2-methyl AP-237-d7 (hydrochloride)
(Synonyms: 2-methyl Buccinazine-d7) 目录号 : GC48735
An Analytical Reference Standard
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
2-methyl AP-237-d7 (hydrochloride) is an analytical reference standard intended for use as an internal standard for the quantification of 2-methyl AP-237 by GC- or LC-MS. 2-methyl AP-237 is categorized as an analgesic.1 This product is intended for research and forensic applications.
1.Furlan, D.Methyl-Piperazino derivatives with analgesic activity(1985)
| Cas No. | SDF | ||
| 别名 | 2-methyl Buccinazine-d7 | ||
| Canonical SMILES | O=C(N1CCN(C/C=C/C2=CC=CC=C2)CC1C)C([2H])([2H])C([2H])([2H])C([2H])([2H])[2H].Cl | ||
| 分子式 | C18H19D7N2O•HCl | 分子量 | 329.9 |
| 溶解度 | DMF: 10 mg/ml,DMSO: 15 mg/ml,Ethanol: 30 mg/ml,PBS (pH 7.2): 10 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 | 3.0312 mL | 15.1561 mL | 30.3122 mL |
| 5 mM | 0.6062 mL | 3.0312 mL | 6.0624 mL |
| 10 mM | 0.3031 mL | 1.5156 mL | 3.0312 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。
Imidazoline Receptor System: The Past, the Present, and the Future
Pharmacol Rev 2020 Jan;72(1):50-79.PMID:31819014DOI:10.1124/pr.118.016311.
Imidazoline receptors historically referred to a family of nonadrenergic binding sites that recognize compounds with an imidazoline moiety, although this has proven to be an oversimplification. For example, none of the proposed endogenous ligands for imidazoline receptors contain an imidazoline moiety but they are diverse in their chemical structure. Three receptor subtypes (I1, I2, and I3) have been proposed and the understanding of each has seen differing progress over the decades. I1 receptors partially mediate the central hypotensive effects of clonidine-like drugs. Moxonidine and rilmenidine have better therapeutic profiles (fewer side effects) than clonidine as antihypertensive drugs, thought to be due to their higher I1/α 2-adrenoceptor selectivity. Newer I1 receptor agonists such as LNP599 [3-chloro-2-methyl-phenyl)-(4-methyl-4,5-dihydro-3H-pyrrol-2-yl)-amine hydrochloride] have little to no activity on α 2-adrenoceptors and demonstrate promising therapeutic potential for hypertension and metabolic syndrome. I2 receptors associate with several distinct proteins, but the identities of these proteins remain elusive. I2 receptor agonists have demonstrated various centrally mediated effects including antinociception and neuroprotection. A new I2 receptor agonist, CR4056 [2-phenyl-6-(1H-imidazol-1yl) quinazoline], demonstrated clear analgesic activity in a recently completed phase II clinical trial and holds great promise as a novel I2 receptor-based first-in-class nonopioid analgesic. The understanding of I3 receptors is relatively limited. Existing data suggest that I3 receptors may represent a binding site at the Kir6.2-subtype ATP-sensitive potassium channels in pancreatic β-cells and may be involved in insulin secretion. Despite the elusive nature of their molecular identities, recent progress on drug discovery targeting imidazoline receptors (I1 and I2) demonstrates the exciting potential of these compounds to elicit neuroprotection and to treat various disorders such as hypertension, metabolic syndrome, and chronic pain.
Ventriculolumbar perfusion of 3-[(4-amino-2-methyl-5-pyrimidinyl)methyl]-1-(2-chloroethyl)-1-nitrosou rea hydrochloride
Neurosurgery 1993 Nov;33(5):817-23.PMID:8264878DOI:10.1227/00006123-199311000-00005.
We report on the toxicity, intrathecal pharmacokinetics, and therapeutic effect of the ventriculolumbar perfusion of 3-[(4-amino-2-methyl-5-pyrimidinyl)methyl]-1-(2-chloroethyl)-1-nitros our ea hydrochloride (ACNU) against the subarachnoid dissemination of primary central nervous system tumors. Fifteen patients received ventriculolumbar perfusion of ACNU. One was treated with ventriculolumbar perfusion of ACNU alone, and the others underwent concomitant systemic chemotherapy; three of these patients received irradiation as well. ACNU was administered at an initial dose of 0.5 and was increased to 1.5 to 10.0 mg in six patients. Because of a lack of Level 2 or greater toxicity, the subsequent seven patients received 8.7 to 10.0 mg of ACNU dissolved in artificial cerebrospinal fluid (CSF) at a concentration of 0.1 mg/ml, from the start of the treatment. During ACNU administration, the lumbar CSF was drained at approximately the same rate as that of the infusion. Twelve patients received from 3 to 42 courses (average, 14 courses). The cumulative dose of ACNU ranged from 5 to 330.4 mg (average, 82.9 mg). One patient had a convulsion; two patients experienced transient headache, nausea, and vomiting; two others reported transient headache, nausea, vomiting, and fecal incontinence; and one experienced transient nausea, vomiting, and fecal incontinence. No side effects were noted in the other nine patients. When 9.0 to 9.5 mg of ACNU, dissolved in 90 to 95 ml of artificial CSF, was administered for 37 to 52 min, the maximum concentration of ACNU in the lumbar CSF was 9.86 to 12.79 micrograms/ml and the area under the drug concentration-time curve was 260.8 to 502.5 micrograms.min/ml.(ABSTRACT TRUNCATED AT 250 WORDS)
2-Methyl-6-(phenylethynyl)pyridine hydrochloride Modulates Metabotropic Glutamate 5 Receptors Endogenously Expressed in Zebrafish Brain
ACS Chem Neurosci 2016 Dec 21;7(12):1690-1697.PMID:27635438DOI:10.1021/acschemneuro.6b00213.
Due to phylogenetic proximity to the human, zebrafish has been recognized as a reliable model to study Alzheimer's disease (AD) and other central nervous system disorders. Furthermore, metabotropic glutamate receptors have been previously reported to be impaired in brain from AD patients. Metabotropic glutamate 5 (mGlu5) receptors are G-protein coupled receptors proposed as potential targets for therapy of different neurodegenerative disorders. Thus, MPEP (2-methyl-6-(phenylethynyl)pyridine hydrochloride), a selective noncompetitive mGlu5 receptor antagonist, has been suggested for pharmacological treatment of AD. The aim of the present work was to quantify mGlu5 receptors in brain from zebrafish and to study the possible modulation of these receptors by MPEP treatment. To this end, radioligand binding assay and open field test were used. Results showed a slightly higher presence of mGlu5 receptors in brain from male than in that from female zebrafish. However, a significant increase of mGlu5 receptor in male without variation in female was observed after MPEP treatment. This gender specific response was also observed in locomotor behavior, being significantly decreased only in male zebrafish. These results confirm the presence of mGlu5 receptors in brain from zebrafish and their gender specific modulation by selective antagonist treatment and suggest a role of these receptors on locomotor activity, which is affected in many disorders. In addition, our data point to zebrafish as a useful model to study mGlu receptor function in both healthy and pathological conditions.
Tapentadol: an initial analysis
J Opioid Manag 2010 May-Jun;6(3):223-6.PMID:20642251DOI:10.5055/jom.2010.0020.
Tapentadol hydrochloride (17(-)-(1R,2R)-3-(3-dimethylamino-1-ethyl-2-methyl-propyl)-phenol) is a newly released analgesic that works at two levels: by acting as a p-opioid agonist and as a modulator of descending inhibitory pathways through its effects on neurotransmitters involved in these pathways. The theoretical advantage is the provision of synergistic analgesic activities, which may lessen the need for opioid escalation. The advantage is its potential as a possible new agent in neuropathic pain. Preclinical models confirm analgesic properties in acute pain and neuropathic pain models, but with less potency than morphine. Tapentadol has minimal CYP 450 interactions limiting potential for drug interactions. Human clinical trial data in nonmalignant pain suggest less potency than a step-3 opioid, and the drug remains to be tested in patients with cancer pain and neuropathic pain.
Identification of major urinary metabolites of ACNU, 3-[(4-amino-2-methyl-5-pyrimidinyl)methyl]-1-(2-chloroethyl)-1-nitroso urea hydrochloride in rats
J Pharmacobiodyn 1985 Jun;8(6):401-8.PMID:3863921DOI:10.1248/bpb1978.8.401.
Metabolites of 3-[(4-amino-2-methyl-5-pyrimidinyl)methyl]-1-(2-chloroethyl)-1- nitrosourea hydrochloride (ACNU) in rat urine were investigated. After intravenous administration of 14C-ACNU into rats, four major radioactive metabolites and two minor ones were detected in the urine by two-dimensional thin-layer chromatographic analysis. The main metabolite was identified to be an imidazolidinone compound, 1-[(4-amino-2-methyl-5-pyrimidinyl)methyl]-5-hydroxy-2-imidazolidinone (M-D). One of the other major metabolites was identified to be a nitrosated compound of the main metabolite i.e., 1-[(4-amino-2-methyl-5-pyrimidinyl)methyl]- 5-hydroxy-3-nitroso-2-imidazolidinone (M-C). These were new types of metabolites which have not been reported in the metabolic study of other chloroethylnitrosourea derivatives. Compared with authentic compounds, two metabolites were identified to be a denitrosated derivative of ACNU i.e., 1-[(4-amino-2-methyl-5-pyrimidinyl)methyl]-3-(2-chloroethyl)urea (M-B), and a cyclized pyrimidopyrimidine compound which lacks the ethylene moiety of ACNU, i.e., 3,4-dihydro-7-methylpyrimido[4,5-d]pyrimidin-2-(1H)-one (M-A). The two minor metabolites were supposed to be compounds derived from M-A. Discussions were made on mechanism of formation of these metabolites in vivo.