MHY1485mTOR activator, autophage inhibitor CAS# 326914-06-1 |
- MTEP hydrochloride
Catalog No.:BCC1780
CAS No.:1186195-60-7
- LY341495
Catalog No.:BCC1724
CAS No.:201943-63-7
- MPEP Hydrochloride
Catalog No.:BCC1777
CAS No.:219911-35-0
- CPPHA
Catalog No.:BCC1501
CAS No.:693288-97-0
- Dipraglurant
Catalog No.:BCC1531
CAS No.:872363-17-2
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 326914-06-1 | SDF | Download SDF |
| PubChem ID | 2834965 | Appearance | Powder |
| Formula | C17H21N7O4 | M.Wt | 387.39 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Solubility | DMSO : 9.5 mg/mL (24.52 mM; Need ultrasonic and warming); | ||
| Chemical Name | 4,6-dimorpholin-4-yl-N-(4-nitrophenyl)-1,3,5-triazin-2-amine | ||
| SMILES | C1COCCN1C2=NC(=NC(=N2)NC3=CC=C(C=C3)[N+](=O)[O-])N4CCOCC4 | ||
| Standard InChIKey | MSSXBKQZZINCRI-UHFFFAOYSA-N | ||
| Standard InChI | InChI=1S/C17H21N7O4/c25-24(26)14-3-1-13(2-4-14)18-15-19-16(22-5-9-27-10-6-22)21-17(20-15)23-7-11-28-12-8-23/h1-4H,5-12H2,(H,18,19,20,21) | ||
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
||
| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
||
| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
MHY1485 Dilution Calculator
MHY1485 Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 2.5814 mL | 12.9069 mL | 25.8138 mL | 51.6276 mL | 64.5344 mL |
| 5 mM | 0.5163 mL | 2.5814 mL | 5.1628 mL | 10.3255 mL | 12.9069 mL |
| 10 mM | 0.2581 mL | 1.2907 mL | 2.5814 mL | 5.1628 mL | 6.4534 mL |
| 50 mM | 0.0516 mL | 0.2581 mL | 0.5163 mL | 1.0326 mL | 1.2907 mL |
| 100 mM | 0.0258 mL | 0.1291 mL | 0.2581 mL | 0.5163 mL | 0.6453 mL |
| * Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. | |||||
Calcutta University
University of Minnesota
University of Maryland School of Medicine
University of Illinois at Chicago
The Ohio State University
University of Zurich
Harvard University
Colorado State University
Auburn University
Yale University
Worcester Polytechnic Institute
Washington State University
Stanford University
University of Leipzig
Universidade da Beira Interior
The Institute of Cancer Research
Heidelberg University
University of Amsterdam
University of Auckland
TsingHua University
The University of Michigan
Miami University
DRURY University
Jilin University
Fudan University
Wuhan University
Sun Yat-sen University
Universite de Paris
Deemed University
Auckland University
The University of Tokyo
Korea University
MHY1485 is a potent mTOR activator that inhibits autophagy with suppression of fusion between autophagosomes and lysosomes. [1]
mTOR (mechanistic target of rapamycin) is a serine/threonine kinase that regulates cellular metabolism, growth ad survival. It mediates the cellular response to stress, growth factor and hormone etc. Inhibition of mTOR strongly induced autophagy. mTOR signaling also plays a role in the promotion of ovarian follicle development.
In Ac2F rat hepatocytes, MHY1485 treatment suppresses the basal autophagic flux, and it also shows inhibitory effect under cell starvation which is an inducer of autophagy. The effects of MHY1485 dose-and time- dependently cause accumulation of LC3II and enlargement of the autophagosomes. [1]
Ovaries of juvenile mice cultured with MHY1485 for 4 days increases ovarian explant weights and follicle development. 2 days pre-incubation of these ovaries with MHY1485 followed by allo-grafting into kidney capsules of adult ovariectomized hosts for 5 days, shows apparent increases in graft weights and promotion of follicle development. [2]
References:
1, Choi YJ, Park YJ, Park JY et al. Inhibitory effect of mTOR activator MHY1485 on
autophagy: suppression of lysosomal fusion. PLoS One. 2012;7(8):e43418. doi:
10. 1371/journal.pone.0043418. Epub 2012 Aug 22. Erratum in: PLoS One. 2013;8(1).
2, Cheng Y, Kim J, Li XX, Hsueh AJ. Promotion of ovarian follicle growth
following mTOR activation: synergistic effects of AKT stimulators. PLoS One. 2015
Feb 24;10(2):e0117769.
- Shz 1
Catalog No.:BCC6334
CAS No.:326886-05-9
- FAAH inhibitor 1
Catalog No.:BCC4254
CAS No.:326866-17-5
- Edpetiline
Catalog No.:BCN6771
CAS No.:32685-93-1
- H-Glu(OtBu)-OtBu.HCl
Catalog No.:BCC2934
CAS No.:32677-01-3
- Mesoridazine Besylate
Catalog No.:BCC3975
CAS No.:32672-69-8
- Fraxamoside
Catalog No.:BCN5247
CAS No.:326594-34-7
- Boc-Ser-OH
Catalog No.:BCC3439
CAS No.:3262-72-4
- Oleuropein
Catalog No.:BCN5246
CAS No.:32619-42-4
- Kaempferol 3-neohesperidoside
Catalog No.:BCN5245
CAS No.:32602-81-6
- GRI 977143
Catalog No.:BCC2401
CAS No.:325850-81-5
- BPIPP
Catalog No.:BCC7730
CAS No.:325746-94-9
- Indiplon
Catalog No.:BCC7720
CAS No.:325715-02-4
- H-Nle-OH
Catalog No.:BCC3295
CAS No.:327-57-1
- Chlorogenic acid
Catalog No.:BCN5906
CAS No.:327-97-9
- TCS-PIM-1-4a
Catalog No.:BCC5461
CAS No.:327033-36-3
- TDZD-8
Catalog No.:BCC4258
CAS No.:327036-89-5
- VU 0285683
Catalog No.:BCC6154
CAS No.:327056-22-4
- Cyclohexanecarboxylic acid
Catalog No.:BCN3443
CAS No.:98-89-5
- tcY-NH2
Catalog No.:BCC5770
CAS No.:327177-34-4
- Heliosupine
Catalog No.:BCN1980
CAS No.:32728-78-2
- Phorbol 13-acetate
Catalog No.:BCN7231
CAS No.:32752-29-7
- Macrocarpal L
Catalog No.:BCN5248
CAS No.:327601-97-8
- BIO 5192
Catalog No.:BCC8002
CAS No.:327613-57-0
- Macrocarpal O
Catalog No.:BCN7371
CAS No.:327622-65-1
MHY1485 activates mTOR and protects osteoblasts from dexamethasone.[Pubmed:27884298]
Biochem Biophys Res Commun. 2016 Dec 9;481(3-4):212-218.
Dexamethasone (Dex) exerts cytotoxic effects to cultured osteoblasts. The potential effect of MHY1485, a small-molecular mammalian target of rapamycin (mTOR) activator, against the process was studied here. In both osteoblastic MC3T3-E1 cells and primary murine osteoblasts, treatment with MHY1485 significantly ameliorated Dex-induced cell death and apoptosis. mTOR inhibition, through mTOR kinase inhibitor OSI-027 or mTOR shRNAs, abolished MHY1485-mediated osteoblast cytoprotection against Dex. Intriguingly, activation of mTOR complex (mTORC1), but not mTORC2, is required for MHY1485's anti-Dex activity. mTORC1 inhibitors (rapamycin and RAD001) or Raptor knockdown almost reversed MHY1485-induced osteoblast cytoprotection. mTORC2 inhibition, via shRNA knockdown of Rictor, failed to affect MHY1485's activity in MC3T3-E1 cells. Further studies showed that MHY1485 treatment in MC3T3-E1 cells and primary murine osteoblasts significantly inhibited Dex-induced mitochondrial death pathway activation, the latter was tested by mitochondrial depolarization, cyclophilin D-ANT-1 association and cytochrome C cytosol release. Together, these results suggest that MHY1485 activates mTORC1 signaling to protect osteoblasts from Dex.
MHY1485 ameliorates UV-induced skin cell damages via activating mTOR-Nrf2 signaling.[Pubmed:28061443]
Oncotarget. 2017 Feb 21;8(8):12775-12783.
Ultra Violet (UV)-caused skin cell damage is a main cause of skin cancer. Here, we studied the activity of MHY1485, a mTOR activator, in UV-treated skin cells. In primary human skin keratinocytes, HaCaT keratinocytes and human skin fibroblasts, MHY1485 ameliorated UV-induced cell death and apoptosis. mTOR activation is required for MHY1485-induced above cytoprotective actions. mTOR kinase inhibitors (OSI-027, AZD-8055 and AZD-2014) or mTOR shRNA knockdown almost abolished MHY1485-induced cytoprotection. Further, MHY1485 treatment in skin cells activated mTOR downstream NF-E2-related factor 2 (Nrf2) signaling, causing Nrf2 Ser-40 phosphorylation, stabilization/upregulation and nuclear translocation, as well as mRNA expression of Nrf2-dictated genes. Contrarily, Nrf2 knockdown or S40T mutation almost nullified MHY1485-induced cytoprotection. MHY1485 suppressed UV-induced reactive oxygen species production and DNA single strand breaks in skin keratinocytes and fibroblasts. Together, we conclude that MHY1485 inhibits UV-induced skin cell damages via activating mTOR-Nrf2 signaling.
Inhibitory effect of mTOR activator MHY1485 on autophagy: suppression of lysosomal fusion.[Pubmed:22927967]
PLoS One. 2012;7(8):e43418.
Autophagy is a major degradative process responsible for the disposal of cytoplasmic proteins and dysfunctional organelles via the lysosomal pathway. During the autophagic process, cells form double-membraned vesicles called autophagosomes that sequester disposable materials in the cytoplasm and finally fuse with lysosomes. In the present study, we investigated the inhibition of autophagy by a synthesized compound, MHY1485, in a culture system by using Ac2F rat hepatocytes. Autophagic flux was measured to evaluate the autophagic activity. Autophagosomes were visualized in Ac2F cells transfected with AdGFP-LC3 by live-cell confocal microscopy. In addition, activity of mTOR, a major regulatory protein of autophagy, was assessed by western blot and docking simulation using AutoDock 4.2. In the result, treatment with MHY1485 suppressed the basal autophagic flux, and this inhibitory effect was clearly confirmed in cells under starvation, a strong physiological inducer of autophagy. The levels of p62 and beclin-1 did not show significant change after treatment with MHY1485. Decreased co-localization of autophagosomes and lysosomes in confocal microscopic images revealed the inhibitory effect of MHY1485 on lysosomal fusion during starvation-induced autophagy. These effects of MHY1485 led to the accumulation of LC3II and enlargement of the autophagosomes in a dose- and time-dependent manner. Furthermore, MHY1485 induced mTOR activation and correspondingly showed a higher docking score than PP242, a well-known ATP-competitive mTOR inhibitor, in docking simulation. In conclusion, MHY1485 has an inhibitory effect on the autophagic process by inhibition of fusion between autophagosomes and lysosomes leading to the accumulation of LC3II protein and enlarged autophagosomes. MHY1485 also induces mTOR activity, providing a possibility for another regulatory mechanism of autophagy by the MHY compound. The significance of this study is the finding of a novel inhibitor of autophagy with an mTOR activating effect.
