SGC-CK2-1
目录号 : GC64382
SGC-CK2-1 是一种高效、ATP 竞争性的 CK2 化学探针，对两种人 CK2 亚型 CK2α 和 CK2α' 具有选择性，IC50分别为 36 和 16 nM。SGC-CK2-1 可用于神经退行性疾病的研究。
Cas No.:2470424-39-4
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
SGC-CK2-1 is a highly potent, ATP-competitive, and cell-active CK2 chemical probe with exclusive selectivity for both human CK2 isoforms, with IC50s of 36 and 16 nM for CK2α and CK2α′respectively in the nanoBRET assay. SGC-CK2-1 can be used for the research of neurodegenerative diseases[1][2].
SGC-CK2-1 inhibits CSNK2A2 and CSNK2A1 with IC50s value of 2.3 and 4.2 nM[1].SGC-CK2-1 inhibits DYRK2 with the IC50 value of 3.7 μM[1].SGC-CK2-1 inhibits blood U-937, MV4-11, MOLM-13, OCI-LY19, OCI-AML5 cells with IC50s of 120, 690, 750, 760 and 810 nM, respectively. SGC-CK2-1 inhibits Head/Neck Detroit562 cells with an IC50 of 550 nM. SGC-CK2-1 inhibits Lung NCI-H2286 cells with an IC50 of 550 nM. SGC-CK2-1 inhibits Brain SK-N-MC cells with an IC50 of 730 nM. SGC-CK2-1 inhibits Breast BT-20 cells with an IC50 of 810 nM. SGC-CK2-1 inhibits Skin A375 cells with an IC50 of 830 nM. SGC-CK2-1 inhibits Stomach SNU-1 cells with an IC50 of 860 nM. SGC-CK2-1 inhibits Duodenum Hutu 80 cells with an IC50 of 920 nM[1].
[1]. Carrow I Wells, et al. Development of a potent and selective chemical probe for the pleiotropic kinase CK2. Cell Chem Biol. 2021 Apr 15;28(4):546-558.e10.
[2]. Marco P Licciardello, et al. A New Chemical Probe Challenges the Broad Cancer Essentiality of CK2. Trends Pharmacol Sci. 2021 May;42(5):313-315.
| Cas No. | 2470424-39-4 | SDF | Download SDF |
| 分子式 | C20H21N7O | 分子量 | 375.43 |
| 溶解度 | DMSO : 100 mg/mL (266.36 mM; Need ultrasonic) | 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 | 2.6636 mL | 13.3181 mL | 26.6361 mL |
| 5 mM | 0.5327 mL | 2.6636 mL | 5.3272 mL |
| 10 mM | 0.2664 mL | 1.3318 mL | 2.6636 mL |
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动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
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| % DMSO % % Tween 80 % saline | ||||||||||
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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。
SGC-CK2-1 Is an Efficient Inducer of Insulin Production and Secretion in Pancreatic β-Cells
Pharmaceutics 2021 Dec 22;14(1):19.PMID:35056914DOI:10.3390/pharmaceutics14010019.
The pyrazolopyrimidine based compound SGC-CK2-1 is a potent and highly specific CK2 inhibitor and a new tool to study the biological functions of protein kinase CK2 irrespective from off-target effects. We used this compound in comparison with the well-established CK2 inhibitor CX-4945 to analyze the importance of CK2 for insulin production and secretion from pancreatic β-cells. Both inhibitors affected the proliferation and viability of MIN6 cells only marginally and downregulated the endogenous CK2 activity to a similar level. Furthermore, both inhibitors increased the message for insulin and boosted the secretion of insulin from storage vesicles. Thus, regarding the high specificity of SGC-CK2-1, we can clearly attribute the observed effects to biological functions of protein kinase CK2.
Targeting CK2 in cancer: a valuable strategy or a waste of time?
Cell Death Discov 2021 Oct 29;7(1):325.PMID:34716311DOI:10.1038/s41420-021-00717-4.
CK2 is a protein kinase involved in several human diseases (ranging from neurological and cardiovascular diseases to autoimmune disorders, diabetes, and infections, including COVID-19), but its best-known implications are in cancer, where it is considered a pharmacological target. Several CK2 inhibitors are available and clinical trials are underway in different cancer types. Recently, the suitability of CK2 as a broad anticancer target has been questioned by the finding that a newly developed compound, named SGC-CK2-1, which is more selective than any other known CK2 inhibitor, is poorly effective in reducing cell growth in different cancer lines, prompting the conclusion that the anticancer efficacy of CX-4945, the commonly used clinical-grade CK2 inhibitor, is to be attributed to its off-target effects. Here we perform a detailed scrutiny of published studies on CK2 targeting and a more in-depth analysis of the available data on SGC-CK2-1 vs. CX-4945 efficacy, providing a different perspective about the actual reliance of cancer cells on CK2. Collectively taken, our arguments would indicate that the pretended dispensability of CK2 in cancer is far from having been proved and warn against premature conclusions, which could discourage ongoing investigations on a potentially valuable drug target.
Inhibition of CK2 Reduces NG2 Expression in Juvenile Angiofibroma
Biomedicines 2022 Apr 21;10(5):966.PMID:35625703DOI:10.3390/biomedicines10050966.
Juvenile angiofibroma (JA) is a rare fibrovascular neoplasm predominately found within the posterior nasal cavity of adolescent males. JA expresses the proteoglycan nerve-glial antigen (NG)2, which crucially determines the migratory capacity of distinct cancer cells. Moreover, it is known that the protein kinase CK2 regulates NG2 gene expression. Therefore, in the present study, we analyzed whether the inhibition of CK2 suppresses NG2-dependent JA cell proliferation and migration. For this purpose, we assessed the expression of NG2 and CK2 in patient-derived JA tissue samples, as well as in patient-derived JA cell cultures by Western blot, immunohistochemistry, flow cytometry and quantitative real-time PCR. The mitochondrial activity, proliferation and migratory capacity of the JA cells were determined by water-soluble tetrazolium (WST)-1, 5-bromo-2'-deoxyuridine (BrdU) and collagen sprouting assays. We found that NG2 and CK2 were expressed in both the JA tissue samples and cell cultures. The treatment of the JA cells with the two CK2 inhibitors, CX-4945 and SGC-CK2-1, significantly reduced NG2 gene and protein expression when compared to the vehicle-treated cells. In addition, the loss of CK2 activity suppressed the JA cell proliferation and migration. These findings indicate that the inhibition of CK2 may represent a promising therapeutic approach for the treatment of NG2-expressing JA.
Evaluation of a Selective Chemical Probe Validates That CK2 Mediates Neuroinflammation in a Human Induced Pluripotent Stem Cell-Derived Mircroglial Model
Front Mol Neurosci 2022 Jun 14;15:824956.PMID:35774866DOI:10.3389/fnmol.2022.824956.
Novel treatments for neurodegenerative disorders are in high demand. It is imperative that new protein targets be identified to address this need. Characterization and validation of nascent targets can be accomplished very effectively using highly specific and potent chemical probes. Human induced pluripotent stem cells (hiPSCs) provide a relevant platform for testing new compounds in disease relevant cell types. However, many recent studies utilizing this platform have focused on neuronal cells. In this study, we used hiPSC-derived microglia-like cells (MGLs) to perform side-by-side testing of a selective chemical probe, SGC-CK2-1, compared with an advanced clinical candidate, CX-4945, both targeting casein kinase 2 (CK2), one of the first kinases shown to be dysregulated in Alzheimer's disease (AD). CK2 can mediate neuroinflammation in AD, however, its role in microglia, the innate immune cells of the central nervous system (CNS), has not been defined. We analyzed available RNA-seq data to determine the microglial expression of kinases inhibited by SGC-CK2-1 and CX-4945 with a reported role in mediating inflammation in glial cells. As proof-of-concept for using hiPSC-MGLs as a potential screening platform, we used both wild-type (WT) MGLs and MGLs harboring a mutation in presenilin-1 (PSEN1), which is causative for early-onset, familial AD (FAD). We stimulated these MGLs with pro-inflammatory lipopolysaccharides (LPS) derived from E. coli and observed strong inhibition of the expression and secretion of proinflammatory cytokines by simultaneous treatment with SGC-CK2-1. A direct comparison shows that SGC-CK2-1 was more effective at suppression of proinflammatory cytokines than CX-4945. Together, these results validate a selective chemical probe, SGC-CK2-1, in human microglia as a tool to reduce neuroinflammation.
Development of a potent and selective chemical probe for the pleiotropic kinase CK2
Cell Chem Biol 2021 Apr 15;28(4):546-558.e10.PMID:33484635DOI:10.1016/j.chembiol.2020.12.013.
Building on the pyrazolopyrimidine CK2 (casein kinase 2) inhibitor scaffold, we designed a small targeted library. Through comprehensive evaluation of inhibitor selectivity, we identified inhibitor 24 (SGC-CK2-1) as a highly potent and cell-active CK2 chemical probe with exclusive selectivity for both human CK2 isoforms. Remarkably, despite years of research pointing to CK2 as a key driver in cancer, our chemical probe did not elicit a broad antiproliferative phenotype in >90% of >140 cell lines when tested in dose-response. While many publications have reported CK2 functions, CK2 biology is complex and an available high-quality chemical tool such as SGC-CK2-1 will be indispensable in deciphering the relationships between CK2 function and phenotypes.