Misonidazole (Ro 7-0582; SR 1354) 是一种缺氧肿瘤细胞放射增敏剂。Misonidazole 还具有抗菌作用。
Misonidazole Chemical Structure
CAS No. : 13551-87-6
规格
是否有货
100 mg
询价
250 mg
询价
500 mg
询价
* Please select Quantity before adding items.
生物活性
Misonidazole (Ro 7-0582; SR 1354) is a hypoxic tumor cell radiosensitizer[1]. Misonidazole also has antimicrobial effects[2].
分子量
201.18
Formula
C7H11N3O4
CAS 号
13551-87-6
中文名称
米索硝唑；丙硝咪唑
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]. Bibo Li, et al. Preparation, Characterization, and In Vitro pH-sensitivity Evaluation of Superparamagnetic Iron Oxide Nanoparticle- Misonidazole pH-sensitive Liposomes. Curr Drug Deliv. 2019;16(3):254-267.
[2]. R C Knight, et al. Mechanism of action of nitroimidazole antimicrobial and antitumour radiosensitizing drugs. Effects of reduced misonidazole on DNA. Int J Radiat Biol Relat Stud Phys Chem Med. 1979 Oct;36(4):367-77.
Misonidazole (Ro 7-0582; SR 1354) 是一种缺氧肿瘤细胞放射增敏剂。Misonidazole 还具有抗菌作用。
Misonidazole Chemical Structure
CAS No. : 13551-87-6
规格
是否有货
100 mg
询价
250 mg
询价
500 mg
询价
* Please select Quantity before adding items.
生物活性
Misonidazole (Ro 7-0582; SR 1354) is a hypoxic tumor cell radiosensitizer[1]. Misonidazole also has antimicrobial effects[2].
分子量
201.18
Formula
C7H11N3O4
CAS 号
13551-87-6
中文名称
米索硝唑；丙硝咪唑
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]. Bibo Li, et al. Preparation, Characterization, and In Vitro pH-sensitivity Evaluation of Superparamagnetic Iron Oxide Nanoparticle- Misonidazole pH-sensitive Liposomes. Curr Drug Deliv. 2019;16(3):254-267.
[2]. R C Knight, et al. Mechanism of action of nitroimidazole antimicrobial and antitumour radiosensitizing drugs. Effects of reduced misonidazole on DNA. Int J Radiat Biol Relat Stud Phys Chem Med. 1979 Oct;36(4):367-77.
Misonidazole (Ro 7-0582; SR 1354) 是一种缺氧肿瘤细胞放射增敏剂。Misonidazole 还具有抗菌作用。
Misonidazole Chemical Structure
CAS No. : 13551-87-6
规格
是否有货
100 mg
询价
250 mg
询价
500 mg
询价
* Please select Quantity before adding items.
生物活性
Misonidazole (Ro 7-0582; SR 1354) is a hypoxic tumor cell radiosensitizer[1]. Misonidazole also has antimicrobial effects[2].
分子量
201.18
Formula
C7H11N3O4
CAS 号
13551-87-6
中文名称
米索硝唑；丙硝咪唑
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]. Bibo Li, et al. Preparation, Characterization, and In Vitro pH-sensitivity Evaluation of Superparamagnetic Iron Oxide Nanoparticle- Misonidazole pH-sensitive Liposomes. Curr Drug Deliv. 2019;16(3):254-267.
[2]. R C Knight, et al. Mechanism of action of nitroimidazole antimicrobial and antitumour radiosensitizing drugs. Effects of reduced misonidazole on DNA. Int J Radiat Biol Relat Stud Phys Chem Med. 1979 Oct;36(4):367-77.
Tezosentan-d4 (RO 610612-d4) is the deuterium labeled Tezosentan. Tezosentan (RO 610612) is an endothelin (ET) receptor antagonist, with pA2s of 9.5, 7.7 for ETA and ETB receptors, respectively[1][2].
体外研究 (In Vitro)
Stable heavy isotopes of hydrogen, carbon, and other elements have been incorporated into drug molecules, largely as tracers for quantitation during the drug development process. Deuteration has gained attention because of its potential to affect the pharmacokinetic and metabolic profiles of drugs[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
609.65
Formula
C27H23D4N9O6S
CAS 号
1794707-10-0
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]. Russak EM, et al. Impact of Deuterium Substitution on the Pharmacokinetics of Pharmaceuticals. Ann Pharmacother. 2019;53(2):211-216.
[2]. Clozel M, et al. Pharmacology of tezosentan, new endothelin receptor antagonist designed for parenteral use. J Pharmacol Exp Ther. 1999 Aug;290(2):840-6.
Acitretin-d3 (Ro 10-1670-d3) is the deuterium labeled Acitretin. Acitretin (Ro 10-1670) is a second-generation, systemic retinoid that has been used in the treatment of psoriasis. Acitretin also can be used for the research of Alzheimer’s disease[1][2][3].
体外研究 (In Vitro)
Stable heavy isotopes of hydrogen, carbon, and other elements have been incorporated into drug molecules, largely as tracers for quantitation during the drug development process. Deuteration has gained attention because of its potential to affect the pharmacokinetic and metabolic profiles of drugs[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
329.45
Formula
C21H23D3O3
中文名称
阿维A d3
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]. Russak EM, et al. Impact of Deuterium Substitution on the Pharmacokinetics of Pharmaceuticals. Ann Pharmacother. 2019;53(2):211-216.
[2]. Lee CS, et al. A review of acitretin, a systemic retinoid for the treatment of psoriasis. Expert Opin Pharmacother. 2005 Aug;6(10):1725-34.
[3]. Sengör B, et al. Effects of acitretin on spermatogenesis of rats. J Eur Acad Dermatol Venereol. 2006 Jul;20(6):689-92.
[4]. Guilherme MDS, et, al. The Synthetic Retinoid Acitretin Increases IL-6 in the Central Nervous System of Alzheimer Disease Model Mice and Human Patients. Front Aging Neurosci. 2019 Jul 23;11:182.
Tezosentan (RO 610612) is an endothelin (ET) receptor antagonist, with pA2s of 9.5, 7.7 for ETA and ETB receptors, respectively.
IC50 & Target
ETA
9.5 (pA2)
ETB
7.7 (pA2)
体外研究 (In Vitro)
Affinity of Tezosentan for the ET receptors is assessed in different cells and tissues. Tezosentan inhibits the specific 125I-labeled ET-1 binding to ETA receptors with an inhibitory potency (Ki) of 0.3 nM on CHO cells and of 18 nM on membranes of baculovirus-infected insect cells. Similarly, Tezosentan inhibits the specific binding of 125I-labeled ET-1, ET-3, or sarafotoxin S6c to ETB receptors with an inhibitory affinity of 10 to 21 nM. Tezosentan up to a concentration of 1 μM did not exhibit any binding inhibitory activity in 27 radioligand binding assays different from ET binding. On H1 central, 5-hydroxytryptamine2A, and vasopressin V1 receptors, Tezosentan (1 μM) induces a weak inhibition of less than 20%[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)
In pithed Wistar rats, Tezosentan dose-dependently inhibits the pressor effect of big ET-1 (P<0.001 at all doses). At the lowest dose tested of 1 mg/kg, Tezosentan inhibits the pressor effect of the various doses of big ET-1 by 50 to 80%. Tezosentan has no effect by itself on blood pressure in these pithed rats. Tezosentan is very effective in a rat model of acute renal failure. ET antagonists have been shown to prevent the vasoconstriction and the renal failure that follow acute renal ischemia in rats[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
605.63
Formula
C27H27N9O6S
CAS 号
180384-57-0
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]. Clozel M, et al. Pharmacology of tezosentan, new endothelin receptor antagonist designed for parenteral use. J Pharmacol Exp Ther. 1999 Aug;290(2):840-6.
Animal Administration [1]
Rats[1] A pseudocrush syndrome is simulated by injection of i.m. glycerol. A control group does not receive glycerol and is used as a reference. Tezosentan or bosentan for comparison or saline as control is injected as two bolus i.v. doses of 10 mg/kg 1 h and 20 min before glycerol. Rats are allowed to recover for 2 h and then are placed in individual metabolic cages for 48 h. Blood samples withdraw from a catheter placed in the abdominal aorta and urine free of food and feces are collected at 24 and 48 h. Plasma and urinary creatinine levels are measured with a centrifugal analyzer. Renal function is assessed by calculating creatinine clearance at 24 and 48 h after glycerol administration[1].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献
[1]. Clozel M, et al. Pharmacology of tezosentan, new endothelin receptor antagonist designed for parenteral use. J Pharmacol Exp Ther. 1999 Aug;290(2):840-6.
Ro-3306 是一种有效，选择性的 CDK1 抑制剂，对 CDK1，CDK1/cyclin B1 和 CDK2/cyclin E 的 Ki 值为分别为 20 nM，35 nM 和 340 nM。
Ro-3306 Chemical Structure
CAS No. : 872573-93-8
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
￥825
In-stock
5 mg
￥750
In-stock
10 mg
￥1030
In-stock
50 mg
￥3200
In-stock
100 mg
￥5200
In-stock
200 mg
询价
500 mg
询价
* Please select Quantity before adding items.
Ro-3306 相关产品
•相关化合物库:
Bioactive Compound Library Plus
Apoptosis Compound Library
Cell Cycle/DNA Damage Compound Library
Kinase Inhibitor Library
Anti-Cancer Compound Library
Anti-Aging Compound Library
Anti-Breast Cancer Compound Library
Anti-Blood Cancer Compound Library
Targeted Diversity Library
生物活性
Ro-3306 is a potent and selective inhibitor of CDK1, with Kis of 20 nM, 35 nM and 340 nM for CDK1, CDK1/cyclin B1 and CDK2/cyclin E, respectively.
IC50 & Target[1]
CDK1
20 nM (Ki)
CDK1/cyclinB1
35 nM (Ki)
CDK1/cyclin A
110 nM (Ki)
CDK2/cyclinE
340 nM (Ki)
PKCδ
318 nM (Ki)
SGK
497 nM (Ki)
ERK
1980 nM (Ki)
体外研究 (In Vitro)
RO-3306 is an ATP-competitive inhibitor, and inhibits CDK1/cyclin A complexes with Ki of 110 nM. RO-3306 blocks the cell cycle in the G2/M phase of human cancer cells. RO-3306 (4 μM) induces apoptosis in cancer cells[1]. RO-3306 (5 μM) induces G2/M-phase cell cycle arrest and apoptosis of AML cells in a time-dependent manner. RO-3306 treatment significantly increases the percentage of Annexin V-positive cells in G1-phase cells without affecting the cell cycle distribution. RO-3306 enhances p53-mediated apoptosis. RO-3306 cooperates with Nutlin-3 in activating Bax and inducing mitochondrial apoptosis. RO-3306 (5 μM) downregulates antiapoptotic p21, Bcl-2 and survivin protein expression in AML. RO-3306 inhibits p53-induced p21 synthesis. RO-3306 does not inhibit RNA polymerase II CTD phosphorylation[2]. RO-3306 (10 μM) effectively arrests oocyte maturation. RO-3306 reduces the blastocyst formation in oocytes[3].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
351.45
Formula
C18H13N3OS2
CAS 号
872573-93-8
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 MCE 网站选购。
参考文献
[1]. Vassilev LT, et al. Selective small-molecule inhibitor reveals critical mitotic functions of human CDK1. Proc Natl Acad Sci U S A. 2006 Jul 11;103(28):10660-5.
[2]. Kojima K, et al. Cyclin-dependent kinase 1 inhibitor RO-3306 enhances p53-mediated Bax activation and mitochondrial apoptosis in AML. Cancer Sci. 2009 Jun;100(6):1128-36.
[3]. Jang WI, et al. A specific inhibitor of CDK1, RO-3306, reversibly arrests meiosis during in vitro maturation of porcine oocytes. Anim Reprod Sci. 2014 Jan 30;144(3-4):102-8.
Kinase Assay [1]
The CDK assays are run by using recombinant human CDK/cyclin complexes (CDK1/cyclin B1, CDK1/cyclin A, CDK2/cyclin E, and CDK4/cyclin D) expressed and isolated from Hi5 insect cells. GST-cyclin B1, CDK1, GST-cyclin-E, CDK2, GST-CDK4, and cyclin D, are used in the assay. The GST-tagged proteins are coexpressed and purified in complex with their partners. All assays use a His-6-tagged fragment of pRB (amino acids 385-928) as a substrate. The protein is expressed from a construct. It is expressed in M15 Escherichia coli cells and bound on a Ni-chalated agarose column pretreated with 1 mM imidazole and eluted with 500 mM imidazole. The eluted protein is dialyzed against 20 mM Hepes, pH 7/6.25 mM MgCl2/1.5 mM DTT, aliquoted, and stored at −80°C.
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献
[1]. Vassilev LT, et al. Selective small-molecule inhibitor reveals critical mitotic functions of human CDK1. Proc Natl Acad Sci U S A. 2006 Jul 11;103(28):10660-5.
[2]. Kojima K, et al. Cyclin-dependent kinase 1 inhibitor RO-3306 enhances p53-mediated Bax activation and mitochondrial apoptosis in AML. Cancer Sci. 2009 Jun;100(6):1128-36.
[3]. Jang WI, et al. A specific inhibitor of CDK1, RO-3306, reversibly arrests meiosis during in vitro maturation of porcine oocytes. Anim Reprod Sci. 2014 Jan 30;144(3-4):102-8.
RO4929097 (RG-4733) is a γ secretase inhibitor with IC50 of 4 nM, inhibiting cellular processing of Aβ40 and Notch with EC50 of 14 nM and 5 nM, respectively[1].
IC50 & Target
IC50: 4 nM (γ secretase)[1]
体外研究 (In Vitro)
RO4929097 inhibits the production of ICN reducing the expression of the downstream Notch target, Hes1, producing a less transformed morphology in A549 cells. RO4929097 inhibits Notch processing in human tumor-derived cells[1]. RO4929097 (1 µM) inhibits the growth of breast cancer cells, and the inhibition is 20% for SUM149 and 10% for SUM190 cells. RO4929097 does not have a marked effect in invasiveness of SUM149 cells. RO4929097 significantly reduces colony formation by both cell lines with the effect being more notable in SUM149 than by SUM190 cells[2]. RO4929097 inhibits proliferation, anchorage independent growth, and sphere formation of primary melanoma cells in vitro[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)
RO4929097 (3-60 mg/kg, p.o.) results in significant tumor growth inhibition in nude mice bearing A549 NSCLC xenografts, compared with vehicle-treated animals. When mice are treated with 60 mg/kg RO4929097 twice daily with the 7+/14- schedule, treatment initially causes regression of established A549 tumors[1]. RO4929097 impairs the growth of primary melanoma cells in vivo. The percentage of secondary tumors formed by RO4929097-treated cells is lower; the secondary tumors formed by RO4929097-treated cells are smaller; a significant delay in tumor formation by the RO4929097-treated cells compared to the vehicle-treated ones is observed in mice injected with 104 cells in vivo[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
469.40
Formula
C22H20F5N3O3
CAS 号
847925-91-1
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Luistro L, et al. Preclinical profile of a potent gamma-secretase inhibitor targeting notch signaling with in vivo efficacy and pharmacodynamic properties. Cancer Res. 2009, 69(19), 7672-7680.
[2]. Debeb BG, et al. Pre-clinical studies of Notch signaling inhibitor RO4929097 in inflammatory breast cancer cells. Breast Cancer Res Treat. 2012.
[3]. Huynh C, et al. The novel gamma secretase inhibitor RO4929097 reduces the tumor initiating potential of melanoma. PLoS One. 2011, 6(9), e25264.
Cell Assay [2]
The IBC cell lines SUM149 and SUM190 are seeded at a density of 5 × 104 cells. The next day, they are treated with vehicle or increasing doses of RO4929097, ranging from 0.1 nM to 10 μM. After 72 hrs, cells are trypsinized and viable cells counted with a hemocytometer.
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: RO4929097-treated mice are orally dosed with suspensions at 3 to 60 mg/kg RO4929097 according to the indicated regimens. In the Calu-6 xenograft model, RO4929097 is dosed at 60 mg/kg/d every other week for 4 weeks (7+/7- × 2 cycles). For all other xenograft models, RO4929097 is dosed once daily at 10 mg/kg for 21 days. Statistical analysis is determined by Mann-Whitney rank-sum test, one-way ANOVA, and post hoc Bonferroni t test. Differences between groups are considered significant when P ≤ 0.05. A549 tumors from vehicle-treated and selected RO4929097-treated groups are collected and fixed in 10% zinc-formalin overnight, processed, paraffin-embedded, sectioned at 5 μM, and stained with H&E for histopathology assessment. An Olympus BX51 microscope (×40 objective) mounted with a Nikon DS-Fi1 using the NIS-Elements F2.20 program collected the histology pictures. For Western blot analysis, three A549 tumors from each group, 7 (60 mg/kg) or 21 days (3 and 30 mg/kg), are flash-frozen. Collagen type V is detected using the H-200 antibody at a dilution of 1:1,000, and MFAP5 is detected using the antibody at a dilution of 1:1,000.
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]. Luistro L, et al. Preclinical profile of a potent gamma-secretase inhibitor targeting notch signaling with in vivo efficacy and pharmacodynamic properties. Cancer Res. 2009, 69(19), 7672-7680.
[2]. Debeb BG, et al. Pre-clinical studies of Notch signaling inhibitor RO4929097 in inflammatory breast cancer cells. Breast Cancer Res Treat. 2012.
[3]. Huynh C, et al. The novel gamma secretase inhibitor RO4929097 reduces the tumor initiating potential of melanoma. PLoS One. 2011, 6(9), e25264.
Ro5-3335, a benzodiazepine, acts as an inhibitor of core binding factor (CBF) leukemia. Ro5-3335 is a RUNX1-CBFβ interaction inhibitor that represses RUNX1/CBFB-dependent transactivation[1].
IC50 & Target
RUNX1-CBFβ interaction[1]
体外研究 (In Vitro)
Ro5-3335 has antiproliferative activity against human CBF leukemia cell lines, with IC50s of 1.1 μM, 21.7 μM and 17.3 μM for ME-1, Kasumi-1 and REH, respectively[1]. Ro5-3335 inhibits definitive hematopoiesis in zebrafish embryos[1]. Ro5-3335 does not completely break apart RUNX1-CBFβ interaction, but changes the conformation of their complex or increases the distance between RUNX1 and CBFβ in the complex[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)
Ro5-3335 is identified as an inhibitor of RUNX1–CBFβ function in zebrafish models[1]. Ro5-3335 rescues preleukemic phenotype in a RUNX1-ETO transgenic zebrafish[1]. Ro5-3335 (300 mg/kg/d; p.o; for 30 days) reduces leukemia burden in a mouse CBFB-MYH11 leukemia model[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:
C57BL/6 mice (leukemic model)[1]
Dosage:
300 mg/kg
Administration:
Oral administration; daily; for 30 days
Result:
Reduced the number of c-kit+ cells in the transplanted mice and leukemic cell infiltration in the livers, bone marrow and spleen.
分子量
259.69
Formula
C13H10ClN3O
CAS 号
30195-30-3
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Cunningham L, et al. Identification of benzodiazepine Ro5-3335 as an inhibitor of CBF leukemia through quantitative high throughput screen against RUNX1-CBFβ interaction. Proc Natl Acad Sci U S A. 2012 Sep 4;109(36):14592-7.
Saquinavir mesylate is an HIV Protease Inhibitor used in antiretroviral therapy. IC50 Value: Target: HIV Protease Saquinavir is a protease inhibitor. Proteases are enzymes that cleave protein molecules into smaller fragments. HIV protease is vital for both viral replication within the cell and release of mature viral particles from an infected cell. Saquinavir binds to the active site of the viral protease and prevents cleavage of viral polyproteins, preventing maturation of the virus. Saquinavir inhibits both HIV-1 and HIV-2 proteases.Studies have also looked at Saquinavir as a possible anti-cancer agent.
Clinical Trial
分子量
766.95
Formula
C39H54N6O8S
CAS 号
149845-06-7
中文名称
沙奎那韦甲磺酸盐
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Kaldor et al (1995) Isophthalic acid derivatives: amino acid surrogates for the inhibition of HIV-1 protease. Bioorg.Med.Chem.Lett. 5 721.
[2]. Yerino GA, Halabe EK, Zini E, Feleder EC. Bioequivalence study of two oral tablet formulations containing saquinavir mesylate boosted with ritonavir in healthy male subjects. Arzneimittelforschung. 2011;61(8):481-7.
[3]. Branham ML, Moyo T, Govender T. Preparation and solid-state characterization of ball milled saquinavir mesylate for solubility enhancement. Eur J Pharm Biopharm. 2012 Jan;80(1):194-202.
[4]. Brouwers J, Vermeire K, Grammen C, Schols D, Augustijns P. Early identification of availability issues for poorly water-soluble microbicide candidates in biorelevant media: a case study with saquinavir. Antiviral Res. 2011 Aug;91(2):217-23.
[5]. Knechten H, Lutz T, Pulik P, Martin T, Tappe A, Jaeger H. Safety and Efficacy in HIV-1-Infected Patients Treated with Ritonavir-Boosted Saquinavir Mesylate.
Ro3280 is a potent, highly selective inhibitor of PLK1 with an IC50 and a Kd of 3 nM and 0.09 nM, respectively, and nearly has no effect on PLK2 and PLK3.
IC50 & Target
PLK1
0.09 nM (Kd)
ALK
230 nM (Kd)
CAMKK1
1100 nM (Kd)
CAMKK2
87 nM (Kd)
DAPK1
100 nM (Kd)
DAPK3
70 nM (Kd)
FER
53 nM (Kd)
GAK
87 nM (Kd)
MYLK
170 nM (Kd)
PTK2
84 nM (Kd)
PTK2B
130 nM (Kd)
RPS6KA6 (KinDom.2)
560 nM (Kd)
TTK
51 nM (Kd)
体外研究 (In Vitro)
Ro3280 (RO3280) inhibits PLK1 activity in NB4 and K562 cells, with an IC50s of 13.45 nM and 301 nM, respectively. RO3280 shows inhibitory activities against the growth of six leukemia cells, with IC50s of 186 nM, 175 nM, 74 nM, 797 nM, 120 nM and 162 nM for U937, HL60, NB4, K562, MV4-11 and CCRF cell lines, respectively. RO3280 also suppresses the growth of primary ALL and AML cells, with IC50s of 35.49-110.76 nM, and 52.80-147.50 nM, respectively. RO3280 (50 or 100 nM) induces apoptosis and cell cycle disorder in acute leukemia cells[1]. Ro3280 shows potent activity in H82, H69, A549 lung cancer cell lines with EC50s of 6 nM, 7 nM and 82 nM. Ro3280 also inhibits several other cancer cell lines, with low concentration[2]. RO3280 is cytotoxic to 5637 and T24 human bladder cancer cells, with IC50s of appr 100 nM.
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)
Ro3280 (RO3280, 40 mg/kg, i.v.) inhibits 72% tumor growth in a mouse xenograft model implanted with HT-29 colorectal cancer cells, and when dosed more frequently, RO3280 completely suppresses the tumor growth[2]. RO3280 (30 mg/kg, once every 5 days, i.p.) shows significant anti-bladder cancer activities in a nude mouse model[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
543.61
Formula
C27H35F2N7O3
CAS 号
1062243-51-9
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Wang NN, et al. Molecular targeting of the oncoprotein PLK1 in pediatric acute myeloid leukemia: RO3280, a novel PLK1 inhibitor, induces apoptosis in leukemia cells. Int J Mol Sci. 2015 Jan 7;16(1):1266-92.
[2]. Chen S, et al. Identification of novel, potent and selective inhibitors of Polo-like kinase 1. Bioorg Med Chem Lett. 2012 Jan 15;22(2):1247-50.
[3]. Zhang Z, et al. Targeted inhibition of Polo-like kinase 1 by a novel small-molecule inhibitor induces mitotic catastrophe and apoptosis in human bladder cancer cells. J Cell Mol Med. 2017 Apr;21(4):758-767.
Cell Assay [1]
Leukemia cells or primary leukemia cells (2 × 104) are seeded in 96-well plates overnight and incubated with DMSO, or increasing concentrations of RO3280 (0.05-120 μM) for 24 h. The same volume of DMSO added to the vehicle treated wells. Each drug concentration is replicated four times. Then, 10 μL CCK8 solution is added to each well, incubated at 37°C for 2-4 h and the optical density (OD) values are measured at 450 nm using a scanning multi-well spectrophotometer. Relative survival rate is calculated from the absorbance values compared with the control group. The proliferation of cells is calculated as a percentage of the DMSO-treated control wells with 50% inhibitory concentration (IC50) values derived after plotting proliferation values on a logarithmic curve. The IC50 of PLK1 inhibitor is calculated by Graph Prism software[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]
Briefly, mice (female, 4-5 weeks of age) are used in the assay. Cells (5 × 106 cells in 150 μL) are suspended in RPMI 1640 and injected subcutaneously into the flank of each BALB/c nude mouse. On day 5, tumour size is measured, the animals are randomized into two groups (n = 15 per group), and RO3280 (40 mg/kg, once every 5 days) treatment is initiated by intraperitoneal injection. The control group is treated with vehicle (1.5% DMSO in PBS). The drug (or vehicle) treatment is performed for 40 days. The length and width of the resulting tumours (in millimetres) are measured every 3 days with callipers. The tumour diameter is measured, and the volume (length × width2 × 0.52) is calculated. The mice are humanely killed on day 45, and the tumours are dissected and weighed. Western blot and immunohistochemistry assays are also performed with these sections. Then, the tumours are fixed, embedded and cut into 3‐μm‐thick sections, which are subsequently stained with haematoxylin and eosin to permit the observation of the tumour margin[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]. Wang NN, et al. Molecular targeting of the oncoprotein PLK1 in pediatric acute myeloid leukemia: RO3280, a novel PLK1 inhibitor, induces apoptosis in leukemia cells. Int J Mol Sci. 2015 Jan 7;16(1):1266-92.
[2]. Chen S, et al. Identification of novel, potent and selective inhibitors of Polo-like kinase 1. Bioorg Med Chem Lett. 2012 Jan 15;22(2):1247-50.
[3]. Zhang Z, et al. Targeted inhibition of Polo-like kinase 1 by a novel small-molecule inhibitor induces mitotic catastrophe and apoptosis in human bladder cancer cells. J Cell Mol Med. 2017 Apr;21(4):758-767.
Sodium nitroprusside (Ro 21-2498) 是血管舒张剂，能促使 NO 释放于血液中。
Sodium nitroprusside Chemical Structure
CAS No. : 14402-89-2
规格
价格
是否有货
数量
Free Sample (0.1-0.5 mg)
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10 mM * 1 mL in DMSO
￥550
In-stock
100 mg
￥500
In-stock
500 mg
￥800
In-stock
1 g
询价
5 g
询价
* Please select Quantity before adding items.
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生物活性
Sodium nitroprusside (Ro 21-2498) is a potent vasodilator working through releasing NO spontaneously in blood.
体外研究 (In Vitro)
Sodium nitroprusside (Ro 21-2498) is a potent vasodilator. Sodium nitroprusside has potent vasodilating effects in arterioles and venules. Sodium nitroprusside breaks down in circulation to release nitric oxide (NO). NO activates guanylate cyclase in vascular smooth muscle and increases intracellular production of cGMP. The end result is vascular smooth muscle relaxation, which allow vessels to dilate [1]. Sodium nitroprusside decreases the proliferation of vascular smooth muscle cells [2]. Sodium nitroprusside (5 mg/kg) significantly reduces the intestinal ischemiareperfusion injury as a nitric oxide donor in rats [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
261.92
Formula
C5FeN6Na2O
CAS 号
14402-89-2
中文名称
硝普钠；亚硝基铁氰化钠
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
4°C, sealed storage, away from moisture and light
*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)
溶解性数据
In Vitro:
H2O : ≥ 100 mg/mL (381.80 mM)
DMSO : 33.33 mg/mL (127.25 mM; Need ultrasonic)
*“≥” 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
3.8180 mL
19.0898 mL
38.1796 mL
5 mM
0.7636 mL
3.8180 mL
7.6359 mL
10 mM
0.3818 mL
1.9090 mL
3.8180 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 and 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：
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]. Wink, D.A., et al., The effect of various nitric oxide-donor agents on hydrogen peroxide-mediated toxicity: a direct correlation between nitric oxide formation and protection. Arch Biochem Biophys, 1996. 331(2): p. 241-8.
[2]. Garg, U.C. and A. Hassid, Nitric oxide-generating vasodilators and 8-bromo-cyclic guanosine monophosphate inhibit mitogenesis and proliferation of cultured rat vascular smooth muscle cells. J Clin Invest, 1989. 83(5): p. 1774-7.
[3]. Namazi, H., Sodium nitroprusside as a nitric oxide donor in a rat intestinal ischemia reperfusion model: a novel molecular mechanism. Clinics (Sao Paulo), 2008. 63(3): p. 405.
Ro 48-8071 is an inhibitor of OSC (Oxidosqualene cyclase) with IC50 of appr 6.5 nM.
IC50 & Target
IC50: appr 6.5 nM (Oxidosqualene cyclase)[1]
体外研究 (In Vitro)
In HepG2 cells, Ro 48-8071 reduces cholesterol synthesis dose dependently with an IC50 value of appr 1.5 nM[1]. Ro 48-8071 (10 μM) significantly reduces the viability of PC-3 prostate cancer cells, but not normal prostate cells. Ro 48-8071 (10-30 μM) induces apoptosis of both LNCaP and C4-2 cell lines in a dose-dependent manner. And castration-resistant PC-3 and DU145 cells also demonstrate significant levels of apoptosis following 24-hour treatment with Ro 48-8071. Ro 48-8071 (10-25 μM) reduces AR protein expression in a dose-dependent manner. Ro 48-8071 (0.1-1 μM) increases ERβ protein expression dose-dependently in both hormone-dependent LNCaP and castration-resistant PC-3 cells[2]. Using mammalian cells engineered to express human ERα or ERβ protein, together with an ER-responsive luciferase promoter, Ro 48-8071 dose-dependently inhibits 17β-estradiol (E2)-induced ERα responsive luciferase activity (IC50, appr 10 µM), under conditions that are non-toxic to the cells[3].
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)
Ro 48-8071 lowers LDL-C maximally appr 60% at 150 μmol/kg per day, with no further reduction up to 300 μmol/kg per day, leaving HDL-C unchanged at all doses in hamsters. Ro 48-8071 (≥00 μmol/kg per day) increases the amount of MOS in liver of hamsters. Ro 48-8071 (300 μmol/kg per day) remarkedly and significantly reduces VLDL secretion of hamsters[1]. Ro 48-8071 (5 or 20 mg/kg) significantly reduces in vivo tumor growth in mice, without weight loss of the mice. Furthermore, Ro 48-8071 at a concentration of 20 mg/kg, completely eradicates two of the 12 tumors being monitored in the mice in the timeframe tested[2]. Ro 48-8071 (20 mg/day/kg body weight) leads to a rapid and sustained inhibition (>50%) of cholesterol synthesis in the whole small intestine of BALB/c mice. Sterol synthesis is also reduced in the large intestine and stomach[4].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
448.37
Formula
C23H27BrFNO2
CAS 号
161582-11-2
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]. Morand OH, et al. Ro 48-8.071, a new 2,3-oxidosqualene:lanosterol cyclase inhibitor lowering plasma cholesterol in hamsters, squirrel monkeys, and minipigs: comparison to simvastatin. J Lipid Res. 1997 Feb;38(2):373-90.
[2]. Liang Y, et al. Cholesterol biosynthesis inhibitor RO 48-8071 suppresses growth of hormone-dependent and castration-resistant prostate cancer cells. Onco Targets Ther. 2016 May 30;9:3223-32.
[3]. Liang Y, et al. Cholesterol biosynthesis inhibitors as potent novel anti-cancer agents: suppression of hormone-dependent breast cancer by the oxidosqualene cyclase inhibitor RO 48-8071. Breast Cancer Res Treat. 2014 Jul;146(1):51-62.
[4]. Chuang JC, et al. Sustained and selective suppression of intestinal cholesterol synthesis by Ro 48-8071, an inhibitor of 2,3-oxidosqualene:lanosterol cyclase, in the BALB/c mouse. Biochem Pharmacol. 2014 Apr 1;88(3):351-63.
Animal Administration [2]
Six-week-old male athymic nude mice (nu/nu) weighing 20-22 g are used in the assay. Castration-resistant PC-3 cells (5×106 in 0.15 mL solution) are mixed with matrigel and RPMI-1640 medium (1/1, v/v) and injected subcutaneously into both flanks of each mouse (n=6 animals/group) and tumors allowed to develop. The tumors are measured twice per week with a digital caliper. Tumor volumes are calculated by the formula (L × W × H) × π/6. Drug treatment is started when tumor volumes reach appr 100 mm3. Mice are given daily tail vein injections of 0.1 mL solution of either 5 or 20 mg/kg Ro 48-8071 for 5 days. This is followed by an injection every other day for six additional treatments and then a final injection 2 hours prior to sacrifice. Control mice receive the same volume of phosphate-buffered saline on the same schedule. The animals are weighed and tumor volumes are measured twice weekly throughout the drug treatment period.
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献
[1]. Morand OH, et al. Ro 48-8.071, a new 2,3-oxidosqualene:lanosterol cyclase inhibitor lowering plasma cholesterol in hamsters, squirrel monkeys, and minipigs: comparison to simvastatin. J Lipid Res. 1997 Feb;38(2):373-90.
[2]. Liang Y, et al. Cholesterol biosynthesis inhibitor RO 48-8071 suppresses growth of hormone-dependent and castration-resistant prostate cancer cells. Onco Targets Ther. 2016 May 30;9:3223-32.
[3]. Liang Y, et al. Cholesterol biosynthesis inhibitors as potent novel anti-cancer agents: suppression of hormone-dependent breast cancer by the oxidosqualene cyclase inhibitor RO 48-8071. Breast Cancer Res Treat. 2014 Jul;146(1):51-62.
[4]. Chuang JC, et al. Sustained and selective suppression of intestinal cholesterol synthesis by Ro 48-8071, an inhibitor of 2,3-oxidosqualene:lanosterol cyclase, in the BALB/c mouse. Biochem Pharmacol. 2014 Apr 1;88(3):351-63.
