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MHY-1685 Sale

(Synonyms: 5-(4-羟基亚苄基)巴比妥酸) 目录号 : GC64402

MHY-1685 is a novel mTOR inhibitor, which attenuates senescence by modulating autophagy through the inhibition of mTOR in human cardiac stem cells.

MHY-1685 Chemical Structure

Cas No.:27406-31-1

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100 mg
¥450.00
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产品描述

MHY-1685 is a novel mTOR inhibitor, which attenuates senescence by modulating autophagy through the inhibition of mTOR in human cardiac stem cells.

[1] Park JH, et al. Exp Mol Med. 2021 Sep;53(9):1423-1436.

Chemical Properties

Cas No. 27406-31-1 SDF Download SDF
别名 5-(4-羟基亚苄基)巴比妥酸
分子式 C11H8N2O4 分子量 232.19
溶解度 DMSO : 62.5 mg/mL (269.18 mM; Need ultrasonic) 储存条件 Store at -20°C
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1 mM 4.3068 mL 21.5341 mL 43.0682 mL
5 mM 0.8614 mL 4.3068 mL 8.6136 mL
10 mM 0.4307 mL 2.1534 mL 4.3068 mL
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Research Update

Human cardiac stem cells rejuvenated by modulating autophagy with MHY-1685 enhance the therapeutic potential for cardiac repair

Exp Mol Med 2021 Sep;53(9):1423-1436.PMID:34584195DOI:10.1038/s12276-021-00676-x.

Stem cell-based therapies with clinical applications require millions of cells. Therefore, repeated subculture is essential for cellular expansion, which is often complicated by replicative senescence. Cellular senescence contributes to reduced stem cell regenerative potential as it inhibits stem cell proliferation and differentiation as well as the activation of the senescence-associated secretory phenotype (SASP). In this study, we employed MHY-1685, a novel mammalian target of rapamycin (mTOR) inhibitor, and examined its long-term priming effect on the activities of senile human cardiac stem cells (hCSCs) and the functional benefits of primed hCSCs after transplantation. In vitro experiments showed that the MHY-1685‒primed hCSCs exhibited higher viability in response to oxidative stress and an enhanced proliferation potential compared to that of the unprimed senile hCSCs. Interestingly, priming MHY-1685 enhanced the expression of stemness-related markers in senile hCSCs and provided the differentiation potential of hCSCs into vascular lineages. In vivo experiment with echocardiography showed that transplantation of MHY-1685‒primed hCSCs improved cardiac function than that of the unprimed senile hCSCs at 4 weeks post-MI. In addition, hearts transplanted with MHY-1685-primed hCSCs exhibited significantly lower cardiac fibrosis and higher capillary density than that of the unprimed senile hCSCs. In confocal fluorescence imaging, MHY-1685‒primed hCSCs survived for longer durations than that of the unprimed senile hCSCs and had a higher potential to differentiate into endothelial cells (ECs) within the infarcted hearts. These findings suggest that MHY-1685 can rejuvenate senile hCSCs by modulating autophagy and that as a senescence inhibitor, MHY-1685 can provide opportunities to improve hCSC-based myocardial regeneration.