Brexpiprazole是一种口服非典型抗精神病药物，是5-HT1A（Ki=0.12nM）和dopamine D2L（Ki=0.3nM）受体的强效部分激动剂，以及5-HT2A受体（Ki=0.47nM）的拮抗剂。
Cas No.:913611-97-9
Sample solution is provided at 25 µL, 10mM.
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Brexpiprazole, an oral atypical antipsychotic agent, is a potent partial agonist of 5-HT1A (Ki=0.12nM) and dopamine D2L (Ki=0.3nM) receptors, and an antagonist of 5-HT2A receptor (Ki=0.47nM) [1]. Brexpiprazole enhances nerve growth by antagonizing 5-HT2A receptors and through IP3 receptor-mediated Ca2+ signaling, thereby promoting nerve growth induced by nerve growth factor (NGF)[2]. Brexpiprazole has been widely used to alleviate the positive and cognitive symptoms of schizophrenia, reduce the severity of aggressive behavior, and improve symptoms and achieve functional remission [3].
In vitro, Brexpiprazole treatment for 24 hours significantly inhibited the viability of HCT116, SW620 and NCM460 cells, with IC50 values of 27.39, 32.33 and 142.5μM, respectively[4]. Treatment with 300nM Brexpiprazole for 14 days reduced the protein expression of 5-HT1A and 5-HT7 receptors as well as the phosphorylation level of AMPK in the plasma membrane components of primary cortical astrocytes, and increased the level of connexin 43[5].
In vivo, Brexpiprazole treatment via daily intragastric administration at a dose of 5mg/kg for 17 days significantly inhibited tumor growth in a HCT116 xenograft mouse model and reduced the expression of phosphorylated AKT, P85, P38, ERK1/2 and RAF in the tumor tissues[6]. When administered orally at a dose of 0.5mg/kg/day for 28 consecutive days, Brexpiprazole caused metabolic disorders in glucose and lipid metabolism in rats, resulting in increased body weight, elevated levels of lipids and blood glucose, accompanied by hormonal imbalances (insulin, glucagon, GLP-1)[7]. For 8 consecutive weeks, a daily oral dose of 5mg/kg of Brexpiprazole was administered to the colorectal cancer mouse model, resulting in a significant reduction in the number of metastatic foci in the lung tissue of the mice[8].
References:
[1] Ishima T, Futamura T, Ohgi Y, et al. Potentiation of neurite outgrowth by brexpiprazole, a novel serotonin–dopamine activity modulator: A role for serotonin 5-HT1A and 5-HT2A receptors[J]. European Neuropsychopharmacology, 2015, 25(4): 505-511.
[2] Das S, Barnwal P, Winston A B, et al. Brexpiprazole: so far so good[J]. Therapeutic advances in psychopharmacology, 2016, 6(1): 39-54.
[3] Siwek M, Wojtasik-Bakalarz K, Krupa A J, et al. Brexpiprazole—pharmacologic properties and use in schizophrenia and mood disorders[J]. Brain Sciences, 2023, 13(3): 397.
[4] Li T, Liu X, Long X, et al. Brexpiprazole suppresses cell proliferation and de novo lipogenesis through AMPK/SREBP1 pathway in colorectal cancer[J]. Environmental Toxicology, 2023, 38(10): 2352-2360.
[5] Fukuyama K, Motomura E, Okada M. Brexpiprazole reduces 5-HT7 receptor function on astroglial transmission systems[J]. International Journal of Molecular Sciences, 2022, 23(12): 6571.
[6] Long X, Liu X, Xia W, et al. Brexpiprazole prevents the Malignant progression of human colorectal cancer cells and increases its sensitivity to egfr inhibition[J]. Frontiers in Bioscience-Landmark, 2024, 29(5): 174.
[7] Li D, Yue Q, Liu L, et al. Brexpiprazole caused glycolipid metabolic disorder by inhibiting GLP1/GLP1R signaling in rats[J]. Acta Pharmacologica Sinica, 2021, 42(8): 1267-1279.
[8] Liu X, He J, Ma A, et al. Brexpiprazole inhibits EMT and migration of colorectal cancer cells by downregulating the SREBP1/SNAI1 signaling pathway[J]. Frontiers in Oncology, 2026, 15: 1734678.
Brexpiprazole是一种口服非典型抗精神病药物，是5-HT1A（Ki=0.12nM）和dopamine D2L（Ki=0.3nM）受体的强效部分激动剂，以及5-HT2A受体（Ki=0.47nM）的拮抗剂[1]。Brexpiprazole通过拮抗5-HT2A受体以及通过IP3受体介导的Ca2+信号通路来增强神经生长，从而促进神经生长因子诱导的神经生长[2]。Brexpiprazole已被广泛用于缓解精神分裂症的阳性和认知症状，降低攻击行为的严重程度，并改善症状以实现功能缓解[3]。
在体外，Brexpiprazole处理24小时显著抑制了HCT116、SW620和NCM460细胞的活力，IC50值分别为27.39、32.33和142.5μM[5]。300nM的Brexpiprazole处理原代皮层星形胶质细胞14天，降低了质膜组分中5-HT1A和5-HT7受体的蛋白表达以及AMPK的磷酸化水平，并增加了connexin 43的水平[6]。
在体内，每日灌胃5mg/kg剂量的Brexpiprazole，连续17天，显著抑制了HCT116异种移植小鼠模型中的肿瘤生长，并降低了肿瘤组织中磷酸化AKT、P85、P38、ERK1/2和RAF的表达[6]。连续28天每日口服0.5mg/kg剂量的Brexpiprazole，导致大鼠葡萄糖和脂质代谢紊乱，表现为体重增加、血脂和血糖水平升高，并伴有激素失衡（胰岛素、胰高血糖素、GLP-1）[7]。连续8周每日口服5mg/kg剂量的Brexpiprazole给药结直肠癌小鼠模型，导致小鼠肺组织中转移灶数量显著减少[8]。
| Cell experiment [1]: | |
Cell lines | HCT116 cells |
Preparation Method | HCT116 cells were grown in McCoy's 5A medium with 10% (v/v) fetal bovine serum (FBS), 0.2mM glutamine, 100U/ml penicillin, and 100μg/ml streptomycin at 37°C in 5% CO2/atmosphere. Cells (5×103 cells/ml) were seeded in 96-well plates and allowed to adhere in a 5% CO2 incubator at 37°C overnight. Cells were treated with different concentrations of Brexpiprazole (0, 10, 20, 30, 40, and 50µM) for 24h. Cell viability was evaluated. |
Reaction Conditions | 0, 10, 20, 30, 40, and 50µM; 24h |
Applications | Brexpiprazole treatment significantly reduced the cell viability of HCT116 cells in a dose-dependent manner. |
| Animal experiment [2]: | |
Animal models | Male nude mice |
Preparation Method | Four-week-old male nude mice weighing 20±2g were routinely maintained in a standard environment with food and water ad libitum. After one week of adaption, 1×107 HCT116 cells were inoculated subcutaneously into each mouse. When the tumor reached 100mm3, the mice were divided into 3 groups, 6 nude mice per group: Group 1, 5% gum arabic was gavaged, and PBS was intraperitoneally injected. Group 2, Brexpiprazole in 5% gum Arabic was gavaged (5mg/kg/day). Group 3, cetuximab was injected intraperitoneally with a dose of 1mg twice a week. Tumor volume was calculated by measuring the length (a) and width (b) with a caliper every 2 days. After 3-week treatment, nude mice were anesthetized with 1% pentobarbital and then killed by cervical dislocation, and tumors were collected for analysis. |
Dosage form | 5mg/kg/day for 3 weeks; i.g. |
Applications | Brexpiprazole treatment significantly attenuated tumor growth in nude mice with HCT116 xenografts. |
References: | |
| Cas No. | 913611-97-9 | SDF | |
| 别名 | 依匹哌唑; OPC-34712 | ||
| 化学名 | 7-[4-[4-(1-benzothiophen-4-yl)piperazin-1-yl]butoxy]-1H-quinolin-2-one | ||
| Canonical SMILES | C1CN(CCN1CCCCOC2=CC3=C(C=C2)C=CC(=O)N3)C4=C5C=CSC5=CC=C4 | ||
| 分子式 | C25H27N3O2S | 分子量 | 433.57 |
| 溶解度 | ≥ 21.68mg/mL in DMSO 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。 |
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| 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 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.3064 mL | 11.5322 mL | 23.0643 mL |
| 5 mM | 461.3 μL | 2.3064 mL | 4.6129 mL |
| 10 mM | 230.6 μL | 1.1532 mL | 2.3064 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。
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