BAY 61-3606 (hydrochloride)
目录号 : GC42897
A Syk inhibitor
Cas No.:1615197-10-8
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
BAY 61-3606 is a cell-permeable, reversible inhibitor of spleen tyrosine kinase (Syk; Ki = 7.5 nM; IC50 = 10 nM). It is 700 to >1,000-fold more selective for Syk over Src, Lyn, Fyn, Itk, and Btk. BAY 61-3606 can inhibit degranulation (IC50 = 5-46 nM) and block cytokine release from mast cells. At 3 mg/kg, oral administration of BAY 61-3606 to rats was shown to suppress antigen-induced passive cutaneous anaphylactic reaction, bronchoconstriction, and bronchial edema. It can also sensitize MCF-7 breast cancer cells to TNF-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis by inhibiting Cdk9. This compound has been used in a pre-clinical model to explore the feasibility of targeting Syk in the treatment of retinoblastoma.
| Cas No. | 1615197-10-8 | SDF | |
| Canonical SMILES | NC(C1=C(NC2=NC(C3=CC(OC)=C(OC)C=C3)=CC4=NC=CN24)N=CC=C1)=O.Cl | ||
| 分子式 | C20H18N6O3•HCl | 分子量 | 426.9 |
| 溶解度 | DMF: 1 mg/mL,DMSO: 30 mg/mL,DMSO:PBS (pH 7.2) (1:30): 0.03 mg/mL,Ethanol: 0.1 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。 |
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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 | 2.3425 mL | 11.7123 mL | 23.4247 mL |
| 5 mM | 0.4685 mL | 2.3425 mL | 4.6849 mL |
| 10 mM | 0.2342 mL | 1.1712 mL | 2.3425 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。
BAY 61-3606, CDKi, and sodium butyrate treatments alter gene expression in human vestibular schwannomas and cause cell death in vitro
Ecancermedicalscience 2012;6:285.PMID:23304241DOI:PMC3530378
Background: Disrupted kinase and signaling pathways are found in many human cancers and they are implicated in carcinogenesis. Therefore, kinases have been important targets for the development of cancer therapeutics. Human vestibular schwannomas (VS) are the third most common intracranial tumours which occur in the vestibular branch of VIII(th ) cranial nerve. Sodium butyrate (Na-Bu) is a potent histone deacetylase inhibitor (HDACi) and with therapeutic efficacy. Spleen tyrosine kinase (Syk) has been implicated in many immunological consequences and is a putative target for cancer treatment. Aims and objectives: The present study was undertaken in order to evaluate the effect Na-Bu, 2,4-Diamino-5-oxo-pyrimidine hydrochloride (CDKi), a broad spectrum kinase inhibitor and BAY 61-3606 (Syk inhibitor) on the survival of VS tumour tissues in vitro and their possible effects on cell survival/death and levels of a few key proteins in the treated cells as compared to the untreated cells. Materials and methods: Fresh tumour tissues were collected randomly from 16 patients with sporadic, VS tumours, minced into pieces and maintained in primary cultures. Twenty four hours later these cells were exposed to Na-Bu, BAY 61-3606 or CDKi. Forty eight hours after exposure, the tissue lysates were analysed by western blotting for expression of pRb and other proteins involved in cell survival/death. SUMMARY AND SIGNIFICANCE OF THE FINDINGS: The tissue samples used were positive for S100A protein, the maker for schwann cells confirming the VS tumour samples. The three individual treatments led to morphological change, DNA fragmentation and cell death and significantly reduced level of total and phosphorylated forms of pRb protein and drastically reduced EGF-R protein. These treatments also modulated levels of other proteins involved in cell survival/death such as PI3K, Caspase 3, TGF-β1, JNK, ASK1, Shh, NF-κB, p21(cip1/waf1). The Untreated cells had uncleaved PARP-1 protein and the treated cells had cleaved PARP-1. The results show that the observed cell death in treated cells perhaps is mediated by modulation of the levels and processing of certain key proteins. The possible development of these components as therapeutics is discussed.