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Sigma-Aldrich

Cathepsin G Inhibitor I

≥98% (HPLC), solid, cathepsin G inhibitor, Calbiochem®

Synonyme(s) :

Cathepsin G Inhibitor I

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About This Item

Formule empirique (notation de Hill):
C36H33N2O6P
Numéro CAS:
Poids moléculaire :
620.63
Code UNSPSC :
12352200
Nomenclature NACRES :
NA.77

product name

Cathepsin G Inhibitor I, The Cathepsin G Inhibitor I, also referenced under CAS 429676-93-7, controls the biological activity of Cathepsin G. This small molecule/inhibitor is primarily used for Protease Inhibitors applications.

Niveau de qualité

Pureté

≥98% (HPLC)

Forme

solid

Puissance

53 nM IC50

Fabricant/nom de marque

Calbiochem®

Conditions de stockage

OK to freeze
protect from light

Couleur

white

Solubilité

DMSO: 5 mg/mL
methanol: soluble

Conditions d'expédition

ambient

Température de stockage

−20°C

InChI

1S/C36H33N2O6P/c1-37(28-18-20-38(21-19-28)35(40)25-11-3-2-4-12-25)36(41)32-23-27-14-6-5-13-26(27)22-31(32)33(39)34(45(42,43)44)30-17-9-15-24-10-7-8-16-29(24)30/h2-17,22-23,28,34H,18-21H2,1H3,(H2,42,43,44)

Clé InChI

GNOZQRKYZJSIPZ-UHFFFAOYSA-N

Description générale

A potent, selective, reversible, and competitive non-peptide inhibitor of cathepsin G (IC50 = 53 nM and Ki = 63 nM). Weakly inhibits chymotrypsin (Ki = 1.5 µM) and does not have any significant inhibitory effect on thrombin, factor Xa, factor IXa, plasmin, trypsin, tryptase, proteinase 3, and human leukocyte elastase (IC50 >100 µM).
A potent, selective, reversible, competitive, non-peptide inhibitor of cathepsin G [IC50 = 53 nM and Ki = 63 nM]. Weakly inhibits chymotrypsin (Ki = 1.5 µM) and poorly inhibits thrombin, factor Xa, factor IXa, plasmin, trypsin, tryptase, proteinase 3, and human leukocyte elastase (IC50 >100 µM).

Actions biochimiques/physiologiques

Cell permeable: no
Primary Target
cathepsin G
Product does not compete with ATP.
Reversible: yes
Target Ki: 63 nM for cathepsin G

Conditionnement

Packaged under inert gas

Avertissement

Toxicity: Standard Handling (A)

Reconstitution

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

Autres remarques

Greco, M.N., et al. 2002. J. Am. Chem. Soc.124, 3810.

Informations légales

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

Code de la classe de stockage

11 - Combustible Solids

Classe de danger pour l'eau (WGK)

WGK 1

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable


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Consulter la Bibliothèque de documents

Stefan J Schunk et al.
Circulation, 144(11), 893-908 (2021-07-02)
Cardiovascular diseases and chronic kidney disease (CKD) are highly prevalent, aggravate each other, and account for substantial mortality. Both conditions are characterized by activation of the innate immune system. The alarmin interleukin-1α (IL-1α) is expressed in a variety of cell
Mira Tohmé et al.
Methods in molecular biology (Clifton, N.J.), 960, 509-515 (2013-01-19)
Proteases generate peptides that bind to MHC class II molecules to interact with a wide diversity of CD4(+) T cells. They are expressed in dedicated organelles: endosomes and lysosomes of professional antigen presenting cells (pAPCs) such as B cells, macrophages
Fabian Gärtner et al.
ACS omega, 5(43), 28233-28238 (2020-11-10)
During an immune response, cathepsin G (CatG) takes on the role of adaptive and innate immunity and the outcome depends on the localization of CatG. Soluble, cell surface-bound, or intracellular CatG is also responsible for pathophysiology conditions. We applied the
Akmaral Assylbekova et al.
Pharmaceuticals (Basel, Switzerland), 15(5) (2022-05-29)
Coronavirus disease 2019 (COVID-19) can lead to multi-organ failure influenced by comorbidities and age. Binding of the severe acute respiratory syndrome coronavirus 2 spike protein (SARS-CoV-2 S protein) to angiotensin-converting enzyme 2 (ACE2), along with proteolytic digestion of the S
Hui Yang et al.
EMBO reports, 24(10), e57032-e57032 (2023-08-31)
Bromodomain-containing protein 4 (BRD4) is overexpressed and functionally implicated in various myeloid malignancies. However, the role of BRD4 in normal hematopoiesis remains largely unknown. Here, utilizing an inducible Brd4 knockout mouse model, we find that deletion of Brd4 (Brd4Δ/Δ )

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