Mitochondrial fusion promoter M1
目录号 : GC50600
Mitochondrial fusion promoter M1是一种具有细胞渗透性的苯腙类化合物，能有效促进线粒体融合。
Cas No.:219315-22-7
Sample solution is provided at 25 µL, 10mM.
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Mitochondrial fusion promoter M1, a cell-permeable phenylhydrazone, effectively promotes mitochondrial fusion[1]. Mitochondrial fusion promoter M1 exerts anti-inflammatory and antioxidant effects by regulating mitochondrial function and blocking the PI3K-AKT signaling pathway[2]. Mitochondrial fusion promoter M1 has been widely used in cell models to enhance the complementary mitochondrial metabolism[3].
In vitro, Mitochondrial fusion promoter M1 treatment for 24 hours induced the elongation of mitochondria in mitofusin 1-knockout mouse embryonic fibroblast (MEF) cells and mitofusin 2-knockout MEF cells, with EC50 values of 5.3μM and 4.42μM, respectively[4]. Treatment with 20μM of the Mitochondrial fusion promoter M1 for 3 days reduced the susceptibility of Jurkat cells to HIV infection, resulting in an increase in the oxygen consumption rate (OCR) of the cells and a decrease in the extracellular acidification rate (ECAR)[5]. Mitochondrial fusion promoter M1 treatment (1μM; 12h) alleviated the mitochondrial damage and fusion inhibition in triphenyl phosphate (TPHP)-induced TM3 cells, reducing the decline in cell viability and the increase in apoptosis rate induced by TPHP[6].
In vivo, Mitochondrial fusion promoter M1 treatment via continuous intraperitoneal injection at a dose of 2mg/kg/day for 6 weeks significantly promoted mitochondrial fusion in the heart tissue of diabetic rats, and weakened the decrease in the expression of optic nerve atrophy 1 (Opa1), alleviated oxidative stress, improved mitochondrial function, and alleviated dilated cardiomyopathy (DCM) in diabetic rats[7]. Intravenous injection of a single dose of Mitochondrial fusion promoter M1 (2mg/kg) 15 minutes before cardiac ischemia/reperfusion (I/R) injury alleviated the brain mitochondrial dysfunction, blood-brain barrier disruption, macrophage infiltration, apoptosis and the expression of Alzheimer's disease-related proteins in rats following cardiac I/R injury[8].
References:
[1] Asalla S, Girada S B, Kuna R S, et al. Restoring mitochondrial function: a small molecule-mediated approach to enhance glucose stimulated insulin secretion in cholesterol accumulated pancreatic beta cells[J]. Scientific Reports, 2016, 6(1): 27513.
[2] Zeng T, Liu L, Xu D, et al. The mitochondrial fusion promoter M1 mitigates cigarette smoke-induced airway inflammation and oxidative stress via the PI3K-AKT signaling pathway[J]. Lung, 2025, 203(1): 12.
[3] Yang L, Long Q, Liu J, et al. Mitochondrial fusion provides an ‘initial metabolic complementation’controlled by mtDNA[J]. Cellular and Molecular Life Sciences, 2015, 72(13): 2585-2598.
[4] Wang D, Wang J, Bonamy G M C, et al. A small molecule promotes mitochondrial fusion in mammalian cells[J]. Angewandte Chemie International Edition, 2012, 51(37): 9302-9305.
[5] Song Z, Wang J, Zheng Z, et al. Mitochondrial fusion reduces T cell susceptibility to HIV infection through citrate modulation[J]. Journal of Leukocyte Biology, 2025, 117(5): qiaf042.
[6] Wang M, Xu J, Zhao Z, et al. Triphenyl phosphate induced apoptosis of mice testicular Leydig cells and TM3 cells through ROS-mediated mitochondrial fusion inhibition[J]. Ecotoxicology and Environmental Safety, 2023, 256: 114876.
[7] Ding M, Liu C, Shi R, et al. Mitochondrial fusion promoter restores mitochondrial dynamics balance and ameliorates diabetic cardiomyopathy in an optic atrophy 1‐dependent way[J]. Acta Physiologica, 2020, 229(1): e13428.
[8] Surinkaew P, Apaijai N, Sawaddiruk P, et al. Mitochondrial fusion promoter alleviates brain damage in rats with cardiac ischemia/reperfusion injury[J]. Journal of Alzheimer’s Disease, 2020, 77(3): 993-1003.
Mitochondrial fusion promoter M1是一种具有细胞渗透性的苯腙类化合物，能有效促进线粒体融合[1]。Mitochondrial fusion promoter M1通过调节线粒体功能并阻断PI3K-AKT信号通路，发挥抗炎和抗氧化作用[2]。Mitochondrial fusion promoter M1已在细胞模型中广泛用于增强互补性线粒体代谢[3]。
在体外，在体外，Mitochondrial fusion promoter M1处理 24 小时诱导mitofusin 1敲除小鼠胚胎成纤维细胞（MEF）和mitofusin 2敲除MEF细胞的线粒体伸长，EC50值分别为5.3μM和4.42μM[4]。用20μM的Mitochondrial fusion promoter M1处理3天降低了Jurkat细胞对HIV感染的易感性，导致细胞耗氧率（OCR）增加和细胞外酸化率（ECAR）降低[5]。Mitochondrial fusion promoter M1处理（1μM；12小时）减轻了triphenyl phosphate（TPHP）诱导的TM3细胞中的线粒体损伤和融合抑制，减少了TPHP诱导的细胞活力下降和凋亡率增加[6]。
在体内，Mitochondrial fusion promoter M1以2mg/kg/day的剂量连续腹腔注射 6 周，显著促进了糖尿病大鼠心脏组织中的线粒体融合，减弱了optic nerve atrophy 1（Opa1）表达的下降，减轻了氧化应激，改善了线粒体功能，并缓解了糖尿病大鼠的扩张型心肌病（DCM）[7]。在心脏缺血/再灌注（I/R）损伤前15 分钟静脉注射单剂量的Mitochondrial fusion promoter M1（2mg/kg）缓解了心脏I/R损伤后大鼠的脑线粒体功能障碍、血脑屏障破坏、巨噬细胞浸润、细胞凋亡和阿尔茨海默病相关蛋白的表达[8]。
| Cell experiment [1]: | |
Cell lines | TM3 cells |
Preparation Method | TM3 cells were cultured in DMEM/F-12 medium containing 5% horse serum, 2.5% fetal bovine serum and 1% penicillin-streptomycin at 37°C in a humidified incubator with 5% CO₂. TM3 cells (5×105) were seeded in 6-well plates. After the TM3 cells reached 80-85% confluence, they were treated with TPHP (100μM) only, TPHP (100μM) and Mitochondrial fusion promoter M1 (1μM), respectively. TM3 cells were pre-treated with Mitochondrial fusion promoter M1 for 12 hours and then incubated with TPHP for 24 hours. The apoptosis and mitochondrial status of the cells were analyzed. |
Reaction Conditions | 1μM; 12h |
Applications | Mitochondrial fusion promoter M1 treatment alleviated the mitochondrial damage and fusion inhibition in TPHP-induced TM3 cells, reducing the decline in cell viability and the increase in apoptosis rate induced by TPHP. |
| Animal experiment [2]: | |
Animal models | Male Sprague-Dawley rats |
Preparation Method | Male Sprague-Dawley rats aged 6-8 weeks were housed in an environment with a temperature controlled at 22±2°C and a 12-hour light/12-hour dark cycle. Diabetes was induced by a single intraperitoneal injection of streptozotocin (STZ; 65mg/kg). Seven weeks after the injection of the vehicle or STZ, the control group and the diabetic group rats were respectively treated with intraperitoneal injections of the vehicle or the Mitochondrial fusion promoter M1 (2mg/kg/day) for 6 weeks. The rat heart tissues were collected for analysis. |
Dosage form | 2mg/kg/day for 6 weeks; i.p. |
Applications | Mitochondrial fusion promoter M1 treatment significantly promoted mitochondrial fusion, and alleviated myocardial hypertrophy and fibrosis in the hearts of diabetic rats. |
References: | |
| Cas No. | 219315-22-7 | SDF | |
| Canonical SMILES | C\C(=N/NC1=C(Cl)C=C(Cl)C=C1Cl)C1=C(O)C=CC(Cl)=C1 | ||
| 分子式 | C14H10Cl4N2O | 分子量 | 364.05 |
| 溶解度 | DMSO : 41.67 mg/mL (114.46 mM; ultrasonic and warming and heat to 60°C) | 储存条件 | Store at -20°C |
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.7469 mL | 13.7344 mL | 27.4688 mL |
| 5 mM | 549.4 μL | 2.7469 mL | 5.4938 mL |
| 10 mM | 274.7 μL | 1.3734 mL | 2.7469 mL |
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