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Merck
CN

G1274

HA-1004 hydrochloride

≥98% (HPLC), powder

Synonym(s):

N-(2-Guanidinoethyl)-5-isoquinolinesulfonamide hydrochloride

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About This Item

Empirical Formula (Hill Notation):
C12H15N5O2S · HCl
CAS Number:
Molecular Weight:
329.81
UNSPSC Code:
12352200
PubChem Substance ID:
MDL number:
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assay

≥98% (HPLC)

form

powder

color

white

solubility

H2O: 10 mM, ethanol: 10 mg/mL

storage temp.

−20°C

SMILES string

Cl.NC(=N)NCCNS(=O)(=O)c1cccc2cnccc12

InChI

1S/C12H15N5O2S.ClH/c13-12(14)16-6-7-17-20(18,19)11-3-1-2-9-8-15-5-4-10(9)11;/h1-5,8,17H,6-7H2,(H4,13,14,16);1H

InChI key

GUGJQAFPKZZOIV-UHFFFAOYSA-N

Biochem/physiol Actions

Shown to be an intracellular calcium antagonist. Reported to induce neurite formation.


Storage Class

13 - Non Combustible Solids

wgk

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

ppe

Eyeshields, Gloves, type N95 (US)

Regulatory Information

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H Tsushima et al.
Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research, 8(12), 1317-1328 (1998-01-07)
Erythropoietin (Epo) is a cytokine known to stimulate proliferation and differentiation of erythroid cells. However, recent gene disruption experiments demonstrated that Epo receptor signaling is not an obligatory step in erythroid differentiation. Here, we describe the role of Epo in
M R Crowley et al.
Journal of cardiovascular pharmacology, 23(5), 806-813 (1994-05-01)
HA1004, an isoquinolinesulfonamide and a cyclic nucleotide-dependent protein kinase inhibitor, is an intracellular calcium antagonist that produces vascular smooth muscle (VSM) relaxation in vitro. We studied the hemodynamic effects of intravenous (i.v.) infusions of HA1004 (0.1-2.0 mg/kg) in vivo in
A Fex Svenningsen et al.
Journal of neuroscience research, 52(5), 530-537 (1998-06-19)
Schwann cell proliferation was studied in cultured segments of the rat sciatic nerve by measurement of [3H] thymidine incorporation or through bromodeoxyuridine-(BrdU)-labelling and immunocytochemistry. The aim was to delineate mechanisms involved in the injury-induced proliferative response of Schwann cells. Removal