Trichostatin A是一种选择性且强效的HDAC抑制剂,IC50约为1.8 nM,HDAC8是HDAC家族中唯一不受TSA影响的成员。


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| 产品名称 | HD1 ↓ ↑ | HD2 ↓ ↑ | HDAC ↓ ↑ | HDAC1 ↓ ↑ | HDAC10 ↓ ↑ | HDAC11 ↓ ↑ | HDAC2 ↓ ↑ | HDAC3 ↓ ↑ | HDAC4 ↓ ↑ | HDAC5 ↓ ↑ | HDAC6 ↓ ↑ | HDAC7 ↓ ↑ | HDAC8 ↓ ↑ | HDAC9 ↓ ↑ | 其他靶点 | 纯度 | |||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Givinostat HCl monohydrate |
++++
HD1-B, IC50: 7.5 nM HD1-A, IC50: 16 nM |
+++
HD2, IC50: 10 nM |
99%+ | ||||||||||||||||
| MC1568 |
++
HD1-B (Maize), IC50: 3.4 μM HD1-A (Maize), IC50: 100 nM |
96% | |||||||||||||||||
| Trichostatin A |
++++
HDAC, IC50: ~1.8 nM |
99%+ | |||||||||||||||||
| Scriptaid | ✔ | 99%+ | |||||||||||||||||
| Valproic acid sodium | ✔ | Autophagy | 97% | ||||||||||||||||
| AR-42 |
+++
HDAC, IC50: 30 nM |
99%+ | |||||||||||||||||
| Dacinostat |
+++
HDAC, IC50: 32 nM |
98+% | |||||||||||||||||
| CUDC-101 |
++++
HDAC, IC50: 4.4 nM |
++++
HDAC1, IC50: 4.5 nM |
+++
HDAC10, IC50: 26.1 nM |
+++
HDAC2, IC50: 12.6 nM |
++++
HDAC3, IC50: 9.1 nM |
+++
HDAC4, IC50: 13.2 nM |
+++
HDAC5, IC50: 11.4 nM |
++++
HDAC6, IC50: 5.1 nM |
+
HDAC7, IC50: 373 nM |
++
HDAC8, IC50: 79.8 nM |
++
HDAC9, IC50: 67.2 nM |
EGFR,HER2 | 99%+ | ||||||
| M344 |
++
HDAC, IC50: 100 nM |
99%+ | |||||||||||||||||
| Splitomicin |
+
Sir2p, IC50: 60 μM |
99% | |||||||||||||||||
| Panobinostat |
++++
HDAC (Reh cells), IC50: 20 nM HDAC (MOLT-4 cells), IC50: 5 nM |
98% | |||||||||||||||||
| Sodium 4-Phenylbutyrate | ✔ | 98% | |||||||||||||||||
| Vorinostat |
+++
HDAC, IC50: ~10 nM |
98% | |||||||||||||||||
| Curcumin | ✔ | Nrf2,NF-κB | 98% | ||||||||||||||||
| Belinostat |
+++
HDAC, IC50: 27 nM |
98% | |||||||||||||||||
| RG-2833 |
++
HDAC1, Ki: 32 nM |
++
HDAC3, Ki: 5 nM |
98% | ||||||||||||||||
| Valproic acid |
+
HDAC1, IC50: 0.4 mM |
98% | |||||||||||||||||
| BG45 |
+
HDAC1, IC50: 2 μM |
+
HDAC2, IC50: 2.2 μM |
+
HDAC3, IC50: 289 nM |
99%+ | |||||||||||||||
| Entinostat |
+
HDAC1, IC50: 0.51 μM |
+
HDAC3, IC50: 1.7 μM |
98% | ||||||||||||||||
| Resminostat |
+++
HDAC1, IC50: 42.5 nM |
++
HDAC3, IC50: 50.1 nM |
++
HDAC6, IC50: 71.8 nM |
98+% | |||||||||||||||
| Romidepsin |
+++
HDAC1, IC50: 36 nM |
+++
HDAC2, IC50: 47 nM |
99%+ | ||||||||||||||||
| Parthenolide | ✔ | NF-κB,p53 | 97% HPLC | ||||||||||||||||
| Tacedinaline |
+
HDAC1, IC50: 0.9 μM |
+
HDAC2, IC50: 0.9 μM |
+
HDAC3, IC50: 1.2 μM |
98% | |||||||||||||||
| Mocetinostat |
++
HDAC1, IC50: 0.15 μM |
+
HDAC11, IC50: 0.59 μM |
+
HDAC2, IC50: 0.29 μM |
+
HDAC3, IC50: 1.66 μM |
98% | ||||||||||||||
| WT-161 |
++++
HDAC1, IC50: 8.35 nM |
+++
HDAC2, IC50: 15.4 nM |
++++
HDAC6, IC50: 0.4 nM |
99%+ | |||||||||||||||
| Fimepinostat |
++++
HDAC1, IC50: 1.7 nM |
++++
HDAC10, IC50: 2.8 nM |
++++
HDAC11, IC50: 5.4 nM |
++++
HDAC2, IC50: 5.0 nM |
++++
HDAC3, IC50: 1.8 nM |
+++
HDAC6, IC50: 27 nM |
99%+ | ||||||||||||
| Tucidinostat |
++
HDAC1, IC50: 95 nM |
++
HDAC10, IC50: 78 nM |
++
HDAC2, IC50: 160 nM |
++
HDAC3, IC50: 67 nM |
99%+ | ||||||||||||||
| Santacruzamate A |
++++
HDAC2, IC50: 119 pM |
99%+ | |||||||||||||||||
| (E,E)-RGFP966 |
++
HDAC3, IC50: 80 nM |
99%+ | |||||||||||||||||
| LMK-235 |
+++
HDAC4, IC50: 11.9 nM |
++++
HDAC5, IC50: 4.2 nM |
99%+ | ||||||||||||||||
| Tasquinimod | ✔ | 99%+ | |||||||||||||||||
| CAY10603 |
++++
HDAC6, IC50: 2 pM |
98% | |||||||||||||||||
| Tubastatin A |
+++
HDAC6, IC50: 15 nM |
98% | |||||||||||||||||
| Tubacin |
++++
HDAC6, IC50: 4 nM |
99%+ | |||||||||||||||||
| ACY-738 |
++++
HDAC6, IC50: 1.7 nM |
99%+ | |||||||||||||||||
| Nexturastat A |
++++
HDAC6, IC50: 5 nM |
99%+ | |||||||||||||||||
| BRD73954 |
+++
HDAC6, IC50: 36 nM |
++
HDAC8, IC50: 120 nM |
99% | ||||||||||||||||
| Tubastatin A HCl |
+++
HDAC6, IC50: 15 nM |
+
HDAC8, IC50: 854 nM |
98% | ||||||||||||||||
| PCI-34051 |
+++
HDAC8, IC50: 10 nM |
99%+ | |||||||||||||||||
| Ricolinostat |
++
HDAC1, IC50: 58 nM |
++
HDAC2, IC50: 48 nM |
++
HDAC3, IC50: 51 nM |
++++
HDAC6, IC50: 4.7 nM |
++
HDAC8, IC50: 100 nM |
99%+ | |||||||||||||
| Droxinostat |
+
HDAC3, IC50: 16.9 μM |
+
HDAC6, IC50: 2.47 μM |
+
HDAC8, IC50: 1.46 μM |
99%+ | |||||||||||||||
| Abexinostat |
++++
HDAC1, Ki: 7 nM |
+++
HDAC10, IC50: 24 nM |
+++
HDAC2, Ki: 19 nM |
++++
HDAC3/SMRT, Ki: 8.2 nM |
+++
HDAC6, Ki: 17 nM |
+
HDAC8, IC50: 280 nM |
98%+ | ||||||||||||
| Citarinostat |
+++
HDAC1, IC50: 35 nM |
+++
HDAC2, IC50: 45 nM |
+++
HDAC3, IC50: 46 nM |
++++
HDAC6, IC50: 2.6 nM |
++
HDAC8, IC50: 137 nM |
99%+ | |||||||||||||
| HPOB |
+
HDAC1, IC50: 2.9 μM |
+
HDAC10, IC50: 3.0 μM |
+
HDAC2, IC50: 4.4 μM |
+
HDAC3, IC50: 1.7 μM |
++
HDAC6, IC50: 56 nM |
+
HDAC8, IC50: 2.8 μM |
97% | ||||||||||||
| Quisinostat 2HCl |
++++
HDAC1, IC50: 0.11 nM |
++++
HDAC10, IC50: 0.46 nM |
++++
HDAC11, IC50: 0.37 nM |
++++
HDAC2, IC50: 0.33 nM |
++++
HDAC3, IC50: 4.86 nM |
++++
HDAC4, IC50: 0.64 nM |
++++
HDAC5, IC50: 3.69 nM |
++++
HDAC8, IC50: 4.26 nM |
97% | ||||||||||
| Domatinostat |
+
HDAC1, IC50: 1.20 μM |
+
HDAC10, IC50: 21 μM |
+
HDAC11, IC50: 9.7 μM |
+
HDAC2, IC50: 1.12 μM |
+
HDAC3, IC50: 0.57 μM |
+
HDAC5, IC50: 11.3 μM |
+
HDAC9, IC50: 50 μM |
99%+ | |||||||||||
| TMP269 |
++
HDAC4, IC50: 157 nM |
++
HDAC5, IC50: 97 nM |
+++
HDAC7, IC50: 43 nM |
+++
HDAC9, IC50: 23 nM |
99%+ | ||||||||||||||
| Pracinostat |
++
HDAC1, IC50: 49 nM |
+++
HDAC10, IC50: 40 nM |
++
HDAC11, IC50: 93 nM |
++
HDAC2, IC50: 96 nM |
+++
HDAC3, IC50: 43 nM |
++
HDAC4, IC50: 56 nM |
+++
HDAC5, IC50: 47 nM |
+
HDAC6, IC50: 1.008 μM |
++
HDAC7, IC50: 137 nM |
++
HDAC8, IC50: 140 nM |
++
HDAC9, IC50: 70 nM |
99%+ | |||||||
| TMP195 |
++
HDAC4, Ki: 59 nM |
++
HDAC5, Ki: 60 nM |
+++
HDAC7, Ki: 26 nM |
+++
HDAC9, Ki: 15 nM |
99%+ | ||||||||||||||
| 1. 鼠标悬停在“+”上可以显示相关IC50的具体数值。"+"越多,抑制作用越强。2. "✔"表示该化合物对相应的亚型有抑制作用,但抑制强度暂时没有相关数据。 | |||||||||||||||||||
| 靶点 |
|
| 描述 | HDACs are a group of enzymes that remove acetyl groups and regulate the histone tail, protein-DNA interaction, chromatin conformation, and even transcription. There are 18 mammalian HDACs divided into four classes: class I (HDACs 1, 2, 3, 8), class II (HDACs 4, 5, 6, 7, 9, 10), class III (sirtuin family: sirt1-sirt7) and class IV (HDAC11)[1]. Trichostatin A (TSA) is the inhibitors of the class I and class II HDACs with IC50 value of 2.4 ± 0.5 nM (measured by HDAC activity in cellular extracts). Trichostatin A treatment with concentration of 2 μM for 24h can increase histone H4 hyperacetylation in all of the breast cancer cell lines tested (MCF-7, T-47D, ZR-75-1, BT-474, MDA-MB-231, MDA-MB-453, CAL 51, and SK-BR-3) significantly and inhibit the cell growth with IC50 values ranging in 26 – 308 nM in 96h. Treatment of 500 μg/kg trichostatin A by s.c injection daily for 4 weeks significantly inhibited tumor growth in Ludwig/Wistar/Olac female rats bearing tumors induced with NMU, compared with control[2]. Trichostatin A is usually used in the study of tumor growth inhibition. The cell death and cell cycle arrest induced by it may involve in several mechanisms including transcription-dependence and -independence, such as cell cycle arrest, apoptosis, the regulation of ROS and the inhibition of angiogenesis[3]. |
| 作用机制 | Trichostatin A comprises a hydroxamic acid-based metal-binding domain that coordinates the catalytic Zn(II) in the HDAC active site[4]. |
| Concentration | Treated Time | Description | References | |
| HT-3 cells | 100 nM | 24 h | SLIT2 gene expression showed minimal reactivation after TSA treatment | Mol Cancer. 2006 May 15;5:16. |
| ME-180 cells | 100 nM | 24 h | SLIT2 gene expression was reactivated after TSA treatment | Mol Cancer. 2006 May 15;5:16. |
| SiHa cells | 100 nM | 24 h | SLIT2 gene expression was not reactivated after TSA treatment | Mol Cancer. 2006 May 15;5:16. |
| mouse primary hepatocytes | 1 μM | To investigate the role of SIRT5 in regulating protein malonylation in hepatocytes, results showed that SIRT5 deficiency led to a significant increase in protein malonylation levels in hepatocytes. | Mol Cell. 2015 Jul 16;59(2):321-32. | |
| IMR90 cells | 100 nM | 10 days | Trichostatin A (TSA) treatment significantly decreased accumulation of CCFs in senescent cells and strongly reduced the expression of key SASP genes. | Genes Dev. 2020 Mar 1;34(5-6):428-445. |
| MG-63 cells | 10 nM | 24 h | As a positive control for histone acetylation, TSA treatment significantly increased histone acetylation levels in MG-63 cells. | Front Immunol. 2023 May 31;14:1138539. |
| NSCLC cell lines | 300 nM | 18 h | To evaluate the effect of TSA on SULF2 expression, partial restoration of SULF2 expression was observed in some cell lines | Oncogene. 2012 Sep 13;31(37):4107-16. |
| HeLa cells | 100 or 300 ng/ml | 4-24 h | TSA treatment reversibly increased the acetylation level of histone H4 globally and at these initiation sites, promoting a more dispersive pattern of initiations. | Nucleic Acids Res. 2005 Jan 13;33(1):325-36. |
| Administration | Dosage | Frequency | Description | References | ||
| C57BL/6N mice | ICCA tumor model | Intraperitoneal and subcutaneous injection | 0.5 mg/kg | Once a week for five weeks | Evaluate the effect of TSA and IFN-α2 combination therapy on ICCA tumor development | J Exp Clin Cancer Res. 2024 May 30;43(1):152 |
| Mice | Not3 knockout mice | Drinking water | 0.71% w/v | 1 week | HDAC inhibitors VPA and TSA rescued the impaired heart function in not3+/? mice, restoring cardiac contractility. | Cell. 2010 Apr 2;141(1):142-53 |
| NOD/SCID mice | A549-luci subcutaneous transplantation model | Intraperitoneal injection | 0.5 mg/kg | Every 3 days until the mice died | To evaluate the inhibitory effect of Trichostatin A combined with ibuprofen on cancer progression | Br J Cancer. 2020 Sep;123(5):730-741 |
| Mice | C57BL/6 mice | Intraperitoneal injection | 0.5 mg/kg | 1 day before and simultaneously with APAP administration, lasting 48 hours | Trichostatin A (TSA) significantly reduced APAP-induced CCF and SASP expression and decreased oxidative stress and inflammation. | Genes Dev. 2020 Mar 1;34(5-6):428-445. |
| Dose | Mice[5] (i.p.): min = 0.5 mg/kg, max = 80 mg/kg | ||||||||||
| Administration | i.p. | ||||||||||
| Pharmacokinetics |
|
| NCT号 | 适应症或疾病 | 临床期 | 招募状态 | 预计完成时间 | 地点 |
| NCT03049124 | Rectal Cancer | Not Applicable | Recruiting | July 31, 2019 | Canada, Ontario ... 展开 >> University of Ottawa Recruiting Ottawa, Ontario, Canada, K1N 6N5 Contact: Amanda Wurz, MSc 613-562-5800 ext 3626 amanda.wurz@uottawa.ca 收起 << |
| NCT02152267 | Craniomandibular Disorders | Not Applicable | Completed | - | Brazil ... 展开 >> Federal University of Bahia Salvador, Bahia, Brazil, 40110-902 收起 << |
| NCT01028014 | Urethral Sphincter Activity | Not Applicable | Completed | - | United States, Alabama ... 展开 >> University of Alabama at Birmingham, The Kirklin Clinic Birmingham, Alabama, United States, 35233 收起 << |
| 计算器 | ||||
| 存储液制备 | ![]() |
1mg | 5mg | 10mg |
|
1 mM 5 mM 10 mM |
3.31mL 0.66mL 0.33mL |
16.54mL 3.31mL 1.65mL |
33.07mL 6.61mL 3.31mL |
|
| CAS号 | 58880-19-6 |
| 分子式 | C17H22N2O3 |
| 分子量 | 302.37 |
| SMILES Code | CN(C1=CC=C(C=C1)C([C@@H](/C=C(/C=C/C(NO)=O)C)C)=O)C |
| MDL No. | MFCD03848392 |
| 别名 | 曲古柳菌素A ;TSA |
| 运输 | 蓝冰 |
| InChI Key | RTKIYFITIVXBLE-QEQCGCAPSA-N |
| Pubchem ID | 444732 |
| 存储条件 |
In solvent -20°C: 3-6个月 -80°C: 12个月 Pure form Inert atmosphere, store in freezer, under -20°C |
| 溶解方案 |
DMSO: 50 mg/mL(165.36 mM),配合低频超声助溶,注意:DMSO长时间开封后,会吸水并导致溶解能力下降,请避免使用长期开封的DMSO 以下溶解方案都请先按照体外实验的方式配制澄清的储备液,再依次添加助溶剂: ——为保证实验结果的可靠性,澄清的储备液可以根据储存条件,适当保存;体内实验的工作液,建议现用现配,当天使用; 以下溶剂前显示的百分比是指该溶剂在终溶液中的体积占比;如在配制过程中出现沉淀、析出现象,可以通过加热和/或超声的方式助溶
|
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