory role of N-acetylcysteine (NAC). Rats received EPI (9.6 mg/kg) by intraperitoneal injection (i.p.) followed 1 h later by NAC (50 or 300 mg/kg, i.p.). Glucose homeostasis was assessed using the Homeostatic Model Assessment (HOMA-IR), and β-cell function was assessed using HOMA-β levels. Plasma insulin levels, as well as insulin, proinsulin, beclin, autophagy-related proteins (ATG5), Microtubule-Associated Protein 1 Light Chain 3 (LC3), phosphorylated Akt (p-Akt), mechanistic target of rapamycin complex 1 (mTOR1), cleaved caspase-3, Zrt/Irt-like Protein 10 (ZIP10), and the proliferation marker Ki-67 in pancreatic tissue, were measured using commercial ELISA kits. Total oxidant status (TOS) and total antioxidant status (TAS) were measured using commercial colorimetric assay kits, and the oxidative stress index (OSI) was calculated. Zn levels in pancreatic tissue and plasma samples were measured using a colorimetric method. Morphological changes in the pancreas were assessed by hematoxylin and eosin staining. As a result, in the EPI group, oxidative stress and ZIP10 levels increased, whereas Zn levels decreased, as well as pancreatic autophagy, proliferation, and insulin synthesis increased. Oxidative stress decreased in both the EN-50 and EN-300 groups, with a more pronounced decrease in the EN-300 group. Furthermore, in the EN-300 group, pancreatic Zn, ZIP10, autophagy, and proliferation levels decreased, whereas mTOR1 levels increased. The pancreatic insulin synthesis observed in the EN-50 group was not observed in the EN-300 group. In conclusion, the increased autophagy observed in the Epi group may reflect an adaptive response to oxidative stress. The effects of NAC on oxidative stress may be dose-dependent, and high-dose NAC administration may suppress EPI-induced autophagy via mTOR1-mediated signaling. Furthermore, the relationship among Zn levels, autophagy, and insulin synthesis observed in the experimental groups may contribute to a better understanding of EPI-associated diabetogenic alterations.

PMID 42286405
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PubMedThe Journal of physiology2026-06-13

Amino acids partially override inhibitory effects of octreotide on islet hormone secretion in healthy individuals.

Reiche Josephine J, Richter Michael M MM, Kjeldsen Sasha A S SAS, Winther-Sørensen Marie M et al.

Hyperaminoacidaemia and hyperglucagonaemia are hallmarks of metabolic dysfunction-associated liver disease and type 2 diabetes. Amino acids potently stimulate glucagon secretion and can stimulate insulin secretion, although less potently than glucose. Endogenous somatostatin released from pancreatic δ-cells inhibits islet hormone output. It remains uncertain whether amino acid-induced stimulation can dominate pharmacological somatostatin receptor (SSTR) activation in humans. To address this we examined hormonal responses to intravenous amino acid infusion (Vamin) with and without concomitant infusion of the somatostatin analogue octreotide in 15 healthy individuals. Plasma glucagon, insulin and C-Peptide were measured during 45 min of amino acid infusion alone, during amino acid infusion combined with a 240‑min octreotide infusion and during octreotide infusion without amino acids. Octreotide alone suppressed glucagon and insulin concentrations by greater than 90% and reduced C‑Peptide by greater than 65%. In contrast amino acids alone significantly increased all three peptides. When amino acids and octreotide were co‑infused, the amino acid-driven elevations in glucagon, insulin and C‑Peptide were reduced to 49%, 43% and 78% of the levels achieved by amino acids alone. These findings demonstrate robust α‑ and β‑cell secretion during SSTR-2‑biased agonism despite profound baseline suppression, indicating partial 'breakthrough' secretion and suggesting that amino acid-driven stimulation can, in part, counteract SSTR‑mediated inhibition in humans. KEY POINTS: Amino acids strongly stimulate glucagon secretion in humans, whereas somatostatin receptor (SSTR) activation potently inhibits basal islet hormone release. During near-maximal suppression with the somatostatin analogue octreotide, amino acid infusion induced substantial 'breakthrough' secretion of glucagon, insulin and C-Peptide. Co-infusion of amino acids and octreotide reduced amino acid-stimulated responses to 49% (glucagon), 47% (insulin) and 78% (C-Peptide) of amino acids alone. Breakthrough secretion was not specific to α-cells, indicating that strong secretagogue stimulation can partially escape somatostatin-mediated inhibition for both α- and β-cells. These in vivo human data support a balance-of-signals model in which elevated amino acids can counteract, but not fully overcome, inhibitory SSTR activation. HIGHLIGHTS: We performed this study to determine why hyperglucagonaemia persists in metabolic diseases despite somatostatin's inhibitory role. We specifically evaluated whether amino acid-induced glucagon secretion can persist during pharmacological somatostatin receptor (SSTR) activation (octreotide) in humans. We found that amino acids strongly stimulated glucagon, insulin and C-Peptide secretion even during somatostatin infusion, reducing but not eliminating the hormonal responses. These findings imply that amino acid-driven stimulation can partially bypass inhibitory signalling downstream of SSTR activation, helping explain persistent glucagon elevation in metabolic disorders.

PMID 42285749
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