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Ambroxol HCl(NA-872)
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
Ambroxol HCl(NA-872)图片
CAS NO:23828-92-4
规格:≥98%
包装与价格:
包装价格(元)
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理化性质和储存条件
Molecular Weight (MW)414.56
FormulaC13H18Br2N2O.HCl
CAS No.23828-92-4 (HCl);
Storage-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)DMSO: 4 mg/mL (9.6 mM)
Water: <1 mg/mL
Ethanol: <1 mg/mL
Other info
Chemical Name: 4-((2-amino-3,5-dibromophenyl)(methyl)amino)cyclohexan-1-ol hydrochloride
InChi Key: BHQINQPCRNWCHB-UHFFFAOYSA-N
InChi Code: InChI=1S/C13H18Br2N2O.ClH/c1-17(9-2-4-10(18)5-3-9)12-7-8(14)6-11(15)13(12)16;/h6-7,9-10,18H,2-5,16H2,1H3;1H
SMILES Code: OC1CCC(N(C2=CC(Br)=CC(Br)=C2N)C)CC1.[H]Cl
SynonymsNA-872; Abrohexal; Duramucal; Ebromin; Ambril; NA872; NA 872; Ambro-Puren Ambrobeta; Mucosolvan
实验参考方法
In Vitro

In vitro activity: Ambroxol inhibits Na+ channels in sensory neurons. The potency for tonic block of TTX-r channels is relatively high. Ambroxol affects the Na+ current kinetics of TTX-r and TTX-s channels differently. In CNaIIA cells, the compound behaves like a charged local anesthetic: the block is dependent on stimulus number and increases with higher frequencies in a train of depolarizing stimuli. In CNaIIA cells, ambroxol inhibits inactivated channels 5.5-fold more potently than resting channels. The corresponding factor for TTX-r channels is only 3.3. Ambroxol inhibits the release of histamine, leukotrienes and cytokines from human leukocytes and mast cells.

In VivoAmbroxol inhibited histamine release by more than 50% from human adenoidal mast cells (1000 microM ambroxol) and skin mast cells (100 microM ambroxol) stimulated by Con A and compound 48/80, respectively. Ambroxol (100 microM) strikingly inhibited anti-IgE induced release of both histamine, LTC4, IL-4 and IL-13 from basophils and reduced both histamine and LTB4 release induced by C5a or Zymosan in monocytes. The drug also reduced LTB4 and superoxide anion production in granulocytes stimulated by zymosan or fMLP.
Animal model
Formulation & Dosage
ReferencesMol Pharmacol. 2002 Sep;62(3):433-8; Inflamm Res. 1999 Feb;48(2):86-93.
 
 
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