MELK-IN-1是母体胚胎亮氨酸拉链激酶 (MELK)的有效抑制剂，IC50 和 Ki 分别为3 nM和0.39 nM。
MELK-IN-1 Chemical Structure
CAS No. : 2095596-44-2
规格
价格
是否有货
5 mg
￥1500
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10 mg
￥2500
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25 mg
￥5500
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50 mg
￥9500
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100 mg
￥15500
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* Please select Quantity before adding items.
生物活性
MELK-IN-1 is a potent inhibitor of maternal embryonic leucine zipper kinase (MELK) with an IC50 and a Ki of 3 nM and 0.39 nM, respectively.
IC50 & Target
IC50: 3 nM (MELK)
Ki: 0.39 nM (MELK)
[1]
分子量
539.62
Formula
C31H33N5O4
CAS 号
2095596-44-2
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. Edupuganti R, et al. Discovery of a potent inhibitor of MELK that inhibits expression of the anti-apoptotic protein Mcl-1 and TNBC cell growth. Bioorg Med Chem. 2017 May 1;25(9):2609-2616.
GRGDSPC, a 7-amino acid peptide, is a thiolated cell adhesion peptide[1].
体外研究 (In Vitro)
GRGDSPC is conjugated to acrylated dextran via thiol-acrylate reaction to regulate the interactions of human mesenchymal stem cells (hMSCs) with the photocrosslinkable hydrogels. To determine the conjugation kinetics and efficiency of GRGDSPC peptide to DEX-MAES16, various GRGDSPC concentrations (i.e., 5, 10 and 20 mg/1 g DEX-MAES16) are conjugated to the acrylated Dextran (DEX) macromer over time (0.25, 0.5, 1 and 3h) in PBS at pH 7.8 and the free thiol groups of unreacted peptides are quantified using Ellman’s assay. In addition, the reaction kinetics of the thiol-peptide to acrylated (DEX-MAES16) and methacrylated (DEX-HEMA16) macromers are compared. As early as 15 min conjugation, with 5, 10 and 20 mg of GRGDSPC peptide/1 g modified DEX, the peptide conjugation efficiencies with DEX-MAES are 105.40, 94.10 and 87.45%, respectively, while for the reaction with the DEX-HEMA they are 0.73, 15.78 and 18.42%, respectively. After 1h, the GRGDSPC conjugation with DEX-MAES is completed with the peptide concentration of 10 mg, but only 35.66% of the thiol groups of the peptide react with DEX-HEMA. The reaction kinetics are also monitored at 3 h of conjugation, and all of the 20 mg GRGDSPC peptide reacts with acrylated DEX compared to only 32.53% for the methacrylated DEX at this time point[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
690.73
Formula
C25H42N10O11S
CAS 号
91575-26-7
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
Solvent & Solubility
In Vitro:
H2O
Peptide Solubility and Storage Guidelines:
1. Calculate the length of the peptide.
2. Calculate the overall charge of the entire peptide according to the following table:
Contents
Assign value
Acidic amino acid
Asp (D), Glu (E), and the C-terminal -COOH.
-1
Basic amino acid
Arg (R), Lys (K), His (H), and the N-terminal -NH2
+1
Neutral amino acid
Gly (G), Ala (A), Leu (L), Ile (I), Val (V), Cys (C), Met (M), Thr (T), Ser (S), Phe (F), Tyr (Y), Trp (W), Pro (P), Asn (N), Gln (Q)
0
3. Recommended solution:
Overall charge of peptide
Details
Negative (<0)
1. Try to dissolve the peptide in water first. 2. If water fails, add NH4OH (<50 μL). 3. If the peptide still does not dissolve, add DMSO (50-100 μL) to solubilize the peptide.
Positive (>0)
1. Try to dissolve the peptide in water first. 2. If water fails, try dissolving the peptide in a 10%-30% acetic acid solution. 3. If the peptide still does not dissolve, try dissolving the peptide in a small amount of DMSO.
Zero (=0)
1. Try to dissolve the peptide in organic solvent (acetonitrile, methanol, etc.) first. 2. For very hydrophobic peptides, try dissolving the peptide in a small amount of DMSO, and then dilute the solution with water to the desired concentration.
参考文献
[1]. Nguyen MK, et al. Photocrosslinkable, biodegradable hydrogels with controlled cell adhesivity for prolonged siRNAdelivery to hMSCs to enhance their osteogenic differentiation. J Mater Chem B. 2017 Jan 21;5(3):485-495.
20-HEDE (WIT 002) is an antagonist of 20-hydroxyeicosatetraenoic acid (20-HETE).
IC50 & Target
20-HEDE (WIT 002)[1].
体外研究 (In Vitro)
ω-hydroxylation activity toward arachidonic acid is high in A549 cells, thus, A549 cells are treated with HET0016 or WIT 002 in the invasion assays, and both of them significantly decrease invasion[2]. WIT 002 inhibits proliferation of 786-O and 769-P renal adenocarcinoma cells, but HET0016 and WIT 002 fail to inhibit proliferation of normal renal epithelial cells RPTC[2][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 effect of the 20-HETE antagonist, WIT 002 on the growth of 786-O clear cell renal carcinoma is assessed in ectopic mouse model of renal tumor. The growth of tumors is significantly suppressed by WIT 002 administered daily to athymic nude mice implanted subcutaneously with cells 786-O. Tumor growth is inhibited by 84%±128%. It is of note that in these experiments WIT 002 treatment start only after the tumor is seeded for 7-14 days and is relatively large 0.1 cm. Thus, WIT 002 is effective at arresting the growth of a fairly advanced tumor[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.
分子量
324.50
Formula
C20H36O3
CAS 号
240427-90-1
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. Ming Yua . et al. Effects of a 20-HETE antagonist and agonists on cerebral vascular tone. Eur J Pharmacol. 2004 Feb 23;486(3):297-306.
[2]. Wei Yu, et al. Cytochrome P450 ω-hydroxylase promotes angiogenesis and metastasis by upregulation of VEGF and MMP-9 in non-small cell lung cancer. Cancer Chemother Pharmacol. 2011 Sep; 68(3): 619-29.
[3]. Anna Alexanian, et al. Down-regulation of 20-HETE Synthesis and Signaling Inhibits Renal Adenocarcinoma Cell Proliferation and Tumor Growth. Anticancer Res. 2009 October ; 29(10): 3819-3824.
Cell Assay [2][3]
Human NSCLC cell lines (e.g A549) are seeded onto the upper well of the chamber. Subsequently, serum-free medium with HET0016 (10 μM), WIT002 (10 μM), WIT003 (0.01, 0.1, 1 μM), or ethanol as a control is added to the upper chamber, while the lower well is filled to the top (500 μL) with RPMI-1640 containing 5% fetal calf serum (FCS) as a chemoattractant. Cells are allowed to migrate for 5 h. Cells that have invaded to the bottom surface of the filter are counted with an ocular micrometer in a blinded manner, counting a minimum of 10 high-powered fields (HPF) [2]. Human renal cell adenocarcinoma lines (RPTC) 786-O or 769-P cells are plated and next day (0 hrs) transferred to serum-free medium containing either EGF or ET-1. Cells are exposed either to 10 μM WIT002 or vehicle. Cell counting is performed at the day of transfer to serum free medium (0 hrs) and 24, 48 and 72 hrs thereafter. Medium is changed to fresh containing mitogens and drugs every 24 hrs. Data presented are characteristic experiment from at least two separate experiments, each performed in triplicate[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.
Animal Administration [3]
Mice[3] Experiments are carried out on 6-week immunodefficient athymic nude mice weighing 20-26 g. Animals are acclimated for 1 week prior to injection with renal cell carcinoma. Immediately before each implantation, the cells are trypsinized, counted and resuspended in 10% serum containing RPMI media. The concentration of cells is adjusted to 40 millions/mL and 4 million cells/animal are injected subcutaneously. The cells are allowed to grow for 7-15 days until the size of the tumors reach approximately 0.1 cm3. The mice then receive daily subcutaneous injection (s.c.) injections of WIT 002 (10 mg/kg/day in 200 μL) in an isotonic NaPO4 buffer (pH 9.0) or vehicle (0.1 M NaPO4 solution pH 9.0). The diameter of the tumor is measured on every 3-4 days for 2 weeks using precision calibers. At the end of the experiment the mice are euthanized with CO2 and the tumors were excised to confirm the diameter measurements[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.
参考文献
[1]. Ming Yua . et al. Effects of a 20-HETE antagonist and agonists on cerebral vascular tone. Eur J Pharmacol. 2004 Feb 23;486(3):297-306.
[2]. Wei Yu, et al. Cytochrome P450 ω-hydroxylase promotes angiogenesis and metastasis by upregulation of VEGF and MMP-9 in non-small cell lung cancer. Cancer Chemother Pharmacol. 2011 Sep; 68(3): 619-29.
[3]. Anna Alexanian, et al. Down-regulation of 20-HETE Synthesis and Signaling Inhibits Renal Adenocarcinoma Cell Proliferation and Tumor Growth. Anticancer Res. 2009 October ; 29(10): 3819-3824.
FLT3-IN-4 is a potent and orally effective Fms-like tyrosine receptor kinase 3 (FLT3; IC50=7 nM) inhibitor for treating acute myelogenous leukemia[1].
体外研究 (In Vitro)
FLT3-IN-4 (Compound 9u) shows potent inhibitory activities against MV4-11 and Molm-13 cells with IC50 values are 0.089±0.001 nM and 0.022±0.003 nM, 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
431.49
Formula
C23H25N7O2
CAS 号
2304799-09-3
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. Yuan X, et al. Identification of Pyrrolo[2,3- d]pyrimidine-Based Derivatives as Potent and Orally Effective Fms-like Tyrosine Receptor Kinase 3 (FLT3) Inhibitors for Treating Acute Myelogenous Leukemia. J Med Chem. 2019 Apr 25;62(8):4158-4173.
GRGDSP, a synthetic linear RGD peptide, is an integrin inhibitor.
IC50 & Target
Integrin[1]
体外研究 (In Vitro)
It is demonstrated that transarterial infusion of GRGDSP (Gly-Arg-Gly-Asp-Ser-Pro integrin-inhibitor which includes RGD-peptide). As a synthetic linear RGD peptide, GRGDSP (Gly-Arg-Gly-Asp-Ser-Pro) can inhibit the adherence of tumor cells to endothelial cells of blood vessels and limit its metastasis[1]. GRGDSP (Gly-Arg-Gly-Asp-Ser-Pro) is used as a soluble integrin-blocking RGD-based peptide. GRGDSP is used widely together with other RGD peptides in integrin research. GRGDSP can be used to modify the surface of cardiovascular implants such as vascular grafts to promote endothelialization[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.
分子量
587.58
Formula
C22H37N9O10
CAS 号
91037-75-1
Sequence
Gly-Arg-Gly-Asp-Ser-Pro
Sequence Shortening
GRGDSP
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. Qian J, et al. Transarterial administration of integrin inhibitor loaded nanoparticles combined with transarterial chemoembolization for treating hepatocellular carcinoma in a rat model. World J Gastroenterol. 2016 Jun 7;22(21):5042-9.
[2]. Patel S, et al. Regulation of endothelial cell function by GRGDSP peptide grafted on interpenetrating polymers. J Biomed Mater Res A. 2007 Nov;83(2):423-33.
PTP1B-IN-3 is a potent and orally active PTP1B inhibitor with IC50s of 120 nM for both PTP1B and TCPTP. PTP1B-IN-3 has antidiabetic and anticancer effects[1][2].
IC50 & Target
IC50: 120 nM (PTP1B), 120 nM (TCPTP) [2]
体内研究 (In Vivo)
In diet-induced obese (DIO) mice, PTP1B-IN-3 (compounds 3g) exhibits dose dependent inhibition (60%, 80% and 100% inhibition at 1, 3 and 10 mg/kg, respectively) of glucose excursion when given orally 2 h before oral glucose challenge with an estimated ED50 of 0.8 mg/kg[1]. In the NDL2 Ptpn1 transgenic mice, PTP1B-IN-3 (compounds 3g; orally; 30 mg/kg for 21 days) shows a significant delay in the onset of tumor development in NDL2 Ptpn1+/+ mice, extending the median tumor free days (T50) from 28 days to 75 days[1]. In diet-induced obese (DIO) mice, PTP1B-IN-3 (compounds 3g) exhibits good oral bioavailability (F of 24%), slow clearance (CL of 0.71 mL/kg/min), and good elimination half live (t1/2 of 6 h). The oral bioavailability in higher species such as rats (F of 4%) and squirrel monkeys (F of 2%) are substantially lower but excellent exposures are achieved with oral dosing[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
362.06
Formula
C12H7BrF2NO3P
CAS 号
809272-64-8
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. Yongxin Han, et al. Discovery of [(3-bromo-7-cyano-2-naphthyl)(difluoro)methyl]phosphonic acid, a potent and orally active small molecule PTP1B inhibitor. Bioorg Med Chem Lett. 2008 Jun 1;18(11):3200-5.
[2]. Patel D, .Discovery of orally active, potent, and selective benzotriazole-based PTP1B inhibitors. ChemMedChem. 2011 Jun 6; 6(6):1011-6.
PDP-Pfp is a reducible ADC linker used for the agents that target for the extracellular loop 1 (ECL1) of TM4SF1 (transmembrane 4 L6 family member 1)[1].
分子量
381.34
Formula
C14H8F5NO2S2
CAS 号
160580-70-1
运输条件
Room temperature in continental US; may vary elsewhere.
BMVC2 (o-BMVC) 是 BMVC 的双取代咔唑衍生物，是一种 G 四联体 (G4) 稳定剂。
BMVC2 Chemical Structure
CAS No. : 850559-51-2
规格
价格
是否有货
5 mg
￥2500
询问价格 & 货期
10 mg
￥3800
询问价格 & 货期
25 mg
￥7500
询问价格 & 货期
50 mg
￥12000
询问价格 & 货期
100 mg
￥18000
询问价格 & 货期
* Please select Quantity before adding items.
生物活性
BMVC2 (o-BMVC) is a bisubstitute carbazole derivative of BMVC. BMVC2 is a G-quadruplex (G4) stabilizer[1].
IC50 & Target
G-quadruplex[1]
体外研究 (In Vitro)
BMVC2 by monitoring the disappearance of the 291 nm CD signals of d[AG3(T2AG3)3] (HT22) after adding Cu2+ is screened, a longer unfolding time would dictate a better G4 stabilizer. The unfolding curve of HT22 in the presence of BMVC2 can be fitted by using two time constants of 133.7 s (29%) and 2816 s (71%), which are similar to the unfolding parameters of BMVC[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
657.33
Formula
C28H25I2N3
CAS 号
850559-51-2
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. Jen-Fei Chu, et al. A Novel Method for Screening G-quadruplex Stabilizers to Human Telomeres. Journal of the Chinese Chemical Society, 2011, 58, 296-300.
QTX125 is a potent and highly selective HDAC6 inhibitor. QTX125 exhibits excellent selectivity over other HDACs. QTX125 has antitumor effects[1].
IC50 & Target[1]
HDAC6
体外研究 (In Vitro)
QTX125 (25-500 nM; 24-48 hours) treatment induces the subsequent apoptosis demonstrated by annexin V/propidium iodide double staining and the cleavage of caspase-9, caspase-8, caspase-3, and PARP[1]. In MCL cell lines MINO, REC-1, IRM-2 and HBL-2 cells, QTX125 (10 nM, 10 μM, 100 μM) induces dose-dependent hyperacetylation of α-tubulin[1]. QTX125 has the strongest growth-inhibitory effect in Burkitt cell lymphoma, follicular lymphoma, and mantle cell lymphoma (MCL)[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
Inhibited the cleavage of caspase-9, caspase-8, caspase-3, and PARP.
体内研究 (In Vivo)
QTX125 (60 mg/kg; i.p.; daily dosing for 5 days; for 4 weeks) treatment inhibits tumor growth in REC-1 or MINO cells xenografted in nude mice[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
Nude mice bearing REC-1 or MINO cells[1]
Dosage:
60 mg/kg
Administration:
Intraperitoneal administration; daily dosing for 5 days; for 4 weeks
Result:
Inhibited tumor growth in REC-1 or MINO cells xenografted in nude mice.
分子量
417.41
Formula
C23H19N3O5
CAS 号
1279698-31-5
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. Montserrat Pérez-Salvia, et al. In vitro and in vivo activity of a new small-molecule inhibitor of HDAC6 in mantle cell lymphoma. Haematologica. 2018 Nov;103(11):e537-e540.
Fimaporfin (TPCS2a) is an endosomal/lysosomal-localizing photosensitizer[1].
体外研究 (In Vitro)
The endosomal/lysosomal localizing photosensitizer Fimaporfin (0.35 μg/ml) is used in the drug delivery technology photochemical internalization (PCI) in combination with drugs that usually are trapped in endosomes and/or lysosomes[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
Clinical Trial
分子量
774.86
Formula
C44H30N4O6S2
CAS 号
1443547-43-0
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[1]. Kaja Lund, et al. 5-FU resistant EMT-like pancreatic cancer cells are hypersensitive to photochemical internalization of the novel endoglin-targeting immunotoxin CD105-saporin. J Exp Clin Cancer Res. 2017 Dec 19;36(1):187.
(±)-ErSO is the racemate of ErSO. ErSO is a selective anticipatory unfolded protein response (a-UPR) activator[1].
分子量
453.33
Formula
C22H13F6NO3
CAS 号
2407860-40-4
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
参考文献
[1]. Boudreau MW, et al. A small-molecule activator of the unfolded protein response eradicates human breast tumors in mice. Sci Transl Med. 2021;13(603):eabf1383.
K-756 is a direct and selective tankyrase (TNKS) inhibitor, which inhibits the ADP-ribosylation activity of TNKS1 and TNKS2 with IC50s of 31 and 36 nM, respectively.
IC50 & Target
TNKS1
31 nM (IC50)
TNKS2
36 nM (IC50)
体外研究 (In Vitro)
K-756 is a novel and selective Wnt/β-catenin pathway inhibitor targeting tankyrase (TNKS). TNKS is one of the members of the PARP family (it is also known as PARP5). K-756 binds to the induced pocket of TNKS and inhibits its enzyme activity. To study the isoform selectivity of K-756, the PARP family enzyme inhibitory activity at 10 μM is evaluated. K-756 inhibits TNKS1 and TNKS2 by 97% and 100%, respectively. In contrast, the inhibitory activity of K-756 against PARP1, PARP2, PARP3, PARP6, PARP7, and PARP11 is less than 13%. K-756 inhibits the cell growth of APC-mutant colorectal cancer COLO 320DM and SW403 cells by inhibiting the Wnt/β-catenin pathway. K-756 strongly inhibits the reporter activity in DLD-1/TCF-Luc cells with an IC50 of 110 nM, but does not inhibit DLD-1/mtTCF-Luc cells, even at 1,000 nM. APC-mutant colorectal cancer cell line COLO 320DM and SW403 cells are treated with K-756 and after 144 hours, cell growth inhibition is measured by an XTT assay. The application of K-756 inhibits the cell growth of COLO 320DM with a GI50 of 780 nM. K-756 also inhibits SW403 with a GI50 of 270 nM[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
DLD-1/TCF-Luc cell xenografts are created in SCID mice. Vehicle (0.5% MC400) or K-756 is administered orally once a day for 3 days at 100, 200, and 400 mg/kg. The Wnt/β-catenin signal inhibition in the tumor is detected by measuring FGF20 and LGR5 and luciferase activity. The expression of FGF20 and reporter activity are significantly decreased at doses of 100 mg/kg and above at 3-day administration. The expression of LGR5 is significantly decreased at doses of 200 mg/kg and above at 3-day administration. The maximum inhibitory activity is reached with the administration of K-756 at a dose of 400 mg/kg at 3-day administration. The Wnt/β-catenin signal inhibition at a dose of 400 mg/kg is observed from 1-day administration[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
433.50
Formula
C24H27N5O3
CAS 号
130017-40-2
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
参考文献
[1]. Okada-Iwasaki R, et al. The Discovery and Characterization of K-756, a Novel Wnt/β-Catenin Pathway Inhibitor Targeting Tankyrase. Mol Cancer Ther. 2016 Jul;15(7):1525-34.
Kinase Assay [1]
The activity of each enzyme is measured using a PARP1, PARP2, PARP3, PARP6, PARP7, and PARP11 Chemiluminescent Assay Kit, and a TNKS1 and TNKS2 Histone Ribosylation Assay Kit. Enzymatic reactions are conducted in duplicate at 30°C for 1 hour in a 50 μL mixture containing an assay buffer, an enzyme-coated plate, and a substrate. After the enzymatic reactions, 50 μL of Streptavidin-HRP is added to each well and the plate is incubated at room temperature for an additional 30 minutes. 100 μLs of developer reagents are added to the wells and luminescence is measured using a Synergy2 microplate reader. The luminescence data are analyzed using the GraphPad Prism software program[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Assay [1]
For the cell viability assay, APC-mutant colorectal cancer cell line COLO 320DM and SW403 cells are seeded in 96-well white plates. siRNAs are reverse transfected by RNAiMax. After 144 hours, a cell viability assay is performed using a Cell Titer-Glo Luminescent Cell Viability Assay Kit. Luciferase activity is measured using a Top count NXT system. For the cell growth inhibition assay, cells are seeded in 96-well plates. The next day, the cells are treated with the compounds (e.g., K-756, 0.1 nM, 1 nM, 10 nM, 100 nM, 1 μM and 10 μM). After 0, 72, or 144 hours of incubation, XTT reagent is added to the cells. After 3 hours of incubation, the formation of formazan dye from tetrazolium salt XTT is measured using a SpectraMax 340PC system[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Administration [1]
Mice[1] SCID mice (CB17/Icr-Prkdcscid/CrlCrlj, male, 5 weeks old) are subcutaneously implanted with 5×106 cells of DLD-1/TCF-Luc cells. After 13 days, the mice with a tumor volume of 236.38 to 595.80 mm3 are divided into groups of 5 animals. On the day after grouping, 0.5% MC 400 or K-756 (100, 200, and 400 mg/kg) is orally administered to the mice once a day for 3 days. Twenty-four hours after the last administration of first and second day and 25 hours after the last administration of the third day, the tumor tissues are collected from the mice and frozen in liquid nitrogen. Tumor total RNA is extracted using an RNeasy mini Kit and reverse-transcribed using VILO reagent. An RT-PCR is performed.
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献
[1]. Okada-Iwasaki R, et al. The Discovery and Characterization of K-756, a Novel Wnt/β-Catenin Pathway Inhibitor Targeting Tankyrase. Mol Cancer Ther. 2016 Jul;15(7):1525-34.
LY2409881 is a selective IκB kinase β (IKK2) inhibitor with an IC50 of 30 nM.
IC50 & Target[1]
IKK2
30 nM (IC50)
体外研究 (In Vitro)
LY2409881 is an IKK2 inhibitor that inhibits TNFα-induced activation of NF-κB. By in vitro kinase assay, LY2409881 potently inhibits IKK2, with an IC50 of 30 nM. In contrast, the IC50 for IKK1 and other common kinases is at least one log higher. The specificity of LY2409881 for NF-κB signaling is further studied in a cell-based assay, by examining the effect of LY2409881 in the TNFα-dependent antiapoptosis function. TNFα is a well-characterized upstream stimulus of NF-κB. In the ovarian cancer cell line SKOV3, LY2409881 demonstrates moderate cytotoxicity, whereas TNFα at 10 ng/mL does not cause any cytotoxicity. In contrast, coadministration of LY2409881 and TNFα results in markedly higher cell killing compared with LY2409881. This is because TNFα-dependent activation of antiapoptotic signals mediated by NF-κB is blocked by LY2409881, while the proapoptotic TNF receptor-associated death domain (TRADD) and FAS-associated death domain (FADD) cascade pathways activated by TNFα are not affected by LY2409881[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
A well-established xenograft model of DLBCL is used to confirm the activity of LY2409881 in vivo. SCID-beige mice implanted with LY10 cell-derived tumors are given intraperitoneal injections of LY2409881 twice weekly at three different doses: 50, 100, and 200 mg/kg. The treatments are well tolerated, resulting in no death or severe morbidity of the mice. The average tumor volume is graphed as a function of time for each treatment group. The rates of tumor volume growth of the treatment groups are all significantly slower than the untreated control group (P≤0.01)[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
485.04
Formula
C24H29ClN6OS
CAS 号
946518-61-2
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
溶解性数据
In Vitro:
DMSO : ≥ 37 mg/mL (76.28 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
2.0617 mL
10.3084 mL
20.6169 mL
5 mM
0.4123 mL
2.0617 mL
4.1234 mL
10 mM
0.2062 mL
1.0308 mL
2.0617 mL
参考文献
[1]. Deng C, et al. The novel IKK2 inhibitor LY2409881 potently synergizes with histone deacetylase inhibitors in preclinical models of lymphoma through the downregulation of NF-κB. Clin Cancer Res. 2015 Jan 1;21(1):134-45.
Cell Assay [1]
OCI-Ly1, OCI-Ly7, and Su-DHL4 are GCB DLBCL cell lines; OCI-Ly3, OCI-Ly10, HBL1, and Su-DHL2 are ABC DLBCL lines. These cell lines are grown in Iscove Modified Dulbecco Medium with 10% FCS. Fresh medium is added every 2 to 3 days, and the cells are kept at a cell concentration of 0.1 to 1×106/mL. Cytotoxicity is evaluated using the CellTiter-Glo Reagent. Experiments are carried out in 96-well plates, with each treatment in triplicate. Samples are taken at typically 24, 48, and 72 hours after treatment. Cytotoxicity is expressed by the decreasing percentage of live cells in each treatment (LY2409881; 0.01, 0.1, 1 and 10 μM) relative to the untreated control from the same experiment, as a function of time. IC50 for each cell line is calculated using the CalcuSyn Version 2.0 software[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Administration [1]
Mice[1] Mouse experiments are carried out. Five- to 7-week-old SCID beige mice are injected with 107 Ly10 cells mixed in Matrigel in the posterior flank subcutaneously. When the tumors approach 150 mm3, the mice are divided into four groups of 8 mice: (i) control group, which receive 5% dextrose in water; (ii) LY2409881 at 50 mg/kg in D5W; (iii) LY2409881 at 100 mg/kg in D5W; and (iv) LY2409881 at 200 mg/kg in D5W. LY2409881 or D5W is administered intraperitoneally on day 1 and 4 of every week for 4 weeks. The data are expressed as average tumor volume (mm3) per group as a function of time. Tumor volume is calculated.
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献
[1]. Deng C, et al. The novel IKK2 inhibitor LY2409881 potently synergizes with histone deacetylase inhibitors in preclinical models of lymphoma through the downregulation of NF-κB. Clin Cancer Res. 2015 Jan 1;21(1):134-45.
SCH-1473759 is an aurora inhibitor with IC50s of 4 and 13 nM for aurora A and B, respectively.
IC50 & Target[1]
Aurora A
4 nM (IC50)
Aurora B
13 nM (IC50)
体外研究 (In Vitro)
SCH-1473759 directly binds to aurora A and B with Kds of 20 and 30 nM, respectively. SCH-1473759 also inhibits the Src family of kinases (IC50<10 nm), chk1 (ic50=13 nM), VEGFR2 (IC50=1 nM), and IRAK4 (IC50=37 nM). It does not have significant activity (IC50>1000 nM) against 34 other kinases representing different families of the kinome. SCH-1473759 inhibits HCT116 cells proliferation with an IC50 of 6 nM[1]. SCH 1473759 inhibits tumor cell lines from different tissues (breast, ovarian, prostate, lung, colon, brain, gastric, renal, skin, and leukemia). The most sensitive cell lines includ A2780, LNCap, N87, Molt4, K562, and CCRF-CEM with IC50 values <5 nm[2].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
SCH-1473759 at a low dose of 5 mg/kg (ip, bid) is well-tolerated in a continuous dosing schedule and shows 50% tumor growth inhibition(TGI) on day 16. A higher dose of 10mg/kg(ip, bid) is well-tolerated in an intermittent schedule (5 days on, 5 days off) and gave 69% TGI on day 16. SCH-1473759 shows good exposure in all species with the clearance being high in rodents and moderate in dog and monkey. The half-life is also moderate, but the tissue distribution is high[1]. SCH 1473759 dose- and schedule-dependent anti-tumor activity in four human tumor xenograft models. Further, the efficacy is enhanced in combination with taxanes and found to be most efficacious when SCH 1473759 is dosed 12-h post-taxane treatment[2].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
426.54
Formula
C20H26N8OS
CAS 号
1094069-99-4
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
参考文献
[1]. Yu T, et al. Discovery of a Potent, Injectable Inhibitor of Aurora Kinases Based on the Imidazo-[1,2-a]-Pyrazine Core. ACS Med Chem Lett. 2010 Jun 7;1(5):214-8.
[2]. Basso AD, et al. SCH 1473759, a novel Aurora inhibitor, demonstrates enhanced anti-tumor activity in combination with taxanes and KSP inhibitors. Cancer Chemother Pharmacol. 2011 Oct;68(4):923-33.
Kinase Assay [1]
Aurora A and Aurora B kinase assays are performed in low protein binding 384-well plates. SCH-1473759 is diluted in 100% DMSO to the desired concentrations. For the Aurora A assay, each reaction consists of 8 nM enzyme Aurora A, 100 nM Tamra-PKAtide, 25μM ATP, 1 mM DTT, and kinase buffer. For the Aurora B assay, each reaction consisted of 26 nM enzyme Aurora B, 100 nM Tamra-PKAtide, 50 μM ATP, 1 mM DTT, and kinase buffer. Dose-response curves are plotted from inhibition data generated in duplicate, from 8 point serial dilutions of SCH-1473759[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Assay [1]
Cells are plated at a cell density ranging from 625 to 3,750 cells per well and treated in triplicate wells with SCH-1473759 (0.1% final DMSO concentration). A plate is stained at the start of the study (zero hour) and a second plate is incubated for 72 hour at 37°C and then stained. Cells are fixed with fixation solution plus 1,000 nM Hoechst 33342 dye and incubated for 30 minutes. The fixation solution is removed and cells are ished twice with PBS. Then 15 immunofluorescence images are captured at 10X using automated fluorescent microscope [1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Administration [2]
Mice: Anti-tumor efficacy of SCH 1473759 dosed i.p. is evaluated in mice bearing established A2780 ovarian tumor xenografts. Three schedules are tested at their respective maximum tolerated doses: 10 mg/kg bid (twice daily), 20 mg/kg qd (daily), and 100 mg/kg day 0, 4, 7. Additionally, 60 mg/kg day 0, 4, 7 is tested[2].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献
[1]. Yu T, et al. Discovery of a Potent, Injectable Inhibitor of Aurora Kinases Based on the Imidazo-[1,2-a]-Pyrazine Core. ACS Med Chem Lett. 2010 Jun 7;1(5):214-8.
[2]. Basso AD, et al. SCH 1473759, a novel Aurora inhibitor, demonstrates enhanced anti-tumor activity in combination with taxanes and KSP inhibitors. Cancer Chemother Pharmacol. 2011 Oct;68(4):923-33.
Naringenin is the predominant flavanone in grapefruit; displays strong anti-inflammatory and antioxidant activities. Naringenin has anti-dengue virus (DENV) activity.
IC50 & Target
Human Endogenous Metabolite
体外研究 (In Vitro)
Naringenin is shown to inhibit the proliferation of HepG2 cells resulted partly from an accumulation of cells in the G0/G1 and G2/M phase of the cell cycle. Naringenin has been shown to induce apoptosis as evidenced by nuclei damage and increased proportion of apoptotic cells. Naringenin triggers the mitochondrial-mediated apoptosis pathway as shown by an increased ratio of Bax/Bcl-2, subsequent release of cytochrome C, and sequential activation of caspase-3[1]. Naringenin exposure significantly reduces the cell viability of A431 cells with a concomitant increase in nuclear condensation and DNA fragmentation in a dose dependent manner. Cell cycle study shows that naringenin induced cell cycle arrest in G0/G1 phase of cell cycle and caspase-3 analysis reveal a dose dependent increment in caspase-3 activity which leads to cell apoptosis[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.
体内研究 (In Vivo)
Naringenin supplementation causes a significant reduction in the amount of total triglyceride and cholesterol in plasma and liver. In addition, naringenin supplementation lowers adiposity and triglyceride contents in parametrial adipose tissue. Naringenin-fed animals show a significant increase in PPARα protein expression in the liver. The expression of CPT-1 and UCP2, known to be regulated by PPARα, is markedly enhanced by naringenin treatment[3]. Naringenin increases hepatic fatty acid oxidation through a PPARγ coactivator 1α/PPARα-mediated transcription program. It prevents sterol regulatory element-binding protein 1c–mediated lipogenesis in both liver and muscle by reducing fasting hyperinsulinemia. Naringenin decreases hepatic cholesterol and cholesterol ester synthesis[4]. Naringenin inhibits TNF-α-induced VSMC proliferation and migration in a dose-dependent manner. Mechanistic study demonstrates that naringenin prevents ERK/MAPK and Akt phosphorylation while left p38 MAPK and JNK unchanged. Naringenin also blocks the increase of ROS generation induced by TNF-α[5].
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
272.25
Formula
C15H12O5
CAS 号
480-41-1
中文名称
柚皮素；柑桔素；柚配制
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Arul D, et al. Naringenin (citrus flavonone) induces growth inhibition, cell cycle arrest and apoptosis in human hepatocellular carcinoma cells. Pathol Oncol Res. 2013 Oct;19(4):763-70.
[2]. Ahamad MS, et al. Induction of apoptosis and antiproliferative activity of naringenin in human epidermoid carcinomacell through ROS generation and cell cycle arrest. PLoS One. 2014 Oct 16;9(10):e110003.
[3]. Cho KW, et al. Dietary naringenin increases hepatic peroxisome proliferators-activated receptor α proteinexpression and decreases plasma triglyceride and adiposity in rats. Eur J Nutr. 2011 Mar;50(2):81-8.
[4]. Mulvihill EE, et al. Naringenin prevents dyslipidemia, apolipoprotein B overproduction, and hyperinsulinemia in LDLreceptor-null mice with diet-induced insulin resistance. Diabetes. 2009 Oct;58(10):2198-210.
[5]. Chen S, et al. Naringenin inhibits TNF-α induced VSMC proliferation and migration via induction of HO-1. Food Chem Toxicol. 2012 Sep;50(9):3025-31.
[6]. Frabasile S, et al. The citrus flavanone naringenin impairs dengue virus replication in human cells. Sci Rep. 2017 Feb 3;7:41864.
Cell Assay [1]
Naringenin is dissolved in DMSO and diluted in cell culture medium. The cells are rinsed with PBS and grown in a medium containing various concentrations of naringenin (50, 100, 150, 200, 250, 300 μM). The solvent DMSO treated cells are served as control. After 24 hrs of treatment, the medium is removed and replaced by another medium containing MTT. Cell viability is measured using the MTT assay[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 [3][4]
Rats: Semi-purified, powdered diets are prepared for concentrations of naringenin: 0, 0.003, 0.006, and 0.012% of diet. After 7 days of acclimatization, rats are assigned to one of four groups, with six animals per group, and fed semi-purified experimental diets for 6 weeks. The experimental diets contain 16% fat, 45.5% sucrose, and different naringenin concentration (0, 0.003, 0.006, or 0.012%) (Table 1). Rats have ad libitum access to food and water during the study period. Food intake and body weight are measured throughout the experiment[3].
Mouse: Eight- to 12-week-old mice are fed ad libitum a rodent standard diet or a high-fat diet containing 42% of calories from fat plus cholesterol (0.05% wt/wt). Naringenin is added to the Western diet at 1 or 3% (wt/wt). Ldlr−/− mice are fed for 4 weeks and C57BL/6J mice for 30 weeks. Food intake is measured daily, and body weight is measured biweekly. Mice are fasted for 6 h before intervention[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.
参考文献
[1]. Arul D, et al. Naringenin (citrus flavonone) induces growth inhibition, cell cycle arrest and apoptosis in human hepatocellular carcinoma cells. Pathol Oncol Res. 2013 Oct;19(4):763-70.
[2]. Ahamad MS, et al. Induction of apoptosis and antiproliferative activity of naringenin in human epidermoid carcinomacell through ROS generation and cell cycle arrest. PLoS One. 2014 Oct 16;9(10):e110003.
[3]. Cho KW, et al. Dietary naringenin increases hepatic peroxisome proliferators-activated receptor α proteinexpression and decreases plasma triglyceride and adiposity in rats. Eur J Nutr. 2011 Mar;50(2):81-8.
[4]. Mulvihill EE, et al. Naringenin prevents dyslipidemia, apolipoprotein B overproduction, and hyperinsulinemia in LDLreceptor-null mice with diet-induced insulin resistance. Diabetes. 2009 Oct;58(10):2198-210.
[5]. Chen S, et al. Naringenin inhibits TNF-α induced VSMC proliferation and migration via induction of HO-1. Food Chem Toxicol. 2012 Sep;50(9):3025-31.
[6]. Frabasile S, et al. The citrus flavanone naringenin impairs dengue virus replication in human cells. Sci Rep. 2017 Feb 3;7:41864.
RA375 is a RPN13 (26S proteasome regulatory subunit) inhibitor. RA375 activates UPR signaling, ROS production and apoptosis. RA375 exhibits ten-fold greater activity against cancer lines than RA190, reflecting its nitro ring substituents and the addition of a chloroacetamide warhead[1].
体内研究 (In Vivo)
RA375 (10 mg/kg, ip) inhibits proteasome function and reduces ovarian tumor burden in mice[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
Animal Model:
RA375 (10 mg/kg, ip) inhibits proteasome function and reduces ovarian tumor burden in mice[1].
Dosage:
10 mg/kg.
Administration:
IP for a 5 days on, 2 days off cycle for two weeks.
The dose of 40 mg/kg on alternate days for two weeks produced no observable toxicities or weight loss.
分子量
589.00
Formula
C30H25ClN4O7
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
溶解性数据
In Vitro:
DMSO : 125 mg/mL (212.22 mM; Need ultrasonic)
配制储备液
浓度溶剂体积质量
1 mg
5 mg
10 mg
1 mM
1.6978 mL
8.4890 mL
16.9779 mL
5 mM
0.3396 mL
1.6978 mL
3.3956 mL
10 mM
0.1698 mL
0.8489 mL
1.6978 mL
参考文献
[1]. Ravi K Anchoori, et al. Structure-function Analyses of Candidate Small Molecule RPN13 Inhibitors With Antitumor Properties. PLoS One. 2020 Jan 15;15(1):e0227727.
NSC16168 is a specific inhibitor of ERCC1-XPF, with an IC50 value of 0.42 μM. NSC16168 inhibits DNA repair and potentiates CDDP efficacy in cancer[1].
IC50 & Target
IC50: 0.42 μM (ERCC1-XPF)[1].
体外研究 (In Vitro)
NSC16168 (0-50 μM) potentiates cisplatin efficacy in cancer cells[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.
Cell Viability Assay[1].
Cell Line:
H460 cells.
Concentration:
0-50 μM.
Incubation Time:
2 h.
Result:
Potentiated cisplatin efficacy in cancer cells.
体内研究 (In Vivo)
NSC16168 (20 mg/kg, ip, twice daily) exhibits significant anti-tumor activity and potentiates cisplatin antitumor activity in H460 lung cancer xenografts[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 Model:
2.5×106 H460 cells were injected s.c. in the right flank of each mouse[1].
Dosage:
20 mg/kg.
Administration:
IP, twice daily for 10 days.
Result:
The tumor growth was minimally affected by compound and the mice displayed no signs of distress or toxic side effects. The combination treatment with 16168 and cisplatin inhibited H460 tumor growth, which was maintained for the duration of the compound injections.
分子量
473.50
Formula
C17H15NO9S3
CAS 号
6837-93-0
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]. Arora S, et al. Identification of small molecule inhibitors of ERCC1-XPF that inhibit DNA repair and potentiate cisplatin efficacy in cancer cells. Oncotarget. 2016 Nov 15;7(46):75104-75117.
LCL521 is an acid ceramidase (ACDase) inhibitor. LCL521 also inhibits the lysosomal acid sphingomyelinase (ASMase)[1].
IC50 & Target
ACDase, ASMase[1]
体外研究 (In Vitro)
LCL521 (1 µM) acts as a potent inhibitor of cellular ACDase activity, whereas 10 µM LCL521 has an additional, decreased affect on the α-form of this enzyme. LCL521 (10 µM) causes a time-dependent (1 hours and 5 hours) decrease of the α-ACDase form in MCF7 cells[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
592.77
Formula
C31H52N4O7
CAS 号
1226851-11-1
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Bai A, et al. Targeting (cellular) lysosomal acid ceramidase by B13: design, synthesis and evaluation of novel DMG-B13 ester prodrugs. Bioorg Med Chem. 2014 Dec 15;22(24):6933-44.
