ACETYLSTROPHANTHIDIN

Details

Stereochemistry	ABSOLUTE
Molecular Formula	C25H34O7
Molecular Weight	446.5333
Optical Activity	UNSPECIFIED
Defined Stereocenters	8 / 8
E/Z Centers	0
Charge	0

SHOW SMILES / InChI

Structure Search

SMILES

CC(=O)O[C@H]1CC[C@]2(C=O)[C@H]3CC[C@]4(C)[C@H](CC[C@]4(O)[C@@H]3CC[C@]2(O)C1)C5=CC(=O)OC5

InChI

InChIKey=JLZAERUVCODZQO-VWCUIIQSSA-N

InChI=1S/C25H34O7/c1-15(27)32-17-3-8-23(14-26)19-4-7-22(2)18(16-11-21(28)31-13-16)6-10-25(22,30)20(19)5-9-24(23,29)12-17/h11,14,17-20,29-30H,3-10,12-13H2,1-2H3/t17-,18+,19-,20+,22+,23-,24-,25-/m0/s1

HIDE SMILES / InChI

Molecular Formula	C25H34O7
Molecular Weight	446.5333
Charge	0
Count

Stereochemistry	ABSOLUTE
Additional Stereochemistry	No
Defined Stereocenters	8 / 8
E/Z Centers	0
Optical Activity	UNSPECIFIED

Description
Sources: https://www.ncbi.nlm.nih.gov/pubmed/239798 | https://www.ncbi.nlm.nih.gov/pubmed/6371896 | https://www.ncbi.nlm.nih.gov/pubmed/13309667

semisynthetic C3 acetyl ester of the aglycone strophanthidin. Acetylstrophanthidin inhibits sodium-potassium adenosinetriphosphatase (Na -K ATPase) and causes an inotropic effect. The effect of acetylstrophanthidin is first seen within half a minute to five minutes and becomes maximal in about ten minutes. This rapid action obviates the effect of time, which is so important for subsidence of precipitationg causes of cardiac failure. Severe pulmonic, coronary, and aortic valvular disease, as well as old age, tended to predispose the patients to unusual acetylstrophanthidin sensitivity. Acetylstrophanthidin may cause nausea and vomiting.

Approval Year

Targets

Primary Target	Pharmacology	Condition	Potency
Sodium/potassium-transporting ATPase (Oryctolagus cuniculus) 1 Target ID: Sodium/potassium-transporting ATPase (Oryctolagus cuniculus) Sources: https://www.ncbi.nlm.nih.gov/pubmed/239798	Inhibitor 8504

Conditions

Condition	Modality	Highest Phase	Product
Acute myocardial infarction 37 Sources: https://www.ncbi.nlm.nih.gov/pubmed/8225670 https://www.ncbi.nlm.nih.gov/pubmed/13309667	Primary	Phase II 1147	Unknown Approved Use Unknown
Congestive heart failure 54 Sources: https://www.ncbi.nlm.nih.gov/pubmed/13309667 https://www.ncbi.nlm.nih.gov/pubmed/13649555 https://www.ncbi.nlm.nih.gov/pubmed/13631061	Primary	Not Provided 511	Unknown Approved Use Unknown
Coronary artery disease 48 Sources: https://www.ncbi.nlm.nih.gov/pubmed/2316465 https://www.ncbi.nlm.nih.gov/pubmed/13309667	Primary	Not Provided 511	Unknown Approved Use Unknown

Doses

Dose	Population	Adverse events
2.7 mg 4 times / hour multiple, intravenous Highest studied dose Dose: 2.7 mg, 4 times / hour Route: intravenous Route: multiple Dose: 2.7 mg, 4 times / hour Sources: https://pubmed.ncbi.nlm.nih.gov/13309667	unhealthy, ADULT Health Status: unhealthy Age Group: ADULT Sex: M+F Food Status: UNKNOWN Sources: https://pubmed.ncbi.nlm.nih.gov/13309667	Other AEs: ventricular bigemin... Other AEs: ventricular bigemin (1 pt) Sources: https://pubmed.ncbi.nlm.nih.gov/13309667

AEs

AE	Significance	Dose	Population
ventricular bigemin	1 pt	2.7 mg 4 times / hour multiple, intravenous Highest studied dose Dose: 2.7 mg, 4 times / hour Route: intravenous Route: multiple Dose: 2.7 mg, 4 times / hour Sources: https://pubmed.ncbi.nlm.nih.gov/13309667	unhealthy, ADULT Health Status: unhealthy Age Group: ADULT Sex: M+F Food Status: UNKNOWN Sources: https://pubmed.ncbi.nlm.nih.gov/13309667

Sourcing

Vendor/Aggregator	ID	URL
eMolecules	4823878	https://orderbb.emolecules.com/search/#?query=4823878
IBScreen	STOCK1N-52599
MolPort	MolPort-001-742-530	https://www.molport.com/shop/molecule-link/MolPort-001-742-530
TimTec	ST50309391	http://www.echemstore.com/catalogsearch/result/?q=ST50309391

PubMed

Title	Date	PubMed
The inotropic effect of cardioactive glycosides in ventricular myocytes requires Na+-Ca2+ exchanger function.	2006-09-15	16825310
Denervation of vagal cardiopulmonary receptors by injection of kainic acid into the nodose ganglia in dogs.	2002-11-29	12492140
Effects of cardiac glycosides on atrial fibrillation.	2001-11	11713174
Biphasic effect of cardiac glycosides on action potential duration in isolated Purkinje fibers.	2001-09	11589786
Regulation of vocal fold transepithelial water fluxes.	2001-09	11509542
Ion transport and regulation of respiratory tract fluid output in dogs.	2001-03	11181589
Transient changes in plasma digoxin concentration and the development of cardiotoxicity.	1977-11	588806
The mechanisms of digitalis-induced ventricular fibrillation.	1968-09	5676466
The mechanics of left ventricular contraction in acute experimental cardiac failure.	1967-03	4381563

Patents

Sample Use Guides

In Vivo Use Guide

The initial dose varied from 0.15 to 0.6 mg. Subsequent doses, if given, varied from 0.1 to 0.6 mg at intervals of one to fifteen minutes.

Route of Administration: Intravenous

In Vitro Use Guide

Acetylstrophanthidin (ACS, 4 uM) alters Ca(2+) transients in completely Na(+)-free conditions in intact ferret and cat ventricular myocytes. In intact ferret myocytes (stimulated at 0.2 Hz), ACS enhanced Ca(2+) transients and cell shortening during twitches. Acute inotropic effects of ACS depend on the presence of Na(+) and a functional Na(+)-Ca(2+) exchanger in ferret and cat myocytes (rather than alternate Na(+)-independent mechanisms).

Substance Class	Chemical Created by `admin` on `Mon Mar 31 23:24:21 GMT 2025` Edited by `admin` on `Mon Mar 31 23:24:21 GMT 2025`
Record UNII	JG33H36364
Record Status	`Validated (UNII)`
Record Version

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Name

Type

Language

ACETYLSTROPHANTHIDIN

Common Name

English

NSC-92954

Preferred Name

English

5.BETA.-CARD-20(22)-ENOLIDE, 3.BETA.,5,14-TRIHYDROXY-19-OXO-, 3-ACETATE

Systematic Name

English

3-ACETYL-STROPHANTHIDIN

Common Name

English

ERYSIMUPICRONE ACETATE

Common Name

English

STROPHANTHIDIN ACETATE

Common Name

English

STROPHANTHIDIN 3-ACETATE

Common Name

English

Code System Code Type Description

CHEBI

59028