Azelastine-13C-d3 (hydrochloride)
(Synonyms: 盐酸氮卓斯汀 13C-d3 (盐酸盐)) 目录号 : GC49057An internal standard for the quantification of azelastine
Sample solution is provided at 25 µL, 10mM.
Quality Control & SDS
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- Purity: >99.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Azelastine-13C-d3 is intended for use as an internal standard for the quantification of azelastine by GC- or LC-MS. Azelastine is a histamine H1 receptor antagonist (Ki = 1.26 nM in bovine cerebral cortex membranes).1 It is selective for histamine H1 over histamine H3 receptors (Ki = 158.49 nM), as well as α1A- and α1B-adrenergic receptors (Ki = 50.12 nM for both). Azelastine (0.14 µg/animal) reduces nose rubbing, sneezing, and nasal mucosa expression of IL-4 in a dust mite-induced mouse model of allergic rhinitis.2 It also reduces infection by a lentivirus pseudotyped with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spike glycoprotein, also known as the surface glycoprotein, in HEK293 cells expressing angiotensin-converting enzyme 2 (ACE2) when used at a concentration of 7 µg/ml.3 Formulations containing azelastine have been used in the treatment of seasonal allergic rhinitis and vasomotor rhinitis.
1.Procopiou, P.A., Browning, C., Buckley, J.M., et al.The discovery of phthalazinone-based human H1 and H3 single-ligand antagonists suitable for intranasal administration for the treatment of allergic rhinitisJ. Med. Chem.54(7)2183-2195(2011) 2.Sun, S., Dean, R., Jia, Q., et al.Discovery of XEN445: A potent and selective endothelial lipase inhibitor raises plasma HDL-cholesterol concentration in miceBioorg. Med. Chem.21(24)7724-7734(2013) 3.Reznikov, L.R., Norris, M.H., Vashisht, R., et al.Identification of antiviral antihistamines for COVID-19 repurposingBiochem. Biophys. Res. Commun.538173-179(2021)
Cas No. | N/A | SDF | |
别名 | 盐酸氮卓斯汀 13C-d3 (盐酸盐) | ||
Canonical SMILES | O=C1N(C2CCCN([13C]([2H])([2H])[2H])CC2)N=C(CC3=CC=C(Cl)C=C3)C4=CC=CC=C41.Cl | ||
分子式 | C21[13C]H21ClD3N3O·HCl | 分子量 | 422.4 |
溶解度 | DMSO: soluble,Methanol: soluble | 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。 |
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1 mg | 5 mg | 10 mg | |
1 mM | 2.3674 mL | 11.8371 mL | 23.6742 mL |
5 mM | 0.4735 mL | 2.3674 mL | 4.7348 mL |
10 mM | 0.2367 mL | 1.1837 mL | 2.3674 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 | |||
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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,
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。
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Antiparasitic activities of new lawsone Mannich bases
Arch Pharm (Weinheim) 2019 Nov;352(11):e1900128.PMID:31536649DOI:10.1002/ardp.201900128.
A series of new lawsone Mannich bases derived from salicylaldehydes or nitrofurfural were prepared and tested for their activities against Leishmania major, Toxoplasma gondii, and Trypanosoma brucei brucei parasites. The hydrochloride salts 5a and 6a of the Mannich bases 2a and 3a, derived from unsubstituted salicylaldehyde and long-chained alkyl amines, were selectively and strongly active against T. gondii cells and appear to be new promising drug candidates against this parasite. Compound 6a showed an even higher activity against T. gondii than the known lawsone Mannich base 1b. Compound 4a, derived from salicylaldehyde and 2-methylaminopyridine, was also distinctly active against T. gondii cells. The derivatives 3a (salicyl derivative), 3b (3,5-dichloro-2-hydroxyphenyl derivative), and 3d (5-nitrofuranyl derivative) as well as the hydrochlorides 6a and 6b were also efficacious against T. b. brucei cells with compounds 3a and 3b being more selective for T. b. brucei over Vero cells when compared with the known control compound 1b. The derivatives 5a, 5c, 6a, and 6c proved to be up to five times more active than 1b against L. major promastigotes and up to four times more efficacious against L. major amastigotes.
[Synthesis of 14C-azelastine hydrochloride]
Arzneimittelforschung 1983;33(11):1515-6.PMID:6686443doi
The synthesis of 4-(p-Chlorobenzyl)-2-(hexahydro-1-methyl-1H-azepin-4-yl)-1(2H)-phthalazinone hydrochloride (14C-azelastine hydrochloride, Asta A 5610) is described Starting material was 14C-phthalic anhydride.
Iodine-Catalyzed Diazenylation with Arylhydrazine Hydrochlorides in Air
J Org Chem 2018 Apr 6;83(7):3537-3546.PMID:29486127DOI:10.1021/acs.joc.7b03149.
A mild approach to diazenylation of active methylene compounds and N-heterocyclic compounds with arylhydrazine hydrochlorides in the presence of iodine under basic aerobic conditions was developed. The reaction could be executed either under heating or in the presence of blue LED light, though the latter condition was found to be relatively efficient. Presumably, the aryldiazene produced by oxidation of arylhydrazine hydrochloride acts as a nitrogen scavenger of the radical intermediate generated from the active methylene compound in the presence of iodine to produce the diazo compounds. The scope and limitations of the protocol are presented.
Green Formation of Novel Pyridinyltriazole-Salicylidene Schiff Bases
Curr Org Synth 2019;16(2):309-313.PMID:31975681DOI:10.2174/1570179416666181207145951.
Aim and objective: In this work, water was used as solvent for the eco-friendly synthesis of imines under microwave irradiation. In the first step of the study, 5-pyridinyl-3-amino-1,2,4-triazole hydrochlorides were synthesized in the reaction of amino guanidine hydrochloride with different pyridine carboxylic acids under acid catalysis. A green method for 5-pyridinyl-3-amino-1,2,4-triazoles was developed with the assistance of microwave synthesis. In the second step, the eco-friendly synthesis of imines was achieved by reacting 5- pyridinyl-2H-1,2,4-triazol-3-amine hydrochlorides with salicylic aldehyde derivatives to produce 2-(5- pyridinyl-2H-1,2,4-triazol-3-ylimino)methyl)phenol imines. Materials and methods: Microwave experiments were done using a monomode Anton Paar Monowave 300 microwave reactor (2.45 GHz). Reaction temperatures were monitored by an IR sensor. Microwave experiments were carried out in sealed microwave process vials G10 with maximum reaction volume of 10 mL. Results: When alternative methods were used, it was impossible to obtain good yields from ethanol. Nevertheless, the use of water was successful for this reaction. After 1-h microwave irritation, a yellow solid was obtained in 82% yield. Conclusion: In this work an eco-friendly protocol for the synthesis of Schiff bases from 5-(pyridin-2-, 3- or 4- yl)-3-amino-1,2,4-triazoles and substituted salicylic aldehydes in water under microwave irradiation was developed. Under the found conditions the high yields for the products were achieved at short reaction time and with an easy isolation procedure.
Nalfurafine hydrochloride, a κ-Opioid Receptor Agonist, Induces Melanophagy via PKA Inhibition in B16F1 Cells
Cells 2022 Dec 29;12(1):146.PMID:36611940DOI:10.3390/cells12010146.
Selective autophagy controls cellular homeostasis by degrading unnecessary or damaged cellular components. Melanosomes are specialized organelles that regulate the biogenesis, storage, and transport of melanin in melanocytes. However, the mechanisms underlying melanosomal autophagy, known as the melanophagy pathway, are poorly understood. To better understand the mechanism of melanophagy, we screened an endocrine-hormone chemical library and identified nalfurafine hydrochlorides, a κ-opioid receptor agonist, as a potent inducer of melanophagy. Treatment with nalfurafine hydrochloride increased autophagy and reduced melanin content in alpha-melanocyte-stimulating hormone (α-MSH)-treated cells. Furthermore, inhibition of autophagy blocked melanosomal degradation and reversed the nalfurafine hydrochloride-induced decrease in melanin content in α-MSH-treated cells. Consistently, treatment with other κ-opioid receptor agonists, such as MCOPPB or mianserin, inhibited excessive melanin production but induced autophagy in B16F1 cells. Furthermore, nalfurafine hydrochloride inhibited protein kinase A (PKA) activation, which was notably restored by forskolin, a PKA activator. Additionally, forskolin treatment further suppressed melanosomal degradation as well as the anti-pigmentation activity of nalfurafine hydrochloride in α-MSH-treated cells. Collectively, our data suggest that stimulation of κ-opioid receptors induces melanophagy by inhibiting PKA activation in α-MSH-treated B16F1 cells.