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Azoxymethane


CAS No. : 25843-45-2

(Synonyms: AOM)

25843-45-2
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Cat. No. : HY-111375
M.Wt: 74.08
Formula: C2H6N2O
Purity: >98 %
Solubility: H2O : 138.89 mg/mL (ultrasonic)
Introduction of 25843-45-2 :

Azoxymethane (AOM) is a colon carcinogen which leads to the formation of DNA adducts. Azomethane is a procarcinogen that requires metabolic activation via cytochrome P450 (P450) enzymes (primarily CYP2E1)[1][2][3]. In Vitro: Azoxymethane is a colon carcinogen which leads to the formation of DNA adducts. On an equal protein basis, hepatic microsomes are much more active than SI and colon microsomes in NADPH-dependent Azoxymethane bioactivation and N7-mG adduct formation. Hepatic microsomes show the highest activity in the hydroxylation of Azoxymethane, followed by SI and colon microsomes[1]. In Vivo: Note:
Please do not refer to only one article to determine the experimental conditions. It is recommended to determine the optimal experimental conditions (animal strain, age, dosage, frequency and cycle, detection time and indicators, etc.) through preliminary experiments before the formal experiment.

Azoxymethane can be used to induce colorectal cancer models.

Induction of Colorectal Cancer
Background
Azomethane (AOM) is oxidatively metabolized by hepatic CYP450 processes to produce methylazomethanol (MAM). MAM is unstable, with a half-life of approximately 12 hours. It subsequently decomposes to produce formaldehyde and a highly reactive methyldiazo ion; this ion can alkylate DNA bases, forming DNA adducts including O6-methylguanine (O6-mG) and N7-methylguanine (N7-mG). The persistent presence of O6-mG can lead to oncogene mutations and tumorigenesis[1]. Azoxymethane induces the conversion of G to A, leading to the activation mutation of K-ras and β-catenin in colon cells. The activation of Wnt signaling through the accumulation of β-catenin is the main mechanism of the Azoxymethane-induced colon cancer model[3].
Specific Modeling Methods
1. Mice: BALB/c mice • male • 6-week-old[2]
Administration: 10 mg/kg• i.p.• weekly for 6 weeks;
2.Mice: A/J mice • male • 20 to 25 g[3]
Administration: 5 mg/kg• i.p.• weekly for 6 weeks;
3. Mice: C57BL/6J mice • male • 8 to 10-week-old[4]
Administration: 10 mg/kg • i.p. • single does on day 0; On day 1, replace the drinking water with 2.5% DSS (HY-116282C) solution for 7 days. On day 8, change the 2.5% DSS solution to normal water for another 10 days. On day 18, replace the drinking water with 2.5% DSS solution for 7 days. On day 25, change the 2.5% DSS solution to normal water for another 10 days. On day 35, replace the drinking water with 2.5% DSS solution for 7 days. On day 42, change the 2.5% DSS solution to normal water until the mice are euthanized. Day 105-119 is a window phase to euthanize mice.
Note
(1) Animals are weighed weekly and sacrificed 18-30 weeks after the first AOM injection, and the recommended criteria can include weight loss of 10%-20%, occult blood in stool and energies.
Modeling Indicators
Phenotypic changes: Weight loss of 10%-20%, occult blood in feces, and lethargy.
Cellular/tissue level: Induced hyperproliferation and microadenoma formation, Increased the cyclin D1 and COX-2 expression.
Molecular changes: Increased the protein expression of pro-TGF-α, pEGFR, pErbB2, pERK, induces K-ras mutations; The level of 6-MeG is elevated in the distal colon tissue.
Histology analysis: Tissue damage, inflammatory cell infiltration in the lamina propria, and an increased number of tumors were observed.
Opposite Product(s): Gefitinib (HY-50895)

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