Silmitasertib | CX-4945 | Casein Kinase 2 Inhibitor | AmBeed-信号通路专用抑制剂

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Silmitasertib {[allProObj[0].p_purity_real_show]}

货号：A103748 同义名： CX-4945

Silmitasertib 是一种选择性的 CK2 抑制剂，对 CK2 具有高亲和力，对 CK2α 和 CK2α' 的 IC50值均为 1 nM。Silmitasertib 具有抗肿瘤和抗炎作用，主要用于癌症和炎症相关疾病的研究。

Silmitasertib 化学结构
CAS号：1009820-21-6

Silmitasertib 3D分子结构
CAS号：1009820-21-6

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Silmitasertib 纯度/质量文件产品仅供科研

货号：A103748 标准纯度： {[allProObj[0].p_purity_real_show]} 产品说明书

批次查询：批次纯度: COA SDS NMR HPLC CNMR LC-MS

全球学术期刊中引用的产品: • Nature, 2025, 645, 793-800. Ambeed. [ A201204 , A444152 , A344107 , A952055 ]; • Cell, 2025. Ambeed. [ A122167 ]; • Science, 2025, 387(6729): eadp5637. Ambeed. [ A875019 ]; • Sig. Transduct. Target. Ther., 2025, 10, 257. Ambeed. [ A104916 ]; • Nat. Nanotechnol., 2025. Ambeed. [ A243018 , A1216705 , A522597 , A125401 , A1355641 ]; 更多 >

Casein Kinase 亚型比较

产品名称	CK1 ↓ ↑	CK2 ↓ ↑	其他靶点	纯度
PF-670462 2HCl	++++ CK1δ, IC50: 13 nM CK1ε, IC50: 90 nM			99%+
D4476	++ CK1 from Schizosaccharomyces pombe, IC50: 200 nM CK1δ, IC50: 300 nM			99%
SR-3029	+++ CK1δ, IC50: 44 nM CK1ε, IC50: 260 nM			99%+
IWP-2	+++ ^M82FCK1δ, IC50: 40 nM		Wnt	99%
LY364947	++ CK1δ, IC50: 0.22 μM			98%
TA-01	++++ CK1δ, IC50: 6.8 nM CK1ε, IC50: 6.4 nM		p38 MAPK	99%+
IC261	+ CK1, IC50: 16 μM			98%
PF-4800567	+++ casein kinase 1 epsilon, IC50: 32 nM casein kinase 1 delta, IC50: 711 nM			99%+
CK1-IN-1	++++ CK1δ, IC50: 15 nM CK1ε, IC50: 16 nM			99%
Longdaysin	+ CKIα, IC50: 5.6 μM CKIδ, IC50: 8.8 μM			99%+
Silmitasertib		++++ CK2, IC50: 1 nM		99%+
Ellagic acid (hydrate)		+++ CK2, IC50: 0.04 μM	PKA	95+%
DMAT		+++ CK2, Ki: ~40 nM		99%
Hematein		++ CK2, IC50: 0.55 μM		40%
Silmitasertib sodium salt		++++ CK2α', IC50: 1 nM CK2α, IC50: 1 nM		99%+
LY294002		+++ CK2, IC50: 98 nM		99%+
A-3 HCl	+ CK1, Ki: 80 μM	++ CK2, Ki: 5.1 μM	PKA,MLCK,PKC	98+%
TBB	+ CK1, Ki: 47 μM	++ CK2, Ki: 0.4 μM		98%
TTP 22		++ CK2, IC50: 100 nM		98%+
DRB		✔		99%+
BioE-1115		+ CK2α, IC50: 10 μM		99%+
(E/Z)-GO289		++++ CK2, IC50: 7 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。

Silmitasertib 生物活性

靶点	CK2 CK2, IC50:1 nM
描述	Silmitasertib (CX-4945) leads to cell-cycle arrest and selectively induces apoptosis in cancer cells compared to normal cells. This action is associated with the attenuation of PI3K/Akt signaling and the antiproliferative activity of Silmitasertib is linked to the expression levels of the CK2α catalytic subunit^[1]. When combined with PS-341, Silmitasertib prevents leukemic cells from initiating a functional unfolded protein response (UPR) to counteract PS-341-induced proteotoxic stress in the ER lumen. It also reduces the expression of the pro-survival ER chaperone BIP/Grp78^[2]. Silmitasertib induces cytotoxicity and apoptosis and exerts antiproliferative effects in hematological tumors. It achieves these effects by downregulating CK2 expression and inhibiting the activation of CK2-mediated PI3K/Akt/mTOR signaling pathways^[3].
体内研究	Administered orally at doses of 25 or 75 mg/kg, Silmitasertib is well-tolerated and shows significant antitumor activity in murine xenograft models. This efficacy is accompanied by reductions in the biomarker phospho-p21 (T145)^[1].
体外研究	Silmitasertib (CX-4945) leads to cell-cycle arrest and selectively induces apoptosis in cancer cells compared to normal cells. This action is associated with the attenuation of PI3K/Akt signaling and the antiproliferative activity of Silmitasertib is linked to the expression levels of the CK2α catalytic subunit^[1]. When combined with PS-341, Silmitasertib prevents leukemic cells from initiating a functional unfolded protein response (UPR) to counteract PS-341-induced proteotoxic stress in the ER lumen. It also reduces the expression of the pro-survival ER chaperone BIP/Grp78^[2]. Silmitasertib induces cytotoxicity and apoptosis and exerts antiproliferative effects in hematological tumors. It achieves these effects by downregulating CK2 expression and inhibiting the activation of CK2-mediated PI3K/Akt/mTOR signaling pathways^[3].
作用机制	CX-4945 acts as an ATP-competitive inhibitor of both isoforms of CK2 catalytic subunits, CK2α and CK2α’, directly blocking the phosphorylation of Akt at Serine 129 in PI3K/Akt signaling pathway.

Silmitasertib 细胞实验

Cell Line U87MG T98G U251 MCF-7 HCT-116 H1299 cells PDX cells (WVUSCC-AR2, WVUSCC-AR5) Cal-27 UM1 HSC-3 HSC-4 HNSCC cells (OSC19, UMSCC1, MDA1586)	Concentration	Treated Time	Description	References
U87MG	25 μM	6 h	To study the effect of CK2 inhibitor on ECE1c stability, results showed that ECE1cK6R exhibited enhanced stability both in the presence and absence of silmitasertib.	Cells. 2023 Feb 3;12(3):506.
T98G	25 μM	6 h	To study the effect of CK2 inhibitor on ECE1c stability, results showed that ECE1cK6R exhibited enhanced stability both in the presence and absence of silmitasertib.	Cells. 2023 Feb 3;12(3):506.
U251	25 μM	6 h	To study the effect of CK2 inhibitor on ECE1c stability, results showed that ECE1cK6R exhibited enhanced stability both in the presence and absence of silmitasertib.	Cells. 2023 Feb 3;12(3):506.
MCF-7	1 μM	24 h	To evaluate the effect of Silmitasertib on cell viability. Results showed a significant reduction in cell viability.	PLoS Pathog. 2019 May 22;15(5):e1007769.
HCT-116	2 μM	48 h	To assess the impact of Silmitasertib on apoptosis. Results indicated an increase in apoptotic cells.	PLoS Pathog. 2019 May 22;15(5):e1007769.
H1299 cells	37 μM	1 h	To investigate the effect of Silmitasertib on N protein LLPS, results showed that Silmitasertib had no detectable effect on N protein LLPS.	Nat Commun. 2021 Apr 9;12(1):2114.
PDX cells (WVUSCC-AR2, WVUSCC-AR5)	0.5-10 µM	24 h	To evaluate the effect of Silmitasertib on PDX cell invasion, results showed that Silmitasertib significantly reduced extracellular matrix (ECM) degradation and invadopodia formation.	Mol Cancer Res. 2019 Apr;17(4):987-1001.
Cal-27	10, 20, 40 µM	24, 48 h	To test the effect of Silmitasertib combined with DDP treatment on the viability of Cal-27 cells, the results showed that the combined treatment significantly reduced cell viability.	Drug Deliv. 2021 Dec;28(1):2480-2494.
UM1	10, 20, 40 µM	24, 48 h	To test the effect of Silmitasertib combined with DDP treatment on the viability of UM1 cells, the results showed that the combined treatment significantly reduced cell viability.	Drug Deliv. 2021 Dec;28(1):2480-2494.
HSC-3	10, 20, 40 µM	12 h	To observe the effect of Silmitasertib on macropinocytosis in HSC-3 cells, the results showed that Silmitasertib induced cell vacuolation.	Drug Deliv. 2021 Dec;28(1):2480-2494.
HSC-4	10, 20, 40 µM	12 h	To observe the effect of Silmitasertib on macropinocytosis in HSC-4 cells, the results showed that Silmitasertib induced cell vacuolation.	Drug Deliv. 2021 Dec;28(1):2480-2494.
HNSCC cells (OSC19, UMSCC1, MDA1586)	0.5-10 µM	12-24 h	To evaluate the effect of Silmitasertib on HNSCC cell invasion, results showed that Silmitasertib significantly reduced extracellular matrix (ECM) degradation and invadopodia formation.	Mol Cancer Res. 2019 Apr;17(4):987-1001.

Silmitasertib 动物实验

Species BALB/c nude mice Mice Mice Nude mice	Animal Model Ovarian cancer xenograft model Xenograft model HNSCC orthotopic tongue tumor model Cal-27 xenograft model	Administration	Dosage	Frequency	Description	References
BALB/c nude mice	Ovarian cancer xenograft model	Oral	60 mg/kg	Twice daily, until the end of the experiment	Silmitasertib significantly inhibited tumor growth	Cell Death Dis. 2025 Jan 18;16(1):27
Mice	Xenograft model	Oral	50 mg/kg	Once daily for 21 days	To determine the efficacy of Silmitasertib in reducing tumor growth. Results showed a significant reduction in tumor volume.	PLoS Pathog. 2019 May 22;15(5):e1007769.
Mice	HNSCC orthotopic tongue tumor model	Oral	50 mg/kg	Twice daily for three weeks	To evaluate the effect of Silmitasertib on HNSCC orthotopic tongue tumor invasion, results showed that Silmitasertib significantly reduced tumor invasion and perineural invasion.	Mol Cancer Res. 2019 Apr;17(4):987-1001.
Nude mice	Cal-27 xenograft model	Peritumoral injection	60 mg/kg	Once every 5 days for 4 weeks	To verify the tumor suppressive effect of Silmitasertib combined with DDP in vivo, the results showed that the combined treatment significantly inhibited tumor growth.	Drug Deliv. 2021 Dec;28(1):2480-2494.

Silmitasertib 动物研究

Dose

Mice: 25 mg/kg - 75 mg/kg^[2] (p.o.)

Administration

p.o.

Pharmacokinetics

Animal	Mice^[2]	Rats^[2]	Dogs^[2]
Dose	5 mg/kg (i.v.) 25 mg/kg (p.o.)	5.2 mg/kg (i.v.) 10.5 mg/kg (p.o.)	1.9 mg/kg (i.v.) 8.2 mg/kg (p.o.)
Administration	i.v. p.o.	i.v. p.o.	i.v. p.o.
F	20% (p.o.)	48% (p.o.)	51% (p.o.)
T_1/2	5 h (i.v.)	11.6 h (i.v.)	8.3 h (i.v.)
AUC	2009 ng·h/ml (p.o.)	42343 ng·h/ml (p.o.)	5646 ng·h/ml (p.o.)
CL	2.5 L/h/kg (i.v.)	0.1 L/h/kg (i.v.)	0.7 L/h/kg (i.v.)
C_max	311 ng/ml (p.o.)	7369 ng/ml (p.o.)	2178 ng/ml (p.o.)
Vss	18.1 L/kg (i.v.)	2.0 L/kg (i.v.)	8.9 L/kg (i.v.)

Silmitasertib 临床研究

NCT号	适应症或疾病	临床期	招募状态	预计完成时间	地点
NCT00891280	Advanced Solid Tumors ... 展开 >> Breast Cancer Inflammatory Breast Cancer Castleman's Disease Multiple Myeloma 收起 <<	Phase 1	Unknown	December 2011	United States, Arizona ... 展开 >> Mayo Clinic Arizona Recruiting Scottsdale, Arizona, United States, 85259 Contact: Clinical Trials Office Mayo Clinic Cancer Center 507-538-7623 Principal Investigator: Donald Northfelt, MD United States, Colorado Front Range Cancer Specialists Recruiting Fort Collins, Colorado, United States, 80528 Contact: P. Zeller 970-212-7609 Principal Investigator: Robert F Marschke, MD Front Range Cancer Specialists Recruiting Loveland, Colorado, United States, 80528 Contact: Pat Zeller 970-212-7609 Principal Investigator: R. McFarland, MD United States, Texas U T M D Anderson Cancer Center Recruiting Houston, Texas, United States, 77030 Contact: R. Alvarez, MD ralvarez@mdanderson.org Principal Investigator: R. Alvarez, MD 收起 <<
NCT03571438	Kidney Cancer	Not Applicable	Recruiting	September 30, 2024	France ... 展开 >> Grenoble Alps Hospital Recruiting Grenoble, France, 38043 Contact: Jean-Luc Descotes, PU-PH 收起 <<
NCT02128282	Cholangiocarcinoma	Phase 1 Phase 2	Recruiting	November 2021	United States, Arizona ... 展开 >> Mayo Clinic Recruiting Scottsdale, Arizona, United States, 85259-5499 Contact: Mayo Clinic Clinical Trials Office 855-776-0015 Principal Investigator: Mitesh Borad, M.D. United States, Colorado University of Colorado- Denver Recruiting Aurora, Colorado, United States, 80045 Contact: Amy Szilard 720-848-0702 Amy.Szilard@ucdenver.edu Principal Investigator: Sarah (Lindsey) Davis, MD United States, Florida Mayo Clinic Recruiting Jacksonville, Florida, United States, 32224 Contact: Mayo Clinic Clinical Trials Office 855-776-0015 Principal Investigator: Kabir Mody, MD United States, Minnesota Mayo Clinic Recruiting Rochester, Minnesota, United States, 55905 Contact: Mayo Clinic Clinical Trials Office 855-776-0015 Principal Investigator: Joleen Hubbard, MD United States, Texas Texas Oncology - Baylor Charles A. Sammons Cancer Center Recruiting Dallas, Texas, United States, 75246 Contact: Tammy Carmical, RN 214-370-1937 tammy.carmical@usoncology.com Principal Investigator: Carlos Becerra, M.D. Texas Oncology-Tyler Recruiting Tyler, Texas, United States, 75702 Contact: Karen Poe, RN 903-579-9869 karen.poe@usoncology.com Principal Investigator: Donald A Richards, M.D. Korea, Republic of Asan Medical Center Recruiting Seoul, Songpa-gu, Korea, Republic of, 138-736 Contact: Heung-Moon Chang, MD 82-3010-3219 ext 3210 changhm@amc.seoul.kr Contact: Seok kyung Jeong 82-2-3010-5634 jsk0213@amc.seoul.kr Samsung Medical Center Recruiting Seoul, Korea, Republic of Contact: Eunyou Lee 82-2-3410-0955 ley0709@samsung.com Principal Investigator: Joon Oh Park, MD Seoul National University Hospital Recruiting Seoul, Korea, Republic of Contact: Myoungsun Choi 82-2-2072-7612 iamyou3@hanmail.net Principal Investigator: Do-Youn Oh, MD Severance Hospital, Yonsei University Health System Recruiting Seoul, Korea, Republic of Contact: So Young Hwang 82-2-2228-8180 syhwang@yuhs.ac Principal Investigator: Sun Young Rha, MD Taiwan China Medical University Hospital Recruiting Taichung City, Taiwan Contact: Pei-Chen Hsu +886-4-2205-2121 peggyshiu0807@gmail.com Principal Investigator: Li-Yuan Bai, M.D. 收起 <<

Silmitasertib 参考文献

[1]Siddiqui-Jain A, et al. CX-4945, an orally bioavailable selective inhibitor of protein kinase CK2, inhibits prosurvival and angiogenic signaling and exhibits antitumor efficacy. Cancer Res. 2010 Dec 15;70(24):10288-98.

[2]Buontempo F, et al. Synergistic cytotoxic effects of PS-341 and CK2 inhibitor CX-4945 in acute lymphoblastic leukemia: turning off the prosurvival ER chaperone BIP/Grp78 and turning on the pro-apoptotic NF-κB. Oncotarget. 2016 Jan 12;7(2):1323-40.

[3]Chon HJ, et al. The casein kinase 2 inhibitor, CX-4945, as an anti-cancer drug in treatment of human hematological malignancies. Front Pharmacol. 2015 Mar 31;6:70.

Silmitasertib 实验方案

计算器

存储液制备

1mg

5mg

10mg

1 mM

5 mM

10 mM

2.86mL

0.57mL

0.29mL

14.30mL

2.86mL

1.43mL

28.59mL

5.72mL

2.86mL

Silmitasertib 技术信息

CAS号	1009820-21-6
分子式	C₁₉H₁₂ClN₃O₂
分子量	349.77
SMILES Code	O=C(C1=CC=C2C(N=C(NC3=CC=CC(Cl)=C3)C4=C2C=NC=C4)=C1)O
MDL No.	MFCD13184796

别名	CX-4945
运输	蓝冰
InChI Key	MUOKSQABCJCOPU-UHFFFAOYSA-N
Pubchem ID	24748573

存储条件

In solvent -20°C: 3-6个月 -80°C: 12个月

Pure form Keep in dark place, sealed in dry, 2-8°C

溶解方案

细胞实验：

DMSO: 35 mg/mL(100.07 mM)，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

0.1 M NaOH: 30 mg/mL(85.77 mM)，配合低频超声，并调节pH至9

动物实验：请根据您的动物给药指南选择适当的溶解方案。
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

方案一

方案二

配制的工作液建议现用现配，短期内尽快用完。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。

方案一

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摩尔计算器

计算溶液所需的质量，体积或浓度。 Ambeed 摩尔浓度计算器基于以下方程式：

浓度 (mol/L) × 体积 (L) × 分子量 (g/mol)=质量 (g)

浓度

体积

分子量

质量

*在制备母液时，请始终参考产品标签或 MSDS / COA（在产品页面可下载）上所显示的对应批次产品的分子量。

靶点

靶点	数值

CK2	CK2, IC50:1 nM

总药量计算器

动物实验：给药剂量 mg/kg 动物体重 g 动物数量只每天给药次给药天

需要的总药量： mg

工作液计算器

动物实验：给药剂量 mg/kg 动物体重 g 给药体积 μL

您需要配制的工作液浓度为：mg/mL

细胞研究

细胞系	浓度	检测类型	检测时间	活性说明	数据源

A431	10 μM	Function Assay	30 min	attenuates PI3K-Akt-mTOR signaling	22387988
A431	10 μM	Function Assay	4-24 h	enhances apoptosis with erlotinib	22387988
A549	3/10 μM	Function Assay	48 h	suppresses the micropillar-induced expression of p-FAK	26318800
A549	10 μM	Function Assay	12/24/48 h	inhibits TGF-β1-induced migration and invasion	24023938
A549	3 μM	Function Assay	48 h	inhibits TGF-β1-induced activation of Smad and expression of Snail and Twist	24023938
A549	0-30 μM	Growth Inhibition Assay	72 h	IC50=4.15 μM, inhibits cell growth concentration dependently	23651443
A549	1/10 μM	Function Assay	48 h	leads to a dose-dependent decrease in Notch reporter activity	23651443
ALL-SIL	1-10 μM	Growth Inhibition Assay	48 h	IC50=5.7 μM	24253024
ALL-SIL	5 μM	Apoptosis Assay	24/48 h	induces apoptosis	24253024
ARPE-19	5/10/20 μM	Kinase Assay	24/48 h	inhibits CK2 kinase activity at a concentration of 5 μM	24686080
ARPE-19	10 μM	Growth Inhibition Assay	24-96 h	inhibits cell growth time dependently	24686080
ARPE-19	10 μM	Function Assay	4 h	causes ER-stress response over the p-eIF2α branch, but does not induce CHOP	24686080
C2C12	3 μM	Function Assay	12/24/48 h	inhibits the expression of osteoclast differentiation markers and Akt phosphorylation	24293011
Calu-1	1/5/10 μM	Growth Inhibition Assay	72 h	inhibits cell growth concentration dependently	25750308
Calu-1	10 μM	Apoptosis Assay	72 h	induces apoptosis	25750308
CEM-R	1-10 μM	Growth Inhibition Assay	48 h	IC50=4 μM	24253024
CEM-S	1-10 μM	Growth Inhibition Assay	48 h	IC50=4.6 μM	24253024
DND-41	1-10 μM	Growth Inhibition Assay	48 h	IC50=9 μM	24253024
DND-41	5 μM	Apoptosis Assay	24/48 h	induces apoptosis	24253024
H1299	1/5/10 μM	Growth Inhibition Assay	72 h	inhibits cell growth concentration dependently	25750308
H1299	10 μM	Apoptosis Assay	72 h	induces apoptosis	25750308
H1299	0-30 μM	Growth Inhibition Assay	72 h	IC50=1.80 μM, inhibits cell growth concentration dependently	23651443
H2052	0.01-30 μM	Growth Inhibition Assay	72 h	IC50=2.0 μM	25422081
H2170	10 μM	Function Assay	30 min	attenuates PI3K-Akt-mTOR signaling	22387988
H2170	10 μM	Function Assay	4-24 h	enhances apoptosis with erlotinib	22387988
H28	0.01-30 μM	Growth Inhibition Assay	72 h	IC50=7.2 μM	25422081
H358	1/5/10 μM	Growth Inhibition Assay	72 h	inhibits cell growth concentration dependently	25750308
H358	10 μM	Apoptosis Assay	72 h	induces apoptosis	25750308
HCT116	10 μM	Growth Inhibition Assay	24-96 h	inhibits cell growth time dependently	24686080
HCT116	10 μM	Function Assay	4 h	causes ER-stress response over the p-eIF2α branch, but does not induce CHOP	24686080
HCT116	10 μM	Apoptosis Assay	24/48 h	induces apoptosis	24686080
HDMEC	0.25/0.5/1 μM	Kinase Assay	24 h	reduces CK2 kinase activity, vWF expression and secretion	26381437
HDMEC	0.25/0.5/1 μM	Function Assay	24 h	reduces expression of VCAM-1 but not ICAM-1	26381437
HDMEC	1 μM	Function Assay	24 h	affects subcellular localization of NFATc1 and phospho-p65	26381437
HDMEC	1-50 μM	Kinase Assay	5 h	decreases CK2 kinase activity without affecting cell viability	26189586
HDMEC	50 μM	Function Assay	1/5 h	decreases the nuclear signal of phosphorylated p65 in TNF-α-stimulated HDMEC	26189586
HEK293	0.5 μM	Kinase Assay	15 min	reduces CK2 kinase activity	25887626
HEK293	3 μM	Function Assay	5 h	CK2 phosphorylates eIF3j at Ser127	25887626
Hela	0.5 μM	Kinase Assay	15 min	reduces CK2 kinase activity	25887626
HPB-ALL	1-10 μM	Growth Inhibition Assay	48 h	IC50=6.1 μM	24253024
INA-6	0-40 μM	Growth Inhibition Assay	48 h	IC50=2.42 µM	24086494
Jeko-1	0-40 μM	Growth Inhibition Assay	48 h	IC50=2.4 µM	24086494
Jurkat	1-10 μM	Growth Inhibition Assay	48 h	IC50=4.9 μM	24253024
LAMA84	0.5 μM	Kinase Assay	15 min	reduces CK2 kinase activity	25887626
LNCap	0-30 μM	Growth Inhibition Assay	4 d	IC50=4.59 μM	22832316
MDA-MB-231	2/5/10 μM	Function Assay	4 h	decreases the constitutive phosphorylation of both p-S529-p65 and p-S129-Akt	25153725
MDA-MB-231	2/5/10 μM	Function Assay	4 h	inhibits serine 529 phosphorylation and the expression of IL-6, IL-8	25153725
MOLT-4	1-10 μM	Growth Inhibition Assay	48 h	IC50=5.7 μM	24253024
MOLT-4	5 μM	Apoptosis Assay	24/48 h	induces apoptosis	24253024
Nalm6	10/20 μM	Function Assay	24 h	results in decreased PTEN phosphorylation at the CK2 target residue S380 and concomitant downregulation of PTEN protein expression	24561792
Nalm6	6/10 μM	Apoptosis Assay	48 h	induces apoptosis	24561792
NU-DUL	5-25 μM	Growth Inhibition Assay	48 h	inhibits cell growth concentration dependently	25788269
Oci Ly 1	5-25 μM	Growth Inhibition Assay	48 h	inhibits cell growth concentration dependently	25788269
Oci Ly 10	5-25 μM	Growth Inhibition Assay	48 h	inhibits cell growth concentration dependently	25788269
Oci Ly 18	5-25 μM	Growth Inhibition Assay	48 h	inhibits cell growth concentration dependently	25788269
Oci Ly 19	5-25 μM	Growth Inhibition Assay	48 h	inhibits cell growth concentration dependently	25788269
Oci Ly 3	5-25 μM	Growth Inhibition Assay	48 h	inhibits cell growth concentration dependently	25788269
PC9/ER	5 µM	Function Assay	48 h	induces autophagy	25486409
PC9/GR	5 µM	Function Assay	48 h	induces autophagy	25486409
PF-382	1-10 μM	Growth Inhibition Assay	48 h	IC50=4.5 μM	24253024
platelets	1/5/10 μM	Kinase Assay	0.5 h	reduces CK2 kinase activity and platelet aggregation	26381437
Raji	5-25 μM	Growth Inhibition Assay	48 h	inhibits cell growth concentration dependently	25788269
Rec-1	0-40 μM	Growth Inhibition Assay	48 h	IC50=1.46 µM	24086494
R-LAMA84	3 μM	Function Assay	24 h	reduces CK2 activity	24012109
R-LAMA84	2.5-10 μM	Growth Inhibition Assay	48 h	inhibits cell growth concentration dependently	24012109
S-LAMA84	3 μM	Function Assay	24 h	reduces CK2 activity	24012109
S-LAMA84	2.5-10 μM	Growth Inhibition Assay	48 h	inhibits cell growth concentration dependently	24012109
SUP-B15	10/20 μM	Function Assay	24 h	results in decreased PTEN phosphorylation at the CK2 target residue S380 and concomitant downregulation of PTEN protein expression	24561792
SUP-B15	6/10 μM	Apoptosis Assay	48 h	induces apoptosis	24561792
U-266	0-40 μM	Growth Inhibition Assay	48 h	IC50=19.8 µM	24086494
U87-MG	1/5/10 μM	Growth Inhibition Assay	24/48/72 h	inhibits cell growth both concentration and time dependently	25241897
UM-SCC1	0.1-30 μM	Growth Inhibition Assay	1-5 d	IC50=4.1 μM	25798061
UM-SCC1	0.5/4/10 μM	Function Assay	72 h	down-regulates the expression of NF-ĸB, Bcl-XL and up-regulates the expression of p53, p21, AP-1 and IL-8 concentration dependently	25798061
UM-SCC-1	0.5-5 μM	Clonogenic Assay	14 d	inhibits clonogenic survival and sphere formation	25379016
UM-SCC46	0.1-30 μM	Growth Inhibition Assay	1-5 d	IC50=3.4 μM	25798061
UM-SCC46	0.5/4/10 μM	Function Assay	72 h	down-regulates the expression of NF-ĸB, Bcl-XL, p53, p21, AP-1 and up-regulates the expression IL-8 concentration dependently	25798061
UM-SCC-46	0.5-5 μM	Clonogenic Assay	14 d	inhibits clonogenic survival and sphere formation	25379016

临床研究

NCT号	适应症或疾病	临床期	招募状态	预计完成时间	地点

NCT00891280	Advanced Solid Tumors ... 展开 >> Breast Cancer Inflammatory Breast Cancer Castleman's Disease Multiple Myeloma 收起 <<	Phase 1	Unknown	December 2011	United States, Arizona ... 展开 >> Mayo Clinic Arizona Recruiting Scottsdale, Arizona, United States, 85259 Contact: Clinical Trials Office Mayo Clinic Cancer Center 507-538-7623 Principal Investigator: Donald Northfelt, MD United States, Colorado Front Range Cancer Specialists Recruiting Fort Collins, Colorado, United States, 80528 Contact: P. Zeller 970-212-7609 Principal Investigator: Robert F Marschke, MD Front Range Cancer Specialists Recruiting Loveland, Colorado, United States, 80528 Contact: Pat Zeller 970-212-7609 Principal Investigator: R. McFarland, MD United States, Texas U T M D Anderson Cancer Center Recruiting Houston, Texas, United States, 77030 Contact: R. Alvarez, MD ralvarez@mdanderson.org Principal Investigator: R. Alvarez, MD 收起 <<
NCT03571438	Kidney Cancer	Not Applicable	Recruiting	September 30, 2024	France ... 展开 >> Grenoble Alps Hospital Recruiting Grenoble, France, 38043 Contact: Jean-Luc Descotes, PU-PH 收起 <<
NCT02128282	Cholangiocarcinoma	Phase 1 Phase 2	Recruiting	November 2021	United States, Arizona ... 展开 >> Mayo Clinic Recruiting Scottsdale, Arizona, United States, 85259-5499 Contact: Mayo Clinic Clinical Trials Office 855-776-0015 Principal Investigator: Mitesh Borad, M.D. United States, Colorado University of Colorado- Denver Recruiting Aurora, Colorado, United States, 80045 Contact: Amy Szilard 720-848-0702 Amy.Szilard@ucdenver.edu Principal Investigator: Sarah (Lindsey) Davis, MD United States, Florida Mayo Clinic Recruiting Jacksonville, Florida, United States, 32224 Contact: Mayo Clinic Clinical Trials Office 855-776-0015 Principal Investigator: Kabir Mody, MD United States, Minnesota Mayo Clinic Recruiting Rochester, Minnesota, United States, 55905 Contact: Mayo Clinic Clinical Trials Office 855-776-0015 Principal Investigator: Joleen Hubbard, MD United States, Texas Texas Oncology - Baylor Charles A. Sammons Cancer Center Recruiting Dallas, Texas, United States, 75246 Contact: Tammy Carmical, RN 214-370-1937 tammy.carmical@usoncology.com Principal Investigator: Carlos Becerra, M.D. Texas Oncology-Tyler Recruiting Tyler, Texas, United States, 75702 Contact: Karen Poe, RN 903-579-9869 karen.poe@usoncology.com Principal Investigator: Donald A Richards, M.D. Korea, Republic of Asan Medical Center Recruiting Seoul, Songpa-gu, Korea, Republic of, 138-736 Contact: Heung-Moon Chang, MD 82-3010-3219 ext 3210 changhm@amc.seoul.kr Contact: Seok kyung Jeong 82-2-3010-5634 jsk0213@amc.seoul.kr Samsung Medical Center Recruiting Seoul, Korea, Republic of Contact: Eunyou Lee 82-2-3410-0955 ley0709@samsung.com Principal Investigator: Joon Oh Park, MD Seoul National University Hospital Recruiting Seoul, Korea, Republic of Contact: Myoungsun Choi 82-2-2072-7612 iamyou3@hanmail.net Principal Investigator: Do-Youn Oh, MD Severance Hospital, Yonsei University Health System Recruiting Seoul, Korea, Republic of Contact: So Young Hwang 82-2-2228-8180 syhwang@yuhs.ac Principal Investigator: Sun Young Rha, MD Taiwan China Medical University Hospital Recruiting Taichung City, Taiwan Contact: Pei-Chen Hsu +886-4-2205-2121 peggyshiu0807@gmail.com Principal Investigator: Li-Yuan Bai, M.D. 收起 <<
NCT01199718	Multiple Myeloma	Phase 1	Unknown	September 2011	United States, Ohio ... 展开 >> Recruiting Kettering, Ohio, United States, 45249 Contact: Michelle Owens, RN michelle.owens@khnetwork.org United States, Oregon Oregon Health Science University Recruiting Portland, Oregon, United States, 97239 Contact: Farnoush Abar, MD abarfa@ohsu.edu Recruiting Springfield, Oregon, United States, 97477 Contact: Jeanne Schaffer, RN jeanne.schaffer@usoncology.com United States, South Carolina Recruiting Greenville, South Carolina, United States, 29605 Contact: Jan Kueber, RN jkueber@ghs.org United States, Virginia Recruiting Norfolk, Virginia, United States, 23502 Contact: Gabrielle Geho, RN Gabrielle.Geho@usoncology.com United States, Washington Recruiting Yakima, Washington, United States, 98902 Contact: Jo Cook jo.cook@yvmh.org 收起 <<

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