(+)-JQ1 | Epigenetic Reader Domain | AmBeed-信号通路专用抑制剂

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(+)-JQ1 {[allProObj[0].p_purity_real_show]}

货号：A529842

(+)-JQ1（JQ1）是一种高效、特异性和可逆的BET溴结构域抑制剂，对BRD4（1/2）的第一个和第二个溴结构域的IC50分别为77 nM和33 nM。它还激活自噬。

(+)-JQ1 化学结构
CAS号：1268524-70-4

(+)-JQ1 3D分子结构
CAS号：1268524-70-4

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(+)-JQ1 纯度/质量文件产品仅供科研

货号：A529842 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 >

表观遗传阅读框亚型比较

产品名称	BET ↓ ↑	bromodomain ↓ ↑	BRPF ↓ ↑	CBP/beta-catenin ↓ ↑	p300/CBP ↓ ↑	其他靶点	纯度
MS436	++ BRD4 (1), Ki: <0.085 μM BRD4 (2), Ki: 0.34 μM						99%+
CPI-203	+++ BRD4, IC50: 37 nM						98+%
GSK1324726A	+++ BRD2, IC50: 31 nM BRD4, IC50: 22 nM						99%+
PFI-1	++ BRD2, IC50: 98 nM BRD4, IC50: 0.22 μM						98%
Apabetalone	+ BD2, IC50: 0.51 μM						99%
(+)-JQ1	+++ BRD4 (2), IC50: 33 nM BRD4 (1), IC50: 77 nM						98%
I-BET151	+ BRD3, IC50: 0.25 μM BRD4, IC50: 0.5 μM						98%
Molibresib	+++ BET proteins, IC50: 35 nM						99%+
I-BRD9	+++ BRD4, pIC50: 5.3 BRD9, pIC50: 7.3						99%+
BI-7273	++++ BRD9, IC50: 19 nM BRD7, IC50: 117 nM						97%
Pelabresib	+++ BRD4-BD1, IC50: 39 nM						98%
ARV-825	+++ BRD4 BD2, Kd: 28 nM BRD4 BD1, Kd: 90 nM						99%+
Birabresib							99%+
BI 2536	+++ BRD4, Kd: 37 nM					c-Myc	99%+
Bromosporine	++ BRD2, IC50: 0.29 μM BRD9, IC50: 0.122 μM	++++ CECR2, IC50: 17 nM					99%+
XMD8-92	++ BRD4 (1), Kd: 170 nM						99%+
Mivebresib	✔						99%+
BI-9564	++++ BRD7, Kd: 73 nM BRD9, Kd: 5.9 nM	++ CECR2, Kd: 77 nM					98%
AZD5153 6-Hydroxy-2-naphthoic acid	++++ FL-BRD4, IC50: 5 nM						99%+
PLX51107	++++ BRD3 BD1, Kd: 2.1 nM BRD4 BD2, Kd: 1.7 nM						99%+
FL-411	+ BRD4(1), IC50: 0.43 μM						99%+
ABBV-744	✔						99%+
dBET6	++++ BRD4, IC50: 14 nM						99%+
dBET1	++++ BRD4, IC50: 20 nM						99%+
MZ1	++++ Brd2(BD2), Kd: 62 nM Brd3(BD2), Kd: 13 nM						99%+
dBET57	+ BRD4_BD1, DC50: 500 nM						99%+
SF2523	+ BRD4, IC50: 241 nM					DNA-PK	99%+
INCB054329	++++ BRD3-BD1, IC50: 9 nM BRD4-BD1, IC50: 119 nM						99%
INCB-057643	✔						99%+
(E/Z)-ZL0420	+++ BRD4 BD1, IC50: 27 nM BRD4 BD2, IC50: 32 nM						99%+
BMS-986158	✔						99%
BRD4 Inhibitor-10	++++ BRD4-BD1, IC50: 5 nM BRD4-BD2, IC50: 41 nM						97%
A1874	✔						99%+
Y06036	++ BRD4 (1), Kd: 82 nM						99%+
Alobresib	✔					NF-κB	95%
ODM-207	✔						98%
GSK778	+++ BRD2-BD1, IC50: 75nM BRD4-BD1, IC50: 143 nM						97%
SRX3207	+ BRD41, IC50: 3070 nM BRD42, IC50: 3070 nM					Syk	98%
GSK046	+++ BRD3_BD2, IC50: 98 nM BRD4_BD2, IC50: 214 nM						98%
GSK620	✔						97%
Trotabresib	✔						99%
NHWD-870	✔						98%
CFT8634	++++ BRD9, DC50: 3 nM						98%
GSK2801		++ BAZ2B, Kd: 136 nM BAZ2A, Kd: 257 nM					99%+
KG-501		✔					99%+
UNC 669		+ L3MBTL4, IC50: 6 μM L3MBTL3, IC50: 35 μM					99%
PFI-3		+++ SMARCA2A, Kd: 72 nM SMARCA4, Kd: 55 nM					99%+
UNC1215		+++ L3MBTL3- D274A, IC50: 3.5 μM L3MBTL3, IC50: 120 nM					99%+
EED226		++ PRC2, Kd: 114 nM EED, Kd: 82 nM					99%+
BRD9539		✔					98%
UNC926		+ L3MBTL1, Kd: 3.9 μM					99%
666-15		++ CREB, IC50: 81 nM					99%+
UNC6852		+ EED, IC50: 247 nM					98%
BAZ1A-IN-1		+ BAZ1A, Kd: 0.52 μM					99%+
PFI-4			++ BRPF1, IC50: 80 nM BRPF2, IC50: 7.9 μM				99%+
OF-1			++ BRPF2, Kd: 500 nM BRPF1B, Kd: 100 nM				99%+
GSK-5959			++ BRPF2, pIC50: 5.2 BRPF3, pIC50: 7.1				99%
GSK6853			++++ BRPF1, pIC50: 8.1				99%+
NI-42			++++ BRPF1, IC50: 48 nM BRPF3, IC50: 260 nM				99%+
E-7386				+++ CBP/beta-catenin, IC50: 0.0484 μM			99%
I-CBP112					++ p300, Kd: 167 nM CBP, Kd: 151 nM		98+%
Histone Acetyltransferase Inhibitor II					+ p300, IC50: 5 μM		98%
C646					+ p300/CBP, Ki: 400 nM		99%+
Anacardic Acid					+ p300/CBP, IC50: 8.5 μM PCAF, IC50: 5 μM		99%+
SGC-CBP30					++++ CREBBP, IC50: 21 nM EP300, IC50: 38 nM		99%+
Nordihydroguaiaretic acid					✔	HER2,IGF-1R	99%+
Curcumin					+ p300, IC50: ~25 μM	Nrf2,Ferroptosis,NF-κB	98%
CPI-637					+++ CBP, IC50: 0.03 μM EP300, IC50: 0.051 μM		99%+
Foscenvivint					✔	β-catenin	99%+
A-485					++ p300 HAT, IC50: 0.06 μM		99%+
GNE-781	+ BRD4(1), IC50: 5100 nM				++++ CBP, IC50: 0.94 nM		99%
NEO2734	+++ BET, IC50: <30 nM				+++ p300/CBP, IC50: <30 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。

(+)-JQ1 生物活性

靶点	BET BRD4 (2), IC50:33 nM BRD4 (1), IC50:77 nM
描述	BRDs (bromodomains) of human proteome can recognize the relaxed chromatin segments and bind to the acetylated nucleosomes, transcription factors and co-activators. (+)-JQ1 is a potent and selective bromodomain inhibitor with IC50 values of 77nM, 33nM and >10uM for BRD4(1), BRD4(2) and CREBBP, respectively^[1]. The (+)-JQ-1-specific inhibition of BRDs can affect the production of the targeted transcription factor-dependent protein, including NRF2-dependent HO-1, NADPH:quinone oxidoreductase-1 as well as GCLC, SOCS3, STAT5-mediated regulation of target genes, RUNX3, SIRT1, MYC and its downstream target genes, etc.^[2]. JQ1 can induce the differentiation and growth arrest in NUT midline carcinoma. Treatment with (+)-JQ-1, 250nM for 48h, potently decreased the expression of both BRD4 target genes, RAD21 and RAN, in NMC cells. Treatment with JQ1, i.p., 50mg/kg for 18 days, can regress the tumor growth and prolong overall survival of NMC797 xenografted mice. In addition, (-)-JQ-1 is the negative control compound of (+)-JQ-1^[1].
作用机制	JQ1 can bind lysine acetylation binding site of BET bromodomains competitively with chromatin in a cellular environment.^[1]

(+)-JQ1 细胞实验

Cell Line ARP-1 JJN3 U266 RPMI-8226 Adult rat ventricular fibroblasts (ARVFs) Adult rat ventricular fibroblasts (ARVFs) KP-4 cells NMC 797 cells U2OS cells SKO-007(J3) cortical neurons cortical neurons C2C12 cells H2081 cells	Concentration	Treated Time	Description	References
ARP-1	0.5 μM	72 h	JQ1 upregulated the expression of MICA in ARP-1 cells.	J Hematol Oncol. 2016 Dec 1;9(1):134.
JJN3	0.5 μM	72 h	JQ1 upregulated the expression of MICA in JJN3 cells.	J Hematol Oncol. 2016 Dec 1;9(1):134.
U266	0.5 μM	72 h	JQ1 upregulated the expression of MICA in U266 cells.	J Hematol Oncol. 2016 Dec 1;9(1):134.
RPMI-8226	0.5 μM	72 h	JQ1 upregulated the expression of MICA in RPMI-8226 cells.	J Hematol Oncol. 2016 Dec 1;9(1):134.
Adult rat ventricular fibroblasts (ARVFs)	10μM to 5nM	72 h	JQ1 inhibited TGF-β1-stimulated α-SMA signal with an IC50 of 94nM.	Circ Res. 2019 Sep 13;125(7):662-677.
Adult rat ventricular fibroblasts (ARVFs)	500nM	72 h	JQ1 significantly reduced basal and TGF-β-mediated collagen gel contraction and profoundly reduced α-SMA protein expression.	Circ Res. 2019 Sep 13;125(7):662-677.
KP-4 cells	500 nM	9 h	JQ1 increased LC3II levels, indicating that JQ1 activates autophagy by inhibiting BRD4	Mol Cell. 2017 May 18;66(4):517-532.e9.
NMC 797 cells	500 nM	48 h	JQ1 induces differentiation in NMC cells, characterized by changes in cell morphology and increased keratin expression	Nature. 2010 Dec 23;468(7327):1067-73.
U2OS cells	500 nM		JQ1 competitively binds to BRD4, leading to its displacement from nuclear chromatin as demonstrated by FRAP experiments	Nature. 2010 Dec 23;468(7327):1067-73.
SKO-007(J3)	0.5 μM	72 h	JQ1 upregulated the expression of MICA in SKO-007(J3) cells, enhancing their sensitivity to NK cell-mediated cytotoxicity.	J Hematol Oncol. 2016 Dec 1;9(1):134.
cortical neurons	250 nM	10 min	JQ1 pretreatment blocked the rapid induction of Arc, Fos, and Nr4a1 after TTX withdrawal	Nat Neurosci. 2015 Oct;18(10):1464-73.
cortical neurons	250 nM	10 min	JQ1 pretreatment blocked the BDNF-induced increase in transcription of Arc, Fos, and Nr4a1	Nat Neurosci. 2015 Oct;18(10):1464-73.
C2C12 cells	200 nM	24 h	JQ1 treatment prevented H2O2-induced oxidative stress, restored LC3II abundance, and reduced p62 levels.	Nat Commun. 2020 Nov 30;11(1):6108.
H2081 cells	1 µM	48 h	JQ1 significantly reduced ASCL1 and IGFBP5 expression, while having no effect on IGFBP3 expression.	Nat Commun. 2019 Jul 19;10(1):3201.

(+)-JQ1 动物实验

Species Mice Mice Mice Mice Nude mice Mouse Zebrafish Zebra fish C57BL/6J mice Mice Mouse NSG mice	Animal Model NMC 797 xenograft model Adult male mice Mdx mouse model ASCL1High SCLC xenograft model Xenograft mouse models Cardiomyocyte-specific BRD4 knockout mouse Hepatocyte ablation model Transgenic zebra fish expressing human 0N/4R-Tau Oxidative stress-induced retina degeneration model Myc-Cap model Fancd2−/− mice HCC70 xenograft model	Administration	Dosage	Frequency	Description	References
Mice	NMC 797 xenograft model	Intraperitoneal injection	50 mg/kg	Once daily for 4 days	JQ1 significantly reduces tumor growth, induces keratin expression, and inhibits tumor proliferation	Nature. 2010 Dec 23;468(7327):1067-73.
Mice	Adult male mice	Intraperitoneal injections	50 mg/kg	Daily for one week or three weeks	JQ1 treatment affected memory formation and decreased seizure susceptibility in mice	Nat Neurosci. 2015 Oct;18(10):1464-73.
Mice	Mdx mouse model	Intraperitoneal injection	20 mg/kg	Once daily for two weeks	JQ1 treatment reduced muscle damage and inflammation in mdx mice, improving muscle function.	Nat Commun. 2020 Nov 30;11(1):6108.
Mice	ASCL1High SCLC xenograft model	Intraperitoneal injection	25 mg/kg	Every other day, continuous treatment	Combination treatment of JQ1 and BMS-754807 significantly inhibited tumor growth, while monotherapy with either JQ1 or BMS-754807 had limited effects.	Nat Commun. 2019 Jul 19;10(1):3201.
Nude mice	Xenograft mouse models	Intraperitoneal injection	50 mg/kg	5 days a week, continuous treatment	To evaluate the resistance of SPOP-mutant tumors to BET inhibitor JQ1, results showed that SPOP-mutant tumors were resistant to JQ1 treatment	Nat Med. 2017 Sep;23(9):1063-1071
Mouse	Cardiomyocyte-specific BRD4 knockout mouse	Intraperitoneal injection	50mg/kg	Once daily for 2 weeks	To evaluate the effect of JQ1 on cardiac function, it was found that JQ1-treated hearts did not affect baseline cardiac function but showed protective effects in the pathological hypertrophy model.	Circulation. 2020 Dec 15;142(24):2356-2370
Zebrafish	Hepatocyte ablation model	Water treatment	3 μM	From A12h to R6h	To study the role of BET proteins in liver regeneration, it was found that JQ1 treatment temporarily inhibited liver regeneration, but regeneration resumed after washout.	J Hepatol. 2016 Feb;64(2):316-325.
Zebra fish	Transgenic zebra fish expressing human 0N/4R-Tau	Bath exposure	2 μM	Continuous exposure from 2 to 5 days	To evaluate the effects of (+)JQ1 on motor function, survival, microgliosis, and synaptic elimination in Tau zebra fish. Results showed that (+)JQ1 improved hypokinesia, increased survival, reduced microgliosis, and prevented brain synapse elimination.	Nat Commun. 2024 Sep 18;15(1):8195
C57BL/6J mice	Oxidative stress-induced retina degeneration model	Intraperitoneal injection	50 mg/kg	Daily for 3 days	JQ1 inhibited SI-induced cGAS-STING activation, reduced retina inflammation and degeneration, and improved retinal integrity.	Cell Death Differ. 2022 Sep;29(9):1816-1833
Mice	Myc-Cap model	Intraperitoneal injection	50 mg/kg	Daily, continuous treatment	To test the combined effect of JQ1 with anti-CTLA-4 immunotherapy, results showed that the combination significantly increased the CD8/Treg ratio and demonstrated a potential survival benefit.	J Immunother Cancer. 2019 Oct 25;7(1):277
Mouse	Fancd2−/− mice	Intraperitoneal injection	50 mg/kg	Daily for 1 month	Reduce DNA damage in LT-HSC, improve survival	Cell Stem Cell. 2021 Jan 7;28(1):33-47. e8
NSG mice	HCC70 xenograft model	Intraperitoneal injection and oral gavage	50 mg/kg	Once daily for 21 days	Evaluate the anti-tumor effect of JQ1 in combination with BEZ235, showing significant reduction in tumor volume and suppression of K14 expressing cell shift	Nat Commun. 2018 Sep 19;9(1):3815

(+)-JQ1 动物研究

Dose	Mice^[1] (i.p.): 50 mg/kg
Administration	i.p.

(+)-JQ1 参考文献

[1]Filippakopoulos P, Qi J, et al. Selective inhibition of BET bromodomains. Nature. 2010;468(7327):1067-73.

[2]Shin DG, Bayarsaihan D. A Novel Epi-drug Therapy Based on the Suppression of BET Family Epigenetic Readers. Yale J Biol Med. 2017;90(1):63-71.

(+)-JQ1 实验方案

计算器

存储液制备

1mg

5mg

10mg

1 mM

5 mM

10 mM

2.19mL

0.44mL

0.22mL

10.94mL

2.19mL

1.09mL

21.88mL

4.38mL

2.19mL

(+)-JQ1 技术信息

CAS号	1268524-70-4
分子式	C₂₃H₂₅ClN₄O₂S
分子量	456.99
SMILES Code	O=C(OC(C)(C)C)C[C@H]1C2=NN=C(C)N2C3=C(C(C)=C(C)S3)C(C4=CC=C(Cl)C=C4)=N1
MDL No.	MFCD22683748

别名
运输	蓝冰
InChI Key	DNVXATUJJDPFDM-KRWDZBQOSA-N
Pubchem ID	46907787

存储条件

In solvent -20°C: 3-6个月 -80°C: 12个月

Pure form Sealed in dry, 2-8°C

溶解方案

细胞实验：

DMSO: 45 mg/mL(98.47 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

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

方案三

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

方案二

细胞研究

细胞系	浓度	检测类型	检测时间	活性说明	数据源

148I		Growth Inhibition Assay	72 h	IC50=0.284±0.035 μM	25944566
148I	0.25/0.5/1.0 μM	Apoptosis Assay	24 h	increases levels of cleaved caspase-3	25944566
148I	1 μM	Apoptosis Assay	48 h	induces cell apoptosis significantly	25944566
148L		Growth Inhibition Assay	72 h	IC50=0.146±0.017 μM	25944566
493H		Growth Inhibition Assay	72 h	IC50=0.047±0.009 μM	25944566
493L		Growth Inhibition Assay	72 h	IC50=0.050±0.011 μM	25944566
494H		Growth Inhibition Assay	72 h	IC50=0.122±0.004 μM	25944566
494H	0.25/0.5/1.0 μM	Apoptosis Assay	24 h	increases levels of cleaved caspase-3	25944566
494H	1 μM	Apoptosis Assay	48 h	induces cell apoptosis significantly	25944566
494L		Growth Inhibition Assay	72 h	IC50=0.317±0.012 μM	25944566
716H		Growth Inhibition Assay	72 h	IC50=0.212±0.034 μM	25944566
858	0-1 μM	Cell Viability Assay	5 d	decreases cell viability in a dose-dependent manner	26206333
89R		Growth Inhibition Assay	72 h	IC50=0.126±0.003 μM	25944566
92.1	0-2 μM	Cell Viability Assay	4 d	decreases cell viability in a dose-dependent manner	26397223
92.1	500 nM	Apoptosis Assay	48 h	induces apoptosis	26397223
92.1	500 nM	Cell Cycle Assay	24/48/72 h	induces the cell accumulation at sub-G1	26397223
98L		Growth Inhibition Assay	72 h	IC50=0.309±0.029 μM	25944566
98Sc		Growth Inhibition Assay	72 h	IC50=0.115±0.004 μM	25944566
A549	0.1-10 μM	Growth Inhibition Assay	72 h	inhibits cell growth in a dose-dependent manner	26415225
A549	1/2.5/5 μM	Function Assay	12 h	weakly decreased Bcl-2 levels	26415225
A549	100/400/1000 nM	Function Assay	24 h	upregulates and activates SIRT1	26212199
BCPAP	250/500/1000 nM	Cell Viability Assay	24/48/72 h	inhibits cell viability in both dose- and time- dependent manner	26707881
BCPAP	250/500/1000 nM	Cell Cycle Assay	72 h	arrests cell cycle at G0/G1 phase	26707881
BE(2)-C	1 μM	Cell Viability Assay	1-4 d	decreases cell viability significantly	26067464
BE(2)-M17	1 μM	Cell Viability Assay	1-4 d	decreases cell viability significantly	26067464
BEL7402	0-10 μM	Growth Inhibition Assay	5 d	IC50=0.47 μM	26575167
C8161	0-2 μM	Cell Viability Assay	4 d	decreases cell viability in a dose-dependent manner	26397223
DDR2L63V	0-1 μM	Cell Viability Assay	5 d	decreases cell viability in a dose-dependent manner	26206333
H1299	0.1-10 μM	Growth Inhibition Assay	72 h	inhibits cell growth in a dose-dependent manner	26415225
H1299	1/2.5/5 μM	Function Assay	12 h	weakly decreased Bcl-2 levels	26415225
H1299	1/2.5/5 μM	Function Assay	12 h	decreased DR4 expression	26415225
H157	0.1-10 μM	Growth Inhibition Assay	72 h	inhibits cell growth in a dose-dependent manner	26415225
H157	1/2.5/5 μM	Function Assay	12 h	decreased DR4 expression	26415225
HBL-1	0-500 nM	Cell Viability Assay	72 h	decreases cell viability in a dose-dependent manner	25009295
HCCLM3	0-10 μM	Growth Inhibition Assay	5 d	IC50=0.14 μM	26575167
HCCLM3	0.1/0.5/2.5 μM	Cell Cycle Assay	48 h	leads to a substantial accumulation of HCC cells in sub-G1 phase	26575167
HCCLM3	0.1/0.5/2.5 μM	Apoptosis Assay	48 h	activates caspase-3 and caspase-9 expression and induced PARP cleavage as well as cytochrome c release into the cytoplasm from mitochondria	26575167
HEK293	100/400/1000 nM	Function Assay	24 h	upregulates and activates SIRT1	26212199
Hela	0-500 nM	Cell Viability Assay	72 h	decreases cell viability in a dose-dependent manner	25009295
Hep3B	0-10 μM	Growth Inhibition Assay	5 d	IC50=0.08 μM	26575167
Hep3B	0.1/0.5/2.5 μM	Cell Cycle Assay	48 h	leads to a substantial accumulation of HCC cells in sub-G1 phase	26575167
Hep3B	0.1/0.5/2.5 μM	Apoptosis Assay	48 h	activates caspase-3 and caspase-9 expression and induced PARP cleavage as well as cytochrome c release into the cytoplasm from mitochondria	26575167
HepG2	0-10 μM	Growth Inhibition Assay	5 d	IC50=0.34 μM	26575167
HLY-1	0-500 nM	Cell Viability Assay	72 h	decreases cell viability in a dose-dependent manner	25009295
HMC-1.1	5-5000 nM	Growth Inhibition Assay	48 h	inhibits cell growth in a dose-dependent manner	26055303
HMC-1.1	200-5000 nM	Apoptosis Assay	48 h	induces cell apoptosis in a dose-dependent manner	26055303
HMC-1.2	5-5000 nM	Growth Inhibition Assay	48 h	inhibits cell growth in a dose-dependent manner	26055303
HMC-1.2	200-5000 nM	Apoptosis Assay	48 h	induces cell apoptosis in a dose-dependent manner	26055303
HuH7	0-10 μM	Growth Inhibition Assay	5 d	IC50=0.21 μM	26575167
IMR-32	1 μM	Cell Viability Assay	1-4 d	decreases cell viability significantly	26067464
JF	1 μM	Cell Viability Assay	1-4 d	decreases cell viability significantly	26067464
K1	250/500/1000 nM	Cell Viability Assay	24/48/72 h	inhibits cell viability in both dose- and time- dependent manner	26707881
K1	250/500/1000 nM	Cell Cycle Assay	72 h	arrests cell cycle at G0/G1 phase	26707881
MCF-7	100/400/1000 nM	Function Assay	24 h	upregulates and activates SIRT1	26212199
Mel202	0-2 μM	Cell Viability Assay	4 d	decreases cell viability in a dose-dependent manner	26397223
Mel270	0-2 μM	Cell Viability Assay	4 d	decreases cell viability in a dose-dependent manner	26397223
Mel285	0-2 μM	Cell Viability Assay	4 d	decreases cell viability in a dose-dependent manner	26397223
Mel290	0-2 μM	Cell Viability Assay	4 d	decreases cell viability in a dose-dependent manner	26397223
MG63		Growth Inhibition Assay	72 h	IC50=0.114±0.025 μM	25944566
MHCC97H	0-10 μM	Growth Inhibition Assay	5 d	IC50=0.41 μM	26575167
MOLM13	250 nM	Apoptosis Assay	48 h	induces significantly apoptosis cotreatment with quizartinib	25053825
MOLM13	250 nM	Function Assay	24 h	enhances quizartinib-induced more p21, BIM, and cleaved PARP	25053825
MOLM13	250 nM	Apoptosis Assay	48 h	induces significantly apoptosis cotreatment with ponatinib	25053825
MV4-11	250 nM	Apoptosis Assay	48 h	induces significantly apoptosis cotreatment with quizartinib	25053825
MV4-11	250 nM	Function Assay	24 h	enhances quizartinib-induced more p21, BIM, and cleaved PARP	25053825
MV4-11	250 nM	Apoptosis Assay	48 h	induces significantly apoptosis cotreatment with ponatinib	25053825
OCI-Ly10	0-500 nM	Cell Viability Assay	72 h	decreases cell viability in a dose-dependent manner	25009295
OCI-Ly3	0-500 nM	Cell Viability Assay	72 h	decreases cell viability in a dose-dependent manner	25009295
OCI-Ly3	172/250/500 nM	Growth Inhibition Assay	2/7 d	induces cell-cycle arrest at sub-G1 with minimal cell death	25009295
OCI-Ly3	172/250 nM	Apoptosis Assay	7d	increases caspase-3/7 activity significantly	25009295
OCI-Ly8	0-500 nM	Cell Viability Assay	72 h	decreases cell viability in a dose-dependent manner	25009295
OCI-Ly8	172/250/500 nM	Growth Inhibition Assay	2/7 d	induces cell-cycle arrest at sub-G1 with minimal cell death	25009295
OCI-Ly8	172/250 nM	Apoptosis Assay	7d	increases caspase-3/7 activity significantly	25009295
OCL-Ly18	0-500 nM	Cell Viability Assay	72 h	decreases cell viability in a dose-dependent manner	25009295
Omm1	0-2 μM	Cell Viability Assay	4 d	decreases cell viability in a dose-dependent manner	26397223
Omm1.3	0-2 μM	Cell Viability Assay	4 d	decreases cell viability in a dose-dependent manner	26397223
Omm1.3	500 nM	Apoptosis Assay	48 h	induces apoptosis	26397223
Omm1.3	500 nM	Cell Cycle Assay	24/48/72 h	induces the cell accumulation at sub-G1	26397223
OS17		Growth Inhibition Assay	72 h	IC50=0.079±0.003 μM	25944566
OS17	0.25/0.5/1.0 μM	Apoptosis Assay	24 h	increases levels of cleaved caspase-3	25944566
OS17	1 μM	Apoptosis Assay	48 h	induces cell apoptosis significantly	25944566
OS9		Growth Inhibition Assay	72 h	IC50=0.406±0.028 μM	25944566
RC-K8	0-500 nM	Cell Viability Assay	72 h	decreases cell viability in a dose-dependent manner	25009295
ROSA KIT D816V	5-5000 nM	Growth Inhibition Assay	48 h	inhibits cell growth in a dose-dependent manner	26055303
ROSA KIT D816V	200-5000 nM	Apoptosis Assay	48 h	induces cell apoptosis in a dose-dependent manner	26055303
ROSA KIT WT	5-5000 nM	Growth Inhibition Assay	48 h	inhibits cell growth in a dose-dependent manner	26055303
ROSA KIT WT	200-5000 nM	Apoptosis Assay	48 h	induces cell apoptosis in a dose-dependent manner	26055303
SAOS2		Growth Inhibition Assay	72 h	IC50=0.217±0.003 μM	25944566
SJSA-1		Growth Inhibition Assay	72 h	IC50=0.100±0.010 μM	25944566
SK-N-DZ	1 μM	Cell Viability Assay	1-4 d	decreases cell viability significantly	26067464
SK-N-SH	1 μM	Cell Viability Assay	1-4 d	decreases cell viability significantly	26067464
SMMC7721	0-10 μM	Growth Inhibition Assay	5 d	IC50=0.41 μM	26575167
SU-DHL-10	0-500 nM	Cell Viability Assay	72 h	decreases cell viability in a dose-dependent manner	25009295
SU-DHL-10	172/250/500 nM	Growth Inhibition Assay	2/7 d	induces cell-cycle arrest at sub-G1 with minimal cell death	25009295
SU-DHL-10	172/250 nM	Apoptosis Assay	7d	increases caspase-3/7 activity significantly	25009295
SU-DHL-4	0-500 nM	Cell Viability Assay	72 h	decreases cell viability in a dose-dependent manner	25009295
SU-DHL-4	172/250/500 nM	Growth Inhibition Assay	2/7 d	induces cell-cycle arrest at sub-G1 with minimal cell death	25009295
SU-DHL-4	172/250 nM	Apoptosis Assay	7d	increases caspase-3/7 activity significantly	25009295
SU-DHL-5	0-500 nM	Cell Viability Assay	72 h	decreases cell viability in a dose-dependent manner	25009295
SU-DHL-6	0-500 nM	Cell Viability Assay	72 h	decreases cell viability in a dose-dependent manner	25009295
U2OS		Growth Inhibition Assay	72 h	IC50=0.198±0.008 μM	25944566

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