Dantrolene Sodium - CAS 14663-23-1
Category:
APIs
Product Name:
Dantrolene Sodium
Catalog Number:
14663-23-1
Synonyms:
sodium;3-[(E)-[5-(4-nitrophenyl)furan-2-yl]methylideneamino]-5-oxo-4H-imidazol-2-olate DANTROLENE SODIUM Dantrolene sodium salt Dantrium Sodium dantrolene 14663-23-1 Dantrolene (sodium) Dantrolene sodium anhydrous UNII-28F0G1E0VF Dantamacrin Dantrix Dantr
CAS Number:
14663-23-1
Description:
Dantrolene Sodium, an inhibitor of calcium channel proteins that markedly suppresses the release of calcium previously sequestered by skeletal, but not cardiac, muscle sarcoplasmic reticulum. In the intact skeletal muscle, dantrolene sodium acts at a site
Molecular Weight:
336.23
Molecular Formula:
C14H9N4NaO5
Quantity:
Grams-Kilos
Quality Standard:
USP
COA:
Inquire
MSDS:
Inquire
Canonical SMILES:
C1C(=O)N=C(N1N=CC2=CC=C(O2)C3=CC=C(C=C3)[N+](=O)[O-])[O-].[Na+]
InChI:
1S/C14H10N4O5.Na/c19-13-8-17(14(20)16-13)15-7-11-5-6-12(23-11)9-1-3-10(4-2-9)18(21)22;/h1-7H,8H2,(H,16,19,20);/q;+1/p-1/b15-7+;
InChIKey:
KSRLIXGNPXAZHD-HAZZGOGXSA-M
Chemical Structure
CAS 14663-23-1 Dantrolene Sodium

Reference Reading


1. Orexin A regulates plasma insulin and leptin levels in a time-dependent manner following a glucose load in mice
Jae-Hyung Park & Hae-Min Shim & Ann-Yae Na. Diabetologia (2015) 58:1542–1550
OXA potentiates glucose-stimulated [Ca2+]i increase via the activation of ryanodine receptors To investigate the downstream signalling mechanism following the OXA-induced cAMP increase, glucose-stimulated [Ca2+]i changes were measured in the presence of various cAMP signaling pathway inhibitors in the primary beta cells. OXA further increased the [Ca2+]i levels in response to high glucose (Fig. 2a).AsshowninFig. 2b, the stimulatory effect of OXA on [Ca2+]i was not observed in the presence of the PLC inhibitor, PKC inhibitor or AC inhibitor or in the presence of H-89 (a non-selective inhibitor of protein kinase A [PKA]) or brefeldin-A (BFA; a non-selective inhibitor of exchange protein activated by cAMP [EPAC]). However, the involvement of EPAC signalling, compared with that of PKA, was more predominant for the stimulatory effect of OXA on the glucose-stimulated [Ca2+]i increase. Because the activation of the Ins(1,4,5)P3 receptor (IP3R) in response to cAMP signalling is a PKA-dependent mechanism and the activation of ryanodine receptors (RyRs) is an EPAC-dependentmechanism, we next investigated the effect of OXA on glucose-stimulated [Ca2+]i increase in the presence of the IP3R antagonist xestospongin C and the RyR antagonist dantrolene sodium. The stimulatory effect of OXA on [Ca2+]i was remarkably reduced not only in the presence of the RyR antagonist but also in the presence of the IP3R antagonist (Fig. 2c, d). However, the involvement of RyR signaling was more predominant than the involvement of IP3Rsignalling for the stimulatory effect of OXA on the [Ca2+]i increase.