1-(3-Chlorophenyl)biguanide (hydrochloride)
(Synonyms: m-Chlorophenylbiguanide hydrochloride, meta-Chlorophenylbiguanide, m-CPBG, meta-CPBG) 目录号 : GC49346
A 5-HT3 receptor agonist
Cas No.:2113-05-5
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >95.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
1-(3-Chlorophenyl)biguanide (m-CPBG) is an agonist of the serotonin (5-HT) receptor subtype 5-HT3.1 It selectively binds 5-HT3 over 5-HT1A and 5-HT2 receptors (Kis = 0.002, 10, and 10 µM, respectively) but also binds to high and low affinity sites on the dopamine transporter (DAT; IC50s = 0.4 and 34.8 µM, respectively, in rat caudate putamen synaptosomal membranes).2,3 m-CPBG induces depolarization of isolated rat vagus nerve and stimulates inositol phosphate formation in rat frontocingulate cortical slices (EC50s = 0.05 and 4.2 µM, respectively).1,4 It induces bradycardia, an effect that can be reversed by the 5-HT3 receptor antagonist ondansetron, in anaesthetized cats (ED50 = 20.3 nmol/kg).1
1.Kilpatrick, G.J., Butler, A., Burridge, J., et al.1-(m-chlorophenyl)-biguanide, a potent high affinity 5-HT3 receptor agonistEur. J. Pharmacol.182(1)193-197(1990) 2.Campbell, A.D., Womer, D.E., and Simon, J.R.The 5-HT3 receptor agonist 1-(m-chlorophenyl)-biguanide interacts with the dopamine transporter in rat brain synaptosomesEur. J. Pharmacol.290(2)157-162(1995) 3.Higgins, G.A., Joharchi, N., and Sellers, E.M.Behavioral effects of the 5-hydroxytryptamine3 receptor agonists 1-phenylbiguanide and m-chlorophenylbiguanide in ratsJ. Pharmacol. Exp. Ther.264(3)1440-1449(1993) 4.Edwards, E., Hampton, E., Ashby, C.R., et al.5-HT3-like receptors in the rat medial prefrontal cortex: Further pharmacological characterizationBrain Res.733(1)21-30(1996)
| Cas No. | 2113-05-5 | SDF | |
| 别名 | m-Chlorophenylbiguanide hydrochloride, meta-Chlorophenylbiguanide, m-CPBG, meta-CPBG | ||
| Canonical SMILES | ClC1=CC=CC(NC(NC(N)=N)=N)=C1.Cl | ||
| 分子式 | C8H10ClN5·HCl | 分子量 | 248.1 |
| 溶解度 | DMF: 30 mg/ml,DMSO: 20 mg/ml,Ethanol: 5 mg/ml,PBS (pH 7.2): 5 mg/ml | 储存条件 | -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 | 4.0306 mL | 20.1532 mL | 40.3063 mL |
| 5 mM | 0.8061 mL | 4.0306 mL | 8.0613 mL |
| 10 mM | 0.4031 mL | 2.0153 mL | 4.0306 mL |
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| 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 |
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| % DMSO % % Tween 80 % saline | ||||||||||
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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，
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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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Roles of 5-hydroxytryptamine (5-HT) receptor subtypes in the inhibitory effects of 5-HT on C-fiber responses of spinal wide dynamic range neurons in rats
J Pharmacol Exp Ther 2007 Jun;321(3):1046-53.PMID:17329553DOI:10.1124/jpet.106.115204.
5-Hydroxytryptamine (5-HT; serotonin) plays an important role in the descending control of nociception. 5-HT and its receptors have been extensively studied in the modulation of nociceptive transmission at the spinal level using behavioral tests that may be affected by the effects of 5-HT on motor performance and skin temperature. Using electrophysiological methods, the present study aimed to systematically investigate the roles of 5-HT receptor subtypes on the inhibitory effects of 5-HT on responses of the spinal wide dynamic range (WDR) neurons to C-fiber inputs in rats. Under basal conditions, topical application of 5-HT to the spinal cord inhibited the C-fiber responses of WDR neurons dose-dependently, whereas antagonists of 5-HT(1A) [WAY 100635 [N-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-N-2-pyridinyl-cyclohexanecarboxamide maleate salt]], 5-HT(1B) [GR 55562 [3-[3-(dimethylamino)propyl]-4-hydroxy-N-[4-(4-pyrid-dinyl)phenyl]benzamide dihydrochloride]], 5-HT(2A) [ketanserin [3-[2-[4-(fluorobenzoyl)-1-piperidinyl]ethyl]-2,4[1H,3H]-quinazolinedione tartrate]], 5-HT(2C) [RS 102221 [8-[5-(2,4-dimethoxy-5-(4-trifluoromethylphenylsulfonamido)phenyl-5-oxopentyl]-1,3,8-triazaspiro[4.5]decane-2,4-dione hydrochloride]], 5-HT(3) [MDL 72222 [3-tropanyl-3,5-dichlorobenzoate]], and 5-HT(4) [GR 113808 ([1-[2-[(methylsulfonyl)-amino]ethyl]-4-piperidinyl]methyl 1-methyl-1H-indole-3-carboxylate)] had no effect on their own. The inhibitory effects of 5-HT were reversed by antagonists of 5-HT(1B) (GR 55562), 5-HT(2A) (ketanserin), 5-HT(2C) (RS 102221), 5-HT(3) (MDL 72222), and 5-HT(4) (GR 113808) but not by 5-HT(1A) (WAY 100635) receptor antagonists. Topical administration of agonists of 5-HT(1A) [(2R)-(+)-8-hydroxy-2-(di-n-propylamino)tetralin hydrobromide], 5-HT(1B) [CGS 12066 [7-trifluoromethyl-4-(4-methyl-1-piperazinyl)pyrrolo-[1,2-a]quinoxaline maleate salt]], 5-HT(2A) (alpha-methyl-5-hydroxytryptamine maleate), 5-HT(2C) [MK 212 [6-chloro-2-(1-piperazinyl)pyrazine hydrochloride]], 5-HT(3) [1-\(3-Chlorophenyl\)biguanide hydrochloride], and 5-HT(4) [2-[1-(4-piperonyl)piperazinyl]benzothiazole] also inhibited the C-responses. These results suggest that, under basal conditions, there is no tonic serotonergic inhibition on the C-responses of dorsal horn neurons, and multiple 5-HT receptor subtypes including 1B, 2A, 2C, 3, and 4 may be involved in mediating the inhibitory effects of 5-HT.
Central 5-HT3 receptor-induced hypothermia in mice: interstrain differences and comparison with hypothermia mediated via 5-HT1A receptor
Neurosci Lett 2009 Nov 6;465(1):50-4.PMID:19735696DOI:10.1016/j.neulet.2009.09.005.
The selective agonist of serotonin 5-HT(3) receptor 1-\(3-Chlorophenyl\)biguanide hydrochloride (m-CPBG) administered intracerebroventricularly (40, 80 or 160 nmol) produced long-lasting dose-dependent hypothermic response in AKR/2J mice. m-CPBG (160 nmol i.c.v.) induced profound hypothermia (delta t=-4 degrees C) that lasted up to 7 h. m-CPBG (40 nmol i.c.v.)-induced hypothermia was attenuated by 5-HT(3) receptor antagonist ondansetron pretreatment. At the same time, intraperitoneal administration of m-CPBG in a wide range of doses (0.5, 1.0, 5.0 or 10.0 mg/kg) did not affect the body temperature. These findings indicate: (1) the implication of central, rather than peripheral 5-HT(3) receptor in the thermoregulation; (2) the inability of m-CPBG to cross blood-brain barrier in mice. The comparison of brain 5-HT(3)-induced hypothermic reaction in six inbred mouse strains (DBA/2J, CBA/Lac, C57BL/6, BALB/c, ICR, AKR/J) was performed and two highly sensitive to m-CPBG strains (CBA/Lac and C57BL/6) were found. In the same six mouse strains the functional activity of 5-HT(1A) receptor was studied. The comparison of hypothermic reactions produced by 5-HT(1A) receptor agonist 8-OH-DPAT (1.0 mg/kg i.p.) and m-CPBG revealed significant correlation between 5-HT(3) and 5-HT(1A)-induced hypothermia in five out of six investigated mouse strains. 5-HT(1A) receptor antagonist p-MPPI pretreatment (1 mg/kg i.p.) diminished hypothermia produced by centrally administered m-CPBG (40 nmol i.c.v.). The data suggest the cross-talk between 5-HT(1A) and 5-HT(3) receptors in the mechanism of 5-HT-related hypothermia.
Involvement of spinal serotonin receptors in the regulation of intraspinal acetylcholine release
Eur J Pharmacol 2005 Feb 21;509(2-3):127-34.PMID:15733547DOI:10.1016/j.ejphar.2004.12.017.
Stimulation of spinal serotonin (5-HT) receptors results in analgesia and release of acetylcholine. We investigated the involvement of 5-HT1, 5-HT2, and 5-HT3 receptor subtypes in the regulation of spinal acetylcholine release. A spinal microdialysis probe was placed dorsally at about the C5 level in anaesthetized rats. The selective serotonin reuptake inhibitor citalopram was found to increase acetylcholine release when infused via the microdialysis probe. Several doses of the 5-HT receptor agonists 8-hydroxy-2-(di-n-propylamino)tetraline (8-OH-DPAT, 5-HT1A), 1,4-dihydro-3-(1,2,3,6-tetrahydro-4-pyridinyl)-5H-pyrrolo[3,2-b]pyridin-5-one dihydrochloride (CP93129, 5-HT1B), alpha-methyl-5-hydroxytryptamine maleate (m5-HT, 5-HT2), 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI, 5-HT2C), and 1-(m-chlorophenyl)-biguanide (5-HT3) were subsequently infused via the microdialysis probe. Only 8-OH-DPAT, CP93129, and m5-HT increased acetylcholine release dose dependently. The 5-HT1A receptor selective antagonist (S)-N-tert-butyl-3-(4-(2-methoxyphenyl)piperazine-1-yl)-2-phenylpropanamide hydrochloride and the 5-HT2A receptor selective antagonist ketanserin tartrate inhibited the 8-OH-DPAT and the m5-HT induced acetylcholine release. The results suggest that 5-HT1A and the 5-HT2A receptors are involved in the regulation of acetylcholine release in the spinal cord.
Serotonin type 3 receptors stimulate offensive aggression in Syrian hamsters
Behav Brain Res 2005 Jan 6;156(1):19-29.PMID:15474647DOI:10.1016/j.bbr.2004.05.003.
Hamsters repeatedly exposed to cocaine during adolescence display high levels of offensive aggression compared to saline-treated littermates. The escalated offensive phenotype observed in adolescent cocaine-treated animals is modulated by serotonin (5-HT) signaling and can be suppressed by inhibiting 5-HT type 3 receptors, suggesting that these receptors might play an important role in the aggression-stimulating effects of adolescent cocaine exposure. The current study examined this hypothesis and extended earlier studies investigating the relationship between 5HT(3) receptor neural signaling and the offensive response patterns of aggressive, adolescent cocaine-treated animals compared to non-aggressive, saline-treated littermates. Adolescent cocaine-treated hamsters and saline-treated littermates were tested for offensive aggression after the administration of either the 5-HT(3) antagonist 3-tropanylindole-3-carboxylate methiodide (tropisetron) or the 5-HT(3) agonist 1-(m-chlorophenyl)-biguanide hydrochloride (mCPBG). Tropisetron significantly reduced the high levels of offensive responding observed in adolescent cocaine-treated animals, whereas treatment with the 5-HT(3) receptor agonist mCPBG failed to affect the escalated offensive response. Conversely, tropisetron failed to affect very low, baseline levels of aggressive responding seen in adolescent saline-treated animals, while 5-HT(3) receptor activation via mCPBG triggered highly escalated levels of offensive aggression in these animals. Together, these data support a stimulatory role for 5-HT(3) neural signaling in offensive aggression.
Serotonin-mediated modulation of Na+/K+ pump current in rat hippocampal CA1 pyramidal neurons
BMC Neurosci 2012 Jan 19;13:10.PMID:22257758DOI:10.1186/1471-2202-13-10.
Background: The aim of this study was to investigate whether serotonin (5-hydroxytryptamine, 5-HT) can modulate Na+/K+ pump in rat hippocampal CA1 pyramidal neurons. Results: 5-HT (0.1, 1 mM) showed Na+/K+ pump current (Ip) densities of 0.40 ± 0.04, 0.34 ± 0.03 pA/pF contrast to 0.63 ± 0.04 pA/pF of the control of 0.5 mM strophanthidin (Str), demonstrating 5-HT-induced inhibition of Ip in a dose-dependent manner in hippocampal CA1 pyramidal neurons. The effect was partly attenuated by ondasetron, a 5-HT3 receptor (5-HT3R) antagonist, not by WAY100635, a 5-HT1AR antagonist, while 1-(3-Chlorophenyl) biguanide hydrochloride (m-CPBG), a 5-HT3R specific agonist, mimicked the effect of 5-HT on Ip. Conclusion: 5-HT inhibits neuronal Na+/K+ pump activity via 5-HT3R in rat hippocampal CA1 pyramidal neurons. This discloses novel mechanisms for the function of 5-HT in learning and memory, which may be a useful target to benefit these patients with cognitive disorder.