Key Documents

View All Documentation

476485

PKA Inhibitor 14-22 Amide

Name: PKA Inhibitor 14-22 Amide
Brand: MM

≥95% (HPLC), PKA Inhibitor, lyophilized

Synonym(s):

PKA Inhibitor 14-22 Amide, Cell-Permeable, Myristoylated, PKI 14-22 Amide, Cell-Permeable, Myristoylated Protein Kinase A Inhibitor Amide 14-22, Cell-Permeable, Myr-GRTGRRNAI-NH₂, Protein Kinase A Inhibitor 14-22 Amide, PKA Inhibitor XIII

Select a Size

Change View

About This Item

Empirical Formula (Hill Notation):

C₅₃H₁₀₀N₂₀O₁₂

Molecular Weight:

1209.49

UNSPSC Code:

12352200

NACRES:

NA.77

Assay:

≥95% (HPLC)

Form:

lyophilized

Quality level:

100

Storage condition:

OK to freeze, desiccated (hygroscopic)

Technical Service

Need help? Our team of experienced scientists is here for you.

Let Us Assist

Properties

Product Name

PKA Inhibitor 14-22 Amide, Cell-Permeable, Myristoylated, PKA Inhibitor 14-22 Amide is myristoylated at the N-terminus that enhances its cell-permeability. The non-myristoylated version is shown to be a specific inhibitor of PKA (K_i = 36 nM).

Quality Level

100

assay

≥95% (HPLC)

form

lyophilized

manufacturer/tradename

Calbiochem^®

storage condition

OK to freeze, desiccated (hygroscopic)

solubility

water: 1 mg/mL

shipped in

ambient

storage temp.

−20°C

Description

General description

Heat-stable protein kinase inhibitor (PKI) peptide sequence (14-22) that has been myristoylated at the N-terminus, enhancing its cell-permeability. The non-myristoylated version of this peptide is a highly specific inhibitor (K_i = 36 nM) of cAMP-dependent protein kinase (PKA).

Biochem/physiol Actions

Cell permeable: yes

Primary Target
cAMP-dependent protein kinase

Product does not compete with ATP.

Reversible: no

Target K_i: 36 nMf or cAMP-dependent protein kinase

Physical form

Supplied as a trifluoroacetate salt.

Preparation Note

Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 3 months at -20°C.

Other Notes

Myr-N-Gly-Arg-Thr-Gly-Arg-Arg-Asn-Ala-Ile-NH₂

Paman, K., et al. 1998. J. Lipid Res. 39, 1091.
Rimon, G., and Rubin M. 1998. Biochim. Biophys. Acta 1380, 289.
Harris, T.E., et al. 1997. Biochem. Biophys. Res. Commun. 232, 648.
Muniz, M., et al. 1997. Proc. Natl. Acad. Sci. USA 94, 14461.
Zoukhri, D., et al. 1997. Am. J. Physiol. 272, C263.
Eichholtz, T., et al. 1993. J. Biol. Chem.268, 1982.
Ward, N.E. and O’Brian, C.A. 1993. Biochemistry32, 11903.
Walsh, D.A. and Glass, D.B. 1991. Methods Enzymol. 201, 304.
Glass, D.B., et al. 1989. J. Biol. Chem.264, 8802.

Legal Information

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

Disclaimer

Toxicity: Standard Handling (A)

Storage Class

11 - Combustible Solids

wgk

WGK 1

flash_point_f

Not applicable

flash_point_c

Not applicable

Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

Already Own This Product?

Find documentation for the products that you have recently purchased in the Document Library.

Visit the Document Library

Intrinsic cardiac adrenergic cells contribute to LPS-induced myocardial dysfunction.

Duomeng Yang et al.

Communications biology, 5(1), 96-96 (2022-01-27)

Intrinsic cardiac adrenergic (ICA) cells regulate both developing and adult cardiac physiological and pathological processes. However, the role of ICA cells in septic cardiomyopathy is unknown. Here we show that norepinephrine (NE) secretion from ICA cells is increased through activation

Exenatide prevents statin-related LDL receptor increase and improves insulin secretion in pancreatic beta cells (1.1E7) in a protein kinase A-dependent manner.

Lukasz Buldak et al.

Journal of applied biomedicine, 20(4), 130-140 (2023-01-29)

Statins are primary drugs in the treatment of hyperlipidemias. This group of drugs is known for its beneficial pleiotropic effects (e.g., reduction of inflammatory state). However, a growing body of evidence suggests its diabetogenic properties. The culpable mechanism is not

Disturbed flow-induced Gs-mediated signaling protects against endothelial inflammation and atherosclerosis.

Akiko Nakayama et al.

JCI insight, 5(23) (2020-12-04)

Atherosclerosis develops preferentially in areas of the arterial system, in which blood flow is disturbed. Exposure of endothelial cells to disturbed flow has been shown to induce inflammatory signaling, including NF-κB activation, which leads to the expression of leukocyte adhesion

View All Related Papers

Global Trade Item Number

SKU	GTIN
476485-500UG	04055977183832