YM-1 tosylate
Based on 1 publication(s) in Google Scholar
YM-1 tosylate is a stable MKT-077 (HY-15096) analog and an orally active Hsp70 inhibitor. YM-1 tosylate induces cell death of HeLa cells and up-regulates the level of p53 and p21 proteins.
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- CAS No.: 1427450-47-2
- Formula: C27H27N3O4S3
- Molecular Weight:553.72
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications Citing Use of MedChemExpress (MCE) YM-1 tosylate
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Biological Activity
Description
IC50 & Target
[1]|
HSP70 3.2 μM (IC50) |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| FM3A | EC50 |
1.1 x 10-5M
Compound: 8d
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Cytotoxicity against mouse mammary tumor FM3A cells representing a model of host
Cytotoxicity against mouse mammary tumor FM3A cells representing a model of host
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[PMID: 11855978] |
In Vitro
YM-1 tosylate promotes Hsp70-dependent steps in nNOS maturation and partially blocks formation of the ATP-bound form[1]. YM-1 (0-200 μM) tosylate activates the binding of Hsp70 to its unfolded substrate[1]. YM-1 (0.001-1000 μM) tosylate converts Hsp70 to its tight-affinity conformation and shows binding efficacy to Hsp70 with an IC50 value of 8.2 μM[1]. YM-1 (0, 0.1, 0.5 and 1 μM; 24 hours) tosylate promotes nNOS ubiquitination[1]. YM-1 (5 and 10 μM; 24 and 48 hours) tosylate induces cell death of HeLa cells and growth arrest of hTERT-RPE1 cells[2]. YM-1 (10 μM; 48 hours) tosylate up-regulates p53 and p21 proteins and down-regulates FoxM1 and survivin[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:MCF7, MCF10A and MDA-MB-231
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Concentration:0-30 μM
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Incubation Time:72 h
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Result:Inhibited viability with EC50s of 2.0 ± 0.2, 3.3 ± 0.3 and 5.2 ± 0.8 μM for MDA-MB-231, MCF10A and MCF7, respectively.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:CD1 mice[1]
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Dosage:20 mg/kg
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Administration:Intravenous injection (Pharmacokinetic Analysis)
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Result:Initial pharmacokinetics of HSP70-IN-4 (Compound YM-01; 20 mg/kg; i.v.)[1]
hour plasma (ng/mL) brain (ng/g) kidney (ng/g) 0.16 359 0 74378 1 324 0 63231
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Animal Model:UAS-hAR52Q flies with polyQ AR-induced dihydrotestosterone (DHT) phenotype[1]
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Dosage:1 mM
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Administration:Oral administration; 1 mM, for 7 days
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Result:Weakened the DHT-dependent eye degeneration phenotype and rescued DHT-dependent pupal toxicity of the polyQ AR.
Chemical Information
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CAS No. 1427450-47-2
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Molecular Weight 553.72
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Formula C27H27N3O4S3
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SMILES
CN(C1=CC=CC=C1S/2)C2=C3C(N(CC)/C(S\3)=C/C4=[N+](C)C=CC=C4)=O.[O-]S(=O)(C5=CC=C(C)C=C5)=O
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications (1)
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Journal Impact Factor
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Most Recent
Protocols
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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Mammalian live/dead viability and cytotoxicity staining
Live/dead viability and cytotoxicity staining assays are based on the simultaneous detection of intracellular esterase activity in metabolically active (viable) cells and membrane integrity loss in non-viable cells. In commonly used dual-staining approaches, membrane-permeant fluorogenic substrates are converted by intracellular esterases into fluorescent products in live cells, while impermeant DNA-binding dyes selectively enter cells with compromised plasma membranes and label nucleic acids in dead or dying cells, enabling discrimination between viable and non-viable populations by fluorescence microscopy or flow cytometry.
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Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)