Resminostat (RAS2410)Potent HDAC inhibitor CAS# 864814-88-0 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 864814-88-0 | SDF | Download SDF |
| PubChem ID | 11609955 | Appearance | Powder |
| Formula | C16H19N3O4S | M.Wt | 349.4 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Synonyms | RAS2410; 4SC-201 | ||
| Solubility | Soluble in DMSO > 10 mM | ||
| Chemical Name | (E)-3-[1-[4-[(dimethylamino)methyl]phenyl]sulfonylpyrrol-3-yl]-N-hydroxyprop-2-enamide | ||
| SMILES | CN(C)CC1=CC=C(C=C1)S(=O)(=O)N2C=CC(=C2)C=CC(=O)NO | ||
| Standard InChIKey | FECGNJPYVFEKOD-VMPITWQZSA-N | ||
| Standard InChI | InChI=1S/C16H19N3O4S/c1-18(2)11-13-3-6-15(7-4-13)24(22,23)19-10-9-14(12-19)5-8-16(20)17-21/h3-10,12,21H,11H2,1-2H3,(H,17,20)/b8-5+ | ||
| 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. |
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| 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. |
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| 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. | ||
| Description | Resminostat is a potent inhibitor of HDAC1, HDAC3 and HDAC6, with mean IC50 values of 42.5, 50.1, 71.8 nM, respectively, and shows less potent activities against HDAC8, with an IC50 of 877 nM.In Vitro:Resminostat hydrochloride (Resminostat [HCl], 5 μM) induces histone acetylation in myeloma cells. Resminostat hydrochloride displays a substrate competitive binding mode with a mean Ki value of 27 nM. Resminostat hydrochloride (5 μM) induces histone hyperacetylation in myeloma cells. Resminostat inhibits cell growth, induces apoptosis and inhibits MM cell proliferation. Resminostat (5 μM) also modulates expression of bcl-2 family proteins and inhibits Akt pathway signalling downstream of Akt. Resminostat exerts synergistic activity against myeloma cells when combined with common and new anti-myeloma agents[1]. Resminostat inhibits cell growth in head and neck squamous cell carcinoma cell lines, with IC50s ranging from 0.775 μM to 1.572 μM (IC50 for SCC25: 0.775 μM; CAL27: 1.572 μM; and FaDu: 0.899 μM). Resminostat (1.25 and 2.5 μM) has a synergistic effect with irradiation on HNSCC cell lines. Resminostat in combination with cisplatin induces a downregulation of survivin. However, Resminostat shows no effect on Mcl-1 and p-AKT expression[2]. Resminostat reduces viability of HCC cells with the co-treatment of AZD-2014, with IC50s ranging from 0.89 ± 0.12 μM to 0.07 ± 0.01 μM[3]. References: | |||||
Resminostat (RAS2410) Dilution Calculator
Resminostat (RAS2410) Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 2.862 mL | 14.3102 mL | 28.6205 mL | 57.241 mL | 71.5512 mL |
| 5 mM | 0.5724 mL | 2.862 mL | 5.7241 mL | 11.4482 mL | 14.3102 mL |
| 10 mM | 0.2862 mL | 1.431 mL | 2.862 mL | 5.7241 mL | 7.1551 mL |
| 50 mM | 0.0572 mL | 0.2862 mL | 0.5724 mL | 1.1448 mL | 1.431 mL |
| 100 mM | 0.0286 mL | 0.1431 mL | 0.2862 mL | 0.5724 mL | 0.7155 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. | |||||
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Resminostat, also known as RAS2410, is a potent inhibitor of histone deacetylase (HDAC) classes I and II (including HDAC1, HDAC3 and HDAC6) with 50% inhibition concentration IC50 values ranging from 43 to 72 nmol/L. Resminostate has the potential to be used for the treatment of multiple myeloma (MM) due to its ability to induce histone H4 hyperacetylation, and apoptosis (IC50 ranging from 2.5 to 3 μmol/L) in MM cells. Recent study results have shown that, in MM cell lines, resminostat abrogates cell growth, suppresses proliferation and induce G0/G1 cell cycle arrest as well as interfering with Akt signaling pathway by decreasing phosphorylation of 4E-BP1 and p70S6k.
Reference
Mandl-Weber S, Meinel FG, Jankowsky R, Oduncu F, Schmidmaier R, Baumann P. The novel inhibitor of histone deacetylase resminostat (RAS2410) inhibits proliferation and induces apoptosis in multiple myeloma (MM) cells. Br J Haematol. 2010; 149(4):518-528.
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The novel inhibitor of histone deacetylase resminostat (RAS2410) inhibits proliferation and induces apoptosis in multiple myeloma (MM) cells.[Pubmed:20201941]
Br J Haematol. 2010 May;149(4):518-28.
Inhibition of histone deacetylase (HDAC) is a promising mechanism for novel, anti-myeloma agents. We investigated the effects of the novel HDAC inhibitor resminostat on multiple myeloma (MM) cells in vitro. Resminostat is a potent inhibitor of HDACs 1, 3 and 6 [50% inhibitory concentration (IC50)=43-72 nmol/l] representing HDAC classes I and II and induces hyperacetylation of histone H4 in MM cells. Low micromolar concentrations of resminostat abrogated cell growth and strongly induced apoptosis (IC50=2.5-3 micromol/l in 3 out of 4 MM cell lines) in MM cell lines as well as primary MM cells. At 1 micromol/l, resminostat inhibited proliferation and induced G0/G1 cell cycle arrest in 3 out of 4 MM cell lines accompanied with decreased levels of cyclin D1, cdc25a, Cdk4 and pRb as well as upregulation of p21. Resminostat decreased phosphorylation of 4E-BP1 and p70S6k indicating an interference with Akt pathway signalling. Treatment with resminostat resulted in increased protein levels of Bim and Bax and decreased levels of Bcl-xL. Caspases 3, 8 and 9 were activated by resminostat. Furthermore, synergistic effects were observed for combinations of resminostat with melphalan and the proteasome inhibitors bortezomib and S-2209. In conclusion, we have identified potent anti-myeloma activity for this novel HDAC inhibitor.
