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Arsenic(III) oxide

SAJ first grade, ≥99.0%

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Arsenic trioxide, Arsenous acid
Empirical Formula (Hill Notation):
CAS Number:
Molecular Weight:
EC Number:
MDL number:
PubChem Substance ID:


SAJ first grade

vapor pressure

0.000001 hPa ( 66 °C)






available only in Japan

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Hazard Classifications

Acute Tox. 2 Oral - Aquatic Acute 1 - Aquatic Chronic 1 - Carc. 1A - Eye Dam. 1 - Skin Corr. 1B - STOT RE 1

Storage Class

6.1A - Combustible, acute toxic Cat. 1 and 2 / very toxic hazardous materials




Not applicable


Not applicable

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Yanfei Jia et al.
PloS one, 8(1), e54774-e54774 (2013-02-06)
Alpha-fetoprotein (AFP)-producing gastric cancer (AFPGC), represented by the production of AFP, has a more aggressive behavior than common gastric cancer. The underlying mechanisms are not well understood. Arsenic trioxide (As(2)O(3)) is used clinically to treat acute promyelocytic leukemia(APL) and has
Michael T Brady et al.
Leukemia research, 37(7), 822-828 (2013-05-01)
Signal transducer and activator of transcription (STAT) 3 inhibits dendritic cell (DC) differentiation and is constitutively activated in blasts of approximately half of AML patients. We investigated the correlation between STAT3 activity, DC maturation and the ability to stimulate T-cells
Y Zhang et al.
Neoplasma, 60(3), 247-253 (2013-02-05)
Arsenic trioxide (ATO) has been demonstrated to induce apoptosis in retinoblastoma cells, however, mechanisms responsible for this phenomenon are not fully understood. In the present study, we determined whether ATO induced apoptosis by abnormal expression of microRNA. In an apoptosis
Jianing Wu et al.
Toxicology letters, 220(1), 61-69 (2013-04-02)
Notch signaling has been demonstrated to have a central role in cancer stem-like cells (CSLCs) in glioblastoma multiforme (GBM). We have recently demonstrated the inhibitory effect of arsenic trioxide (ATO) on CSLCs in glioblastoma cell lines. In this study we
Akio Iwanami et al.
Proceedings of the National Academy of Sciences of the United States of America, 110(11), 4339-4344 (2013-02-27)
Despite their nearly universal activation of mammalian target of rapamycin (mTOR) signaling, glioblastomas (GBMs) are strikingly resistant to mTOR-targeted therapy. We analyzed GBM cell lines, patient-derived tumor cell cultures, and clinical samples from patients in phase 1 clinical trials, and

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