Tonlamarsen
Tonlamarsen (ION-904) is a GalNAc-conjugated antisense oligonucleotide and Angiotensinogen synthesis inhibitor. Tonlamarsen specifically reduces the production of Angiotensinogen in the liver and plasma, and exhibits extremely low activity in the kidneys. Tonlamarsen can be used in research related to hypertension and heart failure.
For research use only. We do not sell to patients.
- CAS No.: 2589926-20-3
- Formula: C241H349N65O12P16S12
- Molecular Weight:7021.13
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
All Angiotensin Receptor Isoforms
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Biological Activity
Description
IC50 & Target
Angiotensinogen[1]
In Vitro
Tonlamarsen significantly reduces plasma AGT levels in subjects, while showing no signals of hyperkalemia, renal dysfunction, hypotension, liver dysfunction or thrombocytopenia (off-target effects)[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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CAS No. 2589926-20-3
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Molecular Weight 7021.13
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Formula C241H349N65O12P16S12
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SMILES
[Tonlamarsen]
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Synonyms
ION-904
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Sequence
DNA, d([2′-O-(2-methoxyethyl)]m5rC-sp-[2′-O-(2-methoxyethyl)]rG-(3′→4′)-[2′,5′-anhydro-6′-deoxy-4′-C-(hydroxymethyl)-α-L-mannofurano]m5C-T-sp-G-sp-A-sp-T-sp-T-sp-T-sp-G-sp-T-sp-m5C-sp-m5C-sp-(3′→4′)-[2′,5′-anhydro-6′-deoxy-4′-C-(hydroxymethyl)-α-L-mannofurano]G-(3′→4′)-[2′,5′-anhydro-6′-deoxy-4′-C-(hydroxymethyl)-α-L-mannofurano]G-sp-[2′-O-(2-methoxyethyl)]rG), 5′-[26-[[2-(acetylamino)-2-deoxy-β-D-galactopyranosyl]oxy]-14,14-bis[[3-[[6-[[2-(acetylamino)-2-deoxy-β-D-galactopyranosyl]oxy]hexyl]amino]-3-oxopropoxy]methyl]-8,12,19-trioxo-16-oxa-7,13,20-triazahexacos-1-yl hydrogen phosphate]
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Research Protocol for Cardiovascular Diseases
Cardiovascular disease can be modeled as maladaptive cardiac remodeling, where ischemic injury or pressure overload activates inflammatory signaling, fibroblast activation, extracellular-matrix deposition, cardiomyocyte hypertrophy, vascular remodeling, and progressive ventricular dysfunction. The TGF-β/SMAD axis is a central profibrotic pathway after myocardial injury and pressure overload, while innate immune and cytokine pathways regulate leukocyte recruitment, scar formation, and adverse remodeling. Key unresolved questions include which inflammatory signals are reparative versus harmful, when fibrosis is protective versus maladaptive, and whether pathway inhibition improves function without weakening necessary infarct healing or compensatory remodeling.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)