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Butein/紫铆因 {[allProObj[0].p_purity_real_show]}

货号:A456537 同义名: 2’,3,4,4’-tetrahydroxy Chalcone

Butein 是一种从 Rhus verniciflua 中提取的植物多酚,是 cAMP 特异性的 PDE 抑制剂(IC50=10.4 μM)和蛋白酪氨酸激酶的抑制剂(对 EGFR 的 IC50=16 μM)。Butein通过 AKT 和 ERK/p38 MAPK 通路增强化疗药物的敏感性,并具有抗炎和抗癌活性。

Butein/紫铆因 化学结构 CAS号:487-52-5
Butein/紫铆因 化学结构
CAS号:487-52-5
Butein/紫铆因 3D分子结构
CAS号:487-52-5
Butein/紫铆因 化学结构 CAS号:487-52-5
Butein/紫铆因 3D分子结构 CAS号:487-52-5
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Butein/紫铆因 纯度/质量文件 产品仅供科研

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产品名称 EGFR/ErbB1 ErbB3 ErbB4 HER2/ErbB2 mutant EGFR 其他靶点 纯度
WZ-3146 ++++

EGFR (E746_A750/T790M), IC50: 14 nM

EGFR (E746_A750), IC50: 2 nM

99%+
Daphnetin +

EGFR, IC50: 7.67 μM

PKA,PKC 95%
Lifirafenib ++

EGFR, IC50: 29 nM

+

EGFR(T790M/L858R), IC50: 495 nM

98%
PD168393 ++++

EGFR, IC50: 0.70 nM

99%+
Nazartinib ++

mutant EGFR, Ki: 0.031 μM

++

mutant EGFR, Ki: 0.031 μM

98%
Norcantharidin 98%
CL-387785 ++++

EGFR, IC50: 370 pM

98%
WHI-P154 +++

EGFR, IC50: 4 nM

Src,VEGFR 98%
Tyrphostin A9 +

EGFR, IC50: 460 μM

PDGFR 98%
AG 555 +

EGFR, IC50: 0.7 μM

98%
AG 494 +

EGFR, IC50: 1.2 μM

99%+
AG-556 +

EGFR, IC50: 5 μM

98%
RG13022 +

EGFR, IC50: 4 μM

99%+
Tyrphostin RG 14620 99%+
Vandetanib +

EGFR, IC50: 500 nM

99%
CNX-2006 ++

mutant EGFR, IC50: <20 nM

++

mutant EGFR, IC50: <20 nM

99%
AZD3759 ++++

EGFR (WT), IC50: 0.3 nM

EGFR (L858R), IC50: 0.2 nM

98%
Erlotinib ++++

EGFR, IC50: 2 nM

95%
Saracatinib +++

EGFR, IC50: 5 nM

EGFR (L861Q), IC50: 4 nM

99%+
AG1557 99%
Rociletinib ++

EGFR (wt), Ki: 303.3 nM

EGFR (L858R/T790M), Ki: 21.5 nM

98%
AG490 +

EGFR, IC50: 0.1 μM

98%
Cetuximab ++++

EGFR, Kd: 0.39 nM

95%
Osimertinib ++

L858R/T790M EGFR, IC50: 11.44 nM

WT EGFR, IC50: 12.92 nM

98%
Osimertinib mesylate 98% (Content MsOH 15.2-18.2%)
Chrysophanol mTOR 98%
PD153035 ++++

EGFR, Ki: 5.2 pM

99%+
Olmutinib BTK 99%+
WZ4002 ++++

EGFR (L858R), IC50: 2 nM

EGFR (L858R/T790M), IC50: 8 nM

99%+
Icotinib +++

EGFR, IC50: 5 nM

99%
Desmethyl Erlotinib HCl ++++

EGFR, IC50: 2 nM

98%
Cyasterone 99%+
PP 3 +

EGFR tyrosine kinase, IC50: 2.7 μM

98%
WZ8040 99%+
(-)-Epigallocatechin Gallate 99%
AG 18 +

EGFR, IC50: 35 μM

99%+
O-Desmethyl gefitinib ++

EGFR, IC50: 36 nM

99%
Falnidamol 99%+
AZ-5104 ++++

EGFR (L858R), IC50: 6 nM

EGFR (L861Q) , IC50: <1 nM

+++

ErbB4, IC50: 7 nM

BRK 99%+
Butein 95%
Genistein 98%
SU5214 +

EGFR, IC50: 36.7 μM

99%+
Naquotinib 99%+
Gefitinib ++

EGFR, IC50: 15.5 nM

+

EGFR (858R/T790M), IC50: 823.3 nM

98%
Theliatinib +++

WT EGFR, IC50: 3 nM

++

EGFR T790M/L858R, IC50: 22 nM

99%
Lazertinib ++++

L858R/T790M EGFR, IC50: 2 nM

WT EGFR, IC50: 76 nM

++++

Del19/T790M, IC50: 1.7 nM

99%+
Gefitinib-based PROTAC 3 ++

EGFR, DC50: 22.3 nM

99%+
MTX-211 PI3K 98%
(E)-AG 99 99%+
Licochalcone D Caspase,PARP 99%
Zipalertinib +++

EGFR WT, IC50: 8 nM

EGFR (L861Q), IC50: 4.1 nM

+++

HER4, IC50: 4 nM

++++

EGFR L858R, IC50: 2 nM

EGFR(d746-750), IC50: 1.4 nM

97%
JND3229 +++

EGFR WT, IC50: 6.8 nM

++

EGFR L858R/T790M, IC50: 30.5 nM

99%+
Firmonertinib mesylate 99%+
Tyrphostin AG30 99%+
EGFR-IN-12 ++

EGFR, IC50: 21 nM

99%+
Mobocertinib 98%
(Rac)-JBJ-04-125-02 95%
(S)-Sunvozertinib 99%
BLU-945 95%
Poziotinib +++

HER1, IC50: 3.2 nM

++

HER4, IC50: 23.5 nM

+++

HER2, IC50: 5.3 nM

98%
TAK-285 ++

EGFR/HER1, IC50: 23 nM

+

HER4, IC50: 260 nM

++

HER2, IC50: 17 nM

99%+
ARRY-380 analog 99%
Canertinib ++++

EGFR, IC50: 1.5 nM

+++

ErbB2, IC50: 9.0 nM

99%+
Dacomitinib +++

EGFR, IC50: 6.0 nM

+

ErbB4, IC50: 73.7 nM

+

ErbB2, IC50: 45.7 nM

98%
EGFR/ErbB-2/ErbB-4 inhibitor-2 +

ErbB4, IC50: 1.91 μM

+

ErbB2, IC50: 0.08 μM

99%+
(E/Z)-CP-724714 ++

HER2/ErbB2, IC50: 10 nM

95%
Lapatinib ++

EGFR, IC50: 10.8 nM

+

ErbB4, IC50: 367 nM

+++

ErbB2, IC50: 9.2 nM

98%
AEE788 ++++

EGFR, IC50: 2 nM

+

HER4/ErbB4, IC50: 160 nM

+++

HER2/ErbB2, IC50: 6 nM

c-Fms/CSF1R 98+%
AV-412 free base ++++

EGFR, IC50: 0.75 nM

++

ErbB2, IC50: 19 nM

++++

EGFRT790M, IC50: 0.79 nM

EGFRL858R/T790M, IC50: 0.51 nM

98+%
Neratinib +

EGFR, IC50: 92 nM

+

HER2, IC50: 59 nM

Src 98%
BMS-599626 ++

HER1, IC50: 20 nM

+

HER4, IC50: 190 nM

++

HER2, IC50: 30 nM

98%
Tucatinib +++

ErbB2, IC50: 8 nM

98%
Allitinib ++++

EGFR, IC50: 0.5 nM

++++

ErbB4, IC50: 0.8 nM

+++

ErbB2, IC50: 3.0 nM

99%
Pelitinib +

EGFR, IC50: 38.5 nM

+

ErbB2, IC50: 1.255 μM

Src,Raf 99%+
Sapitinib +++

EGFR, IC50: 4 nM

+++

ErbB3, IC50: 4 nM

+++

ErbB2, IC50: 3 nM

99%+
CUDC-101 +++

EGFR, IC50: 2.4 nM

++

HER2, IC50: 15.7 nM

HDAC 99%+
Varlitinib +++

ErbB1, IC50: 7 nM

++++

ErbB2, IC50: 2 nM

99%+
Afatinib dimaleate ++++

EGFR (wt), IC50: 0.5 nM

EGFR (L858R/T790M), IC50: 0.4 nM

++

HER2, IC50: 14 nM

98%
Canertinib 2HCl +++

EGFR, IC50: 7.4 nM

+++

ErbB2, IC50: 9 nM

99%
Allitinib tosylate ++++

EGFR, IC50: 0.5 nM

EGFR (T790M/L858R), IC50: 12 nM

++++

ErbB4, IC50: 0.8 nM

+++

ErbB2, IC50: 3.0 nM

99%
Tyrphostin AG 528 +

EGFR, IC50: 4.9 μM

+

HER2, IC50: 2.1 μM

97%
Afatinib ++++

EGFR (wt), IC50: 0.5 nM

EGFR (L858R), IC50: 10 nM

++++

ErbB4, IC50: 1 nM

++

HER2, IC50: 14 nM

99%
Pyrotinib dimaleate ++

EGFR, IC50: 0.013 μM

++

HER2, IC50: 0.038 μM

98%
Epertinib HCl ++++

EGFR, IC50: 1.48 nM

+++

HER4, IC50: 2.49 nM

+++

HER2, IC50: 7.15 nM

99%
Tuxobertinib ++++

EGFR, Kd: 0.2 nM

++++

HER2, Kd: 0.76 nM

99%
ALK-IN-1 ++

EGFR(del19), IC50: 36.8 nM

EGFR(C797S/del19), IC50: 138.6 nM

ALK 99%
Brigatinib +

EGFR(C797S/T790M/del19), IC50: 67.2 nM

EGFR(del19), IC50: 39.9 nM

FLT3,ALK 98%
Avitinib ++++

EGFR L858R/T790M, IC50: 0.18 nM

BTK 99%+
EAI045 97%
Almonertinib 99%
BI-4020 ++++

EGFRdel19 T790M C797S, IC50: 0.2 nM

99%+
EGFR-IN-7 ++++

EGFRL858R/T790M, IC50: 0.19 nM

EGFRd746-750/T790M/C797S, IC50: 0.26 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。

Butein/紫铆因 生物活性

靶点
  • EGFR/ErbB1

描述 Butein is a cAMP-specific PDE inhibitor with an IC50 of 10.4 μM for PDE4[1]. In vitro, Butein is a specific protein tyrosine kinase inhibitor with IC50s of 16 and 65 μM for EGFR and p60c-src in HepG2 cells[2]. Otherwise, Butein also sensitizes HeLa cells to Cisplatin through AKT and ERK/p38 MAPK pathways by targeting FoxO3a[3].
体内研究

In vivo, a combination treatment of Butein (2 mg/kg every 2 days) and cisplatin (2 mg/kg every 2 days) for three weeks notably suppresses tumor growth[3].

体外研究

Butein potently inhibits cAMP-specific phosphodiesterase (type IV) activity with an IC50 of 10.4±0.4 μM. Otherwise, Butein exhibits broader inhibition across PDE types I, III, and V only at concentrations exceeding 100 μM[1].

Butein (10, 20, and 40 μM; 24, 48, and 72 hours) inhibits cell growth in a dose- and time-dependent manner[3]. Butein exhibits anticancer activity through the inhibition of the activation of PKB/AKT and MAPK pathways, which are two pathways known to be involved in resistance to cisplatin. Butein (20 μM) decreases phosphorylation of AKT, ERK and p38 following 24 h of co-treatment with Cisplatin (20 μM)[3].

Butein/紫铆因 细胞实验

Cell Line
Concentration Treated Time Description References
Huh-7 10-60 μM 24-96 h Inhibited cell proliferation and colony formation Int J Biol Sci. 2018 Sep 7;14(11):1521-1534.
C3H10T1/2 adipocytes 20 μM 6 h Induction of Ucp1 mRNA expression, increased mitochondrial contents, and decreased numbers of large lipid droplets Nat Chem Biol. 2016 Jul;12(7):479-81.
HCC-1569 10 μg/ml 24 h To evaluate the effect of Butein on apoptosis of breast cancer cells, results showed that Butein induced apoptosis in HCC-1569 cells J Exp Clin Cancer Res. 2014 Jun 11;33(1):51.
BT-474 10 μg/ml 24 h To evaluate the effect of Butein on apoptosis of breast cancer cells, results showed that Butein induced apoptosis in BT-474 cells J Exp Clin Cancer Res. 2014 Jun 11;33(1):51.
HCC-2218 1 ng/ml to 100 μg/ml 48 h To evaluate the effect of Butein on the viability of breast cancer cells, results showed that Butein did not significantly affect the viability of HCC-2218 cells J Exp Clin Cancer Res. 2014 Jun 11;33(1):51.
HCC-1419 1 ng/ml to 100 μg/ml 48 h To evaluate the effect of Butein on the viability of breast cancer cells, results showed that Butein did not significantly affect the viability of HCC-1419 cells J Exp Clin Cancer Res. 2014 Jun 11;33(1):51.
SKBR-3 1 ng/ml to 100 μg/ml 48 h To evaluate the effect of Butein on the viability of breast cancer cells, results showed that Butein did not significantly affect the viability of SKBR-3 cells J Exp Clin Cancer Res. 2014 Jun 11;33(1):51.
T47D 1 ng/ml to 100 μg/ml 48 h To evaluate the effect of Butein on the viability of breast cancer cells, results showed that Butein reduced the viability of T47D cells J Exp Clin Cancer Res. 2014 Jun 11;33(1):51.
MCF-7 1 ng/ml to 100 μg/ml 48 h To evaluate the effect of Butein on the viability of breast cancer cells, results showed that Butein reduced the viability of MCF-7 cells J Exp Clin Cancer Res. 2014 Jun 11;33(1):51.
Primary cultured astrocytes 50 µM 4 h Inhibited TNF-α-induced pro-inflammatory mediator expression J Neuroinflammation. 2023 Sep 6;20(1):203.
Hep3B 10-60 μM 24-96 h Inhibited cell proliferation and colony formation, induced G2/M arrest and apoptosis Int J Biol Sci. 2018 Sep 7;14(11):1521-1534.
HepG2 10-60 μM 24-96 h Inhibited cell proliferation and colony formation, induced G2/M arrest and apoptosis Int J Biol Sci. 2018 Sep 7;14(11):1521-1534.
HBE cells 20 μM, 40 μM, 60 μM 24 h or 48 h Butein significantly decreased HBE cell viability. Int J Biol Sci. 2019 Jun 4;15(8):1637-1653.
H1299 cells 20 μM, 40 μM, 60 μM 24 h or 48 h Butein significantly decreased NSCLC cell viability and induced cell apoptosis and G2/M phase arrest. Int J Biol Sci. 2019 Jun 4;15(8):1637-1653.
SPC-A1 cells 20 μM, 40 μM, 60 μM 24 h or 48 h Butein significantly decreased NSCLC cell viability and induced cell apoptosis and G2/M phase arrest. Int J Biol Sci. 2019 Jun 4;15(8):1637-1653.
PC-9 cells 20 μM, 40 μM, 60 μM 24 h or 48 h Butein significantly decreased NSCLC cell viability and induced cell apoptosis and G2/M phase arrest. Int J Biol Sci. 2019 Jun 4;15(8):1637-1653.
A549 cells 20 μM, 40 μM, 60 μM 24 h or 48 h Butein significantly decreased NSCLC cell viability and induced cell apoptosis and G2/M phase arrest. Int J Biol Sci. 2019 Jun 4;15(8):1637-1653.
C3H10T1/2 adipocytes 20 μM 6 h To investigate the effect of Butein on the PI3Kα-Akt1 signaling pathway, results showed that Butein increased Prdm4 and Ucp1 expression by inhibiting PI3Kα activity. Cell Death Dis. 2018 Aug 29;9(9):876.
Hepatoma cells (HepG2) 1-10 μM 24 h Butein protected HepG2 cells against ethanol- or acetaldehyde-induced toxicity and inhibited ROS production. J Gastroenterol. 2013 Feb;48(2):222-37.
Hepatic stellate cells (CFSC-2G) 1-10 μM 24 h Butein protected hepatic stellate cells against ethanol- or acetaldehyde-induced toxicity, inhibited ROS production, and suppressed α-SMA and procollagen I production. J Gastroenterol. 2013 Feb;48(2):222-37.
Primary mouse hippocampal neurons 5 or 10 μM 24 h Butein decreased glutamate-induced oxidative damage and ROS production in primary mouse hippocampal neurons. Br J Pharmacol. 2016 Oct;173(19):2894-909.
BV2 microglial cells 1-10 μM 12-24 h Butein suppressed LPS-induced pro-inflammatory enzymes and mediators in BV2 microglia, including IL-6, IL-1β, and TNF-α production and mRNA expression. Br J Pharmacol. 2016 Oct;173(19):2894-909.
HT22 mouse hippocampal cells 1-10 μM 12-24 h Butein decreased glutamate-induced oxidative injury and ROS production in HT22 cells and increased the expression of Bcl-2 and Bcl-xL. Br J Pharmacol. 2016 Oct;173(19):2894-909.
H9c2 cardiomyoblasts 1, 3, 5 µM 24 h To assess the protective effect of Butein against H2O2-induced oxidative stress. Butein pretreatment significantly increased the survival rate of H2O2-treated cells, reduced ROS production and apoptosis, and increased the expression of antioxidant proteins. Antioxidants (Basel). 2022 Jul 23;11(8):1430.
H9c2 cardiomyoblasts 0.5-10 µM 24, 48, 72 h To evaluate the cytotoxicity of Butein on H9c2 cardiomyoblasts. Results showed that all concentrations and durations of Butein treatment did not significantly alter cell viability. Antioxidants (Basel). 2022 Jul 23;11(8):1430.

Butein/紫铆因 动物实验

Species
Animal Model
Administration Dosage Frequency Description References
Nude mice Breast cancer xenograft model Subcutaneous injection 10 μg/ml Twice a week for 20 days To evaluate the effect of Butein on in vivo breast cancer tumor growth, results showed that Butein inhibited the growth of BT-474 tumors but had no significant effect on HCC-1419 tumor growth J Exp Clin Cancer Res. 2014 Jun 11;33(1):51.
Nude mice HCC xenograft model Oral 10 mg/kg Once daily for several weeks Inhibited tumor growth and decreased expressions of Ki67 and phosphor-histone H3 Int J Biol Sci. 2018 Sep 7;14(11):1521-1534.
Nude mice PC-9 xenograft model Intraperitoneal injection 10 mg/kg Once daily for 28 days Butein significantly inhibited the growth of PC-9 xenografts by activating ER stress-dependent ROS generation and apoptosis pathways. Int J Biol Sci. 2019 Jun 4;15(8):1637-1653.
C57BL/6J mice High-fat diet-induced obese mouse model Intraperitoneal injection 5 mg/kg or 15 mg/kg per day Once daily for 8 weeks To investigate the effect of Butein on body weight gain and metabolism in high-fat diet-induced obese mice, results showed that Butein significantly reduced body weight gain and improved metabolic profiles. Cell Death Dis. 2018 Aug 29;9(9):876.

Butein/紫铆因 参考文献

[1]Yu SM, et al. Endothelium-dependent relaxation of rat aorta by butein, a novel cyclic AMP-specific phosphodiesterase inhibitor.Eur J Pharmacol. 1995 Jun 23;280(1):69-77.

[2]Yang EB, et al. Butein, a specific protein tyrosine kinase inhibitor.Biochem Biophys Res Commun. 1998 Apr 17;245(2):435-8.

[3]Zhang L, et al. Butein sensitizes HeLa cells to cisplatin through the AKT and ERK/p38 MAPK pathways by targeting FoxO3a.Int J Mol Med. 2015 Oct;36(4):957-66.

Butein/紫铆因 实验方案

计算器
存储液制备 1mg 5mg 10mg

1 mM

5 mM

10 mM

3.67mL

0.73mL

0.37mL

18.37mL

3.67mL

1.84mL

36.73mL

7.35mL

3.67mL

Butein/紫铆因 技术信息

CAS号487-52-5
分子式C15H12O5
分子量 272.25
SMILES Code OC1=CC=C(C(/C=C/C2=CC(O)=C(O)C=C2)=O)C(O)=C1
MDL No. MFCD00017300
别名 2’,3,4,4’-tetrahydroxy Chalcone
运输蓝冰
InChI Key AYMYWHCQALZEGT-ORCRQEGFSA-N
Pubchem ID 5281222
存储条件

In solvent -20°C: 3-6个月 -80°C: 12个月

Pure form Keep in dark place, inert atmosphere, store in freezer, under -20°C

溶解方案

DMSO: 50 mg/mL(183.65 mM),配合低频超声助溶,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

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
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