2. Apoptosis
  3. Survivin Apoptosis IAP
  4. FL118

FL118  (Synonyms: 10,11-(Methylenedioxy)-20(S)-camptothecin)

目录号: HY-12486 纯度: 99.40%
COA 产品使用指南

摩尔计算器

FL118 (10,11-(Methylenedioxy)-20(S)-camptothecin)，一种喜树碱 (Camptothecin; HY-16560) 类似物，是一种口服有效的 survivin 抑制剂。FL118 与 DDX5 (p68) 结合，去磷酸化并降解 DDX5。FL118 可用于癌症的研究。

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FL118 Chemical Structure

FL118 Chemical Structure

CAS No. : 135415-73-5

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规格 价格 是否有货 数量
1 mg ￥450
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5 mg ￥900
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25 mg ￥2300
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50 mg ￥4200
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Other Forms of FL118:

FL118 相关抗体

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cIAP cIAP-1 cIAP-2 XIAP

  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

FL118 (10,11-(Methylenedioxy)-20(S)-camptothecin), a Camptothecin (HY-16560) analogue, is a potent and orally active survivin inhibitor. FL118 binds to oncoprotein DDX5 (p68) to dephosphorylates and degrades DDX5. FL118 can be used for the research of cancer[1][2].

体外研究
(In Vitro)

FL118 (0-200 nM; 24, 48 and 72 h ) inhibits the cell proliferation of ES-2 and SK-O-V3 cells[1].
FL118 (0-100 nM; 0 and 24 h) inhibits the migration of ES-2 and SK-O-V3 cells[1].
FL118 (0-100 nM; 48 h) affects the expression level of cytoglobin (CYGB)[1].
FL118 (10 and 100 nM; 48 h) inhibits PI3K/AKT/mTOR signaling pathway, and affects the expression level of vimentin and E-cadherin in ovarian cancer cells[1].
FL118 (0-100 nM; 6 and 24 h) dephosphorylates and degrades DDX5[2].
FL118 (0-500 nM; 24, 48, 72 h) regulates survivin, McL-1, XIAP, cIAP2, c-MYc and mKras by regulating DDX5[2].
FL118 (0-1 μM, 24 h) shows significant cytotoxic activity against the three tumor cell lines (A549, MDA-MB-231, and RM-1 cells)[3].
FL118 (0-10 nM, 48 h) increases the production of PARP cleavage, and induces apoptosis in A549[3].
FL118 (0-10 nM, 48 h) arrests A549 cells mainly at the G2/M phase[3].

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

FL118 相关抗体:

Western Blot Analysis[1]

Cell Line: ES-2 and SK-O-V3 cell lines
Concentration: 10 and 100 nM
Incubation Time: 48 h
Result: Effectively inhibited the activation of PI3K/AKT/mTOR signaling pathway in ovarian cancer cells and also inhibited the migration of ES-2 and SK-O-V3 cells.

Cell Migration Assay [1]

Cell Line: ES-2 and SK-O-V3 cell lines
Concentration: 0, 10 and 100 nM
Incubation Time: 0 and 24 h
Result: Inhibited the migration of ES-2 and SK-O-V3 cells dose-dependenly.

RT-PCR[1]

Cell Line: ES-2 and SK-O-V3 cell lines
Concentration: 0, 10 and 100 nM
Incubation Time: 48 h
Result: Promoted CYGB expression.

Cell Proliferation Assay[1]

Cell Line: ES-2 and SK-O-V3 cell lines
Concentration: 0, 1, 10, 50, 100 and 200 nM
Incubation Time: 24, 48 and 72 h
Result: Inhibited the cell proliferation of ES-2 and SK-O-V3 cells time- and dose-dependently.

Western Blot Analysis[2]

Cell Line: SW620 and Mia Paca-2
Concentration: 0, 10 and 100 nM
Incubation Time: 6 and 24 h
Result: Induced dephosphorylation of DDX5 through the ubiquitin-proteasome degradation pathway and degraded DDX5 time-dependently.

Western Blot Analysis[2]

Cell Line: PDAC Panc1, CRC HCT-8, SW620, Mia Paca-2, Panc-1, HCT-8 cell lines
Concentration: 0, 10, 100 and 500 nM
Incubation Time: 24, 48, 72 h
Result: Controled the expression of survivin, Mcl-1, XIAP, cIAP2, c-Myc and mKras by regulated DDX5, as an upstream master regulator in cancer development and malignant networks.

Cell Cytotoxicity Assay[3]

Cell Line: A549, MDA-MB-231, RM-1
Concentration: 0-1 μM
Incubation Time: 24 h
Result: Showed cytotoxicity in A-549 (human lung carcinoma), MDA-MB-231 (human breast carcinoma) and RM-1 (mouse prostate carcinoma), with IC50 values of 8.94 ± 1.54 , 24.73 ± 13.82, and 69.19 ± 8.34 nM, respectively.

Apoptosis Analysis[3]

Cell Line: A549 cells
Concentration: 0, 2.5, 5, 10 nM
Incubation Time: 48 h
Result: Resulted in the downregulation of survivin. Increased the production of PARP cleavage in a concentration-dependent manner, which is the hallmark of apoptosis. Induced apoptosis in A549.

Cell Cycle Analysis[3]

Cell Line: A549 cells
Concentration: 0, 2.5, 5, 10 nM
Incubation Time: 48 h
Result: Increased G2/M cell population in a concentration-dependent manner, and arrested A549 cells mainly at the G2/M phase.
体内研究
(In Vivo)

FL118 (5 and 10 mg/kg; p.o. once a week for 20 days) inhibits antitumor activity[1].
FL118 (0-1.5 mg/kg, i.p. once every other day for five times) effectively eliminates human colon and head-and-neck tumors that acquire irinotecan or topotecan resistance[4].
FL118 (1.5 mg/kg, i.v. once) exhibits favorable pharmacokinetics profiles[4].
Pharmacokinetic Parameters of FL118 in female SCID mice[4].

Sample FaDu SW620 Plasma
T1/2 (hr) 6.852 12.75 1.788
Tmax (hr) 0.167 0.167 0.167
Cmax (ng/g, mL) 115 158 43
AUC (hr*ng/g) 413 842 82
AUC∞ (hr*ng/g) 448 897 104
AUC% Extrap (%) 7.74 6.17 21.7
Vz (g/kg) (ml/kg) 33052 30742 36849
Cl (g/hr/kg) (ml/hr/kg) 3343 1671 14287

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

Animal Model: Fmale BALB/c nude mice[1]
Dosage: 5 and 10 mg/kg
Administration: Oral gavage; 5 mg/kg for once a week; 10 mg/kg for once a week; for 20 days
Result: Showed better antitumor activity than topotecan and dose-dependenly suppressed the growth of ES-2 tumors by upregulating the expression level of CYGB.
Animal Model: SCID (severe combined immunodeficiency) mice bearing human SW620 (colon) and FaDu (head-and-neck) xenograft tumors (ten-week-old, female, 20-25 g, 5 mice per cage)[4]
Dosage: 0, 0.75, 1, 1.5 mg/kg
Administration: IP, once every other day for five times as one cycle (If tumors relapse, mice were treated with FL118 for second or third cycles)
Result: Eliminated human xenograft tumors that acquired irinotecan or topotecan resistance, and was also effective after multiple cycles of treatment without the generation of FL118 resistance.
Animal Model: SCID (severe combined immunodeficiency) mice bearing human SW620 (colon) and FaDu SCID mice bearing human SW620 (colon) and FaDu (head-and-neck) xenograft tumors (ten-week-old, female, 20-25 g, 5 mice per cage)[4]
Dosage: 1.5 mg/kg
Administration: IV, once
Result: Exhibited favorable pharmacokinetics profiles.
分子量

392.36

Formula

C21H16N2O6
CAS 号
性状

固体

颜色

Light brown to brown

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
细胞实验： 

DMSO 中的溶解度 : 1 mg/mL (2.55 mM; 超声助溶 (<60°C); 吸湿的 DMSO 对产品的溶解度有显著影响，请使用新开封的 DMSO)

配制储备液
浓度 溶剂体积 质量 1 mg 5 mg 10 mg
1 mM 2.5487 mL 12.7434 mL 25.4868 mL
5 mM --- --- ---
查看完整储备液配制表

* 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。

  • 摩尔计算器

  • 稀释计算器

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

质量
=
浓度
×
体积
×
分子量 *

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2

浓度 (start)

C1

×
体积 (start)

V1

=
浓度 (final)

C2

×
体积 (final)

V2

动物溶解方案计算器
请输入动物实验的基本信息：

给药剂量

mg/kg

动物的平均体重

g

每只动物的给药体积

μL

动物数量

只
由于实验过程有损耗，建议您多配一只动物的量
计算结果
工作液所需浓度 : mg/mL
纯度 & 产品资料

纯度: 99.40%

COA (200 KB) HNMR (469 KB) RP-HPLC (205 KB)

产品使用指南 (1538 KB)
参考文献

FL118 相关分类

完整储备液配制表

* 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。

可选溶剂 浓度 溶剂体积 质量 1 mg 5 mg 10 mg 25 mg
DMSO 1 mM 2.5487 mL 12.7434 mL 25.4868 mL 63.7170 mL
Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

FL118135415-73-510,11-(Methylenedioxy)-20(S)-camptothecinFL 118FL-118SurvivinApoptosisIAPcamptothecin analoguegrowthmetastasisproliferationmigrationpyroptosisA549 cellMDA-MB-231RM-1Inhibitorinhibitorinhibit

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