Oligomycin, an antifungal antibiotic, is an inhibitor of H+-ATP-synthase. Oligomycin blocks oxidative phosphorylation and the electron transport chain. Oligomycin inhibits HIF-1alpha expression in hypoxic tumor cells[1][2][3][4].
体外研究 (In Vitro)
Oligomycin, inhibitor of the F0 part of H+-ATP-synthase, suppresses the TNF-induced apoptosis[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
CAS 号
1404-19-9
中文名称
寡霉素
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Zhou W, et al. Membrane plasticity facilitates recognition of the inhibitor oligomycin by the mitochondrial ATP synthase rotor. Biochim Biophys Acta Bioenerg. 2018;1859(9):789-796.
[2]. SMITH RM, et al. Oligomycin, a new antifungal antibiotic. Antibiot Chemother (Northfield). 1954;4(9):962-970.
[3]. López de Figueroa P, et al. Autophagy activation and protection from mitochondrial dysfunction in human chondrocytes. Arthritis Rheumatol. 2015;67(4):966-976.
[4]. Gong Y, et al. Oligomycin inhibits HIF-1alpha expression in hypoxic tumor cells. Am J Physiol Cell Physiol. 2005;288(5):C1023-C1029.
[5]. Shchepina LA, et al. Oligomycin, inhibitor of the F0 part of H+-ATP-synthase, suppresses the TNF-induced apoptosis. Oncogene. 2002;21(53):8149-8157.
UNC 0631 is a potent histone methyltransferase G9a inhibitor with an IC50 of 4 nM. UNC 0631 potently reduces H3K9me2 levels in MDA-MB-231 cells with an IC50 of 25 nM[1].
IC50 & Target
G9a
4 nM (IC50)
体外研究 (In Vitro)
UNC 0631 (Compound 7) has high cellular potency and excellent separation of functional potency versus cell toxicity in a variety of cell lines. UNC 0631 is highly potent in reducing H3K9me2 levels and has low cell toxicity. UNC 0631 reduces H3K9me2 levels with ICW IC50 values of 25 nM, 18 nM, 26 nM, 24 nM, 51 nM, 72 nM and 46 nM in MDA-MB-231, MCF7, PC3, 22RV1, HCT116 wt, HCT 116 p53-/- and IMR90 cell lines, respectively[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
635.93
Formula
C37H61N7O2
CAS 号
1320288-19-4
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. OuYang Mingan, et al. Studies on the phenol glycoside constituents of Ligustrum sinense. Guangxi Zhiwu. 01 Jan 2003, 23(3):276-278.
[2]. Chen L, et al. Prediction of anti-tumor chemical probes of a traditional Chinese medicine formula by HPLC fingerprinting combined with molecular docking. Eur J Med Chem. 2014 Aug 18;83:294-306.
Navtemadlin (AMG 232) is a potent, selective and orally available inhibitor of p53-MDM2 interaction, with an IC50 of 0.6 nM. Navtemadlin binds to MDM2 with a Kd of 0.045 nM[1][2].
Induced p53 signaling and inhibits tumor cell proliferation in three p53 wild-type tumor cell lines (SJSA-1, HCT116, and ACHN). Caused robust p21 mRNA induction between 9.76 and 34.9 fold with IC50 values ranging from 12.8 to 46.8 nM.
体内研究 (In Vivo)
Navtemadlin (AMG 232) (10, 25, 75 mg/kg, once daily, p.o.) activates p53 pathway activity in vivo[1]. Navtemadlin (10, 25, 75 mg/kg, once daily, p.o.) potently inhibits growth of tumor xenografts in mice[1]. Navtemadlin (10, 25, 75 mg/kg, once daily, p.o.) blocks DNA synthesis and induces apoptosis in vivo[1]. Navtemadlin causes a dose-dependent tumor growth inhibition with an ED50 of 16 mg/kg[2].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
Female athymic nude mice (n=10/group) based cancer models[1].
Dosage:
10, 25, 75 mg/kg.
Administration:
Once daily by oral gavage.
Result:
Resulted in significant tumor growth inhibition across all models. SJSA-1, an MDM2 amplified osteosarcoma model, was the most sensitive to AMG 232 treatment with an ED50 of 9.1 mg/kg. In the highest dose group of 75 mg/kg, 10/10 tumors completely regressed and were undetectable after 10 days of treatment.
Clinical Trial
分子量
568.55
Formula
C28H35Cl2NO5S
CAS 号
1352066-68-2
运输条件
Room temperature in continental US; may vary elsewhere.
Solubility: 1.5 mg/mL (2.64 mM); Clear solution; Need ultrasonic
*以上所有助溶剂都可在 上海金畔生物科技有限公司 网站选购。
参考文献
[1]. Canon J, et al. The MDM2 Inhibitor AMG 232 Demonstrates Robust Antitumor Efficacy and Potentiates the Activity of p53-Inducing Cytotoxic Agents. Mol Cancer Ther. 2015 Mar;14(3):649-58.
[2]. Rew Y, et al. Discovery of a small molecule MDM2 inhibitor (AMG 232) for treating cancer. J Med Chem. 2014 Aug 14;57(15):6332-41.
Cyasterone, a natural EGFR inhibitor, mainly isolated from Ajuga decumbens Thunb (Labiatae). Cyasterone manifests anti-proliferation effect by induced apoptosis and cell cycle arrests. Cyasterone may serves as a therapeutic anti-tumor agent against human tumors[1].
IC50 & Target
IC50: EGFR[1]
体外研究 (In Vitro)
Cyasterone exerts cytotoxicity on multiple cell lines: HeLa (IC50=77.24 μg/ml); HepG-2 (IC50=52.03 μg/ml); MCF-7 (IC50=82.07 μg/ml) and MCF-7 (IC50=82.07 μg/ml). And It has none cytotoxicity (IC50>400 μg/ml) on 3 types of carcinoma (HT-29, Caco-2, T47D) and 1 type of normal (NIH 3T3) cell lines[1]. Cyasterone (0-60 μg/ml; 48 hours) causes a significantly decreasing of the cell proliferation. It inhibits cell growth as a dose-dependent manner, exhibits IC50 values of 38.50 μg/ml and 32.96 μg/ml, respectively[1]. Cyasterone (0-60 μg/ml; 24 hours) decreases p-EGFR, p-MEK, and p-mTOR as a dose-dependent manner in A549 cells, it affects the MAPK signaling pathway activities[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Viability Assay[1]
Cell Line:
A549 cells and MGC823 cells
Concentration:
0 μg/ml, 20 μg/ml, 40 μg/ml, 60 μg/ml
Incubation Time:
24 hours
Result:
Inhibited cell proliferation as a dose-dependent manner.
Western Blot Analysis[1]
Cell Line:
A549 cells
Concentration:
0 μg/ml, 20 μg/ml, 40 μg/ml, 60 μg/ml
Incubation Time:
24 hours
Result:
Surpressed p-EGFR, p-MEK, and p-mTOR expression.
体内研究 (In Vivo)
Cyasterone (intraperitoneal injection; 5 mg/kg, 10 mg/kg and 15 mg/kg; 21 days) has anti-proliferation effect in vivo and inhibits MGC823 cells xenografted tumor growth in vivo with few changes in body weights[2].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
MGC823 xenograft tumor in BALB/C-nu mice[1]
Dosage:
5 mg/kg, 10 mg/kg and 15 mg/kg
Administration:
Intraperitoneal injection
Result:
Inhibited MGC823 xenograft tumor growth in vivo.
分子量
520.65
Formula
C29H44O8
CAS 号
17086-76-9
中文名称
杯苋甾酮
运输条件
Room temperature in continental US; may vary elsewhere.
Diethylstilbestrol (Stilbestrol), a synthetic nonsteroidal estrogen used in the treatment of menopausal and postmenopausal disorders. Target: Estrogen Receptor/ERR Diethylstilbestrol (DES), a synthetic estrogen that was used in pregnancy, is a prototype endocrine-disrupting chemical. Although prenatal exposure to DES is known to increase risks of vaginal/cervical adenocarcinoma and adverse reproductive outcomes in women, and urogenital anomalies in men, data on nonreproductive medical conditions are lacking. Comparing persons exposed prenatally to DES with those who were not exposed, the hazard ratios were 1.21 (95% confidence interval = 0.96-1.54) for diabetes, 1.27 (1.00-1.62) for all cardiovascular disease, 1.18 (0.88-1.59) for coronary artery disease, 1.28 (0.88-1.86) for myocardial infarction, 1.12 (1.02-1.22) for high cholesterol, 1.14 (1.02-1.28) for hypertension, 1.24 (0.99-1.54) for osteoporosis, and 1.30 (0.95-1.79) for fractures. The associations did not differ by dose and timing of DES exposure, nor, in the women, by the presence or absence of vaginal epithelial changes (a marker of DES host susceptibility) [1]. The role of prenatal exposure to DES as an environmental risk factor for psychiatric disorders requires more evidence before any conclusions can be drawn [2].
Clinical Trial
分子量
268.35
Formula
C18H20O2
CAS 号
56-53-1
中文名称
己烯雌酚；乙烯雌酚；乙芪酚
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Troisi, R., et al., Medical conditions among adult offspring prenatally exposed to diethylstilbestrol. Epidemiology, 2013. 24(3): p. 430-8.
[2]. Kebir, O. and M.O. Krebs, Diethylstilbestrol and risk of psychiatric disorders: a critical review and new insights. World J Biol Psychiatry, 2012. 13(2): p. 84-95.
3-Deazaneplanocin A hydrochloride (DZNep hydrochloride) 是一种有效的组蛋白甲基转移酶 (EZH2) 抑制剂。3-Deazaneplanocin A hydrochloride 是一种有效的 S-腺苷同型半胱氨酸水解酶 (AHCY) 抑制剂。
3-Deazaneplanocin A hydrochloride Chemical Structure
CAS No. : 120964-45-6
规格
价格
是否有货
数量
1 mg
￥900
In-stock
5 mg
￥3500
In-stock
10 mg
￥5500
In-stock
25 mg
￥9900
In-stock
50 mg
询价
100 mg
询价
* Please select Quantity before adding items.
3-Deazaneplanocin A hydrochloride 相关产品
•相关化合物库:
Bioactive Compound Library Plus
生物活性
3-Deazaneplanocin A hydrochloride (DZNep hydrochloride) is a potent histone methyltransferase EZH2 inhibitor[1][2]. 3-Deazaneplanocin A hydrochlorideis a potent S-adenosylhomocysteine hydrolase (AHCY) inhibitor[6].
体外研究 (In Vitro)
3-Deazaneplanocin A (DZNep) hydrochloride is a potent histone methyltransferase EZH2 inhibitor. Treatment of OCI-AML3 cells with 3-Deazaneplanocin A (1.0 μM) results in a significant increase in accumulation of cells in the G0/G1 phase (58.5%) with a concomitant decrease in the number of cells in S phase (35.2%) and G2/M phases (6.3%) of the cell cycle (P<0.05). Treatment with 3-Deazaneplanocin A (200 nM to 2.0 μM) for 48 hours, dose dependently, inhibits colony growth of OCI-AML3 and HL-60 cells[1]. 3-Deazaneplanocin A (DZNep) hydrochloride reduces the expression of EZH2, especially after 72 hours (e.g. 48%, 32% and 36% reduction of EZH2 in PANC-1, MIA-PaCa-2 and LPc006 cells, respectively)[2]. 3-Deazaneplanocin A (DZNep) hydrochloride shows minimal growth inhibition in PANC-1 cells. More than 50% of these cells are still growing after exposure at the highest concentration (20 μM). MIA-PaCa-2 and LPc006 cells are much more sensitive, with IC0 values of 1.0±0.3 and 0.10±0.03 μM, respectively[2]. 3-Deazaneplanocin A (DZNep) hydrochloride causes dose-dependent inhibition of cell proliferation of NSCLC cell lines, and the IC0 values range from 0.08 to 0.24 μM[3].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
The survival of NOD/SCID mice with acute myeloid leukemia (AML) due to HL-60 cells is significantly higher, if treated with 3-Deazaneplanocin A (DZNep) and LBH589 (PS) compare to treatment with PS, 3-Deazaneplanocin A, or vehicle alone (P<0.05). Median survival is as follows: control, 36 days; PS, 42 days; 3-Deazaneplanocin A, 43 days; and 3-Deazaneplanocin A plus PS, 52 days[1]. There is a progressive increase in weight of rats treated with physiological saline in a time-dependent manner (the mean growth rate=3.19% per day). Administration of 20 mg/kg 3-Deazaneplanocin A (DZNep) not only markedly reduces the relative weight of the rats compare to the initial weight (−2.0%, −4.9% and −1.2%) in the first three days post-treatment, but also suppresses the weight growth rate to 2.6% per day from the fourth day onwards post-dose[4].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
298.73
Formula
C12H15ClN4O3
CAS 号
120964-45-6
中文名称
3-去氮腺嘌呤A盐酸盐
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Fiskus W, et al. Combined epigenetic therapy with the histone methyltransferase EZH2 inhibitor 3-deazaneplanocin A and the histone deacetylase inhibitor LBH589 against human AML cells. Blood, 2009, 114(13), 2733-2743.
[2]. Avan A, et al. Molecular mechanisms involved in the synergistic interaction of the EZH2 inhibitor 3-deazaneplanocin A with LY 188011 in pancreatic cancer cells. Mol Cancer Ther. 2012 Aug;11(8):1735-46.
[3]. Kikuchi J, et al. Epigenetic therapy with 3-deazaneplanocin A, an inhibitor of the histone methyltransferase EZH2, inhibits growth of non-small cell lung cancer cells. Lung Cancer. 2012 Nov;78(2):138-43.
[4]. Sun F, et al. Preclinical pharmacokinetic studies of 3-deazaneplanocin A, a potent epigenetic anticancer agent, and its human pharmacokinetic prediction using GastroPlus?. Eur J Pharm Sci. 2015 Sep 18;77:290-302.
[5]. Noriko Uchiyama, et al. Aristeromycin and DZNeP cause growth inhibition of prostate cancer via induction of mir-26a. Eur J Pharmacol. 2017 Oct 5;812:138-146.
Cell Assay [1]
AML HL-60 cells are obtained and maintained. OCI-AML-3 cells are cultured in α minimum essential medium with 10% fetal bovine serum, and 1% nonessential amino acids. To analyze synergism between 3-Deazaneplanocin A and PS in inducing apoptosis, cells are treated with 3-Deazaneplanocin A (100-750 nM) and PS (5-20 nM) at a constant ratio for 48 hours. The percentage of apoptotic cells is determined by flow cytometry. The combination index (CI) for each drug combination is obtained by median dose effect of Chou and Talalay, using the CI equation within the commercially available software Calcusyn[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Administration [1][4]
Mice[1] HL-60 cells (5 million) are injected into the tail vein of female nonobese diabetic/severe combined immunodeficiency (NOD/SCID) mice, and the mice are monitored for 7 days. The following treatments are administered in cohorts of 7 mice for each treatment: vehicle alone, 1 mg/kg 3-Deazaneplanocin A, 10 mg/kg PS, and 3-Deazaneplanocin A plus PS. Treatments are initiated on day 7. 3-Deazaneplanocin A is administered twice per week (Tuesday-Thursday) intraperitoneally for 2 weeks, and then discontinued. PS is administered 3 days per week (Monday, Wednesday, and Friday) for 4 weeks. The survival of mice from the tail vein model is represented with a Kaplan-Meier survival plot. Rats[4] Male wistar rats are used. The acute toxicity study is carried out to determine the NOAEL of 3-Deazaneplanocin A in rats. In total, 20 rats are divided into 4 groups of five each. Three groups are intravenously administered 20, 15, 10 mg/kg body weight (BW) DZNep solution by the tail vein. The remaining group is given physiological saline (0.9% NaCl saline) as the control group. Then, the NOAEL of free DZNep is determined, depending on the following endpoint parameters obtained.
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献
[1]. Fiskus W, et al. Combined epigenetic therapy with the histone methyltransferase EZH2 inhibitor 3-deazaneplanocin A and the histone deacetylase inhibitor LBH589 against human AML cells. Blood, 2009, 114(13), 2733-2743.
[2]. Avan A, et al. Molecular mechanisms involved in the synergistic interaction of the EZH2 inhibitor 3-deazaneplanocin A with LY 188011 in pancreatic cancer cells. Mol Cancer Ther. 2012 Aug;11(8):1735-46.
[3]. Kikuchi J, et al. Epigenetic therapy with 3-deazaneplanocin A, an inhibitor of the histone methyltransferase EZH2, inhibits growth of non-small cell lung cancer cells. Lung Cancer. 2012 Nov;78(2):138-43.
[4]. Sun F, et al. Preclinical pharmacokinetic studies of 3-deazaneplanocin A, a potent epigenetic anticancer agent, and its human pharmacokinetic prediction using GastroPlus?. Eur J Pharm Sci. 2015 Sep 18;77:290-302.
[5]. Noriko Uchiyama, et al. Aristeromycin and DZNeP cause growth inhibition of prostate cancer via induction of mir-26a. Eur J Pharmacol. 2017 Oct 5;812:138-146.
Iohexol is a radiographic contrast agent and can be applied for myelography, computerized tomography (cisternography, ventriculography) and MicroCT imaging in vivo[1].
Clinical Trial
分子量
821.14
Formula
C19H26I3N3O9
CAS 号
66108-95-0
中文名称
碘海醇；碘苯六醇
运输条件
Room temperature in continental US; may vary elsewhere.
(R)-Fangchinoline (Thalrugosine), a alkaloids from genus Stephania，exhibits antimicrobial and hypotensive activity. The roots and stems of several plants from genus Stephania are all used as traditional Chinese medicine and have been used for treatment of fever, diarrhea, dyspepsia and urinary disease[1].
分子量
608.72
Formula
C37H40N2O6
CAS 号
33889-68-8
中文名称
汉防己乙素
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Xiao J, et al. Rapid characterization of TCM Qianjinteng by UPLC-QTOF-MS and its application in the evaluation of three species of Stephania. J Pharm Biomed Anal. 2018 Jul 15;156:284-296.
[1]. Schindler AE, et al. Classification and pharmacology of progestins. Maturitas. 2003 Dec 10;46 Suppl 1:S7-S16.
[2]. Zava DT, et al. Estrogen and progestin bioactivity of foods, herbs, and spices. Proc Soc Exp Biol Med. 1998 Mar;217(3):369-78.
[3]. Komesaroff PA, et al. Effects of wild yam extract on menopausal symptoms, lipids and sex hormones in healthy menopausal women. Climacteric. 2001 Jun;4(2):144-50.
[4]. Girling JE, et al. Progesterone, but not estrogen, stimulates vessel maturation in the mouse endometrium. Endocrinology. 2007 Nov;148(11):5433-41. Epub 2007 Aug 9.
GK921 is a transglutaminase 2 (TGase) inhibitor with an IC50 of 7.71 μM for human recombinant TGase 2.
IC50 & Target
IC50: 7.71 μM (TGase)[1]
体外研究 (In Vitro)
GK921 inhibits the TGase 2-induced polymerization of I-κBα and p53 in a dose-dependent manner. The cytotoxicity of GK921 ranged from GI50 of 10-10 to 10-4 M. The average GI50 is 9.05×10-7 M. GK921 rescues p53 levels and consequently induces apoptosis; a concentration-dependent increase in cleaved poly(ADP-ribose) polymerase (c-PARP) and p53 levels is observed[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
A single treatment with GK921 almost completely reduces tumor growth by stabilizing p53 in the ACHN and CAKI-1 preclinical xenograft tumor models[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
344.41
Formula
C21H20N4O
CAS 号
1025015-40-0
运输条件
Room temperature in continental US; may vary elsewhere.
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
*以上所有助溶剂都可在 上海金畔生物科技有限公司 网站选购。
参考文献
[1]. Ku BM, et al. Transglutaminase 2 inhibitor abrogates renal cell carcinoma in xenograft models. J Cancer Res Clin Oncol. 2014 May;140(5):757-67.
Kinase Assay [1]
TGase 2 from guinea pig liver is preincubated for 10 min with various concentrations of GK13 or GK921 in 0.1 mL of reaction buffer, with or without 10 mM CaCl2, followed by the addition of 0.4 mL of substrate solution containing 2
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Assay [1]
Cells are transfected with a BAX promoter luciferase reporter construct. After exposure to GK921 (0, 0.5, 1, 2.5, 5 μM), firefly and Renilla luciferase activities are measured using a dual luciferase assay kit and pRL-CMV as an internal control[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Administration [1]
Mice: GK921 is dissolved in DMSO. Vehicle alone and GK921 (8 mg/kg) are administered orally once per day, 5 days/week, for 64 days. The size of the primary tumors is measured every 2-3 days using calipers. Tumor volume is calculated[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献
[1]. Ku BM, et al. Transglutaminase 2 inhibitor abrogates renal cell carcinoma in xenograft models. J Cancer Res Clin Oncol. 2014 May;140(5):757-67.
Desmethylglycitein (4′,6,7-Trihydroxyisoflavone), a metabolite of daidzein, sourced from Glycine max with antioxidant, and anti-cancer activities. Desmethylglycitein binds directly to CDK1 and CDK2 in vivo, resulting in the suppresses CDK1 and CDK2 activity[1]. Desmethylglycitein is a direct inhibitor of protein kinase C (PKC)α, against solar UV (sUV)-induced matrix matrix metalloproteinase 1 (MMP1)[2]. Desmethylglycitein binds to PI3K in an ATP competitive manner in the cytosol, where it inhibits the activity of PI3K and downstream signaling cascades, leading to the suppression of adipogenesis in 3T3-L1 preadipocytes[3].
IC50 & Target[1][2][3]
CDK1
CDK2
PKC
体外研究 (In Vitro)
Desmethylglycitein (4′,6,7-Trihydroxyisoflavone)(0-100 μM; 24-72 hours) suppesses anchorage-dependent growth of HCT-116 and DLD1 cells in a dose- and time-dependent manner without cytotoxicity [1]. Desmethylglycitein (4′,6,7-Trihydroxyisoflavone)(0-100 μM; 24-72 hours) suppresses CDK1 activity in a dose-dependent manner and inhibits CDK2 activity in HCT-116 cells[1]. Desmethylglycitein (4′,6,7-Trihydroxyisoflavone)(0-100 μM; 24-72 hours) induces cell cycle arrest at the S and G2/M phases, the percentage of cells in S phase is higher in the 100 μM 6,7,4′-THIF-treated group, and the same pattern is observed in G2/M phase (29.5% versus 19.1% ) [1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Viability Assay[1]
Cell Line:
HCT-116 cells
Concentration:
0, 12.5, 25, 50 or 100 μM
Incubation Time:
24, 48 or 72 hours
Result:
Inhibited anchorage-dependent and -independent growth of HCT-116 cells.
Western Blot Analysis[1]
Cell Line:
HCT-116 and DLD1 cells
Concentration:
0, 25, 50 or 100 μM
Incubation Time:
48 hours
Result:
Inhibited CDK1,CDK2 expression.
Cell Cycle Analysis[1]
Cell Line:
HCT-116 cells
Concentration:
0, 25, 50 or 100 μM
Incubation Time:
24, 48 or 72 hours
Result:
Induces cell cycle arrest of HCT-116 cells at S and G2/M phases.
体内研究 (In Vivo)
Desmethylglycitein (4′,6,7-Trihydroxyisoflavone) (intraperitoneally injection; 5 or 25 mg/kg; once daily; 20 days) suppresses tumor development in mice and serves as an effective anticancer treatment with the potential to inhibit or delay the tumorigenicity of HCT-116 cells in an in vivo system[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
Female athymic nude mice subcutaneously injected with HCT-116 cells[1]
Dosage:
5 or 25 mg/kg
Administration:
Intraperitoneally injection; 5 or 25 mg/kg; once daily; 20 days
Result:
Decreased tumor growth, volume and weight of HCT-116 xenografts.
分子量
270.24
Formula
C15H10O5
CAS 号
17817-31-1
中文名称
4′,6,7-三羟基异黄酮
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Lee DE, et al. 6,7,4′-trihydroxyisoflavone inhibits HCT-116 human colon cancer cell proliferation by targeting CDK1 and CDK2. Carcinogenesis. 2011 Apr;32(4):629-35.
[2]. Lim TG, et al. The daidzein metabolite, 6,7,4′-Trihydroxyisoflavone, is a novel inhibitor of PKCα in suppressing solar UV-induced matrix metalloproteinase 1. Int J Mol Sci. 2014 Nov 19;15(11):21419-32
[3]. Seo SG, et al. A metabolite of daidzein, 6,7,4′-trihydroxyisoflavone, suppresses adipogenesis in 3T3-L1 preadipocytes via ATP-competitive inhibition of PI3K.
Genistein, a soy isoflavone, is a multiple tyrosine kinases (e.g., EGFR) inhibitor which acts as a chemotherapeutic agent against different types of cancer, mainly by altering apoptosis, the cell cycle, and angiogenesis and inhibiting metastasis.
IC50 & Target[1]
EGFR
0.6 μM (IC50, Cell Assay)
Human Endogenous Metabolite
体外研究 (In Vitro)
Genistein inhibits serum-stimulated growth of MCF-7 and T47D ER+ cells with IC50 values of 7.6 and 8.7 μg/mL by dye exclusion, respectively, and 8.7 and 10.6 μg/mL by [3H]thymidmne incorporation, respectively. These values are similar to the IC50 values of 9.4 and 7 μg/mL for MCF-7 and T47D ER+ cells, respectively, obtained with the MTT assay. Additionally, Genistein at concentrations up to 20 μg/mL does not alter MTT mitochondrial reduction when compared to control cells in an 8 h incubation period. Furthermore, neither biochanin A or daidzein are found to interfere with the MTT assay at IC50 concentrations. Therefore, the MTT assay is valid for determining growth inhibition by Genistein at concentrations under 20 μg/mL in the systems studied[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
In the present study, the effective dose of morphine caused a significant decrease in testis weight of mice compared to Saline group (p=0.00). Moreover, testis weight are significantly increase in treated animals with Genistein and Genistein plus morphine in all doses in comparison with morphine group (p=0.028). Morphine caused a significant decrease in the testosterone, LH and FSH hormones compared to saline group (p=0.00). In addition, the testosterone, LH and FSH hormones increased significantly in Genistein (p<0.05) and Genistein plus morphine in all groups administration compared to morphine group (p=0.024)[2]. Bisphenol A (BPA) treatment alone and combined with Genistein had no significant effect on the protein expression of LC3II and PPARα in liver of STD- or HFD-fed rats (P>0.05; P>0.05). Significant decreasing of the protein expression of PPARγ in liver is observed when Genistein is added to rats, compared to either HFD group or HFD-BPA group[3].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Clinical Trial
分子量
270.24
Formula
C15H10O5
CAS 号
446-72-0
中文名称
染料木素；染料木黄酮；金雀异黄酮
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Peterson G, et al. Genistein inhibits both estrogen and growth factor-stimulated proliferation of human breast cancer cells. Cell Growth Differ. 1996 Oct;7(10):1345-51.
[2]. Jalili C, et al. Effect of Genistein on reproductive parameter and serum nitric oxide levels in morphine-treated mice. Int J Reprod Biomed (Yazd). 2016 Feb;14(2):95-102.
[3]. Ding S, et al. Environmentally Relevant Dose of Bisphenol A Does Not Affect Lipid Metabolism and Has No Synergetic or Antagonistic Effects on Genistein’s Beneficial Roles on Lipid Metabolism. PLoS One. 2016 May 12;11(5):e0155352.
Cell Assay [1]
The IC50 values for Genistein are determined by the MTT assay. Briefly, the MTT assay is a colorimetric assay that is based on the ability of living but not dead cells to reduce a tetrazolium-based compound to a blue formazan product. The formazan crystals are solubilized in DMSO, and the absorbance is measured at 540 nm. The absorbance at 540 nm is proportional to the number of viable cells. The lC50 values obtained with the MTT assay are compared with the lC50 values obtained by counting viable cells using trypan blue dye exclusion and by tritiated thymidine incorporation into DNA[1].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Administration [2][3]
Mice[2] Balb/c male mice are used. Genistein is administered as follows: On days 1-30, Genistein once daily, interaperitoneally injecting. Morphine plus Genistein is administered as follows: On days 1-30, Genistein once daily plus morphine, interaperitoneally injecting (17, 18). The same volume of saline is administered. Mice are randomly divided into 8 groups (n=6). 1) Normal saline group (1 mL DW/daily); 2) Morphine treated group; 3) Genistein 1 mg/kg treated group; 4) Genistein 2 mg/kg treated group 5) Genistein 4 mg/kg treated group; 6) Morphine plus Genistein 1 mg/kg treated group; 7) Morphine plus Genistein 2 mg/kg treated group; 8) Morphine plus Genistein 4 mg/kg treated group. Rats[3] Male 8-week-old Wistar rats (150-180g) are used. After one week acclimation, all rats are randomly divided into 8 groups with 10 rats per group and treated for 35 weeks as follows: (1) STD group is fed with rodent standard chow diet (STD); (2) STD-BPA group is fed with STD and administered with BPA (50 μg/kg/day); (3) STD-(BPA+G) group is fed with STD and administered with BPA (50 μg/kg/day) plus Genistein (10 mg/kg/day); (4) STD-G group is fed with STD and administered with Genistein (10 mg/kg/day); (5) HFD group received high-fat diet (HFD); (6) HFD-BPA group is fed with HFD and administered with BPA (50 μg/kg/day); (7) STD-(BPA+G) group is fed with HFD and administered with BPA (50 μg/kg/day) plus Genistein (10 mg/kg/day); (8) HFD-G group is fed with HFD and administrated with Genistein (10 mg/kg/day). All the male genitors are treated for 35 weeks consecutively. The details of BPA (50 μg/kg/day) and Genistein (10 mg/kg/day) treatment methods have been described previously: BPA is dissolved in corn oil and diluted with three stock solutions (20, 40, 80, and 120 μg/mL).
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献
[1]. Peterson G, et al. Genistein inhibits both estrogen and growth factor-stimulated proliferation of human breast cancer cells. Cell Growth Differ. 1996 Oct;7(10):1345-51.
[2]. Jalili C, et al. Effect of Genistein on reproductive parameter and serum nitric oxide levels in morphine-treated mice. Int J Reprod Biomed (Yazd). 2016 Feb;14(2):95-102.
[3]. Ding S, et al. Environmentally Relevant Dose of Bisphenol A Does Not Affect Lipid Metabolism and Has No Synergetic or Antagonistic Effects on Genistein’s Beneficial Roles on Lipid Metabolism. PLoS One. 2016 May 12;11(5):e0155352.
