APHA Compound 8
(Synonyms: 组蛋白去乙酰化酶) 目录号 : GC40674A class I and II HDAC inhibitor
Cas No.:676599-90-9
Sample solution is provided at 25 µL, 10mM.
;)
,-1-7$$$37316672.jpg');)
;)
;)
$$$36806353.jpg');)
;33(7)%EF%BC%9A546-561$$$37156877.jpg');)
;)
;)
;)
%201124-1138.$$$35908550.jpg');)
%20766-780.$$$37100057.jpg');)
%20418-432.$$$36893736.jpg');)
%EF%BC%9A-240-255.$$$35108512.jpg');)
533-545$$$36543525.jpg');)
%201-13.$$$36600053.jpg');)
;)
Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
| Cas No. | 676599-90-9 | SDF | |
| 别名 | 组蛋白去乙酰化酶 | ||
| Canonical SMILES | CN1C=C(C(CC2=CC=CC=C2)=O)C=C1/C=C/C(NO)=O | ||
| 分子式 | C16H16N2O3 | 分子量 | 284.3 |
| 溶解度 | DMSO: >10 mg/ml | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
||
| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 3.5174 mL | 17.5871 mL | 35.1741 mL |
| 5 mM | 0.7035 mL | 3.5174 mL | 7.0348 mL |
| 10 mM | 0.3517 mL | 1.7587 mL | 3.5174 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Histone-deacetylase inhibitors produce positive results in the GADD45a-GFP GreenScreen HC assay
Mutat Res 2013 Mar 18;751(2):96-100.PMID:23340162DOI:10.1016/j.mrgentox.2012.12.009.
Histone-deacetylase inhibitors (HDACi) are able to induce cell-cycle arrest, apoptosis and differentiation in a variety of tumour cell lines. The mechanisms leading to these cellular outcomes are not fully understood, however, it is has been proposed that induction of cell-cycle arrest might be a result of genotoxic stress. Despite the potential for genotoxic activity of this class of compounds, there are very few data available to provide evidence for this, either in vitro or in vivo. In this study, four HDACi, viz. trichostatin A, sodium butyrate, APHA Compound 8 and apicidin, were tested in the human lymphoblastoid TK6 cell line-hosted GADD45a-GFP assay, which has high sensitivity and specificity in the detection of genotoxic carcinogens and in vivo genotoxicants. All four compounds produced positive genotoxicity results within the acceptable toxic dose range of the assay, with APHA Compound 8 producing the weakest response. Taken alongside recent evidence demonstrating that GADD45a is not induced by non-genotoxic apoptogens, this study suggests that genotoxicity contributes to the anti-tumour activity of HDACi drugs.
Contrasting Effects of Histone Deacetylase Inhibitors on Reward and Aversive Olfactory Memories in the Honey Bee
Insects 2014 Jun 10;5(2):377-98.PMID:26462690DOI:10.3390/insects5020377.
Much of what we have learnt from rodent models about the essential role of epigenetic processes in brain plasticity has made use of aversive learning, yet the role of histone acetylation in aversive memory in the honey bee, a popular invertebrate model for both memory and epigenetics, was previously unknown. We examined the effects of histone deacetylase (HDAC) inhibition on both aversive and reward olfactory associative learning in a discrimination proboscis extension reflex (PER) assay. We report that treatment with the HDAC inhibitors APHA Compound 8 (C8), phenylbutyrate (PB) or sodium butyrate (NaB) impaired discrimination memory due to impairment of aversive memory in a dose-dependent manner, while simultaneously having no effect on reward memory. Treatment with C8 1 h before training, 1 h after training or 1 h before testing, impaired aversive but not reward memory at test. C8 treatment 1 h before training also improved aversive but not reward learning during training. PB treatment only impaired aversive memory at test when administered 1 h after training, suggesting an effect on memory consolidation specifically. Specific impairment of aversive memory (but not reward memory) by HDAC inhibiting compounds was robust, reproducible, occurred following treatment with three drugs targeting the same mechanism, and is likely to be genuinely due to alterations to memory as sucrose sensitivity and locomotion were unaffected by HDAC inhibitor treatment. This pharmacological dissection of memory highlights the involvement of histone acetylation in aversive memory in the honey bee, and expands our knowledge of epigenetic control of neural plasticity in invertebrates.