Deslanoside
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Deslanoside
structure -
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CAS No:
17598-65-1
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Formula:
C47H74O19
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Chemical Name:
Deslanoside
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Synonyms:
Card-20(22)-enolide,3-[(O-β-D-glucopyranosyl-(1→4)-O-2,6-dideoxy-β-D-ribo-hexopyranosyl-(1→4)-O-2,6-dideoxy-β-D-ribo-hexopyranosyl-(1→4)-2,6-dideoxy-β-D-ribo-hexopyranosyl)oxy]-12,14-dihydroxy-,(3β,5β,12β)-;Lanatoside C,deacetyl-;(3β,5β,12β)-3-[(O-β-D-Glucopyranosyl-(1→4)-O-2,6-dideoxy-β-D-ribo-hexopyranosyl-(1→4)-O-2,6-dideoxy-β-D-ribo-hexopyranosyl-(1→4)-2,6-dideoxy-β-D-ribo-hexopyranosyl)oxy]-12,14-dihydroxycard-20(22)-enolide;Deacetyllanatoside C;Deslanoside;Cedilanid D;Desacetyllanatoside C;Deslanatoside C;Deslanoside C;De-O-acetyllanatoside C;Deacetylanatoside C;Purpurea glycoside C;Desace;Desaci;35-58-5;1329-81-3;11004-41-4;11029-69-9
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CAS No:
Description
Solution S is clear (2.2.1) and colourless (2.2.2, Method II).ChEBI: A cardenolide glycoside that is lanatoside C with the acetoxy group replaced by a hydroxy group.
Solid
Deslanoside is a cardenolide glycoside that is lanatoside C with the acetoxy group replaced by a hydroxy group. It has a role as an anti-arrhythmia drug, a cardiotonic drug, a metabolite and an EC 3.6.3.9 (Na(+)/K(+)-transporting ATPase) inhibitor. It is a 14beta-hydroxy steroid, a 12beta-hydroxy steroid, a cardenolide glycoside and a tetrasaccharide derivative.|Deacetyllanatoside C. A cardiotonic glycoside from the leaves of Digitalis lanata.
Deslanoside Basic Attributes
943.08
943.08
241-568-1
YGY317RK75
DTXSID1022897
C - Cardiovascular system
2938900000
Characteristics
282
0.2
Solid
1.1255 (rough estimate)
220-235°C
732.1°C (rough estimate)
1.6500 (estimate)
4.68e-01 g/L
2-8°C
D20 +12° (c = 1.084 in 75% alc)
Safety Information
2811
23/25-33
1-22-45
P260, P264, P270, P271, P284, P301+P310, P304+P340, P310, P314, P320, P321, P330, P403+P233, P405, P501
H300
|Danger|H300 (100%): Fatal if swallowed [Danger Acute toxicity, oral]|P260, P264, P270, P271, P284, P301+P310, P304+P340, P310, P314, P320, P321, P330, P403+P233, P405, and P501|The GHS information provided by 1 company from 1 notification to the ECHA C&L Inventory.
Toxicity
Symptoms of overdose include ventricular tachycardia, ventricular fibrillation, progressive bradyarrhythmias, or heart block.
20%
Drug Information
For the treatment and management of Congestive cardiac insufficiency, arrhythmias and heart failure.
Deslanoside is a cardiac glycoside used to treat congestive heart failure and supraventricular arrhythmias due to reentry mechanisms, and to control ventricular rate in the treatment of chronic atrial fibrillation.
Agents used for the treatment or prevention of cardiac arrhythmias. They may affect the polarization-repolarization phase of the action potential, its excitability or refractoriness, or impulse conduction or membrane responsiveness within cardiac fibers. Anti-arrhythmia agents are often classed into four main groups according to their mechanism of action: sodium channel blockade, beta-adrenergic blockade, repolarization prolongation, or calcium channel blockade. (See all compounds classified as Anti-Arrhythmia Agents.)|Agents that have a strengthening effect on the heart or that can increase cardiac output. They may be CARDIAC GLYCOSIDES; SYMPATHOMIMETICS; or other drugs. They are used after MYOCARDIAL INFARCT; CARDIAC SURGICAL PROCEDURES; in SHOCK; or in congestive heart failure (HEART FAILURE). (See all compounds classified as Cardiotonic Agents.)|Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction. (See all compounds classified as Enzyme Inhibitors.)
Little absorption from the gastrointestinal tract (40%).
36 hours
Deslanoside inhibits the Na-K-ATPase membrane pump, resulting in an increase in intracellular sodium and calcium concentrations. Increased intracellular concentrations of calcium may promote activation of contractile proteins (e.g., actin, myosin). Deslanoside also acts on the electrical activity of the heart, increasing the slope of phase 4 depolarization, shortening the action potential duration, and decreasing the maximal diastolic potential.
Cedilanid D
Deslanoside Use and Manufacturing
Cardiotonic.
Human Drugs -> FDA Approved Drug Products with Therapeutic Equivalence Evaluations (Orange Book) -> Active Ingredients
Computed Properties
Molecular Weight:943.1
XLogP3:-0.3
Hydrogen Bond Donor Count:9
Hydrogen Bond Acceptor Count:19
Rotatable Bond Count:10
Exact Mass:942.48243013
Monoisotopic Mass:942.48243013
Topological Polar Surface Area:282
Heavy Atom Count:66
Complexity:1760
Defined Atom Stereocenter Count:26
Covalently-Bonded Unit Count:1
Compound Is Canonicalized:Yes
Drug Function and Efficacy
1. Positive inotropic effect: This product selectively binds to the Na+-K+-ATPase of myocardial cell membrane and inhibits the activity of the enzyme, increasing the concentration of Ca2+ in myocardial cells, stimulating myocardial contractile proteins and thus increasing myocardial contractility; 2. Negative frequency effect: Due to its positive inotropic effect, it increases the cardiac output of the failing heart, improves the hemodynamic state, eliminates the reflex increase of sympathetic nerve tension, and enhances vagal nerve tension, thereby slowing down the heart rate and delaying atrioventricular conduction. In addition, at low doses, it increases the sensitivity of the sinus node to vagal impulses, which can enhance its effect of slowing down the heart rate. Due to its negative frequency effect, the diastole period is relatively prolonged, which is beneficial to increase myocardial blood supply; large doses (usually close to the toxic dose) can directly inhibit the sinoatrial node, atrioventricular node and His bundle to present sinus bradycardia and varying degrees of atrioventricular conduction block; 3 Cardiac electrophysiological effects: through direct effects on myocardial electrical activity and indirect effects on the vagus nerve, it reduces the autonomy of the sinoatrial node; improves the autonomy of Purkinje fibers; slows down the conduction velocity of the atrioventricular node, prolongs its effective refractory period, and leads to an increase in latent conduction of the atrioventricular node, which can slow down the ventricular rate of atrial fibrillation or atrial flutter; since this drug shortens the effective refractory period of the atrium, when used for atrial tachycardia and atrial flutter, it may lead to acceleration of the atrial rate and conversion of atrial flutter to atrial fibrillation; shortens the still effective refractory period of Purkinje fibers.
Registered Holders
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NOBILUS ENT Tomasz Koz(’)luk
Active
Japan
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Weizhi Pharmaceutical Co., Ltd.
Active
China
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Guangdong Leawell Pharmaceutical Co., Ltd.
Active
China
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