1111-39-3 Usage
Originator
Acylanid ,Sandoz ,US ,1954
Manufacturing Process
Acetyldigitoxin-α can be obtained from acetyldigitoxin-β by heating it in an anhydrous or aqueous organic solvent at neutral, weakly acid or weakly
alkaline pH, i.e., at a pH range from about 3.5 to about 8.
The acetylidigitoxin-β used for this purpose is a cardiac glycoside which can be
obtained either by splitting off the glucose residue from lanatoside A, or by
extraction of the leaves of Digitalis ferrugines. It is composed of the aglycone
digitoxigenin and 3 molecules of digitoxose, to one of which an acetyl group is
attached. Acetyldigitoxin-α, obtained from acetyldigitoxin-β by rearrangement,
differs from the latter in the position of the acetyl group.
The process may be carried out, for example, in the following manner: A
solution of acetyldigitoxin-β in a suitable solvent, such as methanol, is boiled
under reflux and then diluted with water. The unchanged acetyldigitoxin-β,
which crystallizes out first, is filtered off and can again be submitted to the
same process. On concentrating the filtrate, acetyldigitoxin-α separates out in
crystalline form and after filtering off and recrystallizing is obtained in a pure
state. The acetyldigitoxin-α crystallizes from aqueous methanol in platelets
melting at 217-221°C.
Brand name
Acylanid (Novartis).
Therapeutic Function
Cardiotonic
Purification Methods
-Acetyldigitoxin is obtained from the commercial mixture [ : (2:1)] [25395-32-8]. The form is obtained from the form by heating in anhydrous or aqueous organic solvent (e.g. aqueous MeOH) at pH 3.5—8. It crystallises from MeOH as plates, CHCl3/Et2O or Me2CO/Et2O. At 20o 1g dissolves in 16mL of MeOH, 66mL of Me2CO and ~880mL of EtOAc. [Stoll & Kreis Helv Chim Acta 35 1318, 1322 1952, Beilstein 18 III/IV 1479.] It is a cardenolide.C5128
Check Digit Verification of cas no
The CAS Registry Mumber 1111-39-3 includes 7 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 4 digits, 1,1,1 and 1 respectively; the second part has 2 digits, 3 and 9 respectively.
Calculate Digit Verification of CAS Registry Number 1111-39:
(6*1)+(5*1)+(4*1)+(3*1)+(2*3)+(1*9)=33
33 % 10 = 3
So 1111-39-3 is a valid CAS Registry Number.
InChI:InChI=1/C43H66O14/c1-21-38(48)33(54-24(4)44)19-37(51-21)57-40-23(3)53-36(18-32(40)46)56-39-22(2)52-35(17-31(39)45)55-27-9-12-41(5)26(16-27)7-8-30-29(41)10-13-42(6)28(11-14-43(30,42)49)25-15-34(47)50-20-25/h15,21-23,26-33,35-40,45-46,48-49H,7-14,16-20H2,1-6H3/t21-,22-,23-,26-,27+,28-,29+,30-,31+,32+,33+,35+,36+,37+,38-,39-,40-,41+,42-,43+/m1/s1
1111-39-3Relevant articles and documents
Perfectly regioselective acylation of a cardiac glycoside, digitoxin, via catalytic amplification of the intrinsic reactivity
Yoshida, Keisuke,Furuta, Takumi,Kawabata, Takeo
body text, p. 4830 - 4832 (2010/10/02)
Organocatalytic regioselective acylation of digitoxin has been developed. This method provides the 4′′′-O-manoacylate as the sole product without the concomitant formation of diacylates. The extremely high regioselectivity was assumed to be the result from the combined effects of the high intrinsic reactivity of C(4′′′)-OH and catalyst-promoted regioselective acylation of the same hydroxy group.
Uses of ouabain and ouabain-like molecules in apoptosis related pathologies
-
, (2008/06/13)
Longterm elevation of the intracellular Na+/K+ratio inhibits macromolecule synthesis and proliferation in the majority of cell types studied so far, including vascular smooth muscle cells (VSMC). We report here that inhibition of the Na+,K+pump in VSMC by ouabain or 1 hour preincubation in K+-depleted medium attenuated apoptosis triggered by serum withdrawal, staurosporine or okadaic acid. In the absence of ouabain, both DNA degradation and caspase-3 activation in VSMC undergoing apoptosis were insensitive to modification of the extracellular Na+/K+ratio as well as to hyperosmotic cell shrinkage. In contrast, protection of VSMC from apoptosis by ouabain was abolished under equimolar substitution of Na+owith K+o, showing that the anti apoptotic action of Na+,K+pump inhibition was caused by inversion of the intracellular Na+/K+ratio. Unlike VSMC, the same level of increment of the [Na+]i/[K+]iratio caused by 2 hours preincubation of Jurkat cells with ouabain did not affect chromatin cleavage and caspase-3 activity triggered by treatment with Fas ligand, staurosporine or hyperosmotic shrinkage. Thus, our results show for the first time that similarly to cell proliferation, maintenance of a physiologically low intracellular Na+/K+ratio is required for progression of VSMC apoptosis.
