Details
| Stereochemistry | ACHIRAL |
| Molecular Formula | AsBr3 |
| Molecular Weight | 314.634 |
| Optical Activity | NONE |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
Br[As](Br)Br
InChI
InChIKey=JMBNQWNFNACVCB-UHFFFAOYSA-N
InChI=1S/AsBr3/c2-1(3)4
| Molecular Formula | AsBr3 |
| Molecular Weight | 314.634 |
| Charge | 0 |
| Count |
|
| Stereochemistry | ACHIRAL |
| Additional Stereochemistry | No |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Optical Activity | NONE |
Arsenic trioxide (ATO) is used to treat acute promyelocytic leukemia in people who have not been helped by other types of chemotherapy or whose condition has improved but then worsened following treatment with other types of chemotherapy. Arsenic trioxide acts through activation of Jun N-terminal kinase (JNK), activator protein-1, and inhibition of dual-specificity phosphatases. Although the exact mechanisms under which ATO exerts its therapeutic effect in acute promyelocytic leukemia cancer cells are not well elucidated. It was shown that apoptotic mechanisms involved the induction of phosphatidylserine externalization, caspase-3 activation, and nucleosomal DNA fragmentation. Adverse reactions described are leukocytosis, nausea, vomiting, diarrhea, and abdominal pain, fatigue, edema, hyperglycemia, dyspnea, cough, rash or itching, headaches, and dizziness.
Approval Year
Targets
| Primary Target | Pharmacology | Condition | Potency |
|---|---|---|---|
Target ID: CHEMBL2096667 Sources: https://www.ncbi.nlm.nih.gov/pubmed/12012315 |
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Target ID: activator protein-1 Sources: https://www.ncbi.nlm.nih.gov/pubmed/12012315 |
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Target ID: dual-specificity phosphatases Sources: https://www.ncbi.nlm.nih.gov/pubmed/12012315 |
Conditions
| Condition | Modality | Targets | Highest Phase | Product |
|---|---|---|---|---|
| Primary | TRISENOX Approved UseAcute promyelocytic leukemia (newly diagnosed) (low-risk disease): Treatment of newly diagnosed low-risk acute promyelocytic leukemia (APL), in combination with tretinoin, in adults whose APL is characterized by the presence of the t(15;17) translocation or PML/RAR-alpha gene expression
Acute promyelocytic leukemia (relapsed or refractory): Remission induction and consolidation treatment of APL in patients who are refractory to, or have relapsed from, retinoid and anthracycline chemotherapy, and whose APL is characterized by the presence of the t(15;17) translocation or PML/RAR-alpha gene expression Launch Date2000 |
Sample Use Guides
Induction Treatment Schedule: TRISENOX™ should be administered intravenously at a dose of 0.15 mg/kg daily until bone marrow remission. Total induction dose should not exceed 60 doses.
Consolidation Treatment Schedule: Consolidation treatment should begin 3 to 6 weeks after completion of induction therapy. TRISENOX™ should be administered intravenously at a dose of 0.15 mg/kg daily for 25 doses over a period up to 5 weeks.
Route of Administration:
Intravenous
| Substance Class |
Chemical
Created
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Mon Mar 31 18:16:09 GMT 2025
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Mon Mar 31 18:16:09 GMT 2025
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| Record UNII |
41CN475O7F
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| Record Status |
Validated (UNII)
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7784-33-0
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DTXSID4064840
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41CN475O7F
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ARSENIC TRIBROMIDE
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425
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232-057-4
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m2061
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24569
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41CN475O7F
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1313315
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ACTIVE MOIETY |