MHY1485

Catalog No.S7811 Batch:S781102

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Technical Data

Formula

C17H21N7O4
Molecular Weight 387.39 CAS No. 326914-06-1
Solubility (25°C)* In vitro DMSO 3.75 mg/mL (9.68 mM)
Water Insoluble
Ethanol Insoluble
In vivo (Add solvents to the product individually and in order)
Homogeneous suspension
CMC-NA
≥5mg/ml Taking the 1 mL working solution as an example, add 5 mg of this product to 1 ml of CMC-Na solution, mix evenly to obtain a homogeneous suspension with a final concentration of 5 mg/ml.
* <1 mg/ml means slightly soluble or insoluble.
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.
* Room temperature shipping (Stability testing shows this product can be shipped without any cooling measures.)

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Biological Activity

Description MHY1485 is a potent, and cell-permeable mTOR activator, and also potently inhibits autophagy.
Targets
mTOR [1]
In vitro

MHY1485 suppresses the basal autophagic flux. MHY1485 causes the accumulation of LC3II and enlargement of the autophagosomes in a dose- and time- dependent manner.[1]

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.[2]
In vivo

MHY1485 is a potent, and cell-permeable mTORC1 agonist.

Protocol (from reference)

Kinase Assay:

[1]
  • Activation of mTOR

    Western blot analysis is performed to detect the change of total protein level and levels of phosphorylated forms of mTOR and 4E-BP1 reflecting the activity of mTOR. Ac2F cells are treated with MHY1485 of different concentrations and rapamycin 5 mM as a positive control for 1 h. Cells are washed with cold PBS and harvested. Cell lysates are prepared using RIPA buffer. Protein concentration is determined by the bicinchoninic acid (BCA) method. Equal amounts of protein are separated on 10-12% sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) gels. The gels are subsequently transferred onto a polyvinylidene difluoride membrane by electroblotting for 2 h at 60-75 V. The membranes are blocked in a 5% nonfat milk solution in Tris-buffered saline (TBS) with 0.5% Tween-20, and incubated with primary antibodies. Pre-stained protein markers are used for molecular-weight determination.
Cell Assay:

[3]
  • Cell lines

    TU177 cells

  • Concentrations

    10 µM

  • Incubation Time

    24 h

  • Method

    Cells were treated with indicated concentration of drug for 24 h.

References

  • https://pubmed.ncbi.nlm.nih.gov/22927967/
  • https://pubmed.ncbi.nlm.nih.gov/25710488/
  • https://pubmed.ncbi.nlm.nih.gov/36438491/
  • https://pubmed.ncbi.nlm.nih.gov/34580888/

Customer Product Validation

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.

Data from [ , , FASEB J, 2018, 32(1):512-528 ]

Phosphorylation level of mTOR detected by western blot.

Data from [ , , Int J Biol Sci, 2017, 13(11):1398-1408 ]

MYH1485, an activator of mTOR, reduced LC3II production and inhibited autophagosome formation in PAR2-knockdown cells.

Data from [ , , Biochem J, 2017, 474(16):2733-2747 ]

The HO8910‑shLSD1 cells were treated with 10 μΜ mTOR specific activator MHY1485 for the indicated time‑points. The expression of p‑p70S6K and p70S6K was detected via western blot analysis.

Data from [ , , Oncol Rep, 2018, 40(1):425-433 ]

Selleck's MHY1485 has been cited by 99 publications

Metformin attenuates alveolar bone destruction in mice with apical periodontitis and inhibits pro-inflammatory cytokine synthesis in lipopolysaccharide-stimulated RAW264.7 through the AMPK-mTOR-NF-κB pathway [ Front Immunol, 2025, 16:1643676] PubMed: 40821823
Natural polyphenol mangiferin delays neuronal cell senescence by inhibiting neuroinflammation mediated by microglial activation [ IBRO Neurosci Rep, 2025, 18:574-591] PubMed: 40271493
Targeted knockdown of PGAM5 in synovial macrophages efficiently alleviates osteoarthritis [ Bone Res, 2024, 12(1):15] PubMed: 38433252
Augmented ERO1α upon mTORC1 activation induces ferroptosis resistance and tumor progression via upregulation of SLC7A11 [ J Exp Clin Cancer Res, 2024, 43(1):112] PubMed: 38610018
Gestational exposure to PM2.5 disrupts fetal development by suppressing placental trophoblast syncytialization via progranulin/mTOR signaling [ Sci Total Environ, 2024, 921:171101] PubMed: 38387595
Multi-omics analyses of cancer-linked clinical salmonellae reveal bacterial-induced host metabolic shift and mTOR-dependent cell transformation [ Cell Rep, 2024, 43(11):114931] PubMed: 39488829
Toosendanin alleviates acute lung injury by reducing pulmonary vascular barrier dysfunction mediated by endoplasmic reticulum stress through mTOR [ Phytomedicine, 2024, 136:156277] PubMed: 39615214
Tetrahydrocurcumin ameliorates hepatic steatosis by restoring hepatocytes lipophagy through mTORC1-TFEB pathway in nonalcoholic steatohepatitis [ Biomed Pharmacother, 2024, 178:117297] PubMed: 39137653
Adenosine kinase protects against acetaminophen-induced acute liver injury by activating autophagy in hepatocytes [ Cell Biol Toxicol, 2024, 40(1):59] PubMed: 39060559
Polyphyllin I alleviates neuroinflammation after cerebral ischemia-reperfusion injury via facilitating autophagy-mediated M2 microglial polarization [ Mol Med, 2024, 30(1):59] PubMed: 38745316

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SHIPPING AND STORAGE
Selleck products are transported at room temperature. If you receive the product at room temperature, please rest assured, the Selleck Quality Inspection Department has conducted experiments to verify that the normal temperature placement of one month will not affect the biological activity of powder products. After collecting, please store the product according to the requirements described in the datasheet. Most Selleck products are stable under the recommended conditions.

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