3-Acetylmorphine
(Synonyms: 3-MAM, O3-Monoacetylmorphine) 目录号 : GC40875
An Analytical Reference Standard
Cas No.:5140-28-3
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
3-Acetylmorphine (3-MAM) is a less active metabolite of heroin compared to the more active 6-MAM and morphine . 3-MAM has relatively weak affinity for µ-opioid receptors due to the placement of the acetyl group in the 3 position. This product is intended only for forensic and research purposes.
| Cas No. | 5140-28-3 | SDF | |
| 别名 | 3-MAM, O3-Monoacetylmorphine | ||
| Canonical SMILES | O[C@@H](C=C[C@@]1([H])[C@H]2CC3=CC=C4OC(C)=O)[C@@]5([H])[C@]1(CCN2C)C3=C4O5 | ||
| 分子式 | C19H21NO4 | 分子量 | 327.4 |
| 溶解度 | DMF: 20 mg/ml,DMF:PBS(pH 7.2)(1:1): 0.5 mg/ml,DMSO: 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 | 3.0544 mL | 15.2718 mL | 30.5437 mL |
| 5 mM | 0.6109 mL | 3.0544 mL | 6.1087 mL |
| 10 mM | 0.3054 mL | 1.5272 mL | 3.0544 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。
Site- and species-specific hydrolysis rates of heroin
Eur J Pharm Sci 2016 Jun 30;89:105-14.PMID:27130543DOI:10.1016/j.ejps.2016.04.028.
The hydroxide-catalyzed non-enzymatic, simultaneous and consecutive hydrolyses of diacetylmorphine (DAM, heroin) are quantified in terms of 10 site- and species-specific rate constants in connection with also 10 site- and species-specific acid-base equilibrium constants, comprising all the 12 coexisting species in solution. This characterization involves the major and minor decomposition pathways via 6-acetylmorphine and 3-Acetylmorphine, respectively, and morphine, the final product. Hydrolysis has been found to be 18-120 times faster at site 3 than at site 6, depending on the status of the amino group and the rest of the molecule. Nitrogen protonation accelerates the hydrolysis 5-6 times at site 3 and slightly less at site 6. Hydrolysis rate constants are interpreted in terms of intramolecular inductive effects and the concomitant local electron densities. Hydrolysis fraction, a new physico-chemical parameter is introduced and determined to quantify the contribution of the individual microspecies to the overall hydrolysis. Hydrolysis fractions are depicted as a function of pH.
Determination of Morphine in Human Urine by the Novel Competitive Fluorescence Immunoassay
J Anal Methods Chem 2019 Feb 3;2019:7826090.PMID:30863655DOI:10.1155/2019/7826090.
A competitive fluorescence immunoassay for the identification and quantification of morphine has been developed on the basis of hapten-coated plate format. Hapten was prepared through covalent conjugating a morphine derivative with albumin bovine. In the immunoassay, the hapten was inoculated on a 96-well plate and then bound with monoclonal antibodies labeled with a signal indicating dye, fluorescein isothiocyanate (FITC). Unbound FITC-antibodies were rinsed off from the plate. The fluorescein intensity decreases in the presence of morphine molecules due to the competitively binding to antibodies against hapten. The intensity is inversely correlated with the concentration of morphine. In quantitative analysis for urine samples, we obtained a linearity range of 0.2 μg/mL∼2.5 μg/mL, along with a detection limit of c.a. 1 ng/mL. The fluorescence immunoassay shows low cross-reactivity (below 10%) to 6-acetylmorphine, 3-Acetylmorphine, and heroine. The developed method produced comparable results to the standard GC-MS/MS method. In conclusion, a rapid and efficient screening tool for morphine in clinical human urine has been established.
Distinct pharmacological properties of morphine metabolites at G(i)-protein and β-arrestin signaling pathways activated by the human μ-opioid receptor
Biochem Pharmacol 2011 May 15;81(10):1248-54.PMID:21396918DOI:10.1016/j.bcp.2011.03.001.
Morphine and several other opioids are important drugs for the treatment of acute and chronic pain. Opioid-induced analgesia is predominantly mediated by the μ-opioid receptor (MOR). When administered to humans, complex metabolic pathways lead to generation of many metabolites, nine of which may be considered major metabolites. While the properties of the two main compounds, morphine-6-glucuronide and morphine-3-glucuronide, are well described, the activity of other morphine metabolites is largely unknown. Here we performed an extensive pharmacological characterization by comparing efficacies and potencies of morphine and its nine major metabolites for the two main signaling pathways engaged by the human MOR, which occur via G(i)-protein activation and β-arrestins, respectively. We used radioligand binding studies and FRET-based methods to monitor MOR-mediated G(i)-protein activation and β-arrestin recruitment in single intact 293T cells. This approach identified two major groups of morphine metabolites, which we classified into "strong" and "weak" receptor ligands. Strong partial agonists morphine, morphine-6-glucuronide, normorphine, morphine-6-sulfate, 6-acetylmorphine and 3-Acetylmorphine showed efficacies in the nanomolar range, while the weak metabolites morphine-N-oxide, morphine-3-sulfate, morphine-3-glucuronide and pseudomorphine activated MOR pathways only in the micromolar range. Interestingly, three metabolites, normorphine, 6-acetylmorphine and morphine-6-glucuronide, had lower potencies for Gi-protein activation but higher potencies and efficacies for β-arrestin recruitment than morphine itself, suggesting that they are biased towards β-arrestin pathways.
Differential influence of N-dealkylation on the stimulus properties of some opioid agonists
J Pharmacol Exp Ther 1992 Apr;261(1):278-84.PMID:1313871doi
The capacity of several opioid agonists and their N-dealkylated derivatives (normetabolites) to substitute for the discriminative and reinforcing stimulus properties of codeine was evaluated in rhesus monkeys, and the affinity of these compounds in binding to mu receptors in rhesus monkey brain membranes was determined. Heroin (0.1 mg/kg), 6-acetylmorphine (0.1 mg/kg), methadone (0.6 mg/kg), 3-Acetylmorphine (1 mg/kg), morphine (1 mg/kg) and codeine (1.8 mg/kg) substituted for the codeine cue, but the normetabolites of heroin, 6-acetylmorphine, morphine and codeine did not (up to 10 mg/kg). l-alpha-Acetylmethadol (3 mg/kg) and its mono (0.1 mg/kg) and double (0.6 mg/kg) N-dealkylated derivatives all substituted. In self administration, subjects responded for morphine (0.1 mg/kg/injection) and codeine (0.3 mg/kg/injection), but not for norcodeine (up to 1 mg/kg/injection) or normophine (up to 3 mg/kg/injection). l-alpha-Acetylmethadol (up to 0.3 mg/kg/injection) did not maintain responding, but its mono (0.1 mg/kg/injection) and double (0.1 mg/kg/injection) normetabolites did. In receptor binding, the normetabolites of morphine and 6-acetylmorphine were less potent than their parent agonists in displacing [3H]Tyr-D-Ala-Gly-(Me)Phe-Gly-ol, but the normetabolites of l-alpha-acetylmethadol had greater affinity than their parent. Codeine and norcodeine were inactive in binding. If l-alpha-acetylmethadol is converted only slowly to its active normetabolites, this may explain the lack of efficacy found with this compound in the self administration procedure.