Bobcat339 hydrochloride
目录号 : GC34498
A cytosine derivative
Cas No.:2436747-44-1
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Bobcat 339 is a cytosine derivative that was originally found to be an inhibitor of ten-eleven translocation methylcytosine dioxygenase 1 (TET1) and TET2 (IC50s = 33 and 73 ?M, respectively, in cell-free assays).1 However, it was found that the TET inhibitory activity was due to residual copper in the Bobcat 339 preparation used for the experiments.2 Copper-containing Bobcat 339 (10 ?M) also reduces DNA 5-hydroxymethylcytosine (5-hmC) levels in HT22 hippocampal neurons, but copper-free preparations of Bobcat 339 (50 ?M) do not reduce DNA 5-hmC levels in Hep3B cells.1,2
1.Chua, G.N.L., Wassarman, K.L., Sun, H., et al.Cytosine-based TET enzyme inhibitorsACS Med. Chem. Lett.10(2)180-185(2019) 2.Weirath, N.A., Hurben, A.K., Chao, C., et al.Small molecule inhibitors of TET dioxygenases: Bobcat339 activity is mediated by contaminating copper(II)ACS Med. Chem. Lett.13(5)792-798(2022)
| Cas No. | 2436747-44-1 | SDF | |
| Canonical SMILES | NC1=NC(N(C2=CC=CC(C3=CC=CC=C3)=C2)C=C1Cl)=O.Cl | ||
| 分子式 | C16H13Cl2N3O | 分子量 | 334.2 |
| 溶解度 | DMSO : 130 mg/mL (388.99 mM) | 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。 |
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| 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 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.9922 mL | 14.9611 mL | 29.9222 mL |
| 5 mM | 0.5984 mL | 2.9922 mL | 5.9844 mL |
| 10 mM | 0.2992 mL | 1.4961 mL | 2.9922 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。
Ferroptosis inhibitor ferrostatin?1 alleviates homocysteine?induced ovarian granulosa cell injury by regulating TET activity and DNA methylation
Polycystic ovary syndrome is one of the most common endocrine and metabolic gynecological disorders, of which dysfunction of ovarian granulosa cells is a key contributing factor. The aim of the present study was to explore the role of ferrostatin?1 (Fer?1), a ferroptosis inhibitor, in a cell injury model established by homocysteine (Hcy)?induced ovarian granulosa KGN cell line and the potential underlying mechanism. Cell viability was measured using Cell Counting Kit?8 assay in the presence or absence of Hcy and Fer?1. Cell apoptosis was assessed using TUNEL staining and the expression levels of apoptosis?related proteins were measured using western blotting. To explore the effects of Fer?1 on oxidative stress in Hcy?treated ovarian granulosa cells, the levels of reactive oxygen species (ROS), malondialdehyde (MDA), lactate dehydrogenase (LDH) and glutathione (GSH) were measured using their corresponding kits. Furthermore, Fe2+ levels were assessed using Phen Green? SK labeling and western blotting was performed to measure the protein expression levels of ferroptosis?associated proteins GPX4, SLC7A11, ASCL4 and DMT1. Subsequently, DNA methylation and ten?eleven translocation (TET) 1/2 demethylase levels were also detected to evaluate the extent of overall DNA methylation in ovarian granulosa cells after Hcy treatment. The TET1/2 inhibitor Bobcat339 hydrochloride was applied to treat ovarian granulosa cells before evaluating the possible effects of Fer?1 on TET1/2 and DNA methylation. Fer?1 was found to markedly elevate ovarian granulosa cell viability following Hcy treatment. The apoptosis rate in Fer?1?treated groups was also markedly decreased, which was accompanied by downregulated Bax and cleaved caspase?3 expression and upregulated Bcl?2 protein expression. In addition, Fer?1 treatment reduced the levels of ROS, MDA and LDH whilst enhancing the levels of GSH. Fe2+ levels were significantly decreased following Fer?1 treatment, which also elevated glutathione peroxidase 4 expression whilst reducing solute carrier family 7 member 11, achaete?scute family BHLH transcription factor 4 and divalent metal transporter 1 protein expression. Fer?1 significantly inhibited DNA methylation and enhanced TET1/2 levels, which were reversed by treatment with Bobcat339 hydrochloride. Subsequent experiments on cell viability, oxidative stress, Fe2+ content, ferroptosis? and apoptosis?related proteins levels revealed that Bobcat339 hydrochloride reversed the effects of Fer?1 on ovarian granulosa Hcy?induced cell injury. These results suggest that Fer?1 may potentially protect ovarian granulosa cells against Hcy?induced injury by increasing TET levels and reducing DNA methylation.
Graphene Quantum Dots Disrupt Embryonic Stem Cell Differentiation by Interfering with the Methylation Level of Sox 2
The tremendous potential for graphene quantum dots (GQDs) in biomedical applications has led to growing concerns of their health risks in human beings. However, present studies mainly focused on oxidative stress, apoptosis, and other general toxicity effects; the knowledge on the developmental toxicity and the related regulatory mechanisms is still far from sufficient. Our study revealed the development retardation of mouse embryonic stem cells (mESCs) caused by GQDs with a novel DNA methylation epigenetic mechanism. Specifically, GQDs were internalized into cells mainly via energy-dependent endocytosis, and a significant fraction of internalized GQDs remained in the cells even after a 48-h clearance period. Albeit with unobservable cytotoxicity or any influences on cell pluripotency, significant retardation was found in the in vitro differentiation of the mESCs into embryoid bodies (EBs) with the upregulation of Sox2 levels in GQD pretreatment groups. Importantly, this effect could be contributed by GQD-induced inhibition in CpG methylation of Sox2 through altering methyltransferase and demethyltransferase transcriptional expressions, and the demethyltransferase inhibitor, bobcat339 hydrochloride, reduced GQD-induced upregulation of Sox2. The current study first demonstrated that GQDs compromised the differentiation program of the mESCs, potentially causing development retardation. Exposure to this nanomaterial during gestation or early developmental period would cause adverse health risks and is worthy of more attention.