1122-90-3

Basic information

• Product Name: p-Aminophenyl Arsenoxide
• Synonyms: 4-aminophenylarsenoxide;PAPAO;4-aminophenylarsine oxide;p-Aminophenylarsenic oxide;4-ArsenosobenzenaMine;NSC 10876;p-Arsenosoaniline
• CAS NO: 1122-90-3
• Molecular Formula: C₆H₆AsNO
• Molecular Weight: 183.041
• Product Categories: Miscellaneous Reagents;Aromatics;Aromatics, Miscellaneous Reagents
• Mol File: 1122-90-3.mol

Chemical Properties

• Melting Point: 93-102°C
• Boiling Point: °Cat760mmHg
• Flash Point: °C
• Appearance: /
• Density: g/cm³
• Storage Temp.: -20°C Freezer
• CAS DataBase Reference: p-Aminophenyl Arsenoxide(CAS DataBase Reference)
• NIST Chemistry Reference: p-Aminophenyl Arsenoxide(1122-90-3)
• EPA Substance Registry System: p-Aminophenyl Arsenoxide(1122-90-3)

Safety Data

• RIDADR: 1557
• HazardClass: 6.1(b)
• PackingGroup: III
• Hazardous Substances Data: 1122-90-3(Hazardous Substances Data)

Usage

Uses

Used in Biochemical Research:
p-Aminophenyl Arsenoxide is used as a research reagent for studying 2-oxoacid dehydrogenase multienzyme complexes. Its application is crucial in understanding the mechanisms and functions of these complexes, which play a vital role in cellular metabolism and energy production.
Used in Pharmaceutical Industry:
In the pharmaceutical industry, p-Aminophenyl Arsenoxide is used as a key intermediate in the synthesis of various drugs. Its unique chemical structure allows for the development of novel compounds with potential therapeutic applications.
Used in Chemical Synthesis:
p-Aminophenyl Arsenoxide is also utilized in chemical synthesis, particularly for the production of organic compounds and materials. Its versatility as a reagent makes it a valuable asset in the development of new chemical entities with diverse applications.

Safety Profile

Poison by intraperitoneal route. When heated to decomposition it emits toxic fumes of NOx and As.

InChI:InChI=1/C6H6AsNO.2H2O/c8-6-3-1-5(7-9)2-4-6;;/h1-4H,8H2;2*1H2

Upstream product

• 98-50-0 p-aminophenylarsonic acid 
• 10034-85-2 hydrogen iodide 
• 7782-99-2 sulphurous acid 
• 79368-82-4 p-aminophenyldichloroarsine 
• 5410-78-6 p-aminophenyldichloroarsine. hydrochloride 
• 127-85-5 p-arsanilic acid monosodium salt 
• 861529-90-0 (4-nitroso-phenyl)-arsonic acid 
• 100-63-0 phenylhydrazine 
• 67-56-1 methanol 

Downstream Products

• 802835-49-0 tris-(4-amino-phenyl)-arsine 
• 62-53-3 aniline 
• 1613402-18-8 2-(4-acetamidophenyl)-1,3,2-dithiarsinane 
• 116975-09-8 4-dibromoarsino-aniline 
• 79368-82-4 p-aminophenyldichloroarsine 
• 153449-97-9 4-arsino-aniline 
• 6052-23-9 (p-NH₂C₆H₄)2Hg 

Relevant articles and documents

Arsenic trioxide targets Hsp60, triggering degradation of p53 and survivin

The mechanisms of action of arsenic trioxide (ATO), a clinically used drug for the treatment of acute promyelocytic leukemia (APL), have been actively studied mainly through characterization of individual putative protein targets. There appear to be no studies at a system level. Herein, we integrate metalloproteomics through a newly developed organoarsenic probe, As-AC (C20H17AsN4O3S2) with quantitative proteomics, allowing 37 arsenic binding and 250 arsenic regulated proteins to be identified in NB4, a human APL cell line. Bioinformatics analysis reveals that ATO disrupts multiple physiological processes, in particular, chaperone-related protein folding and cellular response to stress. Furthermore, we discover heat shock protein 60 (Hsp60) as a vital target of ATO. Through biophysical and cell-based assays, we demonstrate that ATO binds to Hsp60, leading to abolishment of Hsp60 refolding capability. Significantly, the binding of ATO to Hsp60 disrupts the formation of Hsp60-p53 and Hsp60-survivin complexes, resulting in degradation of p53 and survivin. This study provides significant insights into the mechanism of action of ATO at a systemic perspective, and serves as guidance for the rational design of metal-based anticancer drugs. This journal is

Carbohydrate-conjugated 4-(1,3,2-dithiarsolan-2-yl)aniline as a cytotoxic agent against colorectal cancer

Arsenic trioxide (As2O3) has been approved for the treatment of acute promyelocytic leukemia (APL); however, its use in the treatment of solid tumors is limited due to its pharmacokinetic properties. Organic arsenic compounds provide better options for pharmaceutical optimization. p-Aminophenyl arsenoxide (p-APAO), an organic arsenic compound, was found to interact with the promyelocytic leukemia-retinoic acid receptor alpha (PML-RARα) fusion protein in a similar manner to arsenic trioxide. Analogs of p-APAO such as 4-(1,3,2-dithiarsolan-2-yl)aniline (p-APDTAs) were recently found to show improved cytotoxicity toward several solid tumor cell lines with lower toxicity to normal cells. Here, we synthesized a carbohydrate-conjugated 4-(1,3,2-dithiarsolan-2-yl)aniline (p-APDTAs) and showed that it exhibited reduced cytotoxicity to normal cells, suggesting a feasible approach to improve the therapeutic index of arsenic-containing compounds as chemotherapeutic agents.

Structural Modification of Aminophenylarsenoxides Generates Candidates for Leukemia Treatment via Thioredoxin Reductase Inhibition

Upregulation of the selenoprotein thioredoxin reductase (TrxR) is of pathological significance in maintaining tumor phenotypes. Thus, TrxR inhibitors are promising cancer therapeutic agents. We prepared different amino-substituted phenylarsine oxides and evaluated their cytotoxicity and inhibition of TrxR. Compared with our reported p-substituted molecule (8), the o-substituted molecule (10) shows improved efficacy (nearly a fourfold increase) to kill leukemia HL-60 cells. Although the compounds 8 and 10 display similar potency to inhibit the purified TrxR, the o-substitution 10 exhibits higher potency than the p-substitution 8 to inhibit the cellular TrxR activity. Molecular docking results demonstrate the favorable weak interactions of the o-amino group with the TrxR C-terminal active site. Efficient inhibition of TrxR consequently induces the oxidative stress-mediated apoptosis of cancer cells. Silence of the TrxR expression sensitizes the cells to the arsenic compound treatment, further supporting the critical involvement of TrxR in the cellular actions of compound 10.

Thiourea-containing arsenic sugar with anti-tumor activity and preparation method and application thereof

The invention relates to the field of arsenic sugar, and in particular relates to thiourea-containing arsenic sugar with anti-tumor activity and a preparation method and application thereof. The thiourea-containing arsenic sugar is composed of two compounds: 1-(N-(4'-(1'', 3'', 2''-dithiaarsenic pentane-2-yl) phenyl)-thiourea)-2, 3, 4, 6-O-acetyl-beta-D-glucose and 1-(N-(4'-(1'', 3 '', 2''-dithiaarsenic hexane-2-yl) phenyl)-thiourea)-2, 3, 4, 6-O-acetyl-beta-D-glucose. The thiourea-containing arsenic sugar provided by the invention has the advantages of simple reaction operation and high yield. The thiourea-containing arsenic sugar with a specific three-dimensional configuration can be obtained, and the thiourea-containing arsenic sugar has good anti-tumor activity.

Organoarsenic compound and use thereof

The invention discloses an organoarsenic compound. The organoarsenic compound has the following structural formula as shown in the specification, wherein n is 1 or 2; R, R1, R2, R3, R4 and R5 are respectively and independently amino, R6-CO-NH, R7-CO-O, alkyl, aryl, a heterocyclic substituent, alkoxyl, alkylamino, a halogen atom, nitro, hydroxyl or a hydrogen atom; R6 is alkyl, aminoalkyl or aryl;R7 is alkyl, aminoaryl or aryl. The organoarsenic compound has good inhibitory activity for thioredoxin reductase, has strong cytotoxicity for tumor cell HL-60, and can be used for preparing a thioredoxin reductase inhibitor or an antitumor drug with thioredoxin reductase as a target spot.

Dithiaarsanes induce oxidative stress-mediated apoptosis in HL-60 cells by selectively targeting thioredoxin reductase

The selenoprotein thioredoxin reductase (TrxR) plays a pivotal role in regulating cellular redox homeostasis and has attracted increasing attention as a promising anticancer drug target. We report here that 2-(4-aminophenyl)-1,3,2- dithiarsinane (PAO-PDT, 4), a potent and highly selective small molecule inhibitor of TrxR, stoichiometrically binds to the C-terminal selenocysteine/cysteine pair in the enzyme in vitro and induces oxidative stress-mediated apoptosis in HL-60 cells. The molecular action of 4 in cells involves inhibition of TrxR, elevation of reactive oxygen species, depletion of cellular thiols, and activation of caspase-3. Knockdown of TrxR sensitizes the cells to 4 treatment, whereas overexpression of the functional enzyme alleviates the cytotoxicity, providing physiological relevance for targeting TrxR by 4 in cells. The simplicity of the structure and the presence of an easily manipulated amine group will facilitate the further development of 4 as a potential cancer chemotherapeutic agent.

Substantially cell membrane impermeable compound and use thereof

The present invention relates to a compound according to Formula (I): A-(L-Y)p, wherein A comprises at least one substantially cell-membrane impermeable pendant group; L comprises any suitable linker and/or spacer group; Y comprises at least one arsenoxide or arsenoxide equivalent; p is an integer from 1 to 10; and the sum total of carbon atoms in A and L together, is greater than 6.