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CXL-1020
- 2-MSPA
Axon 2653
CAS:
950834-06-7
Purity:
99%
- MF: C7H9NO5S2
- MW: 251.28
Description
CXL-1020 is a specialized nitroxyl (HNO) donor and prodrug that serves as both a therapeutic candidate and an experimental pharmacology tool. It decomposes non-enzymatically to release pure HNO, a reactive nitrogen species that targets cardiovascular function and cellular signaling pathways.
CXL-1020 supports studies linking reactive signaling species to cardiovascular and cellular stress models.
Key Features
- HNO donor
- Pharmacological tool for HNO-dependent mechanism studies
- Decomposes nonenzymatically to release pure nitroxyl (HNO) (pure HNO delivery)
- Boosts both cardiac contraction (inotropic) and relaxation (lusitropic) mechanics
Applications
- HNO pharmacology and target-validation studies
- HNO pathway assays and nitroxyl signaling mapping
- Disease-relevant cellular and translational model systems
- Metabolic pathway and biomarker-response studies
More Information
| Parent CAS No. | 950834-06-7 |
|---|---|
| Chemical Name | N-hydroxy-2-(methylsulfonyl)benzenesulfonamide |
| SMILES | C1(S(NO)(=O)=O)=CC=CC=C1S(C)(=O)=O |
| MFCD | N.A. |
| InChi | InChI=1S/C7H9NO5S2/c1-14(10,11)6-4-2-3-5-7(6)15(12,13)8-9/h2-5,8-9H,1H3 |
| InChiKey | RZRWBKKAFHXNEQ-UHFFFAOYSA-N |
| CID | 52939580 |
| Short Description | HNO donor |
CXL-1020
nitroxyl (HNO) donor prodrug
2-MSPA
2MSPA
CXL1020
CXL 1020
Cysteine residues
Donor
Unclassified
HNO pharmacology
HNO pathway assays and nitroxyl signaling mapping
Metabolic pathway and biomarker-response studies
metabolism
cardiovascular research
signal transduction
CAS 950834-06-7
Axon Medchem
Axon 2653
Supplier
Vendor
References
- A Arcaro et al. Nitroxyl (HNO) for treatment of acute heart failure. Curr Heart Fail Rep. 2014 Sep;11(3):227-35.
- HN Sabbah et al. Nitroxyl (HNO): A novel approach for the acute treatment of heart failure. Circ Heart Fail. 2013 Nov;6(6):1250-8.
- Diering, S. et al. Receptor-independent modulation of cAMP-dependent protein kinase and protein phosphatase signaling in cardiac myocytes by oxidizing agents. J. Biol. Chem. 2020, in press.
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