443797-96-4|JNJ-7706621|JNJ-7706621|MFCD11100270-范德生物科技公司

JNJ-7706621

NMR下载 COA and HPLC MSDS下载
names：
JNJ-7706621
CAS号：
443797-96-4
MDL Number： MFCD11100270
MF(分子式)： C15H12F2N6O3S MW(分子量)： 394.36
EINECS: Reaxys Number:
Pubchem ID:5330790 Brand:BIOFOUNT

JNJ-7706621(cas:443797-96-4) 是一种有效的 aurora kinase 抑制剂，同时能有效抑制 CDK1 和 CDK2，对 CDK1，CDK2，aurora-A 和 aurora-B 的 IC₅₀ 值分别为 9 nM，3 nM，11 nM 和 15 nM。

货品编码	规格	纯度	价格 (¥)	现价(¥)	特价(¥)	库存描述	数量	总计 (¥)
YZM001241-5mg	5mg	99.9%	¥ 1417.00	¥ 1417.00		2-3天	- +	¥ 0.00
YZM001241-2mg	2mg	99.9%	¥ 780.00	¥ 780.00		2-3天	- +	¥ 0.00

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中文别名	JNJ-7706621(443797-96-4);JNJ 7706621
英文别名	JNJ-7706621(443797-96-4)
CAS号	443797-96-4
SMILES	O=S(C1=CC=C(NC2=NN(C(C3=C(F)C=CC=C3F)=O)C(N)=N2)C=C1)(N)=O
Inchi	InChI=1S/C15H12F2N6O3S/c16-10-2-1-3-11(17)12(10)13(24)23-14(18)21-15(22-23)20-8-4-6-9(7-5-8)27(19,25)26/h1-7H,(H2,19,25,26)(H3,18,20,21,22)
InchiKey	KDKUVYLMPJIGKA-UHFFFAOYSA-N
分子式 Formula	C15H12F2N6O3S
分子量 Molecular Weight	394.36
闪点 FP	363.0±34.3 °C
熔点 Melting point	149-155℃
沸点 Boiling point	676.6±65.0 °C at 760 mmHg
Polarizability极化度	36.2±0.5 10-24cm3
密度 Density	1.7±0.1 g/cm3
蒸汽压 Vapor Pressure	0.0±2.1 mmHg at 25°C
溶解度Solubility	生物体外In Vitro:DMSO溶解度≥ 125 mg/mL(316.97 mM)*"≥" means soluble可溶, but saturation unknown溶解度未知.
性状	白色至灰白色固体粉末
储藏条件 Storage conditions	短期1-2周储存在-4℃条件下就行，长期储存（1-2年）需在-20℃条件下存储

JNJ-7706621(443797-96-4)实验注意事项：
1.实验前需戴好防护眼镜，穿戴防护服和口罩，佩戴手套，避免与皮肤接触。
2.实验过程中如遇到有毒或者刺激性物质及有害物质产生，必要时实验操作需要手套箱内完成以免对实验人员造成伤害
3.实验后产生的废弃物需分类存储，并交于专业生物废气物处理公司处理，以免造成环境污染

JNJ-7706621(443797-96-4) Experimental considerations:
1. Wear protective glasses, protective clothing and masks, gloves, and avoid contact with the skin during the experiment.
2. The waste generated after the experiment needs to be stored separately, and handed over to a professional biological waste gas treatment company to avoid environmental pollution.

Tag:JNJ-7706621(443797-96-4),JNJ-7706621试剂,JNJ-7706621的外观,JNJ-7706621的作用,JNJ-7706621的溶解度,JNJ-7706621的生产,JNJ-7706621的合成路线,JNJ-7706621的厂家,JNJ-7706621的价格,JNJ-7706621的MSDS,JNJ-7706621的注意事项

产品说明	JNJ-7706621(443797-96-4)是一种新型的细胞周期抑制剂，它对几种细胞周期蛋白依赖性激酶（CDK）和Aurora激酶具有有效的抑制作用
Introduction	JNJ-7706621 (443797-96-4) is a new type of cell cycle inhibitor, which has an effective inhibitory effect on several cyclin-dependent kinases (CDK) and Aurora kinase
Application1	In human cancer cells, treatment with JNJ-7706621 inhibited cell growth independent of p53, retinoblastoma, or P-glycoprotein status; activated apoptosis; and reduced colony formation.
Application2	At low concentrations, JNJ-7706621 slowed the growth of cells and at higher concentrations induced cytotoxicity.
Application3	JNJ-7706621(443797-96-4)选择性地阻断了各种来源的肿瘤细胞的增殖，但在抑制正常人细胞生长方面的作用却降低了约10倍。

警示图
危险性	warning
危险性警示	Not available
安全声明	H303吞入可能有害+H313皮肤接触可能有害+H2413吸入可能对身体有害
安全防护	P264处理后彻底清洗+P280戴防护手套/穿防护服/戴防护眼罩/戴防护面具+P305如果进入眼睛+P351用水小心冲洗几分钟+P338取出隐形眼镜（如果有）并且易于操作,继续冲洗+P337如果眼睛刺激持续+P2393获得医疗建议/护理
备注	实验过程中防止吸入、食入，做好安全防护

Aurora kinase A and B as new treatment targets in aromatase inhibitor-resistant breast cancer cells(Breast Cancer Research and Treatment,2015)

Allosteric modulation of AURKA kinase activity by a small-molecule inhibitor of its protein-protein interaction with TPX2(Scientific Reports,2016)

Multi-kinase inhibitors, AURKs and cancer(Medical Oncology,2016)

Aurora kinase B is important for antiestrogen resistant cell growth and a potential biomarker for tamoxifen resistant breast cancer(BMC Cancer,2015)

Antiproliferation Inhibitors Targeting Aurora Kinases(Checkpoint Responses in Cancer Therapy,2008)

1.Synthesis and evaluation of N-acyl sulfonamides as potential prodrugs of cyclin-dependent kinase inhibitor JNJ-7706621.
Huang S1, Connolly PJ, Lin R, Emanuel S, Middleton SA. Bioorg Med Chem Lett. 2006 Jul 15;16(14):3639-41. Epub 2006 May 6.
A novel prodrug strategy for cyclin-dependent kinase inhibitor JNJ-7706621 has been explored. Through N-acylation of a sulfonamide substituent, tails containing different solubilizing groups (amino, carboxyl, alkoxyl, and hydroxyl) were attached to JNJ-7706621. Most of the prodrugs exhibited good aqueous solubility and the N-acyl groups on the sulfonamide were metabolically cleaved to generate active drug in rat PK study.

2.Active and passive tumor targeting of a novel poorly soluble cyclin dependent kinase inhibitor, JNJ-7706621.
Danhier F1, Ucakar B, Magotteaux N, Brewster ME, Préat V. Int J Pharm. 2010 Jun 15;392(1-2):20-8. doi: 10.1016/j.ijpharm.2010.03.018. Epub 2010 Mar 11.
The anti-cancer cyclin dependent kinase (CDK) inhibitors are poorly soluble drugs. The aims of this work were (i) to formulate a novel CDK inhibitor, JNJ-7706621, in polymeric micelles and nanoparticles, (ii) to compare passive and active targeting on tumor growth and (iii) to evaluate the potential synergy of JNJ-7706621 with Paclitaxel. Therefore, JNJ-7706621 was encapsulated in self-assembling diblock copolymers made up of epsilon-caprolactone (CL) and trimethylene carbonate (TMC) (PEG-p-(CL-co-TMC)) polymeric micelles and in (poly(lactide-co-glycolide)) (PLGA)-based PEGylated nanoparticles (passive targeting) as well as in RGD-grafted nanoparticles (active targeting). In vivo, the transplantable liver tumor growth was more decreased by active targeting with RGD-grafted nanoparticles than by passive targeting with micelles or ungrafted nanoparticles. Moreover, a synergy between JNJ-7706621 and Paclitaxel was demonstrated. Therefore, active targeting of JNJ-7706621-loaded nanocarriers may be considered as an effective anti-cancer drug delivery system for cancer chemotherapy, particularly in combination with Paclitaxel.

3.Growth suppression and mitotic defect induced by JNJ-7706621, an inhibitor of cyclin-dependent kinases and aurora kinases.
Matsuhashi A1, Ohno T, Kimura M, Hara A, Saio M, Nagano A, Kawai G, Saitou M, Takigami I, Yamada K, Okano Y, Shimizu K. Curr Cancer Drug Targets. 2012 Jul;12(6):625-39.
Aurora kinases and cyclin-dependent kinases, which play critical roles in the cell cycle and are frequently overexpressed in a variety of tumors, have been suggested as attractive targets for cancer therapy. JNJ-7706621, a recently identified dual inhibitor of these kinases, is reported to induce cell cycle arrest, endoreduplication, and apoptosis. In the present study, we further investigated the molecular mechanisms underlying these effects. The inhibitor arrested various cells at G2 phase at low concentration, and at both G1 and G2 phases at high concentration. JNJ-7706621 did not prevent localization of Aurora A to the spindle poles, but did inhibit other centrosomal proteins such as TOG, Nek2, and TACC3 in early mitotic phase. Similarly, the drug did not prevent localization of Aurora B to the kinetochore, but did inhibit other chromosomal passenger proteins such as Survivin and INCENP. In the cells exposed to JNJ-7706621 after nocodazole release, Aurora B, INCENP, and Survivin became relocated to the peripheral region of chromosomes, but Plk1 and Prc1 were localized on microtubules in later mitotic phase.

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