Molecular Weight(MW): 387.39
MHY1485 is a potent, and cell-permeable mTOR activator, and also potently inhibits autophagy.
Cited by 9 Publications
5 Customer Reviews
Exosomal miR-124-3p inhibited neuronal inflammation by suppressing the activity of mTOR signaling. A, B) Immunoblot (A) and quantitative (B) data of p-4E-BP1 and p-P70S6K in neurons after scratch injury and exosomal treatment. Their expression was increased after scratch injury and was suppressed by miR-124-3p–up-regulated exosomes, suggesting that miR-124-3p suppresses the activity of mTOR signaling (n = 6/group). ##P < 0.01 vs. control group; **P < 0.01 vs. injury group. C) Expression levels of inflammatory mediators in the culture medium were detected in the 3 groups of neurons: injured neurons (injury group), injured neurons treated with miR-124-3p–up-regulated exosomes (I+Exo-124), and injured neurons treated with miR-124-3p-up-regulated exosomes and the mTOR activator (MHY1485). Compared with the I+Exo-124 group, the MHY1485 group represented an increased expression on proinflammatory cytokines (TNF-α, IL-1β, and IL-6) and a decreased expression of anti-inflammatory cytokines (IL-10), suggesting that MHY1485 blocks the anti-inflammatory effect of miR-124-3p in injured neurons. Thus, the inhibitory effect of exosomal miR-124-3p on neuronal inflammation was exerted by suppressing the activity of mTOR signaling (n = 6/group). #P < 0.05 vs. injury group; *P < 0.05 vs. I+Exo-124 group.
FASEB J, 2018, 32(1):512-528. MHY1485 purchased from Selleck.
MYH1485, an activator of mTOR, reduced LC3II production and inhibited autophagosome formation in PAR2-knockdown cells.
Biochem J, 2017, 474(16):2733-2747. MHY1485 purchased from Selleck.
Effects of liraglutide treatments and AMPK inhibitor/mTOR activator on matrix mineralization and relative protein levels of Alp, OC, p‑AMPK, p‑mTOR and TGF‑β. Following culture in commercial osteogenic differentiation medium for 14 days, MC3T3‑E1 cells were cultured for a further 14 days in basal culture medium with 4 nM liraglutide, and 4 nM liraglutide plus AMPK inhibitor, 10 μM compound C, or 1 μM mTOR activator, MHY1485. MC3T3‑E1 cells maintained in DMEM for 28 days with no treatment were used as the NC;cells cultured in the commercial osteogenic differentiation medium for 14 days and in DMEM without liraglutide for a further 14 days were used as the PC. (B) Relative protein expression was analyzed by western blot and quantifi ed relative to GAPDH (n=5). Data are presented as the mean ± standard error. Bars with letters means they signifi cantly differ with positive control (P<0.05). *P<0.05, **P<0.05 vs. NC; #P<0.05, ##P<0.01 vs. PC. NC, negative control; PC, positive control; Alp, alkaline phosphatase; OC, osteocalcin; p‑, phosphorylated; AMPK, adenosine monophosphate‑activated protein kinase; mTOR, mechanistic target of rapamycin; TGF‑β, transforming growth factor‑β; GAPDH, glyceraldehyde 3‑phosphate dehydrogenase.
Mol Med Rep, 2016, 14(4):3662-8.. MHY1485 purchased from Selleck.
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|Description||MHY1485 is a potent, and cell-permeable mTOR activator, and also potently inhibits autophagy.|
MHY1485 suppresses the basal autophagic flux. MHY1485 causes the accumulation of LC3II and enlargement of the autophagosomes in a dose- and time- dependent manner. MHY1485 increases phospho-mTOR levels and phosphorylation of downstream S6K1 and rpS6 proteins without affecting total mTOR content, total S6K1 and rpS6 levels. Short-term treatment of ovaries with MHY1485 followed by allo-transplantation promoted secondary follicle growth. Treatment with MHY1485 and subsequent grafting allowed the derivation of mature oocytes and healthy offspring.
|In vitro||DMSO||4 mg/mL (10.32 mM)|
|In vivo||Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
5% DMSO+40% PEG 300+5% Tween 80+ddH2O
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