AS601245是一种强效的ATP竞争性JNK抑制剂，对JNK1、JNK2和JNK3的IC50值分别为0.15µM、0.22µM和0.07µM。
Cas No.:345987-15-7
Sample solution is provided at 25 µL, 10mM.
_1-3.$$$39978408@51.jpg');)
_1-9.$$$38538795@65.jpg');)
_1-9.$$$39112701@51.jpg');)
_1-7.$$$37316672@70.jpg');)
_366-372.$$$36198801@70.jpg');)
.$$$38565142@65.jpg');)
_1867-1883.$$$33248023@67.jpg');)
_eads6055.$$$39977546@45.jpg');)
_eadm9805.$$$40080571@45.jpg');)
_eadj3020.$$$39666821@45.jpg');)
_1-20.$$$39757301@28.jpg');)
_1-24.$$$38898113@28.jpg');)
_273-287.$$$36806353@46.jpg');)
_1-16.$$$37156877@44.jpg');)
_1-19.$$$37460805@44.jpg');)
_1291-1307.$$$34518654@46.jpg');)
AS601245 is a potent ATP-competitive JNK inhibitor with IC50 values of 0.15µM, 0.22, and 0.07µM for JNK1, JNK2, and JNK3, respectively [1]. AS601245 can prevent P-TEFb from being released from the inactive complex formed with HEXIM-1, and interfere with the reactivation of the HIV-1 virus at multiple levels[2]. AS601245 has been widely used to inhibit the growth of follicular cells and interfere with the progression of the cell cycle[3].
In vitro, AS601245 treatment for 96h significantly inhibited the proliferation of CaCo-2 cells, with an IC50 value of 2.5µM[4]. 0.1µM of AS601245 treatment for 24 hours significantly increased the expression of p21 in HepG2 cells and inhibited cell viability[5]. Treatment with 10µM AS601245 for 24 hours significantly promoted apoptosis of SH-SY5Y cells, accompanied by an increase in caspase-3 activity, expression of pro-apoptotic proteins, as well as significant disruptions in oxidative phosphorylation and glycolysis[6].
In vivo, AS601245 treatment via intraperitoneal injection at a dose of 80mg/kg at 15 minutes and 24 hours after restoration of carotid artery flow prevented neurite loss, reduced astrogliosis, and improved long-term memory deficits induced by cerebral ischemia in gerbils [7]. A single oral administration of 10mg/kg dose of AS601245 significantly inhibited the release of TNF-α in mice caused by endotoxins[8].
References:
[1] Malemud C J. Small molecular weight inhibitors of stress-activated and mitogen-activated protein kinases[J]. Mini Reviews in Medicinal Chemistry, 2006, 6(6): 689-698.
[2] Wolschendorf F, Bosque A, Shishido T, et al. Kinase control prevents HIV-1 reactivation in spite of high levels of induced NF-κB activity[J]. Journal of virology, 2012, 86(8): 4548-4558.
[3] Oktem O, Oktay K. c-Jun N-terminal kinase (JNK) pathway controls granulosa cell mitosis: a novel mechanism in regulation of preantral follicle growth[J]. Fertility and Sterility, 2008, 90: S330.
[4] Cerbone A, Toaldo C, Minelli R, et al. Rosiglitazone and AS601245 decrease cell adhesion and migration through modulation of specific gene expression in human colon cancer cells[J]. PLoS One, 2012, 7(6): e40149.
[5] Cerbone A, Toaldo C, Pizzimenti S, et al. AS601245, an anti‐inflammatory JNK inhibitor, and Clofibrate have a synergistic effect in inducing cell responses and in affecting the gene expression profile in CaCo‐2 colon cancer cells[J]. PPAR research, 2012, 2012(1): 269751.
[6] Granek Z, Siwecka N, Saramowicz K, et al. Pharmacological Inhibition of JNK Signalling Exerts Anti-Neoplastic Effects on SH-SY5Y Human Neuroblastoma Cells[J]. International Journal of Molecular Sciences, 2025, 26(24): 11894.
[7] Carboni S, Boschert U, Gaillard P, et al. AS601245, ac‐Jun NH2‐terminal kinase (JNK) inhibitor, reduces axon/dendrite damage and cognitive deficits after global cerebral ischaemia in gerbils[J]. British journal of pharmacology, 2008, 153(1): 157-163.
[8] Carboni S, Hiver A, Szyndralewiez C, et al. AS601245 (1, 3-Benzothiazol-2-yl (2-{[2-(3-pyridinyl) ethyl] amino}-4 pyrimidinyl) Acetonitrile): a c-Jun NH2-terminal protein kinase inhibitor with neuroprotective properties[J]. The Journal of pharmacology and experimental therapeutics, 2004, 310(1): 25-32.
AS601245是一种强效的ATP竞争性JNK抑制剂，对JNK1、JNK2和JNK3的IC50值分别为0.15µM、0.22µM和0.07µM[1]。AS601245可阻止P-TEFb从与HEXIM-1形成的非活性复合物中释放，并在多个水平上干扰HIV-1病毒的再激活[2]。AS601245已被广泛用于抑制滤泡细胞的生长并干扰细胞周期的进程[3]。
在体外，AS601245处理CaCo-2细胞96小时，显著抑制了细胞增殖，IC50值为2.5µM[4]。0.1µM的AS601245处理HepG2细胞24小时，显著增加了p21的表达并抑制了细胞活力[5]。10µM的AS601245 处理SH-SY5Y细胞24小时，显著促进了细胞凋亡，同时伴随着caspase-3活性、促凋亡蛋白表达的增加，以及氧化磷酸化和糖酵解的显著破坏[6]。
在体内，在沙鼠颈动脉血流恢复后15分钟和24小时分别腹腔注射80mg/kg剂量的AS601245，可防止神经突丢失，减少星形胶质细胞增生，并改善脑缺血引起的长期记忆缺陷[7]。单次口服10mg/kg剂量的AS601245显著抑制endotoxins引起的小鼠体内TNF-α释放[8].
| Cell experiment [1]: | |
Cell lines | CaCo-2 cells |
Preparation Method | CaCo-2 cells were grown in DMEM medium with 10% (v/v) fetal bovine serum (FBS), 2 mM glutamine, 1% non-essential amino acids solution, and 1% antibiotic mixture (penicillin-streptomycin) at 37°C in 5% CO2/atmosphere. CaCo-2 cells (3×103 cells) were seeded in 96-well plates, incubated for 24h, and then treated with different concentrations of AS601245 (0.1, 1, 10, and 50µM) at 37°C. After 96h, cell viability was measured. |
Reaction Conditions | 0.1, 1, 10, and 50µM; 96h |
Applications | AS601245 treatment significantly reduced the cell viability of CaCo-2 cells in a concentration-dependent manner. |
| Animal experiment [2]: | |
Animal models | C3H/HEN mice |
Preparation Method | C3H/HEN mice were kept in a temperature-controlled (20-22°C) and light/dark cycle-controlled animal room (lights on at 7:00 AM and off at 7:00 PM). Standard laboratory chow and water were available ad libitum. Mice received an oral treatment with AS601245 (10mg/kg in 0.5% CMC/0.25% Tween 20). Fifteen minutes later, endotoxins (O111:B4; 0.3mg/kg) were i.p. injected. Heparinized whole blood was collected by retroorbital puncture under isoflurane anesthesia. TNF-α was determined in plasma. |
Dosage form | 10mg/kg for once; p.o. |
Applications | AS601245 treatment significantly reduced TNF-α levels in mice after treatment with endotoxins. |
References: | |
| Cas No. | 345987-15-7 | SDF | |
| 别名 | AS-601245, c-Jun N-terminal Kinase Inhibitor V | ||
| 化学名 | (Z)-2-(benzo[d]thiazol-2-yl)-2-(2-((2-(pyridin-3-yl)ethyl)imino)-1,2-dihydropyrimidin-4-yl)acetonitrile | ||
| Canonical SMILES | N#CC(C1=NC2=CC=CC=C2S1)C(C=CN/3)=NC3=N/CCC4=CN=CC=C4 | ||
| 分子式 | C20H16N6S | 分子量 | 372.45 |
| 溶解度 | ≥ 14.25mg/mL in DMSO, ≥ 10mg/mL in Water with gentle warming | 储存条件 | Store at -20°C |
| General tips | 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 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
||
| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 2.6849 mL | 13.4246 mL | 26.8492 mL |
| 5 mM | 537 μL | 2.6849 mL | 5.3698 mL |
| 10 mM | 268.5 μL | 1.3425 mL | 2.6849 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Quality Control & SDS
- View current batch:
- Purity: >98.50% Appearance: A solid
- COA (Certificate of Analysis)
- SDS (Safety Data Sheet)
- Datasheet