Cucurbitacin E | α-Elaterin | Natural Product | AmBeed-信号通路专用抑制剂

Cucurbitacin E/葫芦素 E {[allProObj[0].p_purity_real_show]}

货号：A513376 同义名： α-Elaterin; α-Elaterine

Cucurbitacin E是一种JAK2 和 STAT3的抑制剂，可抑制细胞周期蛋白B1/CDC2复合物的活性。

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There will be a HazMat fee per item when shipping a dangerous goods. The HazMat fee will be charged to your UPS/DHL/FedEx collect account or added to the invoice unless the package is shipped via Ground service. Ship by air in Excepted Quantity (each bottle), which is up to 1g/1mL for class 6.1 packing group I or II, and up to 25g/25ml for all other HazMat items.

Type	HazMat fee for 500 gram (Estimated)
Excepted Quantity	USD 0.00
Limited Quantity	USD 15-60
Inaccessible (Haz class 6.1), Domestic	USD 80+
Inaccessible (Haz class 6.1), International	USD 150+
Accessible (Haz class 3, 4, 5 or 8), Domestic	USD 100+
Accessible (Haz class 3, 4, 5 or 8), International	USD 200+

Cucurbitacin E/葫芦素 E 化学结构
CAS号：18444-66-1

Cucurbitacin E/葫芦素 E 3D分子结构
CAS号：18444-66-1

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CDK 亚型比较

产品名称	Cdc ↓ ↑	CDK1 ↓ ↑	CDK19 ↓ ↑	CDK2 ↓ ↑	CDK3 ↓ ↑	CDK4 ↓ ↑	CDK5 ↓ ↑	CDK6 ↓ ↑	CDK7 ↓ ↑	CDK8 ↓ ↑	CDK9 ↓ ↑	CLK ↓ ↑	其他靶点	纯度
XL413 HCl	++++ Cdc7, IC50: 3.4 nM													99%+
SU9516		+++ CDK1, IC50: 40 nM		+++ CDK2, IC50: 22 nM		++ CDK4, IC50: 200 nM								99%+
RO-3306		+++ CDK1, Ki: 20 nM											ERK,SGK	98%
R547		++++ CDK1/CyclinB, Ki: 2 nM		++++ CDK2/CyclinE, Ki: 3 nM		++++ CDK4/CyclinD1, Ki: 1 nM								99%+
BMS-265246		++++ CDK1/CyclinB, IC50: 6 nM		++++ CDK2/CyclinE, IC50: 9 nM		+ CDK4/CyclinD, IC50: 230 nM								99%+
NU6027		+ CDK1, Ki: 2.5 μM		+ CDK2, Ki: 1.3 μM									DNA-PK	98%
Purvalanol A	++++ Cdc2/CyclinB, IC50: 4 nM			+++ CDK2/CyclinA, IC50: 70 nM CDK2/CyclinE, IC50: 35 nM		+ CDK4/CyclinD1, IC50: 850 nM								99%+
SCH900776				++ CDK2, IC50: 0.16 μM										99%+
AUZ 454				++++ CDK2(A144C), Kd: 9.7 nM CDK2(C118L), Kd: 18.6 nM										99%+
A-674563 HCl				++ CDK2, Ki: 46 nM									PKA	99%
JNJ-7706621		++++ CDK1/CyclinB, IC50: 9 nM		++++ CDK2/CyclinA, IC50: 4 nM CDK2/CyclinE, IC50: 3 nM	++ CDK3/CyclinE, IC50: 58 nM	+ CDK4/CyclinD1, IC50: 253 nM		++ CDK6/CyclinD1, IC50: 175 nM						99%+
AT7519		++ CDK1/CyclinB, IC50: 210 nM		++ CDK2/CyclinA, IC50: 47 nM	+ CDK3/CyclinE, IC50: 360 nM	++ CDK4/CyclinD1, IC50: 100 nM	+++ CDK5/p35, IC50: 13 nM	++ CDK6/CyclinD3, IC50: 170 nM			++++ CDK9/CyclinT, IC50: <10 nM			98+%
PHA-793887		++ CDK1/CyclinB, IC50: 60 nM		++++ CDK2/CyclinA, IC50: 8 nM CDK2/CyclinE, IC50: 8 nM		++ CDK4/CyclinD1, IC50: 62 nM	++++ CDK5/p25, IC50: 5 nM		++++ CDK7/CyclinH, IC50: 10 nM		++ CDK9/CyclinT1, IC50: 138 nM			99%+
Milciclib		+ CDK1/CyclinB, IC50: 398 nM		++ CDK2/CyclinA, IC50: 45 nM CDK2/CyclinE, IC50: 363 nM		++ CDK4/CyclinD1, IC50: 160 nM	+ CDK5/p35, IC50: 265 nM		++ CDK7/CyclinH, IC50: 150 nM					99%+
Kenpaullone		+ CDK1/CyclinB, IC50: 0.4μM		+ CDK2/CyclinA, IC50: 0.68μM CDK2/CyclinE, IC50: 7.5μM			+ CDK5/p35, IC50: 0.85μM							98%
SNS-032				+++ CDK2/CyclinA, IC50: 38 nM CDK2/CyclinE, IC50: 48 nM			+ CDK5/p35, IC50: 340 nM		++ CDK7/CyclinH, IC50: 62 nM		++++ CDK9/CyclinT, IC50: 4 nM			99%+
Dinaciclib		++++ CDK1, IC50: 3 nM		++++ CDK2, IC50: 1 nM			++++ CDK5, IC50: 1 nM				++++ CDK9, IC50: 4 nM			99%+
PHA-767491 HCl	++++ Cdc7, IC50: 10 nM	+ CDK1, IC50: 250 nM		+ CDK2, IC50: 240 nM			+ CDK5, IC50: 460 nM				+++ CDK9, IC50: 34 nM		MK2	99%
(R)-Roscovitine	+ Cdc2/CyclinB, IC50: 0.65 μM			+ CDK2/CyclinA, IC50: 0.7 μM CDK2/CyclinE, IC50: 0.7 μM			++ CDK5/p35, IC50: 0.16 μM							99%+
Narazaciclib						++++ CDK4/CyclinD1, IC50: 3.87 nM		++++ CDK6/CyclinD1, IC50: 9.82 nM					RET	99%+
Palbociclib						++++ CDK4/CyclinD3, IC50: 9 nM CDK4/CyclinD1, IC50: 11 nM		+++ CDK6/CyclinD2, IC50: 15 nM						99%
Abemaciclib						++++ CDK4, IC50: 2 nM		++++ CDK6, IC50: 10 nM						99%
Ribociclib						++++ CDK4, IC50: 10 nM		+++ CDK6, IC50: 39 nM						98%
Palbociclib isethionate						++++ CDK4/CyclinD3, IC50: 9 nM CDK4/CyclinD1, IC50: 11 nM		+++ CDK6/CyclinD2, IC50: 15 nM						99%+
BS-181 HCl									+++ CDK7, IC50: 21 nM					99%+
(E/Z)-THZ1 2HCl									++++ CDK7, IC50: 3.2 nM					99%+
LDC4297									++++ CDK7, IC50: 0.13 nM					99%+
Senexin A			+ CDK19, Kd: 0.31 μM							+ CDK8, Kd: 0.83 μM				99%
MSC2530818										++++ CDK8, IC50: 2.6 nM				99%+
Wogonin											✔			99%+
Riviciclib HCl		++ CDK1/CyclinB, IC50: 79 nM		+ CDK2/CyclinA, IC50: 224 nM CDK2/CyclinE, IC50: 2.54 μM		++ CDK4/CyclinD1, IC50: 63 nM		+ CDK6/CyclinD3, IC50: 396 nM	+ CDK7/CyclinH, IC50: 2.87 μM		+++ CDK9/CyclinT1, IC50: 20 nM			98%
LDC000067				+ CDK2, IC50: 2.441 μM							++ CDK9, IC50: 44 nM			98%
Flavopiridol		+++ CDK1, IC50: 40 nM		+++ CDK2, IC50: 40 nM		+++ CDK4, IC50: 40 nM		+++ CDK6, IC50: 40 nM	+ CDK7, IC50: 300 nM		+++ CDK9, IC50: 20 nM			99%+
LY2857785									+ CDK7, IC50: 0.246 μM	+++ CDK8, IC50: 0.016 μM	+++ CDK9, IC50: 0.011 μM			99%+
AZD-5438		+++ CDK1, IC50: 16 nM		++++ CDK2, IC50: 6 nM							+++ CDK9, IC50: 20 nM			99%+
ML167												++ Dyrk1B , IC50: 1648 nM CLK4, IC50: 136 nM		99%+
(E/Z)-TG003												+++ mCLK1, IC50: 200 nM mCLK4, IC50: 15 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。

Cucurbitacin E/葫芦素 E 生物活性

描述

Cyclin-dependent kinases (CDKs) are a group of multifunctional enzymes consisting of catalytic and regulatory subunits^[3]. Cucurbitacin E is a natural compound which from the climbing stem of Cucumic melo L. Cucurbitacin E significantly suppresses the activity of the cyclin B1/CDC2 complex. in vitro study is initiated in which each of the CRC cell lines is exposed to increasing doses of Cucurbitacin E (0, 2.5, 5, and 7.5 μM) over a period of 24 h. Cucurbitacin E is shown to induce morphological changes in the primary colon cancer cells. A remarkable change in morphology was observed in the period of 6 and 24 h. Cucurbitacin E inhibits tumor growth by arresting the cell cycle in the G2/M phase via GADD45γ gene expression and the blockage of cyclin B1/CDC2 complex in primary CRC cells^[4]. A high fat diet mice model of metabolic syndrome (HFD-MetS) is developed to assess the role of Cucurbitacin E (CuE) on body weight and fat tissue biology. Results showed a significant decrease in body weights of mice treated with Cucurbitacin E (0.5mg/kg) and central obesity is also reduced after the treatment^[5].

Cucurbitacin E/葫芦素 E 细胞实验

Cell Line human chondrocytes A375 human melanoma cells MRC-5 and HS68 cells SAS cells HUVEC cells Huh7 cells AMC-HN-8 cells TU686 cells AMC-HN-8 cells TU686 cells Human primary colorectal cancer cell lines (CP1-CP5) Human brain malignant glioma GBM 8401 cells	Concentration	Treated Time	Description	References
human chondrocytes	1, 5, 10 nM	24 h	Inhibited the expression of inflammatory factors IL-1β and COX-2 induced by IL-1β, alleviated extracellular matrix degradation	J Transl Med. 2023 Dec 4;21(1):880
A375 human melanoma cells	0, 1, 2, 4, 8 μM	24-48 h	Inhibited A375 cell proliferation and induced apoptosis	Chin Med. 2022 Feb 22;17(1):28
MRC-5 and HS68 cells	0, 1.25, 2.5, 5 µM	24 h	To assess the effect of Cucurbitacin E on normal cells, results showed minimal impact on MRC-5 and HS68 cell proliferation.	Int J Mol Sci. 2013 Aug 20;14(8):17147-56
SAS cells	0, 1.25, 2.5, 5 µM	24 to 72 h	To evaluate the inhibitory effect of Cucurbitacin E on SAS cell proliferation, results showed that Cucurbitacin E inhibited SAS cell proliferation in a dose-dependent manner.	Int J Mol Sci. 2013 Aug 20;14(8):17147-56
HUVEC cells	0, 10, 20, 40 nM	6 h	To evaluate the effect of CuE on tube formation in HUVEC cells, results showed that CuE significantly inhibited tube formation.	Molecules. 2020 Jan 28;25(3):560
Huh7 cells	0, 10, 20, 40 nM	24 or 48 h	To evaluate the anti-proliferative effect of CuE on Huh7 cells, results showed that CuE significantly inhibited cell proliferation in a concentration- and time-dependent manner.	Molecules. 2020 Jan 28;25(3):560
AMC-HN-8 cells	0.05, 0.1, 0.2 μM	24 h	To evaluate the effect of Cucurbitacin E on mitochondrial membrane potential, results showed that Cucurbitacin E significantly decreased mitochondrial membrane potential.	Am J Cancer Res. 2024 Aug 25;14(8):3905-3921
TU686 cells	0.05, 0.1, 0.2 μM	24 h	To evaluate the effect of Cucurbitacin E on mitochondrial membrane potential, results showed that Cucurbitacin E significantly decreased mitochondrial membrane potential.	Am J Cancer Res. 2024 Aug 25;14(8):3905-3921
AMC-HN-8 cells	0.05, 0.1, 0.2, 0.4 μM	24, 48, 72 h	To evaluate the effect of Cucurbitacin E on the viability of LSCC cells, results showed that Cucurbitacin E significantly reduced the viability of LSCC cells in a concentration- and time-dependent manner.	Am J Cancer Res. 2024 Aug 25;14(8):3905-3921
TU686 cells	0.05, 0.1, 0.2, 0.4 μM	24, 48, 72 h	To evaluate the effect of Cucurbitacin E on the viability of LSCC cells, results showed that Cucurbitacin E significantly reduced the viability of LSCC cells in a concentration- and time-dependent manner.	Am J Cancer Res. 2024 Aug 25;14(8):3905-3921
Human primary colorectal cancer cell lines (CP1-CP5)	2.5-7.5 μM	24 h	To investigate the inhibitory effect of Cucurbitacin E on the proliferation of colorectal cancer cells and its ability to induce G2/M phase cell cycle arrest. Results showed that Cucurbitacin E inhibited cell proliferation in a dose-dependent manner and induced G2/M phase cell cycle arrest.	Cell Death Dis. 2014 Apr 24;5(4):e1198
Human brain malignant glioma GBM 8401 cells	0, 2.5, 5, 10 μM	24 h	To evaluate the inhibitory effect of Cucurbitacin E on the proliferation of GBM 8401 cells. Results showed that Cucurbitacin E inhibited the proliferation of GBM 8401 cells in a dose-dependent manner and induced G2/M phase cell cycle arrest.	Cell Death Dis. 2014 Feb 27;5(2):e1087

Cell Line

Concentration

Treated Time

Description

References

human chondrocytes

1, 5, 10 nM

24 h

Inhibited the expression of inflammatory factors IL-1β and COX-2 induced by IL-1β, alleviated extracellular matrix degradation

J Transl Med. 2023 Dec 4;21(1):880

A375 human melanoma cells

0, 1, 2, 4, 8 μM

24-48 h

Inhibited A375 cell proliferation and induced apoptosis

Chin Med. 2022 Feb 22;17(1):28

MRC-5 and HS68 cells

0, 1.25, 2.5, 5 µM

24 h

To assess the effect of Cucurbitacin E on normal cells, results showed minimal impact on MRC-5 and HS68 cell proliferation.

Int J Mol Sci. 2013 Aug 20;14(8):17147-56

SAS cells

0, 1.25, 2.5, 5 µM

24 to 72 h

To evaluate the inhibitory effect of Cucurbitacin E on SAS cell proliferation, results showed that Cucurbitacin E inhibited SAS cell proliferation in a dose-dependent manner.

Int J Mol Sci. 2013 Aug 20;14(8):17147-56

HUVEC cells

0, 10, 20, 40 nM

6 h

To evaluate the effect of CuE on tube formation in HUVEC cells, results showed that CuE significantly inhibited tube formation.

Molecules. 2020 Jan 28;25(3):560

Huh7 cells

0, 10, 20, 40 nM

24 or 48 h

To evaluate the anti-proliferative effect of CuE on Huh7 cells, results showed that CuE significantly inhibited cell proliferation in a concentration- and time-dependent manner.

Molecules. 2020 Jan 28;25(3):560

AMC-HN-8 cells

0.05, 0.1, 0.2 μM

24 h

To evaluate the effect of Cucurbitacin E on mitochondrial membrane potential, results showed that Cucurbitacin E significantly decreased mitochondrial membrane potential.

Am J Cancer Res. 2024 Aug 25;14(8):3905-3921

TU686 cells

0.05, 0.1, 0.2 μM

24 h

To evaluate the effect of Cucurbitacin E on mitochondrial membrane potential, results showed that Cucurbitacin E significantly decreased mitochondrial membrane potential.

Am J Cancer Res. 2024 Aug 25;14(8):3905-3921

AMC-HN-8 cells

0.05, 0.1, 0.2, 0.4 μM

24, 48, 72 h

To evaluate the effect of Cucurbitacin E on the viability of LSCC cells, results showed that Cucurbitacin E significantly reduced the viability of LSCC cells in a concentration- and time-dependent manner.

Am J Cancer Res. 2024 Aug 25;14(8):3905-3921

TU686 cells

0.05, 0.1, 0.2, 0.4 μM

24, 48, 72 h

Am J Cancer Res. 2024 Aug 25;14(8):3905-3921

Human primary colorectal cancer cell lines (CP1-CP5)

2.5-7.5 μM

24 h

To investigate the inhibitory effect of Cucurbitacin E on the proliferation of colorectal cancer cells and its ability to induce G2/M phase cell cycle arrest. Results showed that Cucurbitacin E inhibited cell proliferation in a dose-dependent manner and induced G2/M phase cell cycle arrest.

Cell Death Dis. 2014 Apr 24;5(4):e1198

Human brain malignant glioma GBM 8401 cells

0, 2.5, 5, 10 μM

24 h

To evaluate the inhibitory effect of Cucurbitacin E on the proliferation of GBM 8401 cells. Results showed that Cucurbitacin E inhibited the proliferation of GBM 8401 cells in a dose-dependent manner and induced G2/M phase cell cycle arrest.

Cell Death Dis. 2014 Feb 27;5(2):e1087

Cucurbitacin E/葫芦素 E 动物实验

Species C57BL/6 mice BALB/c-nu nude mice BALB/c nu/nu athymic nude mice C57BL/6j mice BALB/c nude mice	Animal Model Medial meniscal instability-induced osteoarthritis model ACC xenograft model Subcutaneous melanoma xenograft model DSS-induced colitis model TU686 cell xenograft model	Administration	Dosage	Frequency	Description	References
C57BL/6 mice	Medial meniscal instability-induced osteoarthritis model	Intra-articular injection	0.5 mg/kg	Twice a week for 3 months	Evaluated the effect of Cucurbitacin E on knee joint degeneration, results showed Cucurbitacin E had a protective effect on knee cartilage in the osteoarthritis model	J Transl Med. 2023 Dec 4;21(1):880
BALB/c-nu nude mice	ACC xenograft model	Intraperitoneal injection	10, 20 mg/kg	Once daily for 3 weeks	To evaluate the inhibitory effect of Cucurbitacin E on ACC xenograft tumors, results showed that Cucurbitacin E dose-dependently inhibited tumor growth, and its combination with mitotane almost completely eliminated the tumors.	J Transl Med. 2022 Oct 2;20(1):444
BALB/c nu/nu athymic nude mice	Subcutaneous melanoma xenograft model	Intraperitoneal injection	5 mg/kg	Once every four days for 3 weeks	Inhibited melanoma growth	Chin Med. 2022 Feb 22;17(1):28
C57BL/6j mice	DSS-induced colitis model	Oral gavage	10 mg/kg	Once daily for 14 days	Alleviated DSS-induced colitis symptoms, improved intestinal barrier function and inflammatory response, modulated gut microbiota composition	J Inflamm Res. 2024 May 6;17:2745-2756
BALB/c nude mice	TU686 cell xenograft model	Intraperitoneal injection	5 or 10 mg/kg	Administered every other day for three weeks	To evaluate the anti-tumor activity of Cucurbitacin E in vivo, results showed that Cucurbitacin E significantly inhibited tumor growth and induced tumor cell apoptosis.	Am J Cancer Res. 2024 Aug 25;14(8):3905-3921

Species

C57BL/6 mice BALB/c-nu nude mice BALB/c nu/nu athymic nude mice C57BL/6j mice BALB/c nude mice

Animal Model

Medial meniscal instability-induced osteoarthritis model ACC xenograft model Subcutaneous melanoma xenograft model DSS-induced colitis model TU686 cell xenograft model

Administration

Dosage

Frequency

Description

References

C57BL/6 mice

Medial meniscal instability-induced osteoarthritis model

Intra-articular injection

0.5 mg/kg

Twice a week for 3 months

Evaluated the effect of Cucurbitacin E on knee joint degeneration, results showed Cucurbitacin E had a protective effect on knee cartilage in the osteoarthritis model

J Transl Med. 2023 Dec 4;21(1):880

BALB/c-nu nude mice

ACC xenograft model

Intraperitoneal injection

10, 20 mg/kg

Once daily for 3 weeks

To evaluate the inhibitory effect of Cucurbitacin E on ACC xenograft tumors, results showed that Cucurbitacin E dose-dependently inhibited tumor growth, and its combination with mitotane almost completely eliminated the tumors.

J Transl Med. 2022 Oct 2;20(1):444

BALB/c nu/nu athymic nude mice

Subcutaneous melanoma xenograft model

Intraperitoneal injection

5 mg/kg

Once every four days for 3 weeks

Inhibited melanoma growth

Chin Med. 2022 Feb 22;17(1):28

C57BL/6j mice

DSS-induced colitis model

Oral gavage

10 mg/kg

Once daily for 14 days

Alleviated DSS-induced colitis symptoms, improved intestinal barrier function and inflammatory response, modulated gut microbiota composition

J Inflamm Res. 2024 May 6;17:2745-2756

BALB/c nude mice

TU686 cell xenograft model

Intraperitoneal injection

5 or 10 mg/kg

Administered every other day for three weeks

To evaluate the anti-tumor activity of Cucurbitacin E in vivo, results showed that Cucurbitacin E significantly inhibited tumor growth and induced tumor cell apoptosis.

Am J Cancer Res. 2024 Aug 25;14(8):3905-3921

Cucurbitacin E/葫芦素 E 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
NCT02858388	Otitis Media With Effusion	Phase 3	Completed	-	Italy ... 展开 >> San Gennaro Hospital Naples, Italy, 80136 收起 <<

NCT号

适应症或疾病

临床期

招募状态

预计完成时间

地点

NCT02858388

Otitis Media With Effusion

Phase 3

Completed

Italy ... 展开 >> San Gennaro Hospital Naples, Italy, 80136 收起 <<

Cucurbitacin E/葫芦素 E 参考文献

Cucurbitacin E/葫芦素 E 实验方案

计算器

存储液制备

1mg

5mg

10mg

1 mM

5 mM

10 mM

1.80mL

0.36mL

0.18mL

8.98mL

1.80mL

0.90mL

17.96mL

3.59mL

1.80mL

Cucurbitacin E/葫芦素 E 技术信息

CAS号	18444-66-1
分子式	C₃₂H₄₄O₈
分子量	556.69
SMILES Code	O[C@H](C1)[C@@]([C@@](C)(O)C(/C=C/C(OC(C)=O)(C)C)=O)([H])[C@](C2)(C)[C@]1(C)[C@]3([H])CC=C4C(C)(C)C(C(O)=C[C@@]4([H])[C@]3(C)C2=O)=O
MDL No.	MFCD00135936

别名	α-Elaterin; α-Elaterine; NSC 521775; NSC 106399
运输	蓝冰
InChI Key	NDYMQXYDSVBNLL-MUYMLXPFSA-N
Pubchem ID	5281319

存储条件

In solvent -20°C: 3-6个月 -80°C: 12个月

Pure form Sealed in dry, store in freezer, under -20°C

溶解方案

细胞实验：

DMSO: 50 mg/mL(89.82 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

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

Cucurbitacin E/葫芦素 E {[allProObj[0].p_purity_real_show]}

Cucurbitacin E/葫芦素 E 纯度/质量文件产品仅供科研

全球学术期刊中引用的产品

Cucurbitacin E/葫芦素 E 质控信息

Cucurbitacin E/葫芦素 E 生物活性

Cucurbitacin E/葫芦素 E 细胞实验

Cucurbitacin E/葫芦素 E 动物实验

Cucurbitacin E/葫芦素 E 临床研究

Cucurbitacin E/葫芦素 E 参考文献

Cucurbitacin E/葫芦素 E 实验方案

Cucurbitacin E/葫芦素 E 技术信息

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Cucurbitacin E/葫芦素 E {[allProObj[0].p_purity_real_show]}

Cucurbitacin E/葫芦素 E 纯度/质量文件 产品仅供科研

全球学术期刊中引用的产品

Cucurbitacin E/葫芦素 E 质控信息

Cucurbitacin E/葫芦素 E 生物活性

Cucurbitacin E/葫芦素 E 细胞实验

Cucurbitacin E/葫芦素 E 动物实验

Cucurbitacin E/葫芦素 E 临床研究

Cucurbitacin E/葫芦素 E 参考文献

Cucurbitacin E/葫芦素 E 实验方案

Cucurbitacin E/葫芦素 E 技术信息

最近浏览的产品

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