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。


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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 |
VEGFR,Src | 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 (L858R), IC50: 0.2 nM EGFR (WT), IC50: 0.3 nM |
98% | |||||||||||||||||
| Erlotinib |
++++
EGFR, IC50: 2 nM |
95% | |||||||||||||||||
| Saracatinib |
+++
EGFR (L861Q), IC50: 4 nM EGFR, IC50: 5 nM |
99%+ | |||||||||||||||||
| AG1557 | ✔ | 99% | |||||||||||||||||
| Rociletinib |
++
EGFR (L858R/T790M), Ki: 21.5 nM EGFR (wt), Ki: 303.3 nM |
98% | |||||||||||||||||
| AG490 |
+
EGFR, IC50: 0.1 μM |
98% | |||||||||||||||||
| Cetuximab |
++++
EGFR, Kd: 0.39 nM |
95% | |||||||||||||||||
| Osimertinib |
++
WT EGFR, IC50: 12.92 nM L858R/T790M EGFR, IC50: 11.44 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 (L861Q) , IC50: <1 nM EGFR (L858R), IC50: 6 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 |
++++
WT EGFR, IC50: 76 nM L858R/T790M EGFR, IC50: 2 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 | ✔ | PARP,Caspase | 99% | ||||||||||||||||
| Zipalertinib |
+++
EGFR (L861Q), IC50: 4.1 nM EGFR WT, IC50: 8 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 |
++++
EGFRL858R/T790M, IC50: 0.51 nM EGFRT790M, IC50: 0.79 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 |
Raf,Src | 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 (L858R/T790M), IC50: 0.4 nM EGFR (wt), IC50: 0.5 nM |
++
HER2, IC50: 14 nM |
98% | ||||||||||||||||
| Canertinib 2HCl |
+++
EGFR, IC50: 7.4 nM |
+++
ErbB2, IC50: 9 nM |
99% | ||||||||||||||||
| Allitinib tosylate |
++++
EGFR (T790M/L858R), IC50: 12 nM EGFR, IC50: 0.5 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 (L858R), IC50: 10 nM EGFR (wt), IC50: 0.5 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 |
ALK,FLT3 | 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。 | |||||||||||||||||||
| 靶点 |
|
| 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]. |
| 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. |
| 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. |
| 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 |
|
| 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 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
|
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