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mitiglinide (Bokangtai)

✓ Approved

Uni-Bio Science Group Ltd. · KCNJ11 · Small Molecule

What is mitiglinide?

mitiglinide is a small molecule developed by Uni-Bio Science Group Ltd.. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesBokangtai
CompanyUni-Bio Science Group Ltd.
Drug ClassSmall Molecule
Molecular TargetKCNJ11, ABCC8
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Uni-Bio Science Group Ltd.

Mechanism of Action

Molecular Targets

mitiglinide acts on 2 molecular targets:

KCNJ11potassium inwardly rectifying channel subfamily J member 11 (BIR, HHF2)
ABCC8ATP binding cassette subfamily C member 8 (MRP8, SUR1delta2)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

mitiglinide is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Metabolism and nutrition disordersType 2 diabetes mellitus✓ Approved

Related Research Articles

PubMedActa pharmacologica Sinica2026-02-28

IG20/MADD gene functional isoform KIAA0358 can promote insulin secretion in glucose and repaglinide-induced pancreatic β-cells.

Sui Yi Y, Weng Zhao-Lei ZL, Qian Li-Xia LX, Hong Wan-Jin WJ et al.

Deletion of IG20 (also known as MADD), which can encode multiple isoforms, causes diabetes in mice by impairing glucose-stimulated insulin secretion. To evaluate the role of IG20 in mediating the therapeutic potential of glinide-class insulin secretagogues, we tested their effects in Ig20/Madd-knockout (KMA1ko) mice. Glucose tolerance tests revealed that repaglinide, mitiglinide, and nateglinide failed to lower blood glucose levels or enhance insulin secretion in KMA1ko mice, suggesting that IG20 deficiency significantly diminishes the therapeutic efficacy of glinides. The functional relevance of at least 6 IG20 isoforms remains to be defined. Interestingly, among the six IG20 splicing isoforms re-expressed in IG20-deficient Min6 cells, only KIAA0358 was capable of restoring glucose-stimulated insulin secretion. Notably, KIAA0358 re-expression also rescued repaglinide-induced insulin secretion in vivo. Further transmission electron microscopy and total internal reflection fluorescence microscopy analyses showed that KIAA0358 significantly promoted insulin granule transport and docking impaired by IG20 knockout. Furthermore, guanine nucleotide exchange assay and GST pull-down demonstrated that KIAA0358 functions as a Rab GEF to convert Rab3A and Rab27A from the GDP-bound to the active GTP-bound state, thereby restoring their interactions with the downstream effector proteins Rim2α and Slac-2a that were impaired by IG20 deficiency. Therefore, by regulating the activation states of Rab3A and Rab27A, KIAA0358 mediated the transport and docking of insulin granules to the plasma membrane. This study also highlights that the genes encoding non-drug target proteins can influence drug efficacy and provides a novel conceptual foundation for precision medicine strategies aimed at reducing drug resistance and enhancing the clinical efficacy of glinides.

PMID 41760779
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PubMedJournal of advanced research2025-12-13

High-throughput screening identifies FDA approved drug mitiglinide as a novel pyroptosis inhibitor and therapeutic agent for osteoarthritis.

Zhang Hanwen H, Yu Tanxin T, Zhuo Nanfang N, Zhu Zongxin Z et al.

Osteoarthritis (OA), a leading cause of joint dysfunction, is characterized by progressive cartilage degradation linked to chondrocyte pyroptosis, yet disease-modifying therapies remain elusive. In this study, we conducted the first systematic drug repurposing screen in chondrocytes, aiming at identifying drugs that may suppress pyroptosis and verifying the therapeutic effects on OA. Mitiglinide's effects on chondrocyte viability were quantified via CCK-8 assays and live/dead staining. Pyroptosis inhibition, extracellular matrix (ECM) homeostasis, and NF-κB activation were measured by western blot and immunofluorescence. Network pharmacology analysis and molecular docking were applied to predict the interacting protein of mitiglinide, while Nrf2 was knocked down by siRNAs to confirm its role in mitiglinide regulated pyroptosis and ECM. In vivo, destabilization of the medial meniscus (DMM) model -induced OA mice received mitiglinide for 8 weeks, with efficacy evaluated through X-ray, OARSI-graded histopathology, immunohistochemistry, Hematoxylin-Eosin and Safranin O-Fast green staining. Through high-throughput screening (HTS) of 1,228 FDA-approved drugs, we identified a list of pyroptosis inhibitors, and mitiglinide was suggested as one of the most potent pyroptosis inhibitors in chondrocyte. Mechanistic studies demonstrated that mitiglinide may directly target Nrf2 and suppress its downstream NF-κB-driven NLRP3 inflammasome activation; it may also promote ECM homeostasis in chondrocytes. In vivo study showed that mitiglinide may effectively attenuate OA pathology in mice. Mitiglinide, identified via FDA-drug-library screening, alleviates OA progression by suppressing NLRP3 inflammasome activation and ECM degradation via activation of the Nrf2/HO-1 signaling pathway. This positions mitiglinide as a repurposed disease-modifying OA drug candidate.

PMID 41386507
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PubMedEuropean journal of clinical pharmacology2025-08-01

Efficacy and safety of insulin sensitisers for treating type 2 diabetes: a network meta-analysis.

Huang Gerile G, Li Yujie Y, Shang YuQi Y, Wang Huiduo H et al.

Thiazolidinediones (TZDs), including pioglitazone and rosiglitazone, and non-TZD insulin sensitisers (chiglitazar sodium) demonstrate potential; however, their comparative efficacy and safety remain unclear. We aimed to analyse the efficacy and safety of commonly used insulin sensitisers, including chiglitazar sodium, sitagliptin, pioglitazone, and rosiglitazone for treating type 2 diabetes mellitus (T2DM). A computer-based search was conducted in the China National Knowledge Infrastructure, Wanfang Data, the VIP database, PubMed, Embase, and Cochrane Library databases from the establishment date of each database to January 2025. Included study quality was evaluated using the Cochrane risk of bias tool. Surface under the cumulative ranking curve was calculated for each outcome indicator to compare the efficacy and safety of different interventions. In reducing haemoglobin A1c, 8 mg of rosiglitazone was superior over 100 mg sitagliptin, 30 mg pioglitazone, and 15 mg pioglitazone (P < 0.05), with no significant differences among the remaining medications. To reduce fasting plasma glucose, 45 mg of pioglitazone was more effective than any dosage of chiglitazar sodium, sitagliptin, or rosiglitazone (P < 0.05). Regarding safety, the incidence rate of adverse reactions was higher with 45 mg of pioglitazone than with 8 mg of rosiglitazone (P < 0.05), with no significant differences in adverse events among other medications. Compared with placebo, all four drugs were safe and effective in the treatment of T2DM. High-dose TZDs may be more effective than mitiglinide and sitagliptin. However, 45 mg of pioglitazone was associated with a higher incidence of adverse events, warranting close monitoring of its safety profile.

PMID 40745111
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PubMedMolecular pharmacology2025-04-06

Structural similarity-based search for glinides exhibiting cis- and trans-inhibitory activity toward uric acid transporter 1.

Sayama Misa M, Suzuki Takaaki T, Reien Yoshie Y, Miyauchi Seiji S et al.

Various types of drugs can affect serum urate levels as side effects. Although these drugs are used to treat different diseases, they might share a structural component that acts on a common target to affect urate levels. Human urate transporter 1 (URAT1) plays an essential role in urate reabsorption at the renal proximal tubule and thus might be a common target for drugs that can affect serum urate levels. Our aim was to elucidate the structural requirements for a compound to show activity toward URAT1 and to identify clinically used drugs that can affect URAT1 activity. Our search was based on structural similarities in the compounds. [14C]Urate uptake by URAT1-expressing human embryonic kidney 293 (HEK-hURAT1) cells in the presence of an analog of a small molecule with known URAT1 activity suggested that structural moieties of salicylic acid can increase URAT1 cis-inhibitory activity. Therefore, we searched a database for drugs with substructures similar to salicylic acid. We were able to predict some types of loop diuretics, statins, and angiotensin receptor blockers as drug candidates that might affect URAT1. In addition, we found that glinides inhibit urate uptake by HEK-hURAT1 cells. Three glinides (nateglinide, mitiglinide, and repaglinide) all inhibited urate uptake by HEK-hURAT1 cells concentration-dependently (IC50: nateglinide, 39 μM; mitiglinide, 63 μM; repaglinide, 3.9 μM). Furthermore, glinides also showed trans-inhibition activity in URAT1-expressing Xenopus oocytes pretreated with the glinides. These findings suggest that glinides sharing a salicylic acid-like substructure might affect serum urate level by acting on URAT1. SIGNIFICANCE STATEMENT: Some types of loop diuretics, statins, angiotensin receptor blockers, and glinides were predicted to affect URAT1, based on their chemical structural similarity to salicylic acid, the structure of which allows it to interact with URAT1. Glinides in particular showed cis- and trans-inhibitory activity toward URAT1.

PMID 40186990
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PubMedDiabetology international2024-01-24

The efficacy of switching basal-bolus insulin therapy to basal insulin-supported oral therapy with a glinide and an α-glucosidase inhibitor in patients with type 2 diabetes depends on insulin secretory capacity, but not on blood glucose profiles and insulin dosages prior to the switching.

Ando Toshihito T, Kondo Masaki M, Asada-Yamada Yuriko Y, Kawai Miyuka M et al.

We aimed to identify patients who would benefit from basal insulin-supported oral therapy (BOT) with a glinide and an α-glucosidase inhibitor (a fixed-dose combination tablet of mitiglinide 10 mg and voglibose 0.2 mg) in Japanese type 2 diabetic patients. Patients who were hospitalized to improve hyperglycemia received basal-bolus insulin therapy. After the reduction of glucose toxicity, a 75 g oral glucose tolerance test and a glucagon test were performed. Thereafter, the basal-bolus insulin therapy was switched to BOT with mitiglinide, followed by further addition of voglibose. Interstitial glucose levels were continuously monitored throughout the study period. Diurnal glucose profile was recorded and analyzed. Patients were divided into two groups according to whether their percentage of time in range (TIR, 70-180 mg/dL) under BOT with mitiglinide/voglibose was higher than 70% or not, and the differences in clinical characteristics between the groups were analyzed. Twenty patients were enrolled, and 19 of them completed the study. BOT with mitiglinide/voglibose achieved ≥ 70% of TIR in thirteen patients. The area under the curve of serum C-peptide levels during the oral glucose tolerance test was significantly higher in the patients with ≥ 70% of TIR. The daily insulin dosages and blood glucose profiles were comparable between the two groups. The efficacy of BOT with mitiglinide/voglibose depended on residual insulin secretory abilities. This therapy would be a useful therapeutic option for patients with type 2 diabetes.

PMID 38264217
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PubMedSaudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society2024-01-05

Preparation, in vitro and in vivo evaluation of a novel mitiglinide microemulsions.

Wang Miaomiao M, Li Hanghang H, Yang Wenzhi W

This study aimed to prepare an o/w mitiglinide microemulsion (MTGME) to improve the drug solubility and bioavailability. The formulation of o/w MTGME was optimized by the solubility study of drug, pseudo-ternary phase diagram and Box-Behnken design successively. MTGME was characterized by dynamic laser light scattering (DLS), zeta potential and transmission electron microscopy (TEM), moreover, the storage stability, pharmacodynamics and pharmacokinetics were investigated. The optimal prescription for MTGME consisted of Maisine 35-1 (oil), Cremophor EL (surfactant) and propylene glycol (PG, cosurfactant). MTGME with a spherical dimension of 58.1 ± 5.86 nm was stable when stored at 4 °C for 3 months. The blood glucose levers (BGL) of diabetic mice were uniformly and significantly decreased by intragastric (i.g.) administration of 1-4 mg/kg MTGME, in which BGL (i.g. 4 mg/kg MTGME) was reduced by 69% during 24 h. The pharmacokinetics study of MTGME (i.g., 20 mg/kg) in Wistar rats showed higher plasma drug concentration (Cmax, 2.9 folds), larger area under curve (AUC, 4.6 folds) and oral bioavailability than those of MTG suspensions. Generally, the MTGME (o/w) showed good effect on controlling hyperglycemia. Therefore, microemulsion can be used as an effective oral drug delivery system to improve the bioavailability of MTG.

PMID 38178852
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