HA-1004

CAT: 0804-HY-123468-01Size: 1 mgDry Ice: NoHazardous: No
CAT#:0804-HY-123468-01Size:1 mg
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Description
HA-1004 is a selective inhibitor of PKA, which can inhibit lipolysis and induce vascular relaxation. HA-1004 is also a dual inhibitor of cyclic GMP-dependent protein kinase and cyclic AMP-dependent protein, and is involved in smooth muscle, second messenger, cyclic AMP and cyclic GMP regulation mechanisms. HA-1004 is an antagonist for calcium, that can be used as a vasodilator to inhibit the contraction of rabbit aortic strips, or to antagonize ERK and tyrosine hydroxylase (TH) phosphorylation in morphine abstinence rat models[1][2][3].
CAS Number
[91742-10-8]
UNSPSC
12352005
Target
Calcium Channel; Cyclic GMP-AMP Synthase; ERK; PKA; Tyrosine Hydroxylase
Type
Reference compound
Related Pathways
Immunology/Inflammation; MAPK/ERK Pathway; Membrane Transporter/Ion Channel; Metabolic Enzyme/Protease; Neuronal Signaling; Stem Cell/Wnt; TGF-beta/Smad
Applications
Metabolism-protein/nucleotide metabolism
Field of Research
Metabolic Disease; Cardiovascular Disease
Assay Protocol
https://www.medchemexpress.com/ha-1004.html
Purity
99.04
Solubility
DMSO : 50 mg/mL (ultrasonic)
Smiles
O=S(C1=CC=CC2=C1C=CN=C2)(NCCNC(N)=N)=O
Molecular Formula
C12H15N5O2S
Molecular Weight
293.34
References & Citations
[1]Almela P, et al. Crosstalk between G protein-coupled receptors (GPCRs) and tyrosine kinase receptor (TXR) in the heart after morphine withdrawal. Front Pharmacol. 2013 Dec 27;4:164. |[2]Goodman HM, et al. The isoquinoline sulfonamide inhibitors of protein phosphorylation, H-7, H-8, and HA-1004, also inhibit RNA synthesis: studies on responses of adipose tissue to growth hormone. Endocrinology. 1990 Jan;126 (1) :441-50. |[3]Ishikawa T, et al. Relaxation of vascular smooth muscle by HA-1004, an inhibitor of cyclic nucleotide-dependent protein kinase. J Pharmacol Exp Ther. 1985 Nov;235 (2) :495-9.
Shipping Conditions
Blue Ice
Storage Conditions
-20°C, 3 years (Powder)
Scientific Category
Reference compound1
Clinical Information
No Development Reported

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