分类目录归档：苯丙素类

天然产物苯丙素类 Phenylpropanoids

Etoposide(Synonyms: 依托泊苷; VP-16; VP-16-213)

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天然产物 天然产物苯丙素类 Phenylpropanoids

Etoposide (Synonyms: 依托泊苷; VP-16; VP-16-213) 纯度: 99.86%

Etoposide (VP-16; VP-16-213) 是一种常用的抗肿瘤化疗剂。Etoposide 抑制拓扑异构酶 II (topoisomerase-II)，从而抑制 DNA 复制。Etoposide 诱导细胞周期停滞，凋亡 (apoptosis) 和自噬 (autophagy)。

Etoposide(Synonyms: 依托泊苷; VP-16; VP-16-213)

Etoposide Chemical Structure

CAS No. : 33419-42-0

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生物活性

Etoposide (VP-16; VP-16-213) is an anti-cancer chemotherapy agent. Etoposide inhibits topoisomerase II, thus stopping DNA replication. Etoposide induces cell cycle arrest, apoptosis and autophagy[1].

IC50 & Target[1]

Topoisomerase II

 

体外研究
(In Vitro)

Etoposide is capable of causing cytotoxicity on pancreatic β-cells by inducing apoptosis through the JNK/ERK-mediated GSK-3 downstream-triggered mitochondria-dependent signaling pathway in RIN-m5F cells[1].
Etoposide and Anti-Human VEGF significantly abolish P1 sphere-forming ability, an effect associated with apoptosis of this subset of cells[2].
Etoposide phosphate (0-1μM; 72 hours) inhibits HCT116 FBXW+/+, FBXW-/- and p53-/- as a dose-dependent manner, exhibits IC50s of 0.945 μM; 0.375 μM; and 1.437 μM, respectively[5].
Etoposide (25 μM; 6 hours) delays p53 recover in FBXW7-deficient cells. In addition, FBXW7 expression is disappeared in FBXW7-/- cells[5].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Viability Assay[5]

Cell Line: HCT116 FBXW+/+, FBXW-/- and p53-/- cells
Concentration: 0.025 μM, 0.05 μM, 0.075 μM, 0.1 μM, 0.2 μM, 0.4 μM, 0.6 μM, 0.8 μM, 1 μM
Incubation Time: 72 hours
Result: Inhibits HCT116 FBXW+/+p>, FBXW-/- and p53-/- cell growth as a concentration manner.

Western Blot Analysis[5]

Cell Line: HCT116 FBXW7+/+ or FBXW7-/- cells
Concentration: 25 μM
Incubation Time: 6 hours
Result: Exhibited that the recovery of p53 levels after DNA damage is mediated by FBXW7.

体内研究
(In Vivo)

Etoposide (50 μM) and Anti-Human VEGF-treated hypoxic cells injected intravenously into immunodeficient mice reveals a reduced capacity to induce lung colonies, which also appear with a longer latency period[2]. Etoposide (10 mg/kg/day, i.v.) with NSC 109724 and NSC 241240, reduces the tumor volume in the hepatoblastoma cell injected NMRI nude mice[3].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Clinical Trial

分子量

588.56

Formula

C29H32O13
CAS 号

33419-42-0
中文名称

依托泊苷；臼乙叉苷；足叶乙甙
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

4°C, protect from light

*In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)
溶解性数据
In Vitro: 

DMSO : ≥ 39 mg/mL (66.26 mM)

* “≥” means soluble, but saturation unknown.

配制储备液
浓度 溶剂体积 质量 1 mg 5 mg 10 mg
1 mM 1.6991 mL 8.4953 mL 16.9906 mL
5 mM 0.3398 mL 1.6991 mL 3.3981 mL
10 mM 0.1699 mL 0.8495 mL 1.6991 mL

*

请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。
储备液的保存方式和期限：-80°C, 6 months; -20°C, 1 month (protect from light)。-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。

In Vivo:

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 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，建议您现用现配，当天使用； 以下溶剂前显示的百
分比是指该溶剂在您配制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

  • 1.

    请依序添加每种溶剂： 10% DMSO    40% PEG300    5% Tween-80    45% saline

    Solubility: ≥ 2.5 mg/mL (4.25 mM); Clear solution

    此方案可获得 ≥ 2.5 mg/mL (4.25 mM，饱和度未知) 的澄清溶液。

    以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀；向上述体系中加入50 μL Tween-80，混合均匀；然后继续加入 450 μL生理盐水定容至 1 mL。

    将 0.9 g 氯化钠，完全溶解于 100 mL ddH₂O 中，得到澄清透明的生理盐水溶液

  • 2.

    请依序添加每种溶剂： 10% DMSO    90% corn oil

    Solubility: ≥ 2.5 mg/mL (4.25 mM); Clear solution

    此方案可获得 ≥ 2.5 mg/mL (4.25 mM，饱和度未知) 的澄清溶液，此方案不适用于实验周期在半个月以上的实验。

    以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中，混合均匀。

  • 3.

    请依序添加每种溶剂： 5% DMSO    40% PEG300    5% Tween-80    50% saline

    Solubility: ≥ 2.5 mg/mL (4.25 mM); Clear solution

  • 4.

    请依序添加每种溶剂： 5% DMSO    95% (20% SBE-β-CD in saline)

    Solubility: ≥ 2.5 mg/mL (4.25 mM); Clear solution

  • 5.

    请依序添加每种溶剂： 1% DMSO    99% saline

    Solubility: ≥ 0.5 mg/mL (0.85 mM); Clear solution

*以上所有助溶剂都可在 MCE 网站选购。
参考文献

  • [1]. Lee KI, et al. Etoposide induces pancreatic β-cells cytotoxicity via the JNK/ERK/GSK-3 signaling-mediated mitochondria-dependent apoptosis pathway. Toxicol In Vitro. 2016 Jul 26. pii: S0887-2333(16)30147-3.

    [2]. Calvani M, det al. Etoposide-Anti-Human VEGF a new strategy against human melanoma cells expressing stem-like traits. Oncotarget. 2016 Jun 9. doi: 10.18632/oncotarget.9939.

    [3]. Fuchs, J., et al. Comparative activity of NSC 119875, NSC 109724, NSC 123127, NSC 241240, and etoposide in heterotransplanted hepatoblastoma. Cancer, 1998. 83(11): p. 2400-7.

    [4]. Hande KR, et al. The Importance of Drug Scheduling in Cancer Chemotherapy: Etoposide as an Example. Oncologist. 1996;1(4):234-239.

    [5]. Cui D, et al. FBXW7 Confers Radiation Survival by Targeting p53 for Degradation.Cell Rep. 2020 Jan 14;30(2):497-509.e4.

Honokiol(Synonyms: 和厚朴酚; NSC 293100)

发表于由

天然产物 天然产物苯丙素类 Phenylpropanoids

Honokiol (Synonyms: 和厚朴酚; NSC 293100) 纯度: 98.92%

Honokiol是一种具有生物活性的双酚类植物化学物质，靶向多种信号分子，具有有效的抗氧化，抗炎，抗血管生成和抗癌活性。 它抑制 Akt 的活化。Honokiol 能透过血脑屏障。

Honokiol(Synonyms: 和厚朴酚; NSC 293100)

Honokiol Chemical Structure

CAS No. : 35354-74-6

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Free Sample (0.1-0.5 mg)   Apply now  
10 mM * 1 mL in DMSO ￥500 In-stock
10 mg ￥450 In-stock
50 mg ￥550 In-stock
100 mg ￥770 In-stock
200 mg ￥990 In-stock
500 mg   询价  
1 g   询价  

* Please select Quantity before adding items.

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生物活性

Honokiol is a bioactive, biphenolic phytochemical that possesses potent antioxidative, anti-inflammatory, antiangiogenic, and anticancer activities by targeting a variety of signaling molecules. It inhibits the activation of Akt. Honokiol can readily cross the blood brain barrier[1][2][3][4].

IC50 & Target[4]

Akt

 

ERK1

 

ERK2

 

Autophagy

 

体外研究
(In Vitro)

Honokiol (0, 12.5, 25 and 50 μM) inhibits the growth of GBM cells and induces apoptosis, with IC50 of appr against 30 μM DBTRG-05MG cell. Honokiol-induced apoptosis of GBM cells is associated with the downregulation of the Rb protein and cleavage of PARP and Bcl-x (S/L). Honokiol (50 μM) increases the level of autophagy markers in GBM cells[1]. Honokiol has anticancer effect, and the IC50 values with MDA-MB-231, MDA-MB-468, and MDA-MB-453 cell lines is 16.99 ± 1.28 μM, 15.94 ± 2.35 μM and 20.11 ±3.13 μM respectively. Honokiol (3, 10 μM) produces significant inhibition on the spheroid number and spheroid sizes in the clonogenic assay[2]. Honokiol (0.1-1.0 μM) specifically inhibits washed human platelet aggregation stimulated by collagen, but not by other agonists. honokiol (0.6 and 1.0 μM) can concentration-dependently inhibit the collagen-induced ATP-release reaction in washed human platelets. Honokiol specifically inhibits platelet aggregation and the phosphorylation of Lyn, PLCγ2, and PKC stimulated with convulxin. Honokiol (5, 10 μM) significantly inhibits convulxin-stimulated MAPKs and Akt activation[3].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究
(In Vivo)

Honokiol-NM (40 mg/kg, p.o.) produces superior anticancer effects, and the PCNA, Cyclin D1 and cleaved caspase 3 expressions are 2.12, 1.92 and 1.68-fold significantly altered in this treated group[2].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.
分子量

266.33

Formula

C18H18O2
CAS 号

35354-74-6
中文名称

和厚朴酚
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式
Powder -20°C 3 years
4°C 2 years
In solvent -80°C 6 months
-20°C 1 month
溶解性数据
In Vitro: 

DMSO : ≥ 50 mg/mL (187.74 mM)

* “≥” means soluble, but saturation unknown.

配制储备液
浓度 溶剂体积 质量 1 mg 5 mg 10 mg
1 mM 3.7547 mL 18.7737 mL 37.5474 mL
5 mM 0.7509 mL 3.7547 mL 7.5095 mL
10 mM 0.3755 mL 1.8774 mL 3.7547 mL

*

请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。
储备液的保存方式和期限：-80°C, 6 months; -20°C, 1 month。-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。

In Vivo:

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 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，建议您现用现配，当天使用； 以下溶剂前显示的百
分比是指该溶剂在您配制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

  • 1.

    请依序添加每种溶剂： corn oil

    Solubility: 16.67 mg/mL (62.59 mM); Clear solution; Need ultrasonic

  • 2.

    请依序添加每种溶剂： 10% DMSO    40% PEG300    5% Tween-80    45% saline

    Solubility: ≥ 2.5 mg/mL (9.39 mM); Clear solution

    此方案可获得 ≥ 2.5 mg/mL (9.39 mM，饱和度未知) 的澄清溶液。

    以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀；向上述体系中加入50 μL Tween-80，混合均匀；然后继续加入 450 μL生理盐水定容至 1 mL。

    将 0.9 g 氯化钠，完全溶解于 100 mL ddH₂O 中，得到澄清透明的生理盐水溶液

  • 3.

    请依序添加每种溶剂： 10% DMSO    90% (20% SBE-β-CD in saline)

    Solubility: ≥ 2.5 mg/mL (9.39 mM); Clear solution

    此方案可获得 ≥ 2.5 mg/mL (9.39 mM，饱和度未知) 的澄清溶液。

    以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL 20% 的 SBE-β-CD 生理盐水水溶液中，混合均匀。

    将 2 g 磺丁基醚 β-环糊精加入 5 mL 生理盐水中，再用生理盐水定容至 10 mL，完全溶解，澄清透明
  • 4.

    请依序添加每种溶剂： 10% DMSO    90% corn oil

    Solubility: ≥ 2.5 mg/mL (9.39 mM); Clear solution

    此方案可获得 ≥ 2.5 mg/mL (9.39 mM，饱和度未知) 的澄清溶液，此方案不适用于实验周期在半个月以上的实验。

    以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中，混合均匀。

*以上所有助溶剂都可在 MCE 网站选购。
参考文献

  • [1]. Chang KH, et al. Honokiol-induced apoptosis and autophagy in glioblastoma multiforme cells. Oncol Lett. 2013 Nov;6(5):1435-1438.

    [2]. Godugu C, et al. Honokiol nanomicellar formulation produced increased oral bioavailability and anticancer effects in triple negative breast cancer (TNBC). Colloids Surf B Biointerfaces. 2017 Jan 23;153:208-219

    [3]. Lee TY, et al. Honokiol as a specific collagen receptor glycoprotein VI antagonist on human platelets: Functional ex vivo and in vivo studies. Sci Rep. 2017 Jan 5;7:40002

    [4]. Zhai H, et al. Honokiol-induced neurite outgrowth promotion depends on activation of extracellular signal-regulated kinases (ERK1/2). Eur J Pharmacol. 2005 Jun 1;516(2):112-7.
Cell Assay
[2]

In cytotoxicity assays, 10,000 cells/well are added to 96 wells plates and incubated overnight, thereafter cells are treated with different concentrations of Honokiol dissolved in dimethylsulphoxide (DMSO). Since Honokiol is not soluble in aqueous solvents, for in vitro studies Honokiol is dissolved in DMSO. To study the possible effect of DMSO on cells, solvent (DMSO) control is used at highest concentration of <0.1%. After 72 h treatment, cells are fixed and cell viability is measured by crystal violet staining (0.05%).

MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Administration
[2]

For anticancer in vivo studies, the MDA-MB-231 cells (2 million) are injected into mammary fat tissue. Two weeks after the tumor cell injections, palpable tumors are observed in mammary tissues, which is an indication of tumor formation. Then drug treatment either in free form or in nanomicellar forms is given orally at the dose of 40 and 80 mg/kg daily. The drug treatment is continued for 4 weeks, and the tumor volumes and body weights are recorded weekly. After 4 weeks of treatment, animals are sacrificed; final tumor volumes and weights are measured. These tumors are used for western blot and immunohistochemical analysis. For western blot experiments, tumor tissues are stored at −80°C till the analysis is done. For IHC, tumors are fixed in formal saline.

MCE has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献

  • [1]. Chang KH, et al. Honokiol-induced apoptosis and autophagy in glioblastoma multiforme cells. Oncol Lett. 2013 Nov;6(5):1435-1438.

    [2]. Godugu C, et al. Honokiol nanomicellar formulation produced increased oral bioavailability and anticancer effects in triple negative breast cancer (TNBC). Colloids Surf B Biointerfaces. 2017 Jan 23;153:208-219

    [3]. Lee TY, et al. Honokiol as a specific collagen receptor glycoprotein VI antagonist on human platelets: Functional ex vivo and in vivo studies. Sci Rep. 2017 Jan 5;7:40002

    [4]. Zhai H, et al. Honokiol-induced neurite outgrowth promotion depends on activation of extracellular signal-regulated kinases (ERK1/2). Eur J Pharmacol. 2005 Jun 1;516(2):112-7.

Picropodophyllin(Synonyms: 苦鬼臼毒素; AXL1717; Picropodophyllin; PPP)

发表于由

天然产物 天然产物苯丙素类 Phenylpropanoids

Picropodophyllin (Synonyms: 苦鬼臼毒素; AXL1717; Picropodophyllin; PPP) 纯度: 99.90%

Picropodophyllin (AXL1717) 是选择性的胰岛素样生长因子-1受体 (IGF-1R)抑制剂，IC50 为1 nM。

Picropodophyllin(Synonyms: 苦鬼臼毒素; AXL1717; Picropodophyllin; PPP)

Picropodophyllin Chemical Structure

CAS No. : 477-47-4

规格 价格 是否有货 数量
Free Sample (0.1-0.5 mg)   Apply now  
10 mM * 1 mL in DMSO ￥715 In-stock
5 mg ￥650 In-stock
10 mg ￥900 In-stock
50 mg ￥3200 In-stock
100 mg ￥5600 In-stock
200 mg   询价  
500 mg   询价  

* Please select Quantity before adding items.

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生物活性

Picropodophyllin (AXL1717) is a selective insulin-like growth factor-1 receptor (IGF-1R) inhibitor with an IC50 of 1 nM.

IC50 & Target

IC50: 1 nM (IGF-1R)
体外研究
(In Vitro)

Picropodophyllin (AXL1717) (0.5, 2.5, 10 μM) potently inhibits IGF-1-stimulated IGF-1R, Akt (Ser 473) and Erk1/2 phosphorylation in intact cells. Picropodophyllin (AXL1717) also inhibits cell growth, and induces apoptosis in cultured IGF-1R-positive tumor cells[1]. Picropodophyllin (AXL1717) synergistically sensitizes HMCL, primary human MM and murine 5T33MM cells to ABT-737 and ABT-199 via further decreasing cell viability and enhancing apoptosis[3]. Picropodophyllin and sorafenib synergistically suppress the proliferation and motility of hepatocellular carcinoma cells[4].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究
(In Vivo)

Picropodophyllin (AXL1717) (20 mg/kg/12 h, i.p.) causes complete tumor regression in SCID mice xenografted with human ES-1, BE, and PC3[1]. Picropodophyllin (AXL1717) shows a potent antitumor activity, increases survival in the 5T33MM mouse model[2].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Clinical Trial

分子量

414.41

Formula

C22H22O8
CAS 号

477-47-4
中文名称

苦鬼臼毒素
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式
Powder -20°C 3 years
4°C 2 years
In solvent -80°C 6 months
-20°C 1 month
溶解性数据
In Vitro: 

DMSO : 50 mg/mL (120.65 mM; Need ultrasonic)

配制储备液
浓度 溶剂体积 质量 1 mg 5 mg 10 mg
1 mM 2.4131 mL 12.0653 mL 24.1307 mL
5 mM 0.4826 mL 2.4131 mL 4.8261 mL
10 mM 0.2413 mL 1.2065 mL 2.4131 mL

*

请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。
储备液的保存方式和期限：-80°C, 6 months; -20°C, 1 month。-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。

In Vivo:

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 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，建议您现用现配，当天使用； 以下溶剂前显示的百
分比是指该溶剂在您配制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

  • 1.

    请依序添加每种溶剂： 10% DMSO    90% corn oil

    Solubility: ≥ 2.5 mg/mL (6.03 mM); Clear solution

    此方案可获得 ≥ 2.5 mg/mL (6.03 mM，饱和度未知) 的澄清溶液，此方案不适用于实验周期在半个月以上的实验。

    以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中，混合均匀。

*以上所有助溶剂都可在 MCE 网站选购。
参考文献

  • [1]. Girnita A, et al. Cyclolignans as inhibitors of the insulin-like growth factor-1 receptor and malignant cell growth. Cancer Res. 2004 Jan 1;64(1):236-42.

    [2]. Menu E, et al. Inhibiting the IGF-1 receptor tyrosine kinase with the cyclolignan PPP: an in vitro and in vivo study in the 5T33MM mouse model. Blood. 2006 Jan 15;107(2):655-60. Epub 2005 Jul 26.

    [3]. Bieghs L, et al. The IGF-1 receptor inhibitor picropodophyllin potentiates the anti-myeloma activity of a BH3-mimetic. Oncotarget. 2014 Nov 30;5(22):11193-208.

    [4]. Tomizawa M, et al. Picropodophyllin and sorafenib synergistically suppress the proliferation and motility of hepatocellular carcinoma cells. Oncol Lett. 2014 Nov;8(5):2023-2026. Epub 2014 Aug 27.

    [5]. Stromberg T, et al. IGF-1 receptor tyrosine kinase inhibition by the cyclolignan PPP induces G2/M-phase accumulation and apoptosis in multiple myeloma cells. Blood. 2006 Jan 15;107(2):669-78. Epub 2005 Sep 15.

    [6]. Kong YL, et al. Insulin deficiency induces rat renal mesangial cell dysfunction via activation of IGF-1/IGF-1R pathway. Acta Pharmacol Sin. 2016 Feb;37(2):217-27.
Animal Administration
[1]

Four to 5-week-old pathogen-free SCID mice are used and housed within plastic isolators in a sterile facility. ES-1, BE, and PC3 cells (all proved to express IGF-1R), or R-v-src (IGF-1R negative) and P12 (overexpressing IGF-1 and IGF-1R), are injected s.c. at 107 cells/mice in a 0.2 mL volume of sterile saline solution. Immunocompetent Balb-c mice are injected with 107JC murine breast cancer cells per mouse in 0.15 mL volume of sterile saline solution. Experimental treatments with Picropodophyllin (AXL1717) (20 mg/kg/12 h) are performed by daily i.p. injections of the compound in 10 μL volume of DMSO: vegetable oil, 10:1 (v/v). Control mice are treated with the vehicle only. Three animals are treated in each group. Tumor growth is measured every second day using vernier calipers, and the tumor volumes are calculated. The mice are carefully observed for the presence of side effects and are sacrificed at the end of the experiments for histological analysis of the lesions. A separate experiment on Picropodophyllin (AXL1717)-treated (systemically and locally) tumor-free mice, including histological analyses of various organs, confirms previous observations that Picropodophyllin (AXL1717) appears to be nontoxic.

MCE has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献

  • [1]. Girnita A, et al. Cyclolignans as inhibitors of the insulin-like growth factor-1 receptor and malignant cell growth. Cancer Res. 2004 Jan 1;64(1):236-42.

    [2]. Menu E, et al. Inhibiting the IGF-1 receptor tyrosine kinase with the cyclolignan PPP: an in vitro and in vivo study in the 5T33MM mouse model. Blood. 2006 Jan 15;107(2):655-60. Epub 2005 Jul 26.

    [3]. Bieghs L, et al. The IGF-1 receptor inhibitor picropodophyllin potentiates the anti-myeloma activity of a BH3-mimetic. Oncotarget. 2014 Nov 30;5(22):11193-208.

    [4]. Tomizawa M, et al. Picropodophyllin and sorafenib synergistically suppress the proliferation and motility of hepatocellular carcinoma cells. Oncol Lett. 2014 Nov;8(5):2023-2026. Epub 2014 Aug 27.

    [5]. Stromberg T, et al. IGF-1 receptor tyrosine kinase inhibition by the cyclolignan PPP induces G2/M-phase accumulation and apoptosis in multiple myeloma cells. Blood. 2006 Jan 15;107(2):669-78. Epub 2005 Sep 15.

    [6]. Kong YL, et al. Insulin deficiency induces rat renal mesangial cell dysfunction via activation of IGF-1/IGF-1R pathway. Acta Pharmacol Sin. 2016 Feb;37(2):217-27.

Novobiocin Sodium(Synonyms: Albamycin; Cathomycin)

发表于由

天然产物 天然产物苯丙素类 Phenylpropanoids

Novobiocin Sodium (Synonyms: Albamycin; Cathomycin) 纯度: 95.32%

Novobiocin Sodium (Albamycin; Cathomycin) 是一种口服抗生素 (antibiotic) 化合物，源于链霉菌，也是一个强效的 DNA gyrase 抑制剂通过结合 ATP 结合位点在 ATP 酶亚基。Novobiocin Sodium 对革兰氏阳性菌有较强的抗菌活性，但由于外膜中含有脂多糖，对革兰氏阴性菌的抗菌活性有限。Novobiocin Sodium 与 Hsp90 的 c 端结合，轻微诱导 Hsp90 依赖的 client 蛋白的降解 (IC50=700 μM)。

Novobiocin Sodium(Synonyms: Albamycin; Cathomycin)

Novobiocin Sodium Chemical Structure

CAS No. : 1476-53-5

规格 价格 是否有货 数量
10 mM * 1 mL in DMSO ￥990 In-stock
100 mg ￥900 In-stock
500 mg ￥2000 In-stock
1 g   询价  
5 g   询价  

* Please select Quantity before adding items.

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生物活性

Novobiocin Sodium (Albamycin; Cathomycin) is an orally active antibiotic compound derived from Streptomyces niveus and a potent DNA gyrase inhibitor by binding the ATP-binding site in the ATPase subunit[1]. Novobiocin Sodium manifests strong anti-bacterial activities effectively against gram-positive pathogens and shows limited activity against gram-negative organisms due to LPS-containing outer membrane.Novobiocin Sodium binds to the C-terminus of Hsp90 and slightly induces degradation of Hsp90-dependent client proteins (IC50=700 µM)[1][2].

IC50 & Target

IC50: 700 μM (HSP90)[2]
体外研究
(In Vitro)

Novobiocin Sodium (0.3 mM; 48 hours) induces a caspase-3/7 enzyme–dependent apoptosis assays with an induction of approximately three- to fivefold of apoptotic cells in K562, HL60, Mutz-2[1].
Novobiocin (0-500 μM; 15-hours) is against wild type, lptB1, lptB1(R144H), and efflux pump-deficient ∆tolC strains with IC50 values of 62.5-125 μM; 0.5 μM; 62.5-125 μM; and 2 μM, respectively[2].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Western Blot Analysis[2]

Cell Line: K562, HL60, Mutz-2 cells
Concentration: 0.3 mM
Incubation Time: 48 hours
Result: Decreased caspase-3/7 activity in K562, HL60, Mutz-2 cells.

分子量

634.61

Formula

C31H35N2NaO11
CAS 号

1476-53-5
中文名称

新生霉素钠
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

4°C, sealed storage, away from moisture

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
溶解性数据
In Vitro: 

H2O : 250 mg/mL (393.94 mM; Need ultrasonic)

DMSO : ≥ 30 mg/mL (47.27 mM)

* “≥” means soluble, but saturation unknown.

配制储备液
浓度 溶剂体积 质量 1 mg 5 mg 10 mg
1 mM 1.5758 mL 7.8789 mL 15.7577 mL
5 mM 0.3152 mL 1.5758 mL 3.1515 mL
10 mM 0.1576 mL 0.7879 mL 1.5758 mL

*

请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。
储备液的保存方式和期限：-80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)。-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。
参考文献

  • [1]. Bhatia S, et al. Targeting HSP90 dimerization via the C terminus is effective in imatinib-resistant CML and lacks the heat shock response.Blood. 2018 Jul 19;132(3):307-320.

    [2]. Burlison JA, et al. Novobiocin: redesigning a DNA gyrase inhibitor for selective inhibition of hsp90.J Am Chem Soc. 2006 Dec 6;128(48):15529-36.

Wedelolactone(Synonyms: 蟛蜞菊内酯)

发表于由

天然产物 天然产物苯丙素类 Phenylpropanoids

Wedelolactone (Synonyms: 蟛蜞菊内酯) 纯度: 99.70%

Wedelolactone，是一种来自 Ecliptae herba 的天然产物，通过直接抑制 IKK 复合物来抑制 LPS 诱导的 caspase-11 表达。Wedelolactone 通过氧自由基清除机制抑制 5-脂氧合酶 (5-lipoxygenase, 5-Lox) (IC50~2.5 μM) 活性。Wedelolactone 通过下调 PKCε 诱导前列腺癌细胞中 caspase 依赖性细胞凋亡 (apoptosis) 而不抑制 Akt。具有抗癌，抗炎和抗氧化活性。

Wedelolactone(Synonyms: 蟛蜞菊内酯)

Wedelolactone Chemical Structure

CAS No. : 524-12-9

规格 价格 是否有货 数量
10 mM * 1 mL in DMSO ￥553 In-stock
5 mg ￥800 In-stock
10 mg ￥1400 In-stock
20 mg ￥2300 In-stock
50 mg   询价  
100 mg   询价  

* Please select Quantity before adding items.

Wedelolactone 相关产品

•相关化合物库:

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  • Targeted Diversity Library

生物活性

Wedelolactone, a natural product from Ecliptae herba, suppresses LPS-induced caspase-11 expression by directly inhibiting the IKK Complex[1]. Wedelolactone inhibits 5-lipoxygenase (5-Lox) (IC50~2.5 μM) activity by an oxygen radical scavenging mechanism. Wedelolactone induces caspase-dependent apoptosis in prostate cancer cells via downregulation of PKCε without inhibiting Akt[2]. Anti-cancer, anti-inflammatory, and antioxidant activities[3].

IC50 & Target[1][2][3]

Caspase-11

 

5-LOX

2.5 μM (IC50)

Apoptosis

 

分子量

314.25

Formula

C16H10O7
CAS 号

524-12-9
中文名称

蟛蜞菊内酯；蟛蜞内酯；蟛蜞菊内脂
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式
Powder -20°C 3 years
In solvent -80°C 6 months
-20°C 1 month
溶解性数据
In Vitro: 

DMSO : 125 mg/mL (397.77 mM; Need ultrasonic)

配制储备液
浓度 溶剂体积 质量 1 mg 5 mg 10 mg
1 mM 3.1822 mL 15.9109 mL 31.8218 mL
5 mM 0.6364 mL 3.1822 mL 6.3644 mL
10 mM 0.3182 mL 1.5911 mL 3.1822 mL

*

请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。
储备液的保存方式和期限：-80°C, 6 months; -20°C, 1 month。-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。

In Vivo:

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 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，建议您现用现配，当天使用； 以下溶剂前显示的百
分比是指该溶剂在您配制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

  • 1.

    请依序添加每种溶剂： 10% DMSO    40% PEG300    5% Tween-80    45% saline

    Solubility: ≥ 2.08 mg/mL (6.62 mM); Clear solution

    此方案可获得 ≥ 2.08 mg/mL (6.62 mM，饱和度未知) 的澄清溶液。

    以 1 mL 工作液为例，取 100 μL 20.8 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀；向上述体系中加入50 μL Tween-80，混合均匀；然后继续加入 450 μL生理盐水定容至 1 mL。

    将 0.9 g 氯化钠，完全溶解于 100 mL ddH₂O 中，得到澄清透明的生理盐水溶液

  • 2.

    请依序添加每种溶剂： 10% DMSO    90% corn oil

    Solubility: ≥ 2.08 mg/mL (6.62 mM); Clear solution

    此方案可获得 ≥ 2.08 mg/mL (6.62 mM，饱和度未知) 的澄清溶液，此方案不适用于实验周期在半个月以上的实验。

    以 1 mL 工作液为例，取 100 μL 20.8 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中，混合均匀。

*以上所有助溶剂都可在 MCE 网站选购。
参考文献

  • [1]. Kobori M, et al. Wedelolactone suppresses LPS-induced caspase-11 expression by directly inhibiting the IKK complex. Cell Death Differ. 2004 Jan;11(1):123-30.

    [2]. Sarveswaran S, et al. Wedelolactone, a medicinal plant-derived coumestan, induces caspase-dependent apoptosis in prostate cancer cells via downregulation of PKCε without inhibiting Akt. Int J Oncol. 2012 Dec;41(6):2191-9.

    [3]. Liu YQ, et al. Wedelolactone enhances osteoblastogenesis by regulating Wnt/β-catenin signaling pathway but suppresses osteoclastogenesis by NF-κB/c-fos/NFATc1 pathway. Sci Rep. 2016 Aug 25;6:32260.

Caffeic acid phenethyl ester(Synonyms: 咖啡酸苯乙酯)

发表于由

天然产物 天然产物苯丙素类 Phenylpropanoids

Caffeic acid phenethyl ester (Synonyms: 咖啡酸苯乙酯) 纯度: 98.19%

Caffeic acid phenethyl ester 是一种 NF-κB 抑制剂。

Caffeic acid phenethyl ester(Synonyms: 咖啡酸苯乙酯)

Caffeic acid phenethyl ester Chemical Structure

CAS No. : 104594-70-9

规格 价格 是否有货 数量
Free Sample (0.1-0.5 mg)   Apply now  
10 mM * 1 mL in DMSO ￥500 In-stock
5 mg ￥450 In-stock
10 mg ￥600 In-stock
100 mg ￥990 In-stock
200 mg   询价  
500 mg   询价  

* Please select Quantity before adding items.

Caffeic acid phenethyl ester 相关产品

•相关化合物库:

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生物活性

Caffeic acid phenethyl ester is a NF-κB inhibitor.

IC50 & Target[1]

NF-κB

 

体外研究
(In Vitro)

Caffeic acid phenethyl ester is a NF-κB inhibitor. Cell survival and proliferation of CRPC cell lines are all significantly suppressed by Caffeic acid phenethyl ester (CAPE) treatment dose-dependently. The growth inhibitory effect of Caffeic acid phenethyl ester is evident within 24 hours of treatment but the suppressive effect accumulates over time. The IC50 of 24, 48, 72, and 96 h Caffeic acid phenethyl ester treatment on LNCaP 104-R1 cells is 64.0, 30.5, 20.5, and 18.0 μM, respectively. Colony formation assay reveals that treatment with 10 μM Caffeic acid phenethyl ester reduces colony formation of LNCaP 104-R1 cells by 90% while treatment with 20 μM Caffeic acid phenethyl ester completely blocks the formation of LNCaP 104-R1 colonies. Flow cytometric analysis reveals a reduction of cells in the S phase and G2/M phase but an increase of cells in the G1 phase population in LNCaP 104-R1 cells under Caffeic acid phenethyl ester treatment. Caffeic acid phenethyl ester treatment also significantly decreases protein levels of fatty acid synthase (FAS), retinoblastoma protein (Rb), phospho-Rb Ser807/811, c-Myc, p70S6kinase, phospho-p70S6kinase Thr421/Ser424, Skp2, p90RSK, and NF-κB p65[1].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究
(In Vivo)

Administration of Caffeic acid phenethyl ester (CAPE) by gavage (10 mg/kg body weight per day) for eight weeks results in 50% reduction of tumor volume, suggesting that Caffeic acid phenethyl ester treatment retards the growth of LNCaP 104-R1 xenografts. Caffeic acid phenethyl ester gavage slows down the tumor growth of LNCaP 104-R1 cells, which is consistent with our observation that Caffeic acid phenethyl ester treatment induces cell cycle arrest but not apoptosis[1].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.
分子量

284.31

Formula

C17H16O4
CAS 号

104594-70-9
中文名称

咖啡酸苯乙酯
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式
Powder -20°C 3 years
4°C 2 years
In solvent -80°C 6 months
-20°C 1 month
溶解性数据
In Vitro: 

DMSO : 100 mg/mL (351.73 mM; Need ultrasonic)

H2O : 1 mg/mL (3.52 mM; ultrasonic and warming and heat to 80°C)

配制储备液
浓度 溶剂体积 质量 1 mg 5 mg 10 mg
1 mM 3.5173 mL 17.5864 mL 35.1729 mL
5 mM 0.7035 mL 3.5173 mL 7.0346 mL
10 mM 0.3517 mL 1.7586 mL 3.5173 mL

*

请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。
储备液的保存方式和期限：-80°C, 6 months; -20°C, 1 month。-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。

In Vivo:

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 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，建议您现用现配，当天使用； 以下溶剂前显示的百
分比是指该溶剂在您配制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

  • 1.

    请依序添加每种溶剂： 10% DMSO    40% PEG300    5% Tween-80    45% saline

    Solubility: ≥ 2.5 mg/mL (8.79 mM); Clear solution

    此方案可获得 ≥ 2.5 mg/mL (8.79 mM，饱和度未知) 的澄清溶液。

    以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀；向上述体系中加入50 μL Tween-80，混合均匀；然后继续加入 450 μL生理盐水定容至 1 mL。

    将 0.9 g 氯化钠，完全溶解于 100 mL ddH₂O 中，得到澄清透明的生理盐水溶液

  • 2.

    请依序添加每种溶剂： 10% DMSO    90% (20% SBE-β-CD in saline)

    Solubility: ≥ 2.5 mg/mL (8.79 mM); Clear solution

    此方案可获得 ≥ 2.5 mg/mL (8.79 mM，饱和度未知) 的澄清溶液。

    以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL 20% 的 SBE-β-CD 生理盐水水溶液中，混合均匀。

    将 2 g 磺丁基醚 β-环糊精加入 5 mL 生理盐水中，再用生理盐水定容至 10 mL，完全溶解，澄清透明
  • 3.

    请依序添加每种溶剂： 10% DMSO    90% corn oil

    Solubility: ≥ 2.5 mg/mL (8.79 mM); Clear solution

    此方案可获得 ≥ 2.5 mg/mL (8.79 mM，饱和度未知) 的澄清溶液，此方案不适用于实验周期在半个月以上的实验。

    以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中，混合均匀。

*以上所有助溶剂都可在 MCE 网站选购。
参考文献

  • [1]. Lin HP, et al. Caffeic acid phenethyl ester induced cell cycle arrest and growth inhibition in androgen-independent prostate cancer cells via regulation of Skp2, p53, p21Cip1 and p27Kip1. Oncotarget. 2015 Mar 30;6(9):6684-707.
Kinase Assay
[1]

LNCaP 104-R1 cells are treated with 0, 10, 20, or 40 μM Caffeic acid phenethyl ester (CAPE) for 96 h. Three biological replicates of cells are lysed in SDS lysis buffer (240 mM Tris-acetate, 1% SDS, 1% glycerol, 5 mM EDTA pH 8.0) with DTT, protease inhibitors, and a cocktail of phosphatase inhibitors. Micro-Western Arrays are performed to measure protein expression and phosphorylation status modification[1].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Assay
[1]

LNCaP 104-R1 cells are seeded at a density of 3×103 cells per well in a 96-well plate. After 24 h, the cells are treated with increasing concentrations of Caffeic acid phenethyl ester (CAPE) for 96 h. Cell viability is assessed by an MTT (3,4,5-dimethylthiazol-2-yl)-2–5-diphenyltetrazolium bromide) assay. The amount of formazan is determined by measuring the absorbance at 560 nm using a plate reader. All results are normalized to the average of the control condition in each individual experiment. All experiments are repeated three times. Each time ten wells are utilized for each condition. The mean and standard deviation represent the results from all 30 wells in the three experiments[1].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Administration
[1]

Male Balb/c nu/nu mice at age 6 to 8 weeks of age are injected subcutaneously in both flanks with 5×105 LNCaP 104-R1 cells suspended in 0.5 mL of Matrigel and are injected subcutaneously into athymic mice to form tumors. After 14 weeks, the average tumor volume exceeds 150 mm3. The mice are then separated into control group and Caffeic acid phenethyl ester (CAPE) treatment group. Control group contains 6 mice and 8 tumors, while Caffeic acid phenethyl ester treatment group contains 6 mice and 9 tumors. Caffeic acid phenethyl ester (10 mg/kg/day in sesame oil) or vehicle (sesame oil) is administered by gavage starting from 14th week after cancer cell injection. Tumor volume and body weight of mice carrying 104-R1 xenografts are measured weekly using calipers and volume is calculated using the formula volume=length×width×height×0.52[1].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献

  • [1]. Lin HP, et al. Caffeic acid phenethyl ester induced cell cycle arrest and growth inhibition in androgen-independent prostate cancer cells via regulation of Skp2, p53, p21Cip1 and p27Kip1. Oncotarget. 2015 Mar 30;6(9):6684-707.

Dicoumarol(Synonyms: 双香豆素; Dicumarol)

发表于由

天然产物 天然产物苯丙素类 Phenylpropanoids

Dicoumarol (Synonyms: 双香豆素; Dicumarol) 纯度: 99.59%

Dicoumarol 是 NAD(P)H: 醌氧化还原酶 1 (NQO1) 和 PDK1 的抑制剂，IC50 值分别为 0.37 和 19.42 μM。

Dicoumarol(Synonyms: 双香豆素; Dicumarol)

Dicoumarol Chemical Structure

CAS No. : 66-76-2

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500 mg ￥500 In-stock
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生物活性

Dicoumarol is an inhibitor of both NAD(P)H:quinone oxidoreductase 1 (NQO1) and PDK1 with IC50s of 0.37 and 19.42 μM, respectively.

IC50 & Target

IC50: 0.37 μM (NQO1)[1], 19.42 μM (PDK1)[2]
体外研究
(In Vitro)

Dicoumarol is an inhibitor of both NAD(P)H:quinone oxidoreductase 1 (NQO1) and PDK1 with IC50s of 0.37±0.15 and 19.42±0.032 μM, respectively. The PDK1 activity is inhibited by Dicoumarol in a dose-dependent manner. The enzymatic activity of PDK1 is reduced by approximately 94% when treated with 200 μM Dicoumarol. Dicoumarol decreases the p-PDHA1 level by 26% (100 μM Dicoumarol) and by 72% (200 μM Dicoumarol), with no statistical difference in the total PDHA1 level. Both 100 μM and 200 μM Dicoumarol markedly induce apoptosis of SKOV3 cells. Similarly, flow cytometric analysis of annexin V+PI+ cells reveals that 100 μM and 200 μM Dicoumarol treatments generate approximately 20.87% and 24.94% apoptotic cells, respectively, significantly higher than vehicle treatment[2]. It is also observed that treatment of MCF-7-TAMR cells with Dicoumarol, a known NQO1 inhibitor, reverses their tamoxifen-resistance phenotype[3].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究
(In Vivo)

Dichloroacetate (DCA) at 100 mg/kg, Dicoumarol at 30 mg/kg, and Dicoumarol at 50 mg/kg all significantly reduce tumor volume and decrease tumor weight, when compare to tumors from control or vehicle groups. Total caspase-3 and total anti-poly (ADP-ribose) polymerase (PARP) are significantly decreased in Dicoumarol-treated SKOV3 xenografts, when compare to tumors from the control or vehicle group[2].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.
分子量

336.29

Formula

C19H12O6
CAS 号

66-76-2
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式
Powder -20°C 3 years
4°C 2 years
In solvent -80°C 6 months
-20°C 1 month
溶解性数据
In Vitro: 

H2O : 25 mg/mL (74.34 mM; ultrasonic and adjust pH to 11 with NaOH)

DMSO : 3.67 mg/mL (10.91 mM; Need ultrasonic)

配制储备液
浓度 溶剂体积 质量 1 mg 5 mg 10 mg
1 mM 2.9736 mL 14.8681 mL 29.7362 mL
5 mM 0.5947 mL 2.9736 mL 5.9472 mL
10 mM 0.2974 mL 1.4868 mL 2.9736 mL

*

请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。
储备液的保存方式和期限：-80°C, 6 months; -20°C, 1 month。-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。
参考文献

  • [1]. Bian J, et al. Affinity-based small fluorescent probe for NAD(P)H:quinone oxidoreductase 1 (NQO1). Design, synthesis and pharmacological evaluation. Eur J Med Chem. 2017 Feb 15;127:828-839.

    [2]. Zhang W, et al. Dicumarol inhibits PDK1 and targets multiple malignant behaviors of ovarian cancer cells. PLoS One. 2017 Jun 15;12(6):e0179672.

    [3]. Fiorillo M, et al. Mitochondrial “power” drives tamoxifen resistance: NQO1 and GCLC are new therapeutic targets in breast cancer. Oncotarget. 2017 Mar 2;8(12):20309-20327.
Cell Assay
[2]

The in vitro cell viability is examined using the standard MTT assay. SKOV3 or A2780 cells are seeded in 96-well plates at 8000 cells/well. The next day, increasing concentrations of Dicoumarol (DIC) are added into each well, and the plate is incubated for 24 h. Then, 10 μL of 10 mg/mL MTT reagent in phosphate-buffered saline (PBS) is added into each well, and the plate is incubated for an additional 4 h. The formazan crystals are dissolved in 150 μL of DMSO, and after the plate is shaken for 5 min, the optical density at 570 nm is recorded by the reader[2].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Administration
[2]

Twenty five female BALB/c-nu mice aged 5 to 6 weeks old and weighing approximately 15 g each are used. A total of 1×107 SKOV3 cells are subcutaneously injected into the upper flank. After 10 days, when the tumor volume reaches approximately 100 mm3, the nude mice are randomized into five groups (n=5/group) and are given the following treatments intraperitoneally (i.p.) every other day, for a total of 12 days: control group, administered with 0.2 mL of 0.9% NaCl; vehicle group, administered with 1 mM NaOH; dichloroacetate (DCA) group, administered with 100 mg/kg DCA; Dicoumarol (DIC)-30 group, administered with 30 mg/kg Dicoumarol; and Dicoumarol-50 group, administered with 50 mg/kg Dicoumarol. The body weights and tumor volumes of each mouse are monitored every other day until sacrifice (on day 12 after the initial treatment)[2].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献

  • [1]. Bian J, et al. Affinity-based small fluorescent probe for NAD(P)H:quinone oxidoreductase 1 (NQO1). Design, synthesis and pharmacological evaluation. Eur J Med Chem. 2017 Feb 15;127:828-839.

    [2]. Zhang W, et al. Dicumarol inhibits PDK1 and targets multiple malignant behaviors of ovarian cancer cells. PLoS One. 2017 Jun 15;12(6):e0179672.

    [3]. Fiorillo M, et al. Mitochondrial “power” drives tamoxifen resistance: NQO1 and GCLC are new therapeutic targets in breast cancer. Oncotarget. 2017 Mar 2;8(12):20309-20327.

Chlorogenic acid(Synonyms: 绿原酸; 3-O-Caffeoylquinic acid; Heriguard; NSC-407296)

发表于由

天然产物 天然产物苯丙素类 Phenylpropanoids

Chlorogenic acid (Synonyms: 绿原酸; 3-O-Caffeoylquinic acid; Heriguard; NSC-407296) 纯度: 99.55%

Chlorogenic acid (3-O-Caffeoylquinic acid) 是咖啡和茶中的主要酚类化合物。Chlorogenic acid 具有一些重要作用，如抗氧化活性，抗菌，保肝，心脏保护，抗炎，解热，神经保护，抗肥胖，抗病毒，抗微生物，抗高血压。

Chlorogenic acid(Synonyms: 绿原酸; 3-O-Caffeoylquinic acid; Heriguard; NSC-407296)

Chlorogenic acid Chemical Structure

CAS No. : 327-97-9

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生物活性

Chlorogenic acid is a major phenolic compound in coffee and tea. It plays several important and therapeutic roles such as antioxidant activity, antibacterial, hepatoprotective, cardioprotective, anti-inflammatory, antipyretic, neuroprotective, anti-obesity, antiviral, anti-microbial, anti-hypertension.

IC50 & Target

Human Endogenous Metabolite

 

Clinical Trial

分子量

354.31

Formula

C16H18O9
CAS 号

327-97-9
中文名称

绿原酸；3-咖啡酰奎尼酸；咖啡单宁酸；咖啡酰奎尼酸；氯吉酸；绿源酸
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式
Powder -20°C 3 years
4°C 2 years
In solvent -80°C 6 months
-20°C 1 month
溶解性数据
In Vitro: 

DMSO : 100 mg/mL (282.24 mM; Need ultrasonic)

配制储备液
浓度 溶剂体积 质量 1 mg 5 mg 10 mg
1 mM 2.8224 mL 14.1119 mL 28.2239 mL
5 mM 0.5645 mL 2.8224 mL 5.6448 mL
10 mM 0.2822 mL 1.4112 mL 2.8224 mL

*

请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。
储备液的保存方式和期限：-80°C, 6 months; -20°C, 1 month。-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。

In Vivo:

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 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，建议您现用现配，当天使用； 以下溶剂前显示的百
分比是指该溶剂在您配制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

  • 1.

    请依序添加每种溶剂： 10% DMSO    40% PEG300    5% Tween-80    45% saline

    Solubility: ≥ 2.5 mg/mL (7.06 mM); Clear solution

    此方案可获得 ≥ 2.5 mg/mL (7.06 mM，饱和度未知) 的澄清溶液。

    以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀；向上述体系中加入50 μL Tween-80，混合均匀；然后继续加入 450 μL生理盐水定容至 1 mL。

    将 0.9 g 氯化钠，完全溶解于 100 mL ddH₂O 中，得到澄清透明的生理盐水溶液

  • 2.

    请依序添加每种溶剂： 10% DMSO    90% (20% SBE-β-CD in saline)

    Solubility: ≥ 2.5 mg/mL (7.06 mM); Clear solution

    此方案可获得 ≥ 2.5 mg/mL (7.06 mM，饱和度未知) 的澄清溶液。

    以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL 20% 的 SBE-β-CD 生理盐水水溶液中，混合均匀。

    将 2 g 磺丁基醚 β-环糊精加入 5 mL 生理盐水中，再用生理盐水定容至 10 mL，完全溶解，澄清透明
  • 3.

    请依序添加每种溶剂： 10% DMSO    90% corn oil

    Solubility: ≥ 2.5 mg/mL (7.06 mM); Clear solution

    此方案可获得 ≥ 2.5 mg/mL (7.06 mM，饱和度未知) 的澄清溶液，此方案不适用于实验周期在半个月以上的实验。

    以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中，混合均匀。

*以上所有助溶剂都可在 MCE 网站选购。
参考文献

  • [1]. Park JJ, et al. Chlorogenic acid inhibits hypoxia-induced angiogenesis via down-regulation of the HIF-1α/AKT pathway. Cell Oncol (Dordr). 2015 Jan 6.

    [2]. Park SH, et al. IRAK4 as a Molecular Target in the Amelioration of Innate Immunity-Related Endotoxic Shock and Acute Liver Injury by Chlorogenic Acid. J Immunol. 2015 Feb 1;194(3):1122-30.

    [3]. Kang JW, et al. Protective Effects of Chlorogenic Acid against Experimental Reflux Esophagitis in Rats. Biomol Ther (Seoul). 2014 Sep;22(5):420-5.

Nordihydroguaiaretic acid(Synonyms: 去甲二氢愈创木酸; NDGA)

发表于由

天然产物 天然产物苯丙素类 Phenylpropanoids

Nordihydroguaiaretic acid (Synonyms: 去甲二氢愈创木酸; NDGA) 纯度: 99.88%

Nordihydroguaiaretic acid 是一种 5-脂氧合酶 (5LOX) (IC50=8 μM) 和酪氨酸激酶抑制剂。

Nordihydroguaiaretic acid(Synonyms: 去甲二氢愈创木酸; NDGA)

Nordihydroguaiaretic acid Chemical Structure

CAS No. : 500-38-9

规格 价格 是否有货 数量
10 mM * 1 mL in DMSO ￥660 In-stock
100 mg ￥600 In-stock
250 mg ￥1200 In-stock
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1 g   询价  

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生物活性

Nordihydroguaiaretic acid is a 5-lipoxygenase (5LOX) (IC50=8 μM) and tyrosine kinase inhibitor.

IC50 & Target[1]

5-LOX

8 μM (IC50)

体外研究
(In Vitro)

The natural dicatechol Nordihydroguaiaretic acid (NDGA) is a selective 5LOX inhibitor from the creosote plant (Larrea tridentata: Zygophyllaceae). The 5LOX-inhibiting natural dicatechol Nordihydroguaiaretic acid is a very effective, non-toxic antagonist of TNFα-stimulated microglial activation. Nordihydroguaiaretic acid is approximately six times more potent than Minocycline in vitro, with an IC50 value of 8±3 μM and no toxicity at 100 μM. Significant NO2– suppression is observed at 800 nM Nordihydroguaiaretic acid. Similar efficacy is observed for natural and synthetic Nordihydroguaiaretic acid, as well as for the acetyl ester of Nordihydroguaiaretic acid. Nordihydroguaiaretic acid also suppresses TNFα-stimulated PGE2 production by EOC-20 cells with an IC50 of 841 nM[1].To test the proliferation effect of prostaglandin E1 and Nordihydroguaiaretic acid (NDGA) on cancer cell lines, HepG2 cell lines are treated with various doses of the two compounds and the positive compounds 8-anilino-1-naphtalene sulfonate (ANS), respectively, for 24 h and cell viability is examined by the MTT assay. ANS displays a dose-dependent inhibition (0, 10, 30, 50, 80, 100, 120, and 150 μM) with the estimated IC50 being 25.888 μM. The tested IC50 of prostaglandin E1 is 41.223 μM and Nordihydroguaiaretic acid is 45.646 μM, respectively, at different concentrations of 0, 30, 60, 80, 100, 120, and 140 μM[2].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究
(In Vivo)

Compared with the control ob/ob chow diet group, there is a significant reduction of body weight starting from 9 wk treatment in the high-dose Nordihydroguaiaretic acid (NDGA) diet group, and from 12 wk in the low-dose group. Nordihydroguaiaretic acid treatment results in higher body (rectal) temperatures of ob/ob mice, especially with the high dose of Nordihydroguaiaretic acid[3].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Clinical Trial

分子量

302.36

Formula

C18H22O4
CAS 号

500-38-9
中文名称

去甲二氢愈创木酸；降二氫癒創木酸；正二氢愈创酸
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式
Powder -20°C 3 years
4°C 2 years
In solvent -80°C 6 months
-20°C 1 month
溶解性数据
In Vitro: 

DMSO : 250 mg/mL (826.83 mM; Need ultrasonic)

配制储备液
浓度 溶剂体积 质量 1 mg 5 mg 10 mg
1 mM 3.3073 mL 16.5366 mL 33.0732 mL
5 mM 0.6615 mL 3.3073 mL 6.6146 mL
10 mM 0.3307 mL 1.6537 mL 3.3073 mL

*

请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。
储备液的保存方式和期限：-80°C, 6 months; -20°C, 1 month。-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。

In Vivo:

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 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，建议您现用现配，当天使用； 以下溶剂前显示的百
分比是指该溶剂在您配制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

  • 1.

    请依序添加每种溶剂： 10% DMSO    40% PEG300    5% Tween-80    45% saline

    Solubility: ≥ 2.08 mg/mL (6.88 mM); Clear solution

    此方案可获得 ≥ 2.08 mg/mL (6.88 mM，饱和度未知) 的澄清溶液。

    以 1 mL 工作液为例，取 100 μL 20.8 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀；向上述体系中加入50 μL Tween-80，混合均匀；然后继续加入 450 μL生理盐水定容至 1 mL。

    将 0.9 g 氯化钠，完全溶解于 100 mL ddH₂O 中，得到澄清透明的生理盐水溶液

  • 2.

    请依序添加每种溶剂： 10% DMSO    90% (20% SBE-β-CD in saline)

    Solubility: ≥ 2.08 mg/mL (6.88 mM); Clear solution

    此方案可获得 ≥ 2.08 mg/mL (6.88 mM，饱和度未知) 的澄清溶液。

    以 1 mL 工作液为例，取 100 μL 20.8 mg/mL 的澄清 DMSO 储备液加到 900 μL 20% 的 SBE-β-CD 生理盐水水溶液中，混合均匀。

    将 2 g 磺丁基醚 β-环糊精加入 5 mL 生理盐水中，再用生理盐水定容至 10 mL，完全溶解，澄清透明
  • 3.

    请依序添加每种溶剂： 10% DMSO    90% corn oil

    Solubility: ≥ 2.08 mg/mL (6.88 mM); Clear solution

    此方案可获得 ≥ 2.08 mg/mL (6.88 mM，饱和度未知) 的澄清溶液，此方案不适用于实验周期在半个月以上的实验。

    以 1 mL 工作液为例，取 100 μL 20.8 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中，混合均匀。

*以上所有助溶剂都可在 MCE 网站选购。
参考文献

  • [1]. West M, et al. The arachidonic acid 5-lipoxygenase inhibitor Nordihydroguaiaretic acid inhibits tumor necrosis factor alpha activation of microglia and extends survival of G93A-SOD1 transgenic mice. J Neurochem. 2004 Oct;91(1):133-43.

    [2]. Lu F, et al. Virtual Screening for Potential Allosteric Inhibitors of Cyclin-Dependent Kinase 2 from Traditional Chinese Medicine. Molecules. 2016 Sep 21;21(9). pii: E1259.

    [3]. Zhang H, et al. Nordihydroguaiaretic acid improves metabolic dysregulation and aberrant hepatic lipid metabolism in mice by both PPARα-dependent and -independent pathways. Am J Physiol Gastrointest Liver Physiol. 2013 Jan 1;304(1):G72-86.
Cell Assay
[2]

MTT assay is used to measure cell growth-inhibitory activity of the selected most promising compounds in HepG2 cell lines. Cells are cultured in 96-well culture plate at 1×104 cells/well. After 24 h cultured at 37 °C in the atmosphere of 5% CO2, cells are adhered and treated with different concentrations of the targeted compounds (e.g., Nordihydroguaiaretic acid, 0, 30, 60, 80, 100, 120, and 140 μM) and incubated for 24 h. Then, the supernatants are discarded and MTT (0.5 mg/mL) is added to each well and incubated at 37°C in 5% CO2 for an additional 4 h. Following, the MTT is removed and 150 μL of formazan in DMSO is added to terminate response and then plates are set to the table shaker for 5 min at low speed. Cell proliferation is evaluated by measuring the absorbance at 570 nm using ELISA Plate Reader. The IC50 values are calculated by SPSS statistics 17.0[2].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Administration
[3]

Mice[3]
Seven-week-old male control C57BL/6J mice, male leptin-deficient (ob/ob) mice, and male Pparα-deficient mutant mice (B6.129S4-Pparatm1Gonz/J) are used. These mice are fed a standard chow diet for 1 wk to allow them to acclimatize to a controlled new environment (25±2°C, 55±5% relative humidity with a 12-h light-dark cycle). Subsequently, one group of ob/ob mice is switched to a chow diet supplemented with either low- (0.83 g/kg chow diet) or high-dose (2.5 g/kg chow diet) Nordihydroguaiaretic acid and maintained on this diet for 16 wk. The other groups of ob/ob mice and control mice continue to be fed a normal chow diet for 16 wk. In another set of studies, C57BL/6J mice and Pparα-deficient mutant mice are fed either a high-fat diet (~60% of total calories come from fat), or the same high-fat diet supplemented with a high dose of Nordihydroguaiaretic acid (2.5 g/kg diet). Food intake and body weights are measured once a week throughout the experiment.

MCE has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献

  • [1]. West M, et al. The arachidonic acid 5-lipoxygenase inhibitor Nordihydroguaiaretic acid inhibits tumor necrosis factor alpha activation of microglia and extends survival of G93A-SOD1 transgenic mice. J Neurochem. 2004 Oct;91(1):133-43.

    [2]. Lu F, et al. Virtual Screening for Potential Allosteric Inhibitors of Cyclin-Dependent Kinase 2 from Traditional Chinese Medicine. Molecules. 2016 Sep 21;21(9). pii: E1259.

    [3]. Zhang H, et al. Nordihydroguaiaretic acid improves metabolic dysregulation and aberrant hepatic lipid metabolism in mice by both PPARα-dependent and -independent pathways. Am J Physiol Gastrointest Liver Physiol. 2013 Jan 1;304(1):G72-86.

Osthole(Synonyms: 蛇床子素; Osthol; NSC 31868)

发表于由

天然产物 天然产物苯丙素类 Phenylpropanoids

Osthole (Synonyms: 蛇床子素; Osthol; NSC 31868) 纯度: 99.95%

Osthole (Osthol) 是一种天然抗组胺药替代试剂。Osthole 可有效抑制组胺 H1 受体 (histamine H1 receptor) 活性。Osthole 还可抑制细胞培养物中 HBV 的分泌。

Osthole(Synonyms: 蛇床子素; Osthol; NSC 31868)

Osthole Chemical Structure

CAS No. : 484-12-8

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10 mM * 1 mL in DMSO ￥500 In-stock
250 mg ￥410 In-stock
1 g ￥1190 In-stock
5 g ￥4200 In-stock
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生物活性

Osthole (Osthol) is a natural antihistamine alternative. Osthole may be a potential inhibitor of histamine H1 receptor activity. Osthole also suppresses the secretion of HBV in cells.

IC50 & Target

Histamine H1 receptor[1]
体外研究
(In Vitro)

Osthole (p<0.0001) and Fexofenadine (p<0.001) inhibit increased HRH-1 mRNA expression induced by histamine in the study group. This result is also observed in cells cultured with histamine/Osthole; where combined substances decreased HRH-1 mRNA expression compared to histamine (p<0.0001)[1]. Assessment of cell viability does not detect obvious toxicity when Osthole is used at a dose up to 100 µM. However, when the dose reached 500 µM, Osthole started to show toxic effect. Based on these observations, Osthole is used in all in vitro studies at the dose range of 10 to 100 µM. Osthole dose-dependently promotes osteoblast differentiation, as shown by the upregulation of osteoblast differentiation marker genes such as type I collagen (col1), bone sialoprotein (BSP) and osteocalcin (OC) (2 days of culture). Osthole promotes ALP activity in mouse primary osteoblasts in a dose-dependent manner[2].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究
(In Vivo)

Subcutaneous injection of Osthole at a dose of 5 mg/kg per day onto mouse calvariae significantly stimulates local bone formation, as shown by histologic analysis of calvarial samples harvested 2 weeks after the last injection and stained with H&E orange G. Histomorphometric analysis reveals that Osthole has a significant effect on bone formation as potent as the positive control, the microtubule inhibitor TN-16. This effect, however, is not seen when Osthole is used at a dose of 1 mg/kg per day. Intraperitoneal injection of Osthole for 8 weeks significantly reverses bone loss in the ovariectomized rats. Histologic examination of the L4samples stained with trinitrophenol poinsettia demonstrates a partial recovery of the trabecular structure in ovariectomized rats treated with Osthole. Histomorphometric analysis shows that treatment with Osthole significantly increases total BMD, trabecular bone volume, and trabecular thickness and decreases trabecular separation[2].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.
分子量

244.29

Formula

C15H16O3
CAS 号

484-12-8
中文名称

蛇床子素；蛇床籽素；欧芹酚甲醚
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式
Powder -20°C 3 years
4°C 2 years
In solvent -80°C 6 months
-20°C 1 month
溶解性数据
In Vitro: 

DMSO : ≥ 100 mg/mL (409.35 mM)

* “≥” means soluble, but saturation unknown.

配制储备液
浓度 溶剂体积 质量 1 mg 5 mg 10 mg
1 mM 4.0935 mL 20.4675 mL 40.9350 mL
5 mM 0.8187 mL 4.0935 mL 8.1870 mL
10 mM 0.4093 mL 2.0467 mL 4.0935 mL

*

请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。
储备液的保存方式和期限：-80°C, 6 months; -20°C, 1 month。-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。

In Vivo:

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 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，建议您现用现配，当天使用； 以下溶剂前显示的百
分比是指该溶剂在您配制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

  • 1.

    请依序添加每种溶剂： 10% DMSO    40% PEG300    5% Tween-80    45% saline

    Solubility: ≥ 2.5 mg/mL (10.23 mM); Clear solution

    此方案可获得 ≥ 2.5 mg/mL (10.23 mM，饱和度未知) 的澄清溶液。

    以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀；向上述体系中加入50 μL Tween-80，混合均匀；然后继续加入 450 μL生理盐水定容至 1 mL。

    将 0.9 g 氯化钠，完全溶解于 100 mL ddH₂O 中，得到澄清透明的生理盐水溶液

  • 2.

    请依序添加每种溶剂： 10% DMSO    90% (20% SBE-β-CD in saline)

    Solubility: ≥ 2.5 mg/mL (10.23 mM); Clear solution

    此方案可获得 ≥ 2.5 mg/mL (10.23 mM，饱和度未知) 的澄清溶液。

    以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL 20% 的 SBE-β-CD 生理盐水水溶液中，混合均匀。

    将 2 g 磺丁基醚 β-环糊精加入 5 mL 生理盐水中，再用生理盐水定容至 10 mL，完全溶解，澄清透明
  • 3.

    请依序添加每种溶剂： 10% DMSO    90% corn oil

    Solubility: ≥ 2.5 mg/mL (10.23 mM); Clear solution

    此方案可获得 ≥ 2.5 mg/mL (10.23 mM，饱和度未知) 的澄清溶液，此方案不适用于实验周期在半个月以上的实验。

    以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中，混合均匀。

*以上所有助溶剂都可在 MCE 网站选购。
参考文献

  • [1]. Kordulewska NK, et al. Changes in gene expression induced by histamine, fexofenadine and osthole: Expression of histamine H1 receptor, COX-2, NF-κB, CCR1, chemokine CCL5/RANTES and interleukin-1β in PBMC allergic and non-allergic patients. Immunobiology.

    [2]. Tang DZ, et al. Osthole stimulates osteoblast differentiation and bone formation by activation of beta-catenin-BMP signaling. J Bone Miner Res. 2010 Jun;25(6):1234-45.

    [3]. Sun W, et al. Osthole pretreatment alleviates TNBS-induced colitis in mice via both cAMP/PKA-dependent and independent pathways. Acta Pharmacol Sin. 2017 Aug;38(8):1120-1128.

    [4]. Zhang ZR, et al. Osthole: A Review on Its Bioactivities, Pharmacological Properties, and Potential as Alternative Medicine. Evid Based Complement Alternat Med. 2015;2015:919616.
Cell Assay
[1]

Peripheral blood samples are collected from participants between 7.00 and 9.00 a.m. on the first study day and these are concentrated in grouping tubes with K3EDTA. Fresh PBMCs are then prepared. Isolated cells are seeded on 24-well plates at 1×106 per well with RPMI-1640 and supplemented with 1% heat inactivated human AB serum, 1% gentamicin and 0.25% PHA. Active reagents are added to each well after 24 h and pure medium formed the control for each substance. Cells are then harvested after a further three days[1].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Administration
[2]

Mice[2]
Four-week-old ICR Swiss mice are injected subcutaneously over the calvarial surface with or without the treatment of Osthole twice a day for 5 consecutive days at the doses of 1 and 5 mg/kg per day (3 mice per group). Microtubule inhibitor TN-16 is used as a positive control (5 mg/kg per day, by subcutaneous injection, twice a day for 2 days; 3 mice per group). All mice are euthanized 3 weeks after treatment, and calvariae are dissected, fixed in 10% phosphate-buffered formalin for 2 days, decalcified in 10% EDTA for 2 weeks, and embedded in paraffin. Histologic sections are cut and stained with hematoxylin and eosine orange G. New bone area over the calvarial surface is quantified by histomorphometry using the OsteoMeasure System. To measure mineral appositional rate (MAR) and bone-formation rate (BFR), double calcein labeling is performed at days 7 and 14 by intraperitoneal injection (20 mg/kg), and mice are euthanized 7 days after the second labeling. The labeling is examined in plastic sections. The dissected calvarial samples are fixed in 75% ethanol and embedded in methyl methacrylate. Unstained transverse sections (3 µm thick) are examined with a fluorescent microscope. MAR and BFR are measured using the OsteoMeasure System.
Rats[2]
Thirty 6-month-old female Sprague-Dawley rats are used. After anesthesia with intraperitoneal nembutal injection (30 mg/kg), the rats are randomized by body weight into three groups for the surgery (n=10/group): group 1: sham surgery followed by PBS vehicle treatment (sham+VEH); group 2: ovariectomy followed by vehicle treatment (OVX+VEH); and group 3: ovariectomy followed by Osthole treatment (OVX+OST). The treatment is started 1 month after surgery and continued for 8 weeks. Vehicle or Osthole (100 mg/kg per day) is administered orally once a day for 8 weeks. Before rats are euthanized at the end of the experiments, the total bone mineral density (BMD, g/m2) is measured using dual-energy X-ray absorptiometry. The fourth lumbar vertebrae (L4) then are dissected for histomorphometric and micro-computed tomographic (µCT) analysis, and the left femoral shafts are used for biomechanical testing.

MCE has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献

  • [1]. Kordulewska NK, et al. Changes in gene expression induced by histamine, fexofenadine and osthole: Expression of histamine H1 receptor, COX-2, NF-κB, CCR1, chemokine CCL5/RANTES and interleukin-1β in PBMC allergic and non-allergic patients. Immunobiology.

    [2]. Tang DZ, et al. Osthole stimulates osteoblast differentiation and bone formation by activation of beta-catenin-BMP signaling. J Bone Miner Res. 2010 Jun;25(6):1234-45.

    [3]. Sun W, et al. Osthole pretreatment alleviates TNBS-induced colitis in mice via both cAMP/PKA-dependent and independent pathways. Acta Pharmacol Sin. 2017 Aug;38(8):1120-1128.

    [4]. Zhang ZR, et al. Osthole: A Review on Its Bioactivities, Pharmacological Properties, and Potential as Alternative Medicine. Evid Based Complement Alternat Med. 2015;2015:919616.