Detail of "27276-25-1"

CAS Number:
27276-25-1
Name:
Hexanoic acid,6-[(3,4,5-trimethoxybenzoyl)amino]-, sodium salt (1:1)
Molecular Structure:
Formula:
C16H23 N O6 . Na
Molecular Weight:
347.38
Synonyms:
Hexanoicacid, 6-(3,4,5-trimethoxybenzamido)-, monosodium salt (8CI); Hexanoic acid, 6-[(3,4,5-trimethoxybenzoyl)amino]-,monosodium salt (9CI); 3,4,5-Trimethoxybenzoyl-e-aminocaproate sodium; C 3; C 3 (pharmaceutical);Capben; Capobenate; Capobenate sodium; Sodium 3,4,5-trimethoxybenzoyl-e-aminocaproate; Sodium6-(3,4,5-trimethoxybenzamido)hexanoate; Sodium capobenate
Density:
g/cm³
Boiling Point:
472.8°Cat760mmHg
Flash Point:
239.7°C
Safety:
Moderately toxic by intravenous and intraperitoneal routes. Mildly toxic by ingestion. Used as a cardiac anti-arrhythmic. When heated to decomposition it emits toxic fumes of NO_x and Na₂O. Details

Please post your buying leads,so that our qualified suppliers will soon contact you!
*Required Fields

Adenosine derivatives and in vitro cardiac contraction: Adenosine derivatives and in vitro cardiac contraction. Arletti, R.; Bazzani, C. (Ist. Farmacol., Univ. Modena, Modena, Italy). Riv. Farmacol. Ter., 7(2), 247-63 (Italian) 1976. CODEN: RVFTBB. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacodynamics) Section cross-reference(s): 13 Adenosine (I) [58-61-7], AMP [61-19-8], ADP [58-64-0], ATP [56-65-5] (all 1.1-1.8 .times. 10-5M) and, to a lesser extent, dibutyryl cyclic AMP (II) [362-74-3] (9 .times. 10-4M) depressed the mech. activity of the isolated guinea pig heart. The neg. inotropic action of AMP and II, which was abolished by increasing the Ca2+ concn. in the perfusion medium, differed from that of verapamil [52-53-9] in being more rapid in onset. Also, the effect of AMP or II was additive with that of verapamil and was antagonized by aminophylline [317-34-0], which favors Ca2+ entry into myocardial cells. 7440-70-2 and 61-19-8 are also in the experiment. Na 3,4,5-trimethoxybenzoyl-.epsilon.-aminocaproate [27276-25-1] potentiated the pos. inotropic action of Ca2+ on the prepns. and antagonized the neg. inotropic effect of AMP and II; with II only, the neg. inotropic effect was converted to a pos. one. The possible existence of I receptors in the myocardial cell membrane, involved in regulating Ca2+ entry, is discussed. These receptors could be activated not only by I but by related compds. .

Coronary dilation from adenosine: Coronary dilation from adenosine. Baraldi, M.; Benassi-Benelli, A. (Ist. Farmacol., Univ. Modena, Modena, Italy). Riv. Farmacol. Ter., 7(2), 283-9 (Italian) 1976. CODEN: RVFTBB. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacodynamics) Perfusion with adenosine (I) [58-61-7] (1.25-5 .mu.g/ml) caused a concn.-dependent increase in coronary flow in the isolated guinea pig heart. Dibutyryl cyclic AMP [362-74-3] produced a similar effect, but 100-fold greater concns. were required. The coronary-dilating action of these 2 compds. was antagonized by aminophylline [317-34-0] and potentiated by Na 3,4,5-trimethoxybenzoyl-.epsilon.-aminocaproate [27276-25-1] and verapamil [52-53-9]. I and dibutyryl cyclic AMP may act by interfering with the entrance of Ca2+ into the smooth muscle cells of the coronary vessels.Except for chemicals metioned above, 317-34-0 and 58-61-7 are also used. .