Flutoprazepam
(Synonyms: 氟托西泮) 目录号 : GC43694An Analytical Reference Standard
Cas No.:25967-29-7
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
Flutoprazepam is an analytical reference standard categorized as a benzodiazepine.[1] This product is intended for research and forensic applications.
Reference:
[1]. Lee, X.-P., Shouji, Y., Kumazawa, T., et al. Rapid and highly sensitive analysis of benzodiazepines and tandospirone in human plasma by automated on-line column-switching UFLC-MS/MS. Leg. Med. (Tokyo) 24, 36-55 (2017).
| Cas No. | 25967-29-7 | SDF | |
| 别名 | 氟托西泮 | ||
| 化学名 | 7-chloro-1-(cyclopropylmethyl)-5-(2-fluorophenyl)-1,3-dihydro-2H-1,4-benzodiazepin-2-one | ||
| Canonical SMILES | ClC1=CC(C(C2=CC=CC=C2F)=NC3)=C(C=C1)N(CC4CC4)C3=O | ||
| 分子式 | C19H16ClFN2O | 分子量 | 342.8 |
| 溶解度 | 25 mg/m in DMSO, 30 mg/m in DMF, 1 mg/m in Ethanol | 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 | 2.9172 mL | 14.5858 mL | 29.1715 mL |
| 5 mM | 0.5834 mL | 2.9172 mL | 5.8343 mL |
| 10 mM | 0.2917 mL | 1.4586 mL | 2.9172 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。
Muscle relaxants for pain management in rheumatoid arthritis
Cochrane Database Syst Rev 2012 Jan 18;1:CD008922.PMID:22258993DOI:10.1002/14651858.CD008922.pub2.
Background: Pain management is a high priority for patients with rheumatoid arthritis (RA). Muscle relaxants include drugs that reduce muscle spasm (for example benzodiazepines such as diazepam (Valium), alprazolam (Xanax), lorazepam (Ativan) and non-benzodiazepines such as metaxalone (Skelaxin) or a combination of paracetamol and orphenadrine (Muscol)) and drugs that prevent increased muscle tone (baclofen and dantrolene). Despite a paucity of evidence supporting their use, antispasmodic and antispasticity muscle relaxants have gained widespread clinical acceptance as adjuvants in the management of patients with chronic musculoskeletal pain. Objectives: The aim of this review was to determine the efficacy and safety of muscle relaxants in pain management in patients with RA. The muscle relaxants that were included in this review are the antispasmodic benzodiazepines (alprazolam, bromazepam, chlordiazepoxide,cinolazepam, clonazepam, cloxazolam, clorazepate, diazepam, estazolam, flunitrazepam, flurazepam, Flutoprazepam, halazepam, ketazolam, loprazolam, lorazepam, lormetazepam, medazepam, midazolam, nimetazepam, nitrazepam, nordazepam, oxazepam, pinazepam, prazepam, quazepam, temazepam, tetrazepam, triazolam), antispasmodic non-benzodiazepines (cyclobenzaprine, carisoprodol, chlorzoxazone, meprobamate, methocarbamol, metaxalone, orphenadrine, tizanidine and zopiclone), and antispasticity drugs (baclofen and dantrolene sodium). Search methods: We performed a search of the Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library, 4th quarter 2010), MEDLINE (1950 to week 1 November 2010), EMBASE (Week 44 2010), and PsycINFO (1806 to week 2 November 2010). We also searched the 2008 to 2009 American College of Rheumatology (ACR) and European League Against Rheumatism (EULAR) abstracts and performed a handsearch of reference lists of relevant articles. Selection criteria: We included randomised controlled trials which compared a muscle relaxant to another therapy (active, including non-pharmacological therapies, or placebo) in adult patients with RA and that reported at least one clinically relevant outcome. Data collection and analysis: Two blinded review authors independently extracted data and assessed the risk of bias in the trials. Meta-analyses were used to examine the efficacy of muscle relaxants on pain, depression, sleep and function, as well as their safety. Main results: Six trials (126 participants) were included in this review. All trials were rated at high risk of bias. Five cross-over trials evaluated a benzodiazepine, four assessed diazepam (n = 71) and one assessed triazolam (n = 15). The sixth trial assessed zopiclone (a non-benzodiazepine) (n = 40) and was a parallel group study. No trial duration was longer than two weeks while three single dose trials assessed outcomes at 24 hours only. Overall the included trials failed to find evidence of a beneficial effect of muscle relaxants over placebo, alone (at 24 hrs, 1 or 2 weeks) or in addition to non-steroidal anti-inflammatory drugs (NSAIDs) (at 24 hrs), on pain intensity, function, or quality of life. Data from two trials of longer than 24 hours duration (n = 74) (diazepam and zopiclone) found that participants who received a muscle relaxant had significantly more adverse events compared with those who received placebo (number needed to harm (NNTH) 3, 95% CI 2 to 7). These were predominantly central nervous system side effects, including dizziness and drowsiness (NNTH 3, 95% CI 2 to 11). Authors' conclusions: Based upon the currently available evidence in patients with RA, benzodiazepines (diazepam and triazolam) do not appear to be beneficial in improving pain over 24 hours or one week. The non-benzodiazepine agent zopiclone also did not significantly reduce pain over two weeks. However, even short term muscle relaxant use (24 hours to 2 weeks) is associated with significant adverse events, predominantly drowsiness and dizziness.
Pharmacokinetics of Flutoprazepam, a novel benzodiazepine drug, in normal subjects
Eur J Drug Metab Pharmacokinet 1989 Oct-Dec;14(4):293-8.PMID:2633923DOI:10.1007/BF03190114.
The single dose pharmacokinetics of Flutoprazepam and its active N-desalkyl metabolite were determined in 8 normal subjects by using newly developed, highly sensitive, GC-MS and HPLC techniques. Following a 2 mg dose of the drug, the concentrations of unchanged Flutoprazepam in serum were extremely low (below 5 ng/ml at 2 h) and declined rapidly to undetectable levels within 6-9 h after dosing. At all sampling times, the serum concentration of the N-dealkylated metabolite (N-desalkylflurazepam) was much greater than that of the parent compound. This metabolite appeared in serum rapidly (within 2 h), reached a peak between 2 and 12 h and declined slowly, with an elimination half-life of about 90 h on average. The serum concentration of two additional putative metabolites (3-hydroxy-flutoprazepam and N-desalkyl-3-hydroxy-flutoprazepam) was below the limit of detection (2 ng/ml) in all samples. Mild CNS effects (documented by prolonged choice reaction time) were present at 2 and 4 h but were no longer detectable at 9 h. It is suggested that unchanged Flutoprazepam is unlikely to contribute significantly to clinical effects and that the drug exerts its therapeutic activity through conversion to the slowly eliminated N-desalkyl metabolite.
In vitro and ex vivo inhibition by Flutoprazepam of [3H]flunitrazepam binding to mouse brain receptors
Arch Int Pharmacodyn Ther 1984 Jun;269(2):180-6.PMID:6148044doi
The ability of Flutoprazepam, a new antianxiety drug of the benzodiazepine class, to inhibit [3H]flunitrazepam binding to mouse brain receptors was investigated in vitro and ex vivo (measurement of [3H]flunitrazepam binding in vitro after in vivo treatment of animals with unlabelled drugs). The Ki values for [3H]flunitrazepam binding in vitro were as follows: Flutoprazepam (13.0 nM), diazepam (2.7 nM), nitrazepam (5.3 nM), prazepam (68.5 nM) and chlordiazepoxide (234 nM). Two metabolites of Flutoprazepam, N-desalkyl-flutoprazepam (Ki = 3.1 nM) also inhibited [3H]flunitrazepam binding in vitro with higher potencies than that of Flutoprazepam. Flutoprazepam was found to be more active in inhibiting [3H]flunitrazepam binding ex vivo and in preventing pentetrazol convulsions than predicted from Ki values. The ID50 values for inhibiting [3H]flunitrazepam binding ex vivo were 0.32 mg/kg, p.o. (Flutoprazepam), 0.89 mg/kg, p.o. (diazepam), 0.94 mg/kg, p.o. (nitrazepam), 1.98 mg/kg, p.o. (prazepam) and 23.3 mg/kg, p.o. (chlordiazepoxide), respectively. The correlation between ID50 values ex vivo and ED50 values for preventing pentetrazol convulsions was highly significant (r = 0.929). These results suggest that Flutoprazepam can exert its pharmacological activities by itself and that two metabolites also play an important role in the effects of Flutoprazepam in vivo.
Propranolol does not alter Flutoprazepam kinetics and metabolism in the rat
Eur J Drug Metab Pharmacokinet 1991 Jan-Mar;16(1):53-8.PMID:1936062DOI:10.1007/BF03189875.
The influence of propranolol on the disposition of Flutoprazepam, a benzodiazepine derivative extensively biotransformed by hepatic microsomal oxidation, was evaluated in the rat. Propranolol was infused subcutaneously with osmotic minipumps (5 mg/day) to obtain steady-state concentrations of about 200 ng/ml. Flutoprazepam (5 mg/kg) was given intraperitoneally on the third day of propranolol infusion. There was some variability in Flutoprazepam disposition, consistent with the concept of an extensive first-pass metabolism of high-extraction drugs. Propranolol had no significant effects on the kinetics of Flutoprazepam or norflutoprazepam, an active metabolite possibly accounting for a substantial part of the parent compound's pharmacological and clinical effects. It was concluded that there is no evidence of any pharmacokinetic interaction between this beta-adrenoceptor blocker and Flutoprazepam in the rat.
Effect of Flutoprazepam on skills essential for driving motor vehicles
Arzneimittelforschung 1990 May;40(5):533-5.PMID:1974429doi
The effects of the 1,4-benzodiazepine derivative Flutoprazepam on the skills essential for driving motor vehicles were tested 2.5 h after intake of 1 x 2 mg and 1 x 4 mg, comparing with placebo. 18 healthy subjects who had homogeneous results in psychological/physical tests took part in the study. The study had a double-blind, randomized crossover design with 7-day washout periods. 2.5 h after intake of 4 mg Flutoprazepam, the ability to drive was impaired. Only a very slight reduction in skill was found at the same time under the influence of 2 mg of the drug.