NBD-FTY720 phenoxy (hydrochloride)
目录号 : GC44323
Fluorescently-labeled FTY720 analog
Cas No.:2319882-09-0
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >96.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
FTY720 is an immune modulator that down-regulates sphingosine-1-phosphate (S1P) receptors, enhances the activity of the sphingosine transporter Abcb1 and the leukotriene C4 transporter Abcc1, and inhibits cytosolic phospholipase A2 activity. It is known that some of the effects of FTY720 require its phosphorylation by sphingosine kinases in vivo, with FTY720-phosphate binding to and down-regulating S1P receptors. NBD-FTY720 is a fluorescently-labeled analog of FTY720. The hydroxy methyl side chain of FTY720 that is targeted for phosphorylation by sphingosine kinases is retained in this analog, suggesting that it would likewise be phosphorylated in vivo.
| Cas No. | 2319882-09-0 | SDF | |
| Canonical SMILES | OCC(N)(CO)CCC1=CC=C(C=C1)OCCCCCCNC2=CC=C([N+]([O-])=O)C3=NON=C23.Cl | ||
| 分子式 | C23H31N5O6•HCl | 分子量 | 510 |
| 溶解度 | DMF: 20 mg/ml,DMSO: 10 mg/ml,Ethanol: 20 mg/ml,Ethanol:PBS(pH 7.2) (1:1): 0.5 mg/ml | 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 | 1.9608 mL | 9.8039 mL | 19.6078 mL |
| 5 mM | 0.3922 mL | 1.9608 mL | 3.9216 mL |
| 10 mM | 0.1961 mL | 0.9804 mL | 1.9608 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。
Paroxetine hydrochloride
Profiles Drug Subst Excip Relat Methodol 2013;38:367-406.PMID:23668408DOI:10.1016/B978-0-12-407691-4.00008-3.
Paroxetine hydrochloride (3S-trans)-3-[(1,3-benzodioxol-5-yloxy)methyl]-4-(4-fluorophenyl)-piperidine hydrochloride (or (-)-(3S,4R)-(4-(p-fluorophenyl)-3-[[3,4-(methylenedioxy)-phenoxy]methyl]piperidine hydrochloride), a phenylpiperidine derivative, is a selective serotonin reuptake inhibitor. Paroxetine is indicated for the treatment of depression, generalized anxiety disorder, obsessive-compulsive disorder, panic disorder, posttraumatic stress disorder, and social anxiety disorder. The physicochemical properties, spectroscopic data (1D and 2D NMR, UV, FT-IR, MS, PXRD), stability, methods of preparation and chromatographic methods of analysis of pharmaceutical, and biological samples of paroxetine are documented in this review. Pharmacokinetics, metabolism, and pharmacological effects are also discussed.
Nonhormonal selective estrogen receptor modulator 1-(2-[4-{(3R,4S)-7-Methoxy-2, 2-dimethyl-3-phenyl-chroman-4yl}phenoxy]ethyl)pyrrolidine hydrochloride (ormeloxifene hydrochloride) for the treatment of breast cancer
Drug Dev Res 2018 Sep;79(6):275-286.PMID:30284735DOI:10.1002/ddr.21440.
Breast cancer is the most common type of diagnosed cancers in women, difficult to treat, and has received international attention because of its aggressive nature and inherent drug resistance mechanisms. Development of a better selective estrogen receptor modulator with good therapeutic profile and less toxicity is very crucial in this scenario. This study was undertaken to evaluate and compare the in vitro and in vivo antitumor activities of ormeloxifene with other clinically used breast cancer drugs. Cytotoxic activity of ormeloxifene was compared with standard drugs, 4-hydroxytamoxifene and Adriamycin. Ormeloxifene (50 μM) concentration showed cytotoxicity of 75% and 82% in MDAMB-231 and 24% and 80% in MCF-7 cells, respectively, after 72 and 144 hr of incubation as displayed by cell viability assay. The same concentration of ormeloxifene was shown to exert 74% caspase-7 activation in MCF-7 cells after 24 hr of incubation by fluorescence resonance energy transfer assay. Cell cycle analysis proved that there was an increase in sub-G1 peak to 64.4% and 33.9% in MDAMB-231 and MCF-7 cells, respectively, after treatment using ormeloxifene (50 μM) for 48 hr. The nonobese diabetic-severe combined immunodeficiency mice bearing tumor xenografts of triple negative MDAMB-231 cells treated with ormeloxifene (3 mg/kg bw) showed significant regression in relative tumor volume compared to control. From the results obtained and as evidenced from prior literature, ormeloxifene in addition to contraceptive use, can be repositioned for the development of an efficacious anticancer drug. These data present the preclinical part of a well concerted effort to place ormeloxifene into further clinical trials.
A review of the animal pharmacology of roxatidine acetate
Drugs 1988;35 Suppl 3:30-40.PMID:2905247DOI:10.2165/00003495-198800353-00008.
Roxatidine acetate (TZU 0460/HOE 760) [N-(3-[3-(1-piperidinylmethyl)-phenoxy]-propyl)acetoxyacetamide hydrochloride] is a specific and competitive H2-receptor antagonist with a chemical structure different from those of cimetidine, ranitidine and famotidine. Roxatidine acetate and its main metabolite roxatidine inhibit histamine-induced gastric acid secretion in vitro with a potency greater than that of cimetidine, and in the range of that produced by ranitidine. Gastric acid secretion following stimulation with dibutyryl cyclic adenosine monophosphate remains unaffected by roxatidine acetate. In vivo experiments in rats and dogs confirm these in vitro findings. Thus, in rats roxatidine acetate inhibits gastric acid secretion with similar values following intraduodenal or intraperitoneal injection, indicating excellent absorption of the drug from the gastrointestinal tract. In all studies it was shown that roxatidine acetate was more potent than cimetidine. In rats single or repeated dosing with roxatidine acetate did not influence drug metabolising enzymes in the liver nor did the drug show antiandrogenic activity in long term animal studies. Extensive general pharmacological studies with roxatidine acetate demonstrate the lack of effects on the central nervous system, on gastrointestinal motility, the autonomic nervous system and the cardiovascular and urogenital systems. Studies on the pharmacokinetics and metabolism of roxatidine acetate demonstrate that there is a presystemic deacetylation producing the main metabolite roxatidine, which is responsible for the in vivo effects of the drug.
Discovery of 4-[4-({(3R)-1-butyl-3-[(R)-cyclohexyl(hydroxy)methyl]-2,5-dioxo-1,4,9-triazaspiro[5.5]undec-9-yl}methyl)phenoxy]benzoic acid hydrochloride: a highly potent orally available CCR5 selective antagonist
Bioorg Med Chem 2011 Jul 1;19(13):4028-42.PMID:21658961DOI:10.1016/j.bmc.2011.05.022.
Based on the original spirodiketopiperazine design framework, further optimization of an orally available CCR5 antagonist was undertaken. Structural hybridization of the hydroxylated analog 4 derived from one of the oxidative metabolites and the new orally available non-hydroxylated benzoic acid analog 5 resulted in another potent orally available CCR5 antagonist 6a as a clinical candidate. Full details of a structure-activity relationship (SAR) study and ADME properties are presented.
Hydrogen Bonds, Topologies, Energy Frameworks and Solubilities of Five Sorafenib Salts
Int J Mol Sci 2021 Jun 22;22(13):6682.PMID:34206574DOI:10.3390/ijms22136682.
Sorafenib (Sor) is an oral multi-kinase inhibitor, but its water solubility is very low. To improve its solubility, sorafenib hydrochloride hydrate, sorafenib hydrobromide and sorafenib hydrobromide hydrate were prepared in the mixed solvent of the corresponding acid solution, and tetrahydrofuran (THF). The crystal structures of sorafenib hydrochloride trihydrate (Sor·HCl.3H2O), 4-(4-{3-[4-chloro-3-(trifluoro-methyl)phenyl]ureido}phenoxy)-2-(N-methylcarbamoyl) pyridinium hydrochloride trihydrate, C21H17ClF3N4O3+·Cl-.3H2O (I), sorafenib hydrochloride monohydrate (Sor·HCl.H2O), C21H17ClF3N4O3+·Cl-.H2O (II), its solvated form (sorafenib hydrochloride monohydrate monotetrahydrofuran (Sor·HCl.H2O.THF), C21H17ClF3N4O3+·Cl-.H2O.C4H8O (III)), sorafenib hydrobromide (Sor·HBr), 4-(4-{3-[4-chloro-3-(trifluoro-methyl)phenyl]ureido}phenoxy)-2-(N-methylcarbamoyl) pyridinium hydrobromide, C21H17ClF3N4O3+·Br- (IV) and sorafenib hydrobromide monohydrate (Sor·HBr.H2O), C21H17ClF3N4O3+·Br-.H2O (V) were analysed. Their hydrogen bond systems and topologies were investigated. The results showed the distinct roles of water molecules in stabilizing their crystal structures. Moreover, (II) and (V) were isomorphous crystal structures with the same space group P21/n, and similar unit cell dimensions. The predicted morphologies of these forms based on the BFDH model matched well with experimental morphologies. The energy frameworks showed that (I), and (IV) might have better tabletability than (II) and (V). Moreover, the solubility and dissolution rate data exhibited an improvement in the solubility of these salts compared with the free drug.