Chloropyramine hydrochloride
(Synonyms: 盐酸氯吡胺) 目录号 : GC32979
Chloropyramine hydrochloride (Halopyramine) is a histamine receptor H1 antagonist and has anti-cholinergic, antispasmodic, and antiallergic effects.
Cas No.:6170-42-9
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Kinase experiment: | Cells are incubated in presence or absence of Chloropyramine hydrochloride and stained with anti-FAK antibody 4.47 or in combination with paxillin or VEGFR-3. Detection is done with Alexa Fluor 546 secondary antibody and for dual staining combination of Alexa Fluor 488 and Alexa Fluor 546 secondary antibody is used[1]. |
Cell experiment: | Cell survival is assayed in MTS assay by measuring mitochondrial dehydrogenase activity of metabolically active cells. 5.0×103 (100 µL) cells are plated in 96-well plates and are allowed to attach overnight. One hundred microliters of fresh media with or without Chloropyramine hydrochloride is added to each well. Cells are treated for designated amount of time. MTS assay is performed according the manufacturers protocol[1]. |
Animal experiment: | BT474 and MCF7-VEGFR-3 cells at a concentration of 2 to 5×106 cells per 200 µL are subcutaneously injected into the right flank of the 5 to 6 week old mice, 5 in each group. Treatment with Chloropyramine hydrochloride is started next day after cells injection via intraperitoneal injection (IP) once a day. Tumor size is measured thrice weekly and volume is calculated using the formula length×width2×0.5. Animals are sacrificed after 21 days of treatment or when tumor size reaches protocol end point. Tumor is excised, measured and preserved for protein and RNA preparation and cytochemistry[1]. |
References: [1]. Kurenova EV, et al. Small molecule chloropyramine hydrochloride (C4) targets the binding site of focal adhesion kinase and vascular endothelial growth factor receptor 3 and suppresses breast cancer growth in vivo. J Med Chem. 2009 Aug 13;52(15):4716-24. | |
Chloropyramine hydrochloride (Halopyramine) is a histamine receptor H1 antagonist and has anti-cholinergic, antispasmodic, and antiallergic effects.
| Cas No. | 6170-42-9 | SDF | |
| 别名 | 盐酸氯吡胺 | ||
| Canonical SMILES | CN(C)CCN(CC1=CC=C(Cl)C=C1)C2=NC=CC=C2.[H]Cl | ||
| 分子式 | C16H21Cl2N3 | 分子量 | 326.26 |
| 溶解度 | DMSO : 30 mg/mL (91.95 mM) | 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 | 3.065 mL | 15.3252 mL | 30.6504 mL |
| 5 mM | 0.613 mL | 3.065 mL | 6.1301 mL |
| 10 mM | 0.3065 mL | 1.5325 mL | 3.065 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。
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Small molecule Chloropyramine hydrochloride (C4) targets the binding site of focal adhesion kinase and vascular endothelial growth factor receptor 3 and suppresses breast cancer growth in vivo
J Med Chem 2009 Aug 13;52(15):4716-24.PMID:19610651DOI:10.1021/jm900159g.
FAK is a tyrosine kinase that functions as a key orchestrator of signals leading to invasion and metastasis. Since FAK interacts directly with a number of critical proteins involved in survival signaling in tumor cells, we hypothesized that targeting a key protein-protein interface with druglike small molecules was a feasible strategy for inhibiting tumor growth. In this study, we targeted the protein-protein interface between FAK and VEGFR-3 and identified compound C4 (Chloropyramine hydrochloride) as a drug capable of (1) inhibiting the biochemical function of VEGFR-3 and FAK, (2) inhibiting proliferation of a diverse set of cancer cell types in vitro, and (3) reducing tumor growth in vivo. Chloropyramine hydrochloride reduced tumor growth as a single agent, while concomitant administration with doxorubicin had a pronounced synergistic effect. Our data demonstrate that the FAK-VEGFR-3 interaction can be targeted by small druglike molecules and this interaction can provide the basis for highly specific novel cancer therapeutics.
Allergy to Carbidopa
Clin Neuropharmacol 2018 Mar/Apr;41(2):75-79.PMID:29432287DOI:10.1097/WNF.0000000000000270.
Background: D-Decarboxylase inhibitors, such as carbidopa or benserazide, have been used as adjunct therapy in Parkinson disease shortly after levodopa synthesis in the 1960s. These compounds increase intracerebral drug concentration and decrease adverse effects by blocking peripheral conversion to dopamine. Skin rash as part of an allergic reaction was previously described in subjects who were using levodopa in combination with carbidopa or benserazide; however, etiology was never clear. Allergic reactions to carbidopa have not previously been reported. Methods: We report a case of a 77-year-old woman with a diagnosis of idiopathic Parkinson disease, who developed autonomic and dermatological signs: conjunctival injection, rhinorrhea, excessive sweating, hypertension, and pruritic generalized rash, among others, immediately after carbidopa/levodopa administration regardless of the manufacturer. Treatment with dexamethasone combined with Chloropyramine hydrochloride resulted in complete resolution of the hypersensitivity reaction each time it presented. The autonomic and dermatological manifestations did not reappear after treatment was replaced with benserazide/levodopa. Conclusions: To the best of our knowledge, this is the first case report of an allergic reaction specific to carbidopa. Our case highlights the importance of identifying the source of a hypersensitivity drug response, whether it is caused by the active component or by the excipients.
Inhibition of FAK and VEGFR-3 binding decreases tumorigenicity in neuroblastoma
Mol Carcinog 2015 Jan;54(1):9-23.PMID:23868727DOI:10.1002/mc.22070.
Neuroblastoma is the most common extracranial solid tumor of childhood and is responsible for over 15% of pediatric cancer deaths. Focal adhesion kinase (FAK) is a nonreceptor tyrosine kinase that is important in many facets of tumor development and progression. Vascular endothelial growth factor receptor-3 (VEGFR-3), another tyrosine kinase, has also been found to be important in the development of many human tumors including neuroblastoma. Recent reports have found that FAK and VEGFR-3 interact, and we have previously shown that both of these kinases interact in neuroblastoma. We have hypothesized that interruption of the FAK-VEGFR-3 interaction would lead to decreased neuroblastoma cell survival. In the current study, we examined the effects of a small molecule, Chloropyramine hydrochloride (C4), designed to disrupt the FAK-VEGFR-3 interaction, upon cellular attachment, migration, and survival in two human neuroblastoma cell lines. We also utilized a murine xenograft model to study the impact of C4 upon tumor growth. In these studies, we showed that disruption of the FAK-VEGFR-3 interaction led to decreased cellular attachment, migration, and survival in vitro. In addition, treatment of murine xenografts with Chloropyramine hydrochloride decreased neuroblastoma xenograft growth. Further, this molecule acted synergistically with standard chemotherapy to further decrease neuroblastoma xenograft growth. The findings from this current study help to further our understanding of the regulation of neuroblastoma tumorigenesis, and may provide novel therapeutic strategies and targets for neuroblastoma and other solid tumors of childhood.