Details
| Stereochemistry | ACHIRAL |
| Molecular Formula | C3H8O6S2 |
| Molecular Weight | 204.222 |
| Optical Activity | NONE |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
OS(=O)(=O)CCCS(O)(=O)=O
InChI
InChIKey=MGNVWUDMMXZUDI-UHFFFAOYSA-N
InChI=1S/C3H8O6S2/c4-10(5,6)2-1-3-11(7,8)9/h1-3H2,(H,4,5,6)(H,7,8,9)
Eprodisate (1,3-propanedisulfonate) is a negatively charged, sulfonated molecule of low molecular weight that has structural similarities to heparin sulfate; it is a glycosaminoglycan mimetic that binds to the glycosaminoglycan (GAG) binding site on serum A amyloid (AA) to prevent its interaction with glycosaminoglycan and arrest amyloidosis, or inhibit amyloid deposition. In nonclinical toxicity studies in two animal species (i.e., rat and dog), eprodisate was administered orally at doses of up to 2000 mg/kg/day for 39 weeks: eprodisate showed low toxicity potential at doses several fold higher than the anticipated clinical dose, was well tolerated upon chronic exposure and was found to be nonmutagenic and nonclastogenic. Furthermore, a series of safety pharmacology studies showed that eprodisate does not have any clinically
significant effect on major organ function.
Approval Year
Targets
| Primary Target | Pharmacology | Condition | Potency |
|---|---|---|---|
Target ID: 111345.0 Gene Symbol: Saa Sources: https://www.ncbi.nlm.nih.gov/pubmed/18671471 |
Conditions
| Condition | Modality | Targets | Highest Phase | Product |
|---|---|---|---|---|
| Primary | Unknown Approved UseUnknown |
PubMed
| Title | Date | PubMed |
|---|---|---|
| Systemic AA amyloidosis: epidemiology, diagnosis, and management. | 2014 |
|
| Review of eprodisate for the treatment of renal disease in AA amyloidosis. | 2012 |
|
| Two cationic metal-organic frameworks based on cadmium and α,ω-alkanedisulfonate anions and their photoluminescent properties. | 2010-12-14 |
|
| [Amyloidosis in rheumatic diseases]. | 2010 |
|
| [Diagnostics and therapy of AA amyloidosis]. | 2009-05 |
|
| Preventing beta-amyloid fibrillization and deposition: beta-sheet breakers and pathological chaperone inhibitors. | 2008-12-03 |
|
| Eprodisate in amyloid A amyloidosis: a novel therapeutic approach? | 2008-08 |
|
| Eprodisate in amyloid A amyloidosis: a novel therapeutic approach? | 2008-08 |
|
| [A new treatment of renal disease in AA amyloidosis...and not only that?]. | 2008-02-12 |
|
| Amyloid deposition in transplanted human pancreatic islets: a conceivable cause of their long-term failure. | 2008 |
|
| Eprodisate slows the progression of renal disease in patients with AA amyloidosis. | 2007-11 |
|
| Eprodisate slows the progression of renal disease in patients with AA amyloidosis. | 2007-11 |
|
| Eprodisate in AA amyloidosis. | 2007-09-13 |
|
| Eprodisate for the treatment of renal disease in AA amyloidosis. | 2007-06-07 |
|
| Advances in the treatment of amyloidosis. | 2007-06-07 |
|
| Eprodisate for the treatment of renal disease in AA amyloidosis. | 2007-06-07 |
|
| Diagnostic performance of amyloid A protein quantification in fat tissue of patients with clinical AA amyloidosis. | 2007-06 |
|
| [Multisystemic amyloidosis in 2007]. | 2007-05 |
|
| Dissimilation of C3-sulfonates. | 2006-03 |
|
| Nordihydroguaiaretic acid potently breaks down pre-formed Alzheimer's beta-amyloid fibrils in vitro. | 2002-05 |
|
| Ethanedisulfonate is degraded via sulfoacetaldehyde in Ralstonia sp. strain EDS1. | 2001-07 |
|
| Arresting amyloidosis in vivo using small-molecule anionic sulphonates or sulphates: implications for Alzheimer's disease. | 1995-02 |
Patents
Sample Use Guides
In Vivo Use Guide
Sources: http://www.ncbi.nlm.nih.gov/pubmed/7585011
Curator's Comment: Animals recieved amyloid enhancing factor (AEF) and an inflammatory stimulus to initiate amyloid development. In the acute model, animals were treated with the test compaund 24 hours after induction, and for the next five days. After the sixth days they were killed and their spleens were assessed for amyloid. Eprodisate sodium (Sodium 1,3-propanedisulphonate) was effective in this model (35+/-6% of amyloid found in the untreated controls). This inhibition of steroidogenesis is not a result of a reduction of hepatic serum A amyloid (SAA).
Swiss white mice 25-30 g; 50 mM in 7-8 ml of drinking water per animal per day
Route of Administration:
Oral
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FDA ORPHAN DRUG |
118998
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428573
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DB06405
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DTXSID4048301
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21668-77-9
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C520274
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100000178030
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C166957
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1,3-Propanedisulfonic acid
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6QFP76V7S7
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CHEMBL2111092
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8630
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ACTIVE MOIETY
SALT/SOLVATE (PARENT)