2-(3-(trifluoromethyl)phenyl)piperazine (hydrochloride)
(Synonyms: 2-(3-Trifluorophenyl)piperazine (hydrochloride), 2-(m-Trifluorophenyl)piperazine, 2-(meta-Trifluorophenyl)piperazine) 目录号 : GC42052An Analytical Reference Standard
Cas No.:2517636-54-1
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
2-(3-(trifluoromethyl)phenyl)piperazine (hydrochloride) is an analytical reference standard categorized as a piperazine. This product is intended for research and forensic applications.
| Cas No. | 2517636-54-1 | SDF | |
| 别名 | 2-(3-Trifluorophenyl)piperazine (hydrochloride), 2-(m-Trifluorophenyl)piperazine, 2-(meta-Trifluorophenyl)piperazine | ||
| Canonical SMILES | FC(C1=CC(C2CNCCN2)=CC=C1)(F)F.Cl.Cl | ||
| 分子式 | C11H13F3N2•2HCl | 分子量 | 303.2 |
| 溶解度 | DMSO: 33 mg/ml,PBS (pH 7.2): 10 mg/ml | 储存条件 | Store at -20°C; protect from light |
| 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 | 3.2982 mL | 16.4908 mL | 32.9815 mL |
| 5 mM | 0.6596 mL | 3.2982 mL | 6.5963 mL |
| 10 mM | 0.3298 mL | 1.6491 mL | 3.2982 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。
Roles of serotonin receptor subtypes for the antinociception of 5-HT in the spinal cord of rats
Eur J Pharmacol 2004 Oct 19;502(3):205-11.PMID:15476746DOI:10.1016/j.ejphar.2004.08.048.
The contribution of 5-HT (5-hydroxytryptamine) receptor subtypes to the antinociception produced by intrathecal 5-HT in the formalin test was investigated in rats. Intrathecal 5-HT suppressed both phases of behaviors produced by 5% formalin, and this was blocked by antagonists for 5-HT(1B) (3-[3-(Dimethylamino)propyl]-4-hy-droxy-N-[4-(4-pyridinyl)phenyl]benzamide dihydrochloride, GR 55562), 5-HT(2C) (N-ormethylclozapine/8-Chloro-11-(1-piperazinyl)-5H-dibenzo[b,e][1,4]diazepine, D-MC), 5-HT3 (1-Methyl-N-(8-methyl-8-azabicyclo[3.2.1]-oct-3-yl)-1H-indazole-3-carboxamide maleate, LY-278,584) and 5-HT4 receptors (4-Amino-5-chloro-2-metho-xy-benzoic acid 2-(diethylamino)ethyl ester hydrochloride, SDZ-205,557), but not the 5-HT(1D) receptor antagonist 3-[4-(4-Chlorophenyl)piperazin-1-yl]-1,1-diphenyl-2-propanol hydrochloride (BRL 15572). The 5-HT(1A) receptor antagonist N-[2-[4-(2-Methoxyphenyl)-1-piperazinyl]-N-2-pyridinyl-cyclohexanecarboxamide maleate (WAY-100635) decreased only the second phase antinociception of 5-HT. Intrathecal administration of agonists for 5-HT(1A) (3-(N,N-Dipropylaminoethyl)-1H-indole-5-carboxamide maleate, Dipropyl-5CT), 5-HT(1B) (7-Trifluoromethyl-4(4-met-hyl-1-piperazinyl)-pyrrolo[1,2-a]quinoxaline maleate, CGS-12066A), 5-HT(2C) (6-Ch-loro-2-(1-piperazinyl)pyrazine hydrochloride, MK 212), 5-HT3 (N-(3-Chlorophenyl)imidodicarbonimidic diamide hydrochloride, m-CPBG) and 5-HT4 receptors (2-[1-(4-Piperonyl)piperazinyl]benzothiazole, BZTZ) suppressed both phases of the formalin response. The results of the present study indicate that spinal 5-HT(1B,) 5-HT(2C,) 5-HT3 and 5-HT4 receptors, but not the 5-HT(1D) receptor, mediate antinociception produced by 5-HT in the formalin test. The relevance of the 5-HT(1A) receptor is less clear because of the different effects of antagonist and agonist.
Identification and characterization of INCB9471, an allosteric noncompetitive small-molecule antagonist of C-C chemokine receptor 5 with potent inhibitory activity against monocyte migration and HIV-1 infection
J Pharmacol Exp Ther 2011 Jul;338(1):228-39.PMID:21459966DOI:10.1124/jpet.111.179531.
C-C chemokine receptor 5 (CCR5) is a clinically proven target for inhibition of HIV-1 infection and a potential target for various inflammatory diseases. In this article, we describe 5-[(4-{(3S)-4-[(1R,2R)-2-ethoxy-5-(trifluoromethyl)-2,3-dihydro-1H-inden-1-yl]-3-methylpiperazin-1-yl}-4-methylpiperidin-1-yl)carbonyl]-4,6-dimethylpyrimidine dihydrochloride (INCB9471), a potent and specific inhibitor of human CCR5 that has been proven to be safe and efficacious in viral load reduction in phase I and II human clinical trails. INCB9471 was identified using a primary human monocyte-based radioligand competition binding assay. It potently inhibited macrophage inflammatory protein-1β-induced monocyte migration and infection of peripheral blood mononuclear cells by a panel of R5-HIV-1 strains. The results from binding and signaling studies using incremental amounts of INCB9471 demonstrated INCB9471 as a noncompetitive CCR5 inhibitor. The CCR5 residues that are essential for interaction with INCB9471 were identified by site-specific mutagenesis studies. INCB9471 rapidly associates with but slowly dissociates from CCR5. When INCB9471 was compared with three CCR5 antagonists that had been tested in clinical trials, the potency of INCB9471 in blocking CCR5 ligand binding was similar to those of 4,6-dimethyl-5-{[4-methyl-4-((3S)-3-methyl-4-{(1R0-2-(methyloxy)-1-[4-(trifluoromethyl) phenyl]ethyl}-1-piperazingyl)-1-piperidinyl]carbonyl}pyrimidine (SCH-D; vicriviroc), 4-{[4-({(3R)-1-butyl-3-[(R)-cyclohexyl(hydroxyl)methyl]-2, 5-dioxo-1,4,9-triazaspiro[5.5]undec-9-yl}methyl)phenyl]oxy}benzoic acid hydrochloride (873140; aplaviroc), and 4,4-difluoro-N-((1S)-3-{(3-endo)-3-[3-methyl-5-(1-methylethyl)-4H-1,2,4-triazol-4-yl]-8-azabicyclo[3.2.1]oct-8-yl}-1-phenylpropyl)cyclohexanecarboxamide (UK427857; maraviroc). Its inhibitory activity against CCR5-mediated Ca(2+) mobilization was also similar to those of SCH-D and 873140. Further analysis suggested that INCB9471 and UK427857 may have different binding sites on CCR5. The significance of two CCR5 antagonists with different binding sites is discussed in the context of potentially overcoming drug-resistant HIV-1 strains.
The CCR5 receptor-based mechanism of action of 873140, a potent allosteric noncompetitive HIV entry inhibitor
Mol Pharmacol 2005 Apr;67(4):1268-82.PMID:15644495DOI:10.1124/mol.104.008565.
4-{[4-({(3R)-1-Butyl-3-[(R)-cyclohexyl(hydroxy)methyl]-2,5dioxo-1,4,9-triazaspiro[5.5]undec-9-yl}methyl)phenyl]oxy}benzoic acid hydrochloride (873140) is a potent noncompetitive allosteric antagonist of the CCR5 receptor (pK(B) = 8.6 +/- 0.07; 95% CI, 8.5 to 8.8) with concomitantly potent antiviral effects for HIV-1. In this article, the receptor-based mechanism of action of 873140 is compared with four other noncompetitive allosteric antagonists of CCR5. Although (Z)-(4-bromophenyl){1'-[(2,4-dimethyl-1-oxido-3-pyridinyl)carbonyl]-4'-methyl-1,4'-bipiperidin-4-yl}methanone O-ethyloxime (Sch-C; SCH 351125), 4,6-dimethyl-5-{[4-methyl-4-((3S)-3-methyl-4-{(1R)-2-(methyloxy)-1-[4-(trifluoromethyl)phenyl]ethyl}-1-piperazinyl)-1-piperidinyl]carbonyl}pyrimidine (Sch-D; SCH 417,690), 4,4-difluoro-N-((1S)-3-{(3-endo)-3-[3-methyl-5-(1-methylethyl)-4H-1,2,4-triazol-4-yl]-8-azabicyclo[3.2.1]oct-8-yl}-1-phenyl-propyl)cyclohexanecarboxamide (UK-427,857), and N,N-dimethyl-N-[4-[[[2-(4-methylphenyl)-6,7-dihydro-5H-benzocyclo-hepten-8-yl]carbonyl]amino]benzyl]tetrahydro-2H-pyran-4-aminium chloride (TAK779) blocked the binding of both chemokines (125)I-MIP-1alpha (also known as (125)I-CCL3, (125)I-LD78) and (125)I-RANTES ((125)I-CCL5), 873140 was an ineffectual antagonist of (125)I-RANTES (regulated on activation normal T cell expressed and secreted) binding (but did block binding of (125)I-MIP-1alpha). Furthermore, 873140 blocked the calcium response effects of CCR5 activation by CCL5 (RANTES) (as did the other antagonists), indicating a unique divergence of blockade of function and binding with this antagonist. The antagonism of CCR5 by 873140 is saturable and probe-dependent, consistent with an allosteric mechanism of action. The blockade of CCR5 by 873140 was extremely persistent with a rate constant for reversal of <0.004 h(-) (1) (t(1/2) > 136 h). Coadministration studies of 873140 with the four other allosteric antagonists yielded data that are consistent with the notion that all five of these antagonists bind to a common allosteric site on the CCR5 receptor. Although these ligands may have a common binding site, they do not exert the same allosteric effect on the receptor, as indicated by their differential effects on the binding of (125)I-RANTES. This idea is discussed in terms of using these drugs sequentially to overcome HIV viral resistance in the clinic.
Serotonin enhances gastric acid response to TRH analogue in dorsal vagal complex through 5-HT2 receptors in rats
Am J Physiol 1995 Jul;269(1 Pt 2):R1-6.PMID:7631881DOI:10.1152/ajpregu.1995.269.1.R1.
The effect of serotonin (5-HT) and thyrotropin-releasing hormone (TRH) analogue, p-Glu-His-[3,3'-dimethyl]-Pro-NH2 (RX-77368), injected into the dorsal vagal complex (DVC) on gastric acid secretion was assessed in urethan-anesthetized rats with gastric cannula. 5-HT (0.1, 0.2, 1, or 10 nmol into the DVC) enhanced the acid response to RX-77368 (25 pmol, DVC) by 54, 100, 147, and 144%, respectively, whereas 5-HT given alone had no effect. The 5-HT2 receptor agonists (1 nmol, DVC), ( +/- )-1-(4-iodo-2,5-dimethoxyphenyl)-2-aminopropane hydrochloride, 1-(alpha, alpha, alpha-trifluoro-m-tolyl)-piperazine hydrochloride, and alpha-methyl-5-HT increased the gastric acid response to coinjection of RX-77368 (25 pmol) by 153, 108, and 96%, respectively, whereas 8-hydroxy-2-(di-n-propylamino)tetralin (5-HT1A), 7-trifluoromethyl-4(4-methyl-1-piperazinyl)- pyrrolo[1,2-a]quinoxaline (5-HT1A/1B), and 3-(2-aminoethyl)-2-methyl-1-H-indol-5-ol hydrochloride hydrate (2-methyl-5-HT3) did not. The 5-HT2 receptor antagonist, 3-[2-(4-fluorobenzoyl)-1-piperdinyl]ethyl]-2,4(1H,3H)-quinazoli nedone tartrate (ketanserin; 20 nmol), injected intracisternally abolished the potentiating action of 5-HT injected into the DVC with RX-77368, whereas the 5-HT antagonists 8-[4-(4-fluorophenyl)-4-oxobutyl]-1-phenyl-1,3,8-triazaspiro[4,5]- decan-4-one (spiperone; 5-HT2/1A) and 1,2,3,9-tetrahydro-9-methyl-3-[(2-methyl-1H-imidazol-1- yl)methyl]-4H-carbazol-4-one hydrochloride dihydrate (ondansetron; 5-HT3) did not. Ketanserin (1 nmol/site bilaterally into the DVC) decreased the acid response to kainic acid injected into the raphe pallidus by 62%. These data suggest that 5-HT acting at 5-HT2 receptors in the DVC potentiates the gastric acid response to exogenous and endogenous TRH.
Serotonin receptor subtypes in spinal antinociception in the rat
J Pharmacol Exp Ther 1994 Jun;269(3):1182-9.PMID:8014862doi
The aim of the present study was to clarify the subtypes of serotonin (5-HT) receptors involved in spinal antinociception in the rat. 1) Intrathecal (i.t.) injection of 5-HT (25-200 micrograms) produced a dose-dependent increase in tail-flick latency. 2) Intrathecal injection of fluoxetine, a 5-HT uptake blocker (25-40 micrograms), resulted in a bell-shaped dose-related antinociception with peak effects occurring at 10 micrograms. 3) A bell-shaped antinociceptive effect was obtained by i.t. injection of the 5-HT1A agonist (+)-hydroxy-2-(di-N-propylamino)tetralin (0.25-2 micrograms), with the maximal effect occurring at 0.5 micrograms, which can be prevented by the 5-HT1A antagonist spiperone (25 micrograms i.t.). 4) A similar dose-response curve was obtained following the i.t. injection of the 5-HT1B agonist 1-[3-(trifluoromethyl)phenyl]-piperazine maleate (1-125 micrograms) with the maximal effect observed at 25 micrograms. 5) Neither the 5-HT2 agonist (+/-)-alpha-methyl-5-HT-maleate nor the 5-HT3 agonist (+/-)-2-methyl-5-HT-maleate produced significant antinociceptive effects at doses up to 50 micrograms. Spontaneous tail-flicks emerged at doses higher than 50 micrograms. 6) The antinociceptive effect induced by 5-HT (200 micrograms i.t.) could be attenuated dose-dependently either by the 5-HT1A antagonist spiperone (5 and 25 micrograms i.t.) or by the 5-HT1C/2 antagonist mianserin (0.5-50 micrograms i.t.), but not by the 5-HT2 antagonist 1-(1-naphthyl)piperazine hydrochloride or the 5-HT3 antagonist 3-tropanyl-indole-3-carboxylate.(ABSTRACT TRUNCATED AT 250 WORDS)