1-(3-Trifluoromethylphenyl)piperazine (hydrochloride)
(Synonyms: TFMPP, 1-(m-Trifluoromethylphenyl)piperazine, 1-(meta-Trifluoromethylphenyl)piperazine) 目录号 : GC41755An Analytical Reference Standard
Cas No.:76835-14-8
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
1-(3-Trifluoromethylphenyl)piperazine (TFMPP) is an entactogenic drug which selectively promotes the release of serotonin. When used in combination with 1-benzylpiperazine, TFMPP increases both serotonin and dopamine, mirroring the effects of 3,4-methylenedioxymethamphetamine. Drug-drug synergism may induce seizures. TFMPP has been identified in party pills and powders. Its metabolism in rats has been described. This product is intended for forensic applications.
| Cas No. | 76835-14-8 | SDF | |
| 别名 | TFMPP, 1-(m-Trifluoromethylphenyl)piperazine, 1-(meta-Trifluoromethylphenyl)piperazine | ||
| Canonical SMILES | FC(C1=CC=CC(N2CCNCC2)=C1)(F)F.Cl.Cl | ||
| 分子式 | C11H13F3N2•2HCl | 分子量 | 303.2 |
| 溶解度 | DMF: 20 mg/ml,DMSO: 20 mg/ml,Ethanol: 20 mg/ml,PBS (pH 7.2): 10 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 | 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。
The effects of intraventricular administration of eltoprazine, 1-\(3-Trifluoromethylphenyl\)piperazine hydrochloride and 8-hydroxy-2-(di-n-propylamino)tetralin on resident intruder aggression in the rat
Eur J Pharmacol 1992 Mar 3;212(2-3):295-8.PMID:1534769DOI:10.1016/0014-2999(92)90348-8.
Various serotonergic agents may reduce aggression in rats, but how they act in different parts of the brain is unknown. This study attempted to unravel part of this question by application of different serotonergic ligands into the lateral ventricle (i.c.v.) of male rats (resident-intruder aggression). 8-OH-DPAT (8-hydroxy-2-(di-n-propylamino)tetralin; 1 and 10 micrograms), a specific 5-HT1A agonist, affected neither aggression nor any other behaviour. The mixed 5-HT1A,B,C agonist, TFMPP (1-\(3-Trifluoromethylphenyl\)piperazine hydrochloride), and the 5-HT1A/1B agonist, eltoprazine ((1-(2,3)-dihydro-1,4-benzodioxin-5-yl)piperazine hydrochloride), suppressed aggression at i.c.v. doses of 10 and 30 micrograms. This reduction was not caused by sedation. These data suggest a role of postsynaptic 5-HT1B receptors in mediating the anti-aggressive effects of mixed 5-HT1 agonists.
Modulation of 5-HT(2A) receptor-mediated head-twitch behaviour in the rat by 5-HT(2C) receptor agonists
Pharmacol Biochem Behav 2001 Jul-Aug;69(3-4):643-52.PMID:11509227DOI:10.1016/s0091-3057(01)00552-4.
The pharmacology of several commonly described 5-hydroxytryptamine (5-HT)(2C) receptor agonists was investigated in vivo and in vitro at rat 5-HT(2A), 5-HT(2B), and 5-HT(2C) receptors. The 5-HT(2C) receptor agonist, (S)-2-(6-chloro-5-fluoroindol-1-yl)-1-methylethylamine fumarate (Ro 60-0175), did not induce a significant head-twitch response when given alone, yet when administered to rats subsequent to an acute challenge with the selective 5-HT(2C) receptor antagonist, 6-chloro-5-methyl-1-[6-(2-methylpyridin-3-yloxy) pyridin-3-yl carbomyl] indoline (SB-242084), a robust head-twitch response was observed which was blocked by the selective 5-HT(2A) receptor antagonists R(+)-alpha-(2,3-dimethoxyphenyl)-1-[2-(4-fluorophenyl-ethyl)]-4-piperidine-methanol (MDL 100907) or ketanserin. The preferential 5-HT(2C) receptor agonists Ro 60-0175, 6-chloro-2-[1-piperazinyl]-pyrazine HCl (MK-212), 1-(3-chlorophenyl)piperazine hydrochloride (mCPP), 1-\(3-Trifluoromethylphenyl\)piperazine hydrochloride (TFMPP), and (S)-3-[(2,3-dihydro-5-methoxy-1H-inden-4-yl)oxy]-pyrollidine HCl (ORG-37684), the 5-HT(2A/2C) receptor agonist 2,5-dimethoxy-4-iodoamphetamine (DOI), the 5-HT(2B) receptor agonist 1-[5-thienylmethoxy-1-1H-3-indoyl] propan-2-amine hydrochloride (BW-723C86), and nor-D-fenfluramine were administered to rats subsequent to an acute challenge of SB-242084. Under such conditions, each agonist, with the exception of BW-723C86, induced a dose-dependent increase in the incidence of head twitches. The pharmacology of the same agonists was determined at cloned rat 5-HT(2) receptors using a fluorometric imaging plate reader (FLIPR). Both the in vivo and in vitro data suggest that for some ligands, previous reports have overestimated their in vivo selectivity for the 5-HT(2C) receptor.
Serotonin 5-HT2c agonists mimic the effect of light pulses on circadian rhythms
Brain Res 1998 Sep 28;806(2):257-70.PMID:9739147DOI:10.1016/s0006-8993(98)00746-x.
The serotonin agonist quipazine has been shown to cause phase shifts in melatonin and activity rhythms and to induce c-fos in the suprachiasmatic nucleus of rats. In this study, in vivo pharmacological characterisation of the phase shifting properties of serotonin agonists has been performed, with a view to determining the receptor sub-types involved. Agonists for the 5-HT2a/2c receptors, (+/-)-1-(4-iodo-2,5-dimethoxyphenyl)-2-aminopropane hydrochloride (DOI, 0.1 mg/k), 1-(3-chlorophenyl)-piperazine HCl (mCPP, 2 mg/kg) and N-(3-trifluoromethylphenyl)-piperazine HCl (TFMPP, 2 mg/kg) injected at CT18 resulted in acute transient inhibition of melatonin production and delays in the onset of production on the following nights of 1.2+/-0.2, 1.7+/-0.3 and 1. 4+/-0.8 h respectively. Drugs specific for 5-HT1a/7 and 5-HT3 receptors failed to affect melatonin production. At a dose of 0.07 micromole/kg, the serotonin antagonist, ritanserin inhibited the DOI induced phase delay whereas ketanserin was ineffective at this dose, providing strong evidence that DOI was acting through 5-HT2c receptors. DOI (0.5 mg/kg) at CT18 provoked a phase delay in the core body temperature rhythm of similar magnitude to that following a light pulse. Administration of DOI but not agonists active at other receptor sites resulted in the appearance of c-Fos in the ventrolateral division of the suprachiasmatic nucleus (SCN) at CT18 but not at CT6. Ritanserin was more potent than ketanserin at inhibiting the DOI induced increase in c-Fos labelled cells in the SCN. When rats were pre-treated with metergoline (15 mg/kg), ritanserin (3 mg/kg) or LY 53,857 (3 mg/kg) prior to a 2 lx/ 1 min light pulse, none of the drugs significantly inhibited the responses to light. The results of these experiments indicate that serotonergic agonists active at the 5-HT2c receptor mimic the effects of light on 2 independent rhythms and activate SCN neurones in the rat.
Inhibition of N- and P-type calcium currents and the after-hyperpolarization in rat motoneurones by serotonin
J Physiol 1995 Jun 15;485 ( Pt 3)(Pt 3):635-47.PMID:7562606DOI:10.1113/jphysiol.1995.sp020758.
1. We investigated the effects of serotonin (5-hydroxytryptamine, 5-HT) on whole-cell barium currents through calcium channels in visualized neonatal rat hypoglossal motoneurones (HMs) in a thin brainstem slice preparation. 2. High voltage-activated (HVA) currents were elicited by depolarizing voltage steps from -70 to 0 mV; low voltage-activated (LVA) currents were evoked using steps to between -30 and -40 mV from hyperpolarized potentials (< -80 mV). 5-HT (1.0 microM) inhibited HVA currents by at least 10% in 70% of HMs tested (n = 99); in those responsive neurones, 5-HT decreased HVA current by 22 +/- 1.3% (mean +/- S.E.M.). In contrast, 5-HT had no effect on LVA current amplitude in HMs (n = 7). 3. Calcium current inhibition was mimicked by 5-carboxamidotryptamine maleate (5-CT), a 5-HT1 receptor agonist, and by R(+)-8-hydroxydipropylaminotetralin hydrobromide (8-OH-DPAT), a specific 5-HT1A agonist; N-(3-trifluoromethylphenyl) piperazine hydrochloride (TFMPP), a 5-HT1B agonist, was without effect. The effect of 5-HT was blocked by the 5-HT1A antagonist 1-(2-methoxyphenyl)-4-[4-(2-phthalimido)butyl]piperazine hydrobromide (NAN-190) but not by ketanserin, a 5-HT2A/2C antagonist. Although R(-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane hydrochloride (DOI), a 5-HT2A/2C agonist, mimicked the current inhibition by 5-HT, it was ineffective in the presence of NAN-190. These data indicate that 5-HT1A receptors mediate calcium current inhibition by 5-HT. 4. Following application of either omega-conotoxin-GVIA (omega-CgTX) or omega-agatoxin-IVA (omega-Aga-IVA), to block N- and P-type components of calcium current, the 5-HT-sensitive current was reduced; 5-HT had no effect on the current remaining after application of both toxins. Thus, 5-HT inhibits both N- and P-type calcium currents in neonatal HMs. 5. Inhibition of HVA current by 5-HT was irreversible, and subsequent applications of 5-HT were occluded, when GTP gamma S was substituted for GTP in the pipette. In addition, inhibition of HVA current by 5-HT was relieved following depolarizing prepulses. These data indicate that inhibition of calcium channels by 5-HT is mediated by G proteins. 6. Under current clamp, both 5-HT and 8-OH-DPAT decreased the amplitude of the after-hyperpolarization (AHP) that followed action potentials, indicating involvement of a 5-HT1A receptor.(ABSTRACT TRUNCATED AT 400 WORDS)
Quinpirole attenuates striatal c-fos induction by 5-HT, opioid and muscarinic receptor agonists
Eur J Pharmacol 1998 May 15;349(1):41-7.PMID:9669494DOI:10.1016/s0014-2999(98)00184-8.
Pretreatment with the dopamine D2 receptor agonist quinpirole (0.025-2.5 mg/kg) produced a marked, dose-dependent, attenuation of the striatal Fos expression induced by the serotonin (5-Hydroxytryptamine, 5-HT) releasing agent fenfluramine (25 mg/kg). Quinpirole (2.5 mg/kg) was also able to drastically attenuate the striatal Fos response produced by injections of the direct 5-HT1/2 receptor agonist N-(3-trifluoromethylphenyl)piperazine hydrochloride (TFMPP) (5 mg/kg), the selective 5-HT2 receptor agonist 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane hydrochloride (DOI) (6.64 mg/kg), the 5-HT1A/1B receptor agonist RU-24969 (5-methoxy-3-(1,2,3,6-tetrahydropyridin-4-yl)1H-indole) (5 mg/kg), the mu-opioid receptor agonist morphine (5 mg/kg) and the muscarinic cholinergic receptor agonist pilocarpine (50 mg/kg). These results are in marked contrast to the previously reported ability of quinpirole to potentiate the response to D1 dopamine receptor agonists and demonstrate that stimulation of D2-like receptors can have differential effects on the Fos responses induced by various drugs.