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Dextrorphan (tartrate) Sale

(Synonyms: 去甲右美沙芬酒石酸盐,d-3-hydroxy-N-Methylmorphinan tartrate) 目录号 : GC18213

An Analytical Reference Material

Dextrorphan (tartrate) Chemical Structure

Cas No.:143-98-6

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Sample solution is provided at 25 µL, 10mM.

产品文档

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实验参考方法

Animal experiment [2]:

Animal models

Rat

Preparation Method

Slow i.v. injection of 4-6 mg/kg of dextrorphan (tartrate)

Dosage form

Intravenous injection, 4-6 mg/kg

Applications

I.v. injection of 4-6 mg/kg of dextrorphan (tartrate) resulted in a selective reduction of NMA-induced excitation similar to that seen during the local administration of the drug by electrophoresis.

References:

[1]: J.D. Church, D. Lodge, S.C. Berry.Differential effects of dextrorphan and levorphanol on the excitation of rat spinal neurons by amino acids.Eur J Pharmacol, 111 (1985), pp. 185-190

产品描述

Dextrorphan (tartrate) is a phencyclidine-like metabolite of dextromethorphan, kwoun as an antitussive in cough medicines [1]. Dextrorphan (tartrate) is a noncompetitive N-methyl-d-aspartate (NMDA) antagonist that is neuroprotective in experimental models of focal brain ischemia [2]. Dextrorphan (tartrate) concentrations producing IC50 of K+-stimulated 45Ca 2+ uptake into brain synaptosomes was 200±27μM [3].

Dextrorphan (tartrate) inhibit excitatory amino acid (EAA) evoked neuronal responses 3, apparently by acting at a site on the NMDA-preferring EAA receptor or its associated Ca 2+ channel. Dextromethorphan and dextrorphan (tartrate) protect neurons from EAA-induced cytotoxicity [3].

In dextrorphan-treated patients, transient and reversible adverse effects, including nystagmus, nausea, vomiting, somnolence, hallucinations, and agitation, commonly occurred. Loading-dose escalation was stopped because of rapid-onset, reversible, symptomatic hypotension in 7 of 21 patients treated with doses of 200 to 260 mg/h. Maximum plasma levels of 750 to 1000 ng/mL were obtained in 9 patients [2].

References:
[1]. Shin, E.J., Lee, P.H., Kim, H.J., et al. Neuropsychotoxicity of abused drugs: Potential of dextromethorphan and novel neuroprotective analogs of dextromethorphan with improved safety profiles in terms of abuse and neuroprotective effects. Journal of Pharmacological Sciences 106(1), 22-27 (2008).
[2]. Albers GW, Atkinson RP, Kelley RE, Rosenbaum DM; Dextrorphan Study Group. Safety, tolerability, and pharmacokinetics of the N-methyl-d-aspartate antagonist dextrorphan in patients with acute stroke.Stroke. 1995; 26:254-258.
[3]. Carpenter CL, Marks SS, Watson DL, Greenberg DA. Dextromethorphan and dextrorphan as calcium channel antagonists. Brain Res.1988; 439:372-375.

右啡烷(酒石酸盐)是右美沙芬的苯环利定样代谢物,在止咳药中用作镇咳剂 [1]。右啡烷(酒石酸盐)是一种非竞争性 N-甲基-d-天冬氨酸 (NMDA) 拮抗剂,在局灶性脑缺血的实验模型中具有神经保护作用[2]。产生 K+- 刺激 45Ca 2+ 摄入脑突触体的 IC50 的右啡烷(酒石酸盐)浓度为 200±27μM [3]

右啡烷(酒石酸盐)抑制兴奋性氨基酸 (EAA) 诱发的神经元反应 3,显然是通过作用于偏好 NMDA 的 EAA 受体或其相关 Ca 2+ 通道上的一个位点。右美沙芬和右啡烷(酒石酸盐)保护神经元免受 EAA 诱导的细胞毒性[3]

在接受右啡烷治疗的患者中,通常会发生短暂和可逆的不良反应,包括眼球震颤、恶心、呕吐、嗜睡、幻觉和激越。在接受 200 至 260 mg/h 剂量治疗的 21 名患者中,有 7 名因快速发作、可逆、有症状的低血压而停止负荷剂量增加。 9 名患者[2] 的最大血浆浓度为 750 至 1000 ng/mL。

Chemical Properties

Cas No. 143-98-6 SDF
别名 去甲右美沙芬酒石酸盐,d-3-hydroxy-N-Methylmorphinan tartrate
化学名 (9α,13α,14α)-17-methyl-morphinan-3-ol 2R,3R-dihydroxybutanedioate
Canonical SMILES CN1[C@@H]2[C@@]3([H])CCCC[C@@]3(CC1)C4=CC(O)=CC=C4C2.O[C@H]([C@@H](O)C(O)=O)C(O)=O
分子式 C17H23NO.C4H6O6 分子量 407.5
溶解度 20mg/mL in DMSO, 10mg/mL in DMF 储存条件 Store at -20°C
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1 mM 2.454 mL 12.2699 mL 24.5399 mL
5 mM 0.4908 mL 2.454 mL 4.908 mL
10 mM 0.2454 mL 1.227 mL 2.454 mL
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Research Update

Dextrorphan binds to opioid receptors in guinea-pig brain membranes and is an antagonist at opioid receptors in myenteric plexus

Dextrorphan (+)-tartrate, purified by repeated crystallization to remove all traces of the enantiomer levorphanol, binds to mu, delta, and kappa sites on guinea-pig brain membranes with lower affinities (by a factor of 400-3200) than levorphanol. In the guinea-pig ileum myenteric plexus longitudinal muscle preparation (GPI), dextrorphan, at 100-200 microM, inhibits the electrically stimulated twitch, but this action is not blocked or reversed by naloxone; both (+)- and (-)-naloxone produce similar non-opioid twitch inhibition at comparable concentrations. At 10-20 microM, dextrorphan blocks and reverses the twitch inhibition due to mu and kappa agonists, but the blockade can be overcome only partially by increasing the agonist concentration. We conclude that dextrorphan is an opioid ligand with low affinity and with antagonist effect on opioid receptors in the GPI.

Identification of Additional Anti-Persister Activity against Borrelia burgdorferi from an FDA Drug Library

Lyme disease is a leading vector-borne disease in the United States. Although the majority of Lyme patients can be cured with standard 2-4 week antibiotic treatment, 10%-20% of patients continue to suffer from prolonged post-treatment Lyme disease syndrome (PTLDS). While the cause for this is unclear, persisting organisms not killed by current Lyme antibiotics may be involved. In our previous study, we screened an FDA drug library and reported 27 top hits that showed high activity against Borrelia persisters. In this study, we present the results of an additional 113 active hits that have higher activity against the stationary phase B. burgdorferi than the currently used Lyme antibiotics. Many antimicrobial agents (antibiotics, antivirals, antifungals, anthelmintics or antiparasitics) used for treating other infections were found to have better activity than the current Lyme antibiotics. These include antibacterials such as rifamycins (3-formal-rifamycin, rifaximin, rifamycin SV), thiostrepton, quinolone drugs (sarafloxacin, clinafloxacin, tosufloxacin), and cell wall inhibitors carbenicillin, tazobactam, aztreonam; antifungal agents such as fluconazole, mepartricin, bifonazole, climbazole, oxiconazole, nystatin; antiviral agents zanamivir, nevirapine, tilorone; antimalarial agents artemisinin, methylene blue, and quidaldine blue; antihelmintic and antiparasitic agents toltrazuril, tartar emetic, potassium antimonyl tartrate trihydrate, oxantel, closantel, hycanthone, pyrimethamine, and tetramisole. Interestingly, drugs used for treating other non-infectious conditions including verteporfin, oltipraz, pyroglutamic acid, pidolic acid, and dextrorphan tartrate, that act on the glutathione/γ-glutamyl pathway involved in protection against free radical damage, and also the antidepressant drug indatraline, were found to have high activity against stationary phase B. burgdorferi. Among the active hits, agents that affect cell membranes, energy production, and reactive oxygen species production are more active against the B. burgdorferi persisters than the commonly used antibiotics that inhibit macromolecule biosynthesis. Future studies are needed to evaluate and optimize the promising active hits in drug combination studies in vitro and also in vivo in animal models. These studies may have implications for developing more effective treatments of Lyme disease.

Drug reinforcement studied by the use of place conditioning in rat

Rats display a preference for an environment in which they previously received morphine. The present report provides behavioral and pharmacological data for this simple model of reinforcement produced by opiates and describes an aversion in rats for an environment in which they previously received naloxone. Preferences were produced with intravenous (i.v.) morphine sulfate at doses of 0.08-15 mg/kg and durations of the pairing between environment and morphine of 10 min to 1.5 h. Preferences were also seen with other opiate agonists (etorphine-HCl and levorphanol-tartrate), another route of drug administration (subcutaneous), and after 1-4 administrations of morphine. Cocaine-HCl (i.v.), a non-narcotic drug, known to be self-administered by humans, also produced a place preference. Lithium chloride (i.v.), an agent found to be a punishing stimulus in other situations, produced a place aversion. There was no appreciable preference for an environment paired with dextrorphan-tartrate and naloxone-HCl (2 mg/kg, i.p.) blocked the production of the preference produced by i.v. morphine. In contrast to the effect produced by morphine, aversions were produced with (-)-naloxone-HCl alone at doses of 0.1-45 mg/kg (i.v.). The aversion was not produced at (+)-naloxone. Implantation of rats with a 75 mg morphine pellet 3 days prior to place conditioning potentiated the aversive effect of naloxone. It was concluded that place conditioning produced by morphine and naloxone is mediated by specific opiate receptors and that stimulating and decreasing activity of the endogenous opioid peptide system with systemically administered drugs is positively reinforcing and aversive, respectively. The discussion emphasizes application of the simple and sensitive place conditioning model to drug reinforcement research, including analyses of reinforcement produced by microinjection of opiates into the brain.

Pharmacology of the allodynia in rats evoked by high dose intrathecal morphine

Morphine sulfate in doses of 90 to 150 micrograms/3 microliters evoke a prominent behavioral syndrome characterized by 1) periodic bouts of spontaneous agitation during which the rat scratches and bites at the skin of the caudal dermatomes and 2) vigorous agitation, vocalization and coordinated efforts to bite and escape evoked by a light tactile stimulus applied to the flank, suggestive of a pain state (allodynia). The phenomenon is not reversed by naltrexone or is it subject to tolerance. The ordering of activity of an opioid alkaloid related agent in producing this touch-evoked agitation is: noroxymorphone-3-glucuronide, morphine-3-glucuronide, morphine-3-ethereal sulfate, dihydromorphine, noroxymorphone dihydrate, hydromorphone, dihydrocodeine tartrate, morphine sulfate, dihydroisomorphine, morphine-HCl, 6-acetylmorphine, N-normorphine-HCl and (+)-morphine. The following agents were essentially without effect at the highest doses examined: 3,6-diacetylmorphine, N-normeperidine-HCl, nalorphine-HCl, alfentanil, sufentanil, naloxone, naltrexone, methadone, dextrorphan tartrate, meperidine-HCl, oxycodone, levorphanol, oxymorphone, codeine phosphate, thebaine, nalbuphine and naltrexone-3-glucuronide. The observations that the sulfated and conjugated metabolites are 10 to 50 times more potent than their unmetabolized precursor suggest the possibility that, in high concentrations certain phenanthrene opioid alkaloids with a free 3-OH position, an ether bridge and no N-methyl extension will be subject to conjugation and this metabolite will alter the processing of otherwise innocuous tactile stimuli. The fact that the phenomenon appeared at least partially stereospecific may reflect upon the fact that other laboratories have shown that glucuronyl transferase may preferentially convert (-)-morphine to the 3-glucuronide and (+)-morphine to the 6-glucuronide which may be less active.(ABSTRACT TRUNCATED AT 250 WORDS)

A sensitive assay of metoprolol and its major metabolite alpha-hydroxy metoprolol in human plasma and determination of dextromethorphan and its metabolite dextrorphan in urine with high performance liquid chromatography and fluorometric detection

A reverse-phase High Performance Liquid Chromatographic (HPLC) method was developed for the analysis of metoprolol in the large number of human plasma samples obtained in in vitro-in vivo correlations (IVIVC) and bioavailability studies of extended release formulations of metoprolol tartrate. The metabolite, alpha-hydroxy metoprolol (OH-met), could also be quantified. The analytes were extracted from the plasma using solid phase columns, separated on a C-4 analytical column followed by fluorimetric detection. The linearity, precision, accuracy, stability, selectivity and ruggedness were validated for the concentration ranges of 1-400 ng ml-1 for metoprolol and 0.5-200 ng ml-1 for OH-met. The same chromatographic conditions were slightly modified to quantify dextromethorphan and its metabolite dextrorphan in urine in the concentration range 0.052-0.05 microgram ml-1 as a method for screening for fast metabolizers.