ChidamideNovel HDAC inhibitor CAS# 743420-02-2 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 743420-02-2 | SDF | Download SDF |
| PubChem ID | 9800555 | Appearance | Powder |
| Formula | C22H19FN4O2 | M.Wt | 390.41 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Synonyms | CS055; HBI-8000 | ||
| Solubility | DMSO : ≥ 41 mg/mL (105.02 mM) *"≥" means soluble, but saturation unknown. | ||
| Chemical Name | N-(2-amino-5-fluorophenyl)-4-[[[(E)-3-pyridin-3-ylprop-2-enoyl]amino]methyl]benzamide | ||
| SMILES | C1=CC(=CN=C1)C=CC(=O)NCC2=CC=C(C=C2)C(=O)NC3=C(C=CC(=C3)F)N | ||
| Standard InChIKey | WXHHICFWKXDFOW-BJMVGYQFSA-N | ||
| Standard InChI | InChI=1S/C22H19FN4O2/c23-18-8-9-19(24)20(12-18)27-22(29)17-6-3-16(4-7-17)14-26-21(28)10-5-15-2-1-11-25-13-15/h1-13H,14,24H2,(H,26,28)(H,27,29)/b10-5+ | ||
| 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 | Chidamide is a synthetic benzamide-type HDAC inhibitor, inhibits HDAC1, 2, 3 and 10 with IC50 of 95, 160, 67 and 78 nM, respectively).In Vitro:Chidamide (CS055) at low concentrations dramatically inhibits cell proliferation in each cell line. After Chidamide treatment, cells arrest at the G0/G1 phase in a dose-dependent manner. Western blot analysis indicats that cyclin E1 and E2 protein expression is down-regulated after Chidamide treatment, which is consistent with the cell-cycle analysis. As the changes in cyclin E1 are much more significant than cyclin E2, cyclin E1 is up-regulated in HL60 and K562 cells by lentiviral transduction. The effect on leukaemia proliferation by Chidamide inhibition are largely weakened when cyclin E1 is overexpressed. It is therefore likely that cyclin E1 levels are decreased by Chidamide which induces cell-cycle arrest at the G0/G1 phase[2]. Chidamide causes a significant concentration-dependent inhibitory effect on cell proliferation in comparison to the vehicle-treated cells (P<0.05). The maximal inhibitory effect is reached at 5 μM[3].In Vivo:Inhibition of tumor growth by Chidamide (CS055) treatment is observed in a dose-dependent manner, demonstrating the anti-tumor activity of Chidamide. Control tumors grow to an average volume of 14.51 cm3 after 20 days, and Chidamide-treated tumors grow to 11.68, 11.05 and 8.45 cm3, corresponding to 19.54%, 23.83% and 41.80% growth inhibition respectively. The average tumor mass in animals treated with vehicle is 9.4±2.7 g and is 8.4±2.4 g for animals treated with low-dose Chidamide. In animals treated with a moderate dose of Chidamide, tumor mass is 7.6±1.6 g and those receiving high-dose Chidamide has a tumor mass of 5.4±1.5 g (P<0.01). Additionally, Chidamide treatment prolongs the survival of nude mice bearing HL60 xenografts. Moreover, the level of lipid peroxidation product (MDA), which is a presumptive measure of ROS-mediated injury, is increased in tumor tissue accompanied by treatment of Chidamide, suggesting that Chidamide-induced ROS generation might play a role[2]. References: | |||||
Chidamide Dilution Calculator
Chidamide Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 2.5614 mL | 12.807 mL | 25.6141 mL | 51.2282 mL | 64.0352 mL |
| 5 mM | 0.5123 mL | 2.5614 mL | 5.1228 mL | 10.2456 mL | 12.807 mL |
| 10 mM | 0.2561 mL | 1.2807 mL | 2.5614 mL | 5.1228 mL | 6.4035 mL |
| 50 mM | 0.0512 mL | 0.2561 mL | 0.5123 mL | 1.0246 mL | 1.2807 mL |
| 100 mM | 0.0256 mL | 0.1281 mL | 0.2561 mL | 0.5123 mL | 0.6404 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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Chidamide is a novel benzamide-type histone deacetylase (HDAC) inhibitor. People have investigated the effects of CS055 on proliferation, differentiation and apoptosis in human leukaemia cell lines and primary myeloid leukaemia cells.[1]
Histone deacetylases (HDACs) is a series of enzymes functioning to acetylate and deacetylate the amino-terminal lysine residues of histones, which result in the remodeling of the chromatin structures and affect the accessibility of the chromatin to transcription factors to start gene transcription.[2]
Chidamide has effect on cell cycle, it significantly reduced the S phase cell fraction, while inducing a marked increase in the G1 phase cell fraction in BEL-7402 and HCC-9204 cells with different p53 statuses. Chidamide signifiantly altered the number of cells in the phase fractions with an increase in dose.[2]
The results of the present study suggest that Chidamide is a HDACi with potential therapeutic value in several haematological malignancies via the inhibition of cell proliferation, inducing differentiation and apoptosis in human cells. Chidamide is a new HDACi with potential therapeutic values in several haematological malignancies via the inhibition of cell proliferation, inducing differentiation and apoptosis in human leukaemia cells.[1]
References:
[1] Gong K, Xie J, Yi H, Li W. CS055 (Chidamide/HBI-8000), a novel histone deacetylase inhibitor, induces G1 arrest, ROS-dependent apoptosisand differentiation in human leukaemia cells. Biochem J. 2012 May 1;443(3):735-46.
[2] Wang H1, Guo Y, Fu M, Liang X, etal. , Antitumor activity of Chidamide in hepatocellular carcinoma cell lines. Mol Med Rep. 2012 Jun;5(6):1503-8.
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Chidamide in relapsed or refractory peripheral T cell lymphoma: a multicenter real-world study in China.[Pubmed:28298231]
J Hematol Oncol. 2017 Mar 15;10(1):69.
The efficacy and safety of Chidamide, a new subtype-selective histone deacetylase (HDAC) inhibitor, have been demonstrated in a pivotal phase II clinical trial, and Chidamide has been approved by the China Food and Drug Administration (CFDA) as a treatment for relapsed or refractory peripheral T cell lymphoma (PTCL). This study sought to further evaluate the real-world utilization of Chidamide in 383 relapsed or refractory PTCL patients from April 2015 to February 2016 in mainland China. For patients receiving Chidamide monotherapy (n = 256), the overall response rate (ORR) and disease control rate (DCR) were 39.06 and 64.45%, respectively. The ORR and DCR were 51.18 and 74.02%, respectively, for patients receiving Chidamide combined with chemotherapy (n = 127). For patients receiving Chidamide monotherapy and Chidamide combined with chemotherapy, the median progression-free survival (PFS) was 129 (95% CI 82 to 194) days for the monotherapy group and 152 (95% CI 93 to 201) days for the combined therapy group (P = 0.3266). Most adverse events (AEs) were of grade 1 to 2. AEs of grade 3 or higher that occurred in >/=5% of patients receiving Chidamide monotherapy included thrombocytopenia (10.2%) and neutropenia (6.2%). For patients receiving Chidamide combined with chemotherapy, grade 3 to 4 AEs that occurred in >/=5% of patients included thrombocytopenia (18.1%), neutropenia (12.6%), anemia (7.1%), and fatigue (5.5%). This large real-world study demonstrates that Chidamide has a favorable efficacy and an acceptable safety profile for refractory and relapsed PTCL patients. Chidamide combined with chemotherapy may be a new treatment choice for refractory and relapsed PTCL patients but requires further investigation.
Chidamide in the treatment of peripheral T-cell lymphoma.[Pubmed:28138258]
Onco Targets Ther. 2017 Jan 12;10:347-352.
Mature T-cell lymphomas are aggressive malignancies. Treatment outcome is poor with conventional chemotherapy. They are about twice as common in Asia as compared with other non-Asian countries. Histone proteins form the basic structure of chromatin, and their acetylation at lysine residues relaxes chromatin structure, facilitating gene transcription. Conversely, histone deacetylation, catalyzed by histone deacetylases, compacts chromatin and represses gene transcription. Histone deacetylase inhibitors are an important class of antineoplastic agents. Chidamide is a novel orally active benzamide-type histone deacetylase inhibitor that has shown in vitro activities against a wide array of neoplasms. In Phase I trials, Chidamide showed preferential efficacy in mature T-cell lymphomas. In a pivotal Phase II trial of Chidamide in 79 patients with relapsed or refractory mature T-cell lymphomas, an overall response rate of 28% (complete remission/complete remission unconfirmed: 14%) was achieved, with most responses occurring within the first 6 weeks of treatment. The median duration of response (DOR) was 9.9 (1.1-40.8) months. Of 22 responders, 19 patients (86%) had a DOR of >/=3 months and eight patients (36%) had a DOR of >12 months. Angioimmunoblastic T-cell lymphoma and anaplastic large cell lymphoma (anaplastic lymphoma kinase-negative) showed better response rates, with the most durable responses observed in angioimmunoblastic T-cell lymphoma patients. Safety profile was favorable, with very few cases of grade 3/4 toxicities observed. Chidamide is approved by the China Food and Drug Administration for the treatment of relapsed and refractory peripheral T-cell lymphomas.
A novel histone deacetylase inhibitor Chidamide induces G0/G1 arrest and apoptosis in myelodysplastic syndromes.[Pubmed:27541047]
Biomed Pharmacother. 2016 Oct;83:1032-1037.
Chidamide as a newly designed and synthesized histone deacetylase inhibitor induces an antitumor effect in various cancer, and it has been used in several clinical trials such as peripheral T cell lymphoma (PTCL). Here we demonstrate that Chidamide was able to increase the acetylation levels of histone H3 and decrease HDAC activity in MDS cell lines(SKM-1,MUTZ-1)and AML cell line(KG-1). In vitro, at low concentration (<250nM) of Chidamide inhibited cell proliferation and delayed G0/G1 cell cycle progression by down-regulating CDK2 and regulating p-P53 and P21 protein expression. Meanwhile,it also induced cell apoptosis by down-regulating Bcl-2 and up-regulating cleaved Caspase-3 and Bax protein expression.The results of the present study demonstrates the potential utility of Chidamide for the treatment of Myelodysplastic syndromes.
Chidamide Inhibits Aerobic Metabolism to Induce Pancreatic Cancer Cell Growth Arrest by Promoting Mcl-1 Degradation.[Pubmed:27875574]
PLoS One. 2016 Nov 22;11(11):e0166896.
Pancreatic cancer is a fatal malignancy worldwide and urgently requires valid therapies. Previous research showed that the HDAC inhibitor Chidamide is a promising anti-cancer agent in pancreatic cancer cell lines. In this study, we elucidate a probable underlying anti-cancer mechanism of Chidamide involving the degradation of Mcl-1. Mcl-1 is frequently upregulated in human cancers, which has been demonstrated to participate in oxidative phosphorylation, in addition to its anti-apoptotic actions as a Bcl-2 family member. The pancreatic cancer cell lines BxPC-3 and PANC-1 were treated with Chidamide, resulting in Mcl-1 degradation accompanied by induction of Mcl-1 ubiquitination. Treatment with MG132, a proteasome inhibitor reduced Mcl-1 degradation stimulated by Chidamide. Chidamide decreased O2 consumption and ATP production to inhibit aerobic metabolism in both pancreatic cancer cell lines and primary cells, similar to knockdown of Mcl-1, while overexpression of Mcl-1 in pancreatic cancer cells could restore the aerobic metabolism inhibited by Chidamide. Furthermore, Chidamide treatment or Mcl-1 knockdown significantly induced cell growth arrest in pancreatic cancer cell lines and primary cells, and Mcl-1 overexpression could reduce this cell growth inhibition. In conclusion, our results suggest that Chidamide promotes Mcl-1 degradation through the ubiquitin-proteasome pathway, suppressing the maintenance of mitochondrial aerobic respiration by Mcl-1, and resulting in inhibition of pancreatic cancer cell proliferation. Our work supports the claim that Chidamide has therapeutic potential for pancreatic cancer treatment.
