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HDAC-IN-7

Catalog No. T2025 CAS 743420-02-2

Synonyms: HBI-8000, CS055, Chidamide impurity

HDAC-IN-7 (HBI-8000) (Chidamide impurity) is an impurity of Chidamide. Chidamide is a potent and orally bioavailable inhibitor of HDAC enzymes class I (HDAC1/2/3) and class IIb (HDAC10).

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HDAC-IN-7, CAS 743420-02-2

Pack Size	Availability	Price/USD
1 mg	In stock	$ 56.00
2 mg	In stock	$ 79.00
5 mg	In stock	$ 139.00
10 mg	In stock	$ 239.00
25 mg	In stock	$ 477.00
50 mg	In stock	$ 698.00
100 mg	In stock	$ 993.00
1 mL * 10 mM (in DMSO)	In stock	$ 119.00

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Purity: 98.45%

Purity: 97.86%

Biological Description

Chemical Properties

Storage & Solubility Information

Description	HDAC-IN-7 (HBI-8000) (Chidamide impurity) is an impurity of Chidamide. Chidamide is a potent and orally bioavailable inhibitor of HDAC enzymes class I (HDAC1/2/3) and class IIb (HDAC10).
Targets&IC50	HDAC8:733nM, HDAC1:95nM, HDAC10:78 nM, HDAC11:432 nM, HDAC3:67nM, HDAC2:160nM
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].
Kinase Assay	HDAC activity is detected as described in the Colorimetric HDAC Activity Assay kit. Each reaction (100 μL) contains nuclear protein (50 μg) extract from leukaemia cells and HDAC substrate. To test the effect of HDACis, Chidamide (CS055) and MS-275 are added to the mixtures and incubated at 37°C for 1 h. The HDAC activities are measured by a microplate readers at 405 nm. The positive control (only nuclear extract and vehicle) is set as 100% and double-distilled water containing 10 μM Trichostatin A, a known strong HDACi, is used as a negative control and set as 0%[2].
Cell Research	Chidamide (CS055) is dissolved in DMSO and stored, and then diluted with appropriate medium before use[2]. Proliferation of the PaTu8988 cells is evaluated using CCK-8 assay. PaTu8988 cells are randomly into 4 groups and incubated in the absence or presence of concentrations of 0, 1.25, 2.5 and 5 μM) of Chidamide for 48 h. Subsequently, 10 μL CCK-8 is added in each well and incubated for 2 h. The optical density of each well is then measured with a microplate reader at 450 nm. The cell survival rate is calculated using the formula: Cell survival rate (%)=1-(ODctrl-ODsample)/ODctrl×100%[2].

Synonyms	HBI-8000, CS055, Chidamide impurity
Molecular Weight	390.41
Formula	C22H19FN4O2
CAS No.	743420-02-2

Storage

Powder: -20°C for 3 years | In solvent: -80°C for 1 year

Solubility Information

DMSO: 41 mg/mL

References and Literature

1. Ning ZQ, et al. Chidamide (CS055/HBI-82000): a new histone deacetylase inhibitor of the benzamide class with antitumor activity and the ability to enhance immune cell-mediated tumor cell cytotoxicity. Cancer Chemother Pharmacol. 2012 Apr;69(4):901-9. 2. Gong K, et al. CS055 (Chidamide/HBI-8000), a novel histone deacetylase inhibitor, induces G1 arrest, ROS-dependent apoptosis and differentiation in human leukaemia cells. Biochem J. 2012 May 1;443(3):735-46. 3. Zhao B, et al. Chidamide, a histone deacetylase inhibitor, functions as a tumor inhibitor by modulating the ratio of Bax/Bcl-2 and P21 in pancreatic cancer. Oncol Rep. 2015 Jan;33(1):304-10. 4. Chang Y Y, Wu H L, Fang H, et al. Comparison of three chemometric methods for processing HPLC-DAD data with time shifts: Simultaneous determination of ten molecular targeted anti-tumor drugs in different biological samples[J]. Talanta. 2021, 224: 121798.

Citations

1. Chang Y Y, Wu H L, Fang H, et al. Comparison of three chemometric methods for processing HPLC-DAD data with time shifts: Simultaneous determination of ten molecular targeted anti-tumor drugs in different biological samples. Talanta. 2021, 224: 121798.

Related compound libraries

This product is contained In the following compound libraries：

Anti-Cancer Approved Drug Library Inhibitor Library Anti-Cancer Clinical Compound Library Anti-Cancer Active Compound Library Anti-Cancer Drug Library Drug Repurposing Compound Library Bioactive Compounds Library Max Hematonosis Compound Library Orally Active Compound Library Anti-Pancreatic Cancer Compound Library

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Keywords

HDAC-IN-7 743420-02-2 Chromatin/Epigenetic DNA Damage/DNA Repair HDAC HBI-8000 CS-055 HDAC IN 7 HBI 8000 CS 055 HBI8000 CS055 Chidamide impurity HDACIN7 inhibitor inhibit

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